Oesophageal and gastric endoscopic foreign body removal: complications

and follow-up of 102 dogs

P. GIANELLA, N. S. PFAMMATTER AND I. A. BURGENER

Journal of Small Animal Practice (2009) 50, (12) 649–654

¿Dónde se alojan los cuerpos extraños esofágicos?

, FBs tend to lodge in the narrowest points: the thoracic inlet, the heart
base and just cranial to the lower oesophageal sphincter.

¿Cuándo practicaremos una esofagotomía ante la presencia de un cuerpo

extraño?

The surgery procedure latter, although more aggressive, appears to be a

necessary approach if endoscopic removal fails or if oesophageal or gastric
perforation is present

¿Cuál es la raza más afectada por la presencia de cuerpos extraños

esofágicos?

WHWT

¿Cuál es la complicación más frecuente ante la presencia de un cuerpo

extraño esofágico y qué sintomatología tiene asociada?

La perforación esofágica, mediatinitis, pneumotorax y derrame pleural son

los síntomas asociados

Indica los tres factores de riesgo que dificultan la extracción de un

cuerpo extraño esofágico

Tiempo que hace que se tragó el cuerpo extraño, más de tres días, mal
pronóstico, cuanto menos mejor

Peso del perro, si pasa de 10 Kilos, no hay problema

Tipo de cuerpo extraño, lo peor los huesos

¿Qué tipo de cuerpo extraño esofágico es especialmente difícil de poder

ser extraido por la boca y debe ser empujado al estómago y por qué?

Los juguetes de consistencia gomosa para limpiarse los dientes ya que

carecen de aristas donde engancharse, son redondeados por todos los
lados y es más fácil empujarlos.

¿Qué porcentaje de éxito obtienen los autores en la extracción de cuerpos

extraños?¿Es comparable con otros estudios?

Es una pasada, del 86%, los anteriores de un 26 ó un 63% no establece

motivos

¿Cómo trata pequeñas perforaciones esofágicas?

Cierran espontaneamente

¿Las estenosis esofágicas son frecuentes tras la extracción de un cuerpo

extraño?
No. Sólo encontró una, las ve más frecuentes como resultado de
regurgitaciones durante cirugías.

Dice que otro autor apuntó las estenosis como complicación de los cuerpos
extraños gomosos

Esophagitis and esophageal strictures.

Glazer A, Walters P.

Compend Contin Educ Vet. 2008 May;30(5):281-92.

¿Cómo pasa el bolo alimenticio a través del esófago?

Gracias a un peristaltismo primario, el bolo estimula el vago que paraliza la

respiración y produce el movimiento esofágico. La propia distnsión del
esófago produce un peristaltismo secundario que acerca el bolo al estómago
y produce la relajación del LES

¿Qué drogas anestésicas incrementan el riesgo de reflujo por disminuir lel

tono del LES?
morphine, thiopentone, propofol, xylazine, and atropine

¿Qué otras drogas pueden producir estenosis?

Los antibióticos, en concreto la tetraciclina ya que está formulada muy
ácida.

Indica cómo varía la capa muscular del esófago dependiendo si se trata de

un perro o un gato.
En el perro todo el músculo del esófago es estriado, mientras que en el
gato el tercio distal es liso

¿Cómo puede influir el ayuno en el reflujo gástrico durante la

anestesia?¿Cuánto tiempo recomiendan los autores?

One study in animals suggests that fasting for longer than 24 hours
before surgery is more likely to cause reflux under anesthesia than
fasting less than 4 hours. The ideal fasting interval suggested by the
authors of this study is 8 to 12 hours.17

¿Cuáles son los síntomas más típicos de la enfermedad esofágica?¿Por qué

puede haber síntomas respiratorios?

Animals with esophageal disease often have a variety of clinical signs,

including ptyalism, regurgitation, dysphagia, repetitive swallowing,
odynophagia (painful swallowing), and weight loss.

Por aspiración nasal o deglución desviada.

¿Es interesante la administración de córticos en las estenosis esofágica?

Theoretically, corticosteroids could prevent stricture recurrence after

dilation because steroids reduce fibrosis and collagen formation. However,
in a controlled study of children with esophagitis induced by caustic
substance ingestion, oral steroids were not shown to be beneficial.42 No
controlled studies in animals have evaluated the use of systemic steroids
after esophageal stricture dilation.

Interest has turned from systemic steroid therapy to local injection of

steroids into the stricture using endoscopic guidance. In keloids and
dermal scars, intralesional steroid injections have been shown to reduce
scar formation. The procedure involves the use of an endoscopic
sclerotherapy needle to inject triamcinolone acetonide or dexamethasone
at three or four sites around the stricture before or immediately after
the dilation procedure. In humans, studies have shown a significant
reduction in the number of repeat dilation procedures needed after the
use of local steroid injection.43"46

Cuando hay una estenosis esofágica, ¿Qué capas del esófago están
afectadas?
¿Cuál es la causa más frecuente de esa estenosis esofágica?

Las capas afectadas en una estenosis esofágica son la mucosa, submucosa

y muscular
La causa más frecuente de la estenosis esofágica es el contacto
prolongado de sustancias caústicas por ejemplo, los líquidos gástricos
durante la anestesia o cuerpos extraños en la luz esofágica

Define los esfínters esofágicos que conoces, e indica por quién están
formados?

The esophagus has upper and lower sphincters. The upper esophageal
sphincter is composed of the cricopharyngeus and thyropharyngeus muscles.
The lower esophageal sphincter (LES) is made up of muscle layers around
the esophagus and diaphragmatic crura

Explica los objetivos que persigue el tratamiento médico de la esofagitis.

Treatment of esophagitis is directed at healing inflammation and

preventing further injury while supporting the animal's nutritional needs.
Esophageal healing is promoted by decreasing mechanical trauma to the
esophagus through feeding soft or blenderized food or placing a
gastrostomy tube. Sucralfate may assist healing of the mucosal surface
through stimulation of prostaglandins.

¿Por qué es mejor el tratamiento de la esofagitis con omeprazol que con

ranitidina?

Porque el omeprazol ha demostrado mejor acción terapéutica en la curación

y prevención de las úlceras y debe darse con menos frecuencia, por lo que
el propietario lo suministra mejor.

¿Qué complicaciones puede tener la dilatación con bujías?

Potential complications of bougienage or balloon dilation include bleeding,

esophageal tear, esophageal diverticulum formation, infection, aspiration,
and pain. Mild bleeding is usually self-limiting.

¿Qué porcentaje de éxitos podemos insinuarle al propietario? moderate to

complete resolution of clinical signs, has been reported in 74% to 88% of
animal patients

Signalment, history, and outcome of cats with gastrointestinal tract

intussusception: 20 cases (1986–2000)
Jamie M. Burkitt; Kenneth J. Drobatz; H. Mark Saunders; Robert J.
Washabau.

J Am Vet Med Assoc 2009;234 (6) 771–776

¿Cuáles son las causas de invaginación intestinal en los gatos?¿Éstas

dependen de la edad de los animales?

Si los animales son menores de un año la principal causa es idiopàtica, si

los animales son mayores de seis años, siete de ocho animales tuvieron
linfoma alimentario o enfermedad inflamatoria intestinal.

¿Qué signos clínicos han presentado los gatos con invaginación y hasta
cuánto tiempo han podido durar antes de diagnosticarse?
The most common historical findings were poor appetite (14 cats),
lethargy (12), and vomiting (12). Other signs included weight loss (7 cats),
diarrhea (6), polydipsia (6), melena or hematochezia (2),
decreased fecal output (2), nasal or ocular discharge (2), regurgitation (2),
and polyphagia, polyuria, hypersalivation, and increased borborygmus (1
each).

Historical information was available for 17 cats.

Median duration of clinical signs was 5.5 days (range, 1 to 30 days).

¿En qué porcentaje de animales se puede solucionar la invaginación

manualmente?

En un 50%

¿Cuáles fueron los motivos por los que los animales necesitaron resección
intestinal tras una invaginación?

Reasons for intestinal resection and anastomosis included an inability to

reduce the intussusception (4), intestinal mass or mural thickening
(3), vascular compromise (2), and intestinal wall defect.

¿Qué método de diagnóstico por imagen es más acertado ante una

invaginación?

The ultrasonographic appearance of intestinal intussusception in dogs and

cats has been described, and intussusception was evident on ultrasound
images from all 7 cats in the present study for which such images were
available for review. Consistent with findings in previous reports,abdominal
radiography was useful in recognizing intestinal obstruction in cats in the
present study. However, intussusception could not be definitively
diagnosed on survey radiographs from any of the 10 cats in which it was
performed, and results of contrast radiography were specific for
intussusception in only 1 of 3 cats. Therefore, abdominal ultrasonography
appeared more likely than radiography to provide a specific diagnosis of
intussusception.

¿Cómo se puede conocer la causa de una invaginación?

Por el estudio histológico de la pieza resecada.

Signalment, history, and outcome of cats with gastrointestinal tract
intussusception: 20 cases (1986–2000)
Jamie M. Burkitt; Kenneth J. Drobatz; H. Mark Saunders; Robert J.
Washabau.

J Am Vet Med Assoc 2009;234 (6) 771–776

Clica:
https://avmajournals-avma-org.are.uab.cat/view/journals/javma/
javma-overview.xml?tab_body=toc

¿Cuáles son las causas de invaginación intestinal en los gatos?¿Éstas

dependen de la edad de los animales?

¿Qué signos clínicos han presentado los gatos con invaginación y hasta
cuánto tiempo han podido durar antes de diagnosticarse?

¿En qué porcentaje de animales se puede solucionar la invaginación

manualmente?

¿Cuáles fueron los motivos por los que los animales necesitaron
resección intestinal tras una invaginación?

¿Qué método de diagnóstico por imagen es más acertado ante una

invaginación?

¿Cómo se puede conocer la causa de una invaginación?

 Signalment, history, and outcome of cats

SMALL ANIMALS
with gastrointestinal tract intussusception:
20 cases (1986–2000)
Jamie M. Burkitt, dvm, dacvecc; Kenneth J. Drobatz, dvm, ms, dacvim, dacvecc;
H. Mark Saunders, vmd, ms, dacvr; Robert J. Washabau, vmd, phd, dacvim

Objective—To determine signalment, history, and outcome of cats with gastrointestinal

tract intussusception and to identify physical examination, diagnostic imaging, surgical, his-
tologic, and necropsy findings in affected cats.
Design—Retrospective case series.
Animals—20 cats with intussusception.
Procedures—Medical records were evaluated for information on signalment; history;
physical examination, diagnostic imaging, surgical, histologic, and necropsy findings; and
outcome.
Results—Ten cats were < 1 year old, and 9 were ≥ 6 years old. Anorexia (14/17), lethargy
(12/17), and vomiting (12/17) were the most common reasons for examination. Dehydra-
tion (13/18), poor body condition (12/18), signs of abdominal pain (8/18), and an abdominal
mass (8/18) were the most common physical examination findings. Abdominal radiography
revealed intestinal obstruction in all 10 cats in which it was performed; abdominal ultra-
sonography revealed intussusception in all 7 cats in which it was performed. The most
common intussusception was jejuno-jejunal (8/20), and no intussusceptions were found
proximal to the duodenum. Eleven of 13 cats that underwent laparotomy required intestinal
resection and anastomosis. Histologic examination revealed intestinal lymphoma or inflam-
matory bowel disease in 7 of 8 cats ≥ 6 years old and idiopathic intussusception in 7 of 8
cats < 1 year old.
Conclusions and Clinical Relevance—Results suggested that in cats, intussusception
has a bimodal age distribution, is most commonly jejuno-jejunal, often requires surgical
resection and anastomosis, is often associated with alimentary lymphoma or inflammatory
bowel disease in older cats, and is readily diagnosed by means of ultrasonography. (J Am
Vet Med Assoc 2009;234:771–776)

G astrointestinal tract intussusception in dogs has

been well characterized in the veterinary literature.
Intussusception is most common in young dogs,1–6 with
the German Shepherd Dog being the most commonly
reported breed,2,5–8 although a true breed predisposition
has not been proven. In dogs, intussusception has been
associated with intestinal parasitic infestation,2–6,9–11 ali-
mentary foreign bodies,1,3–6,12 viral enteritis,2–5,7,13 intesti-
nal masses,1,3,6,14,15 recent abdominal or extra-abdominal
surgery,1–3,6,9,16 and nonspecific gastroenteritis.1,2,6,7,9 How-
ever, many previous studies2,4,5 have reported that most
cases of intussusception involving dogs are idiopathic. It
appears that most intussusceptions in dogs are entero-
colic,2–8 although some studies1,9 report a higher preva-
lence of enteroenteric intussusceptions. Correction of
From the Department of Clinical Studies, School of Veterinary Medi-
cine, University of Pennsylvania, Philadelphia, PA 19104. Dr. Burkitt’s
present address is Critical Consultations, Davis, CA 95616. Dr. Saun-
ders’ present address is Lynks Group PLC, Veterinary Imaging, 148
Cheesefactory Ln, Shelburne, VT 05482. Dr. Washabau’s present ad-
dress is Department of Veterinary Clinical Sciences, College of Veteri-
nary Medicine, University of Minnesota, Saint Paul, MN 55108.
Presented in abstract form as a poster at the American College of Vet-
erinary Internal Medicine Annual Forum, Denver, May 2001.
Address correspondence to Dr. Burkitt.
IBD
Abbreviation
Inflammatory bowel disease
intussusception usually requires surgery, and recurrence
rates in dogs of up to 27% have been reported, even after
surgical correction of the intussusception.3
Less information is available in the literature regarding
intussusception in cats. The largest case series published to
date included only 12 cats,17 and most publications describ-
ing intussusception in cats have been individual case reports
or small case series.18–36 As in dogs, intussusception has
been reported most commonly in cats ≤ 1 year old2,17,26,31,35;
however, many cases involving older cats have also been
reported.2,23,24,32,34,36,37 Most cats in previous reports2,17,26
have been domestic shorthairs, but Siamese2,5,31,35,37 and
Burmese17,19,28 cats may be overrepresented. Predisposing
factors for intussusception in cats are poorly described,
although many of the underlying causes reported in dogs
have also been identified in cats.17,37 The ileocolic junction
is the most commonly reported site in cats with intussus-
ception,2,17,31,37 but 4 of 5 queens in a previous report26 had
enteroenteric intussusception, and case reports18,27,33,34,38 of
gastroesophageal intussusception in cats have also been
published.

JAVMA, Vol 234, No. 6, March 15, 2009 Scientific Reports 771
 Given the paucity of published information on in-
tussusception in cats, additional study of predisposing
SMALL ANIMALS
factors, clinical abnormalities, and outcome of treatment
is needed. The purposes of the study reported here were
to determine signalment, history, and outcome of cats
with gastrointestinal tract intussusception and to iden-
tify physical examination, diagnostic imaging, surgical,
histologic, and necropsy findings in affected cats.
Materials and Methods
Criteria for case selection—Medical records and
necropsy reports of cats examined at the Veterinary
Hospital of the University of Pennsylvania between Jan-
uary 1986 and September 2000 were searched to iden-
tify cats in which a diagnosis of gastrointestinal tract
intussusception had been made. Cats were included in
the study only if the diagnosis had been confirmed dur-
ing surgical exploration or necropsy and were excluded
if the diagnosis had been made on the basis of physical
examination or diagnostic imaging findings alone.
Medical records review—Medical records of cats
included in the study were reviewed for information on
signalment; history; initial physical examination, fecal
examination, plain and contrast radiographic, abdomi-
nal ultrasonographic, surgical, histologic, and necropsy
findings; and outcome. Information was recorded on a
standardized spreadsheet.
Historical information that was recorded included
duration and type of clinical signs and any medical
conditions that had been identified in the preceding 30
days. Initial physical examination findings that were re-
corded included vital signs, hydration status, body con-
dition, results of abdominal palpation, and any other
physical abnormalities recorded in the medical record.
Hydration status had been subjectively classified at the
time of initial examination by selecting 1 of 3 options
(ie, good, fair, or poor) on the intake physical examina-
tion form. For purposes of the present study, the terms
adequately hydrated, moderately dehydrated, and se-
verely dehydrated were used to categorize hydration
status. Similarly, body condition had been subjectively
classified by selecting 1 of 5 options (cachetic, under-
weight, normal, overweight, or obese) on the intake
physical examination form. For purposes of the present
study, any cat categorized on the initial physical exami-
nation form as cachectic or underweight was classified
as underweight, and any cat categorized as overweight
or obese was classified as overweight. This classifica-
tion system was used for the present study because
some intake physical examination forms had > 1 of the
5 options circled.
A single board-certified radiologist (HMS) re-
viewed all abdominal radiographs, and abnormalities
were recorded on a standardized spreadsheet. During
the time of the study, abdominal ultrasonography rou-
tinely involved imaging of all intra-abdominal organs,
the peritoneal cavity, and intra-abdominal lymph nodes.
All ultrasound examinations had been performed with
commercially available units.a,b Written reports and re-
corded still images were reviewed by the same board-
certified radiologist (HMS), and abnormalities were
recorded on a standardized spreadsheet. Identification
772 Scientific Reports JAVMA, Vol 234, No. 6, March 15, 2009
of 1 gastrointestinal tract segment invaginating into an
adjoining portion of the gastrointestinal tract was con-
sidered consistent with intussusception.
In all cats that underwent exploratory surgery, a
ventral midline laparotomy with routine examination
of the gastrointestinal tract and abdominal viscera had
been performed. Intussusceptions were characterized
on the basis of location, length, associated lesions, and
(in most instances) whether they could be manually re-
duced. Method of correction of the intussusception (ie,
simple reduction, reduction followed by resection and
anastomosis, or resection and anastomosis without re-
duction) was recorded, along with whether enteroplica-
tion was performed. Other atypical findings identified
during exploratory surgery were also recorded.
All necropsies were performed within 24 hours af-
ter death, and location and length of the intussuscep-
tion, along with any associated lesions, were recorded,
along with results of histologic examination of intus-
suscepted bowel and other grossly abnormal tissues
collected during surgery or necropsy.
Results
Medical records for 21 cats in which a diagnosis of
intussusception had been made were identified, but 1 cat
was excluded from the study because the diagnosis had
been made on the basis of results of abdominal palpation
only. Therefore, 20 cats met the criteria for inclusion in
the study, of which 18 had been brought to the veterinary
teaching hospital for evaluation and treatment and 2 had
been brought for necropsy only. There were 11 domes-
tic shorthair cats, 3 Siamese, 2 domestic longhair cats,
2 Oriental Shorthairs, 1 Persian, and 1 Himalayan. Five
of the cats were sexually intact males, 6 were neutered
males, 5 were sexually intact females, and 4 were spayed
females. Median age was 1.5 years (range, 11 weeks to
16 years), but there was a bimodal age distribution with
10 cats < 12 months old and 9 cats ≥ 6 years old. The
remaining cat was 2 years old.
Historical information was available for 17 cats.
Median duration of clinical signs was 5.5 days (range, 1
to 30 days). The most common historical findings were
poor appetite (14 cats), lethargy (12), and vomiting
(12). Other signs included weight loss (7 cats), diar-
rhea (6), polydipsia (6), melena or hematochezia (2),
decreased fecal output (2), nasal or ocular discharge
(2), regurgitation (2), and polyphagia, polyuria, hyper-
salivation, and increased borborygmus (1 each).
Fourteen cats reportedly had had medical conditions
in the preceding 30 days. Two cats had chronic diarrhea
of unknown origin, and a third cat was being treated for
intestinal neoplasia, although gastrointestinal tract signs
were not specified in the history. Two cats were lactating,
having queened within the previous 6 weeks. Two cats
had clinical signs of upper respiratory tract infection, 1
was being treated for bronchopneumonia, and 1 had a
10-day history of regurgitation, wheezing, and cough.
Conditions in the remaining 5 cats included multiple
oral and foot abscesses, fever of unknown cause, derma-
tophytosis, vaccination, and general anesthesia within
the past month.
Information on initial physical examination find-
ings was available for all 18 cats that had been brought
to the veterinary teaching hospital for diagnosis and
treatment. Twelve of these cats were underweight, 4
had normal body condition, and 2 were overweight.
Seven cats were severely dehydrated, 6 were moderately
dehydrated, and 5 were adequately hydrated. Median
rectal temperature was 38.0°C (100.4°F; range, < 32.2°
to 39.1°C [< 90.0° to 102.4°F]). Eight cats were hypo-
thermic (ie, rectal temperature < 37.8°C [100.0°F]) and
10 were normothermic (ie, rectal temperature between
37.8° and 39.2°C [100.0° to 102.5°F]); none of the cats
was febrile. Seventeen of the 18 cats had abnormalities
evident during abdominal palpation, including a dis-
crete abdominal mass or single thickened bowel loop
(8 cats), signs of abdominal pain (8), distended or dif-
fusely thickened intestinal loops (5), abdominal disten-
tion (3), and findings consistent with free peritoneal
fluid (1). Five cats had signs consistent with shock,
including abnormal heart rate, poor pulses, prolonged
capillary refill time, and obtundation; all 5 of these cats
had rectal temperatures ≤ 37.2°C (99°F). Other physi-
cal examination findings included dyspnea (3), periph-
eral lymphadenopathy (1), a palpable thyroid nodule
(1), small kidneys (1), cranial abdominal organomegaly
(1), and a heart murmur (1). One cat had multiple ad-
ditional physical examination abnormalities, including
oral ulcers, a soft, pliable hemi-mandible, an abscess on
a rear paw, icterus, and ataxia.
A fecal examination for parasites was performed in
2 cats, and results were negative in both. Both of these
cats were > 1 year old, and both were determined to
have intestinal lymphoma on the basis of results of his-
tologic examination of resected bowel segments.
Abdominal radiographs from 10 cats were available
for review, and all 10 had radiographic abnormalities.
Small intestinal distention or dilation was identified
in all 10 cats. Four cats had foreign material visible in
the small intestines. Two cats each had gastric dilation,
poor peritoneal detail, and a small intestinal mass effect.
Intussusception could not be definitively diagnosed on
survey radiographs from any of the 10 cats. In 3 cats,
radiographs had been obtained following administra-
tion of barium. In all 3, contrast radiography confirmed
the small intestinal obstruction suspected on the basis
of survey radiography, but results of contrast radiogra-
phy were specific for intussusception in only 1 cat.
Intussusception was evident on ultrasound images
from all 7 cats for which abdominal ultrasonographic
images were available for review (Figure 1). Other clin-
ically important ultrasonographic findings included in-
testinal mass or focal thickening (3 cats), mesenteric
lymphadenopathy (2), and abdominal effusion (1). A
hepatic mass was identified in 1 cat.
Thirteen of the 18 cats brought to the veterinary
teaching hospital for evaluation and treatment under-
went laparotomy. Of these, 5 were < 1 year old, 1 was 2
years old, and 7 were ≥ 6 years old. Manual reduction
of the intussusception was possible in 7 of the 13 cats
that underwent surgery and impossible in 4; whether
the intussusception could be reduced was not recorded
for the remaining 2 cats. Median duration of clinical
signs was 7 days (range, 1 to 19 days) in the 7 cats
in which the intussusception could be reduced and 12
days (range, 2 to 30 days) in the 4 cats in which the in-
JAVMA, Vol 234, No. 6, March 15, 2009 Scientific Reports 773
tussusception could not be reduced. Manual reduction
SMALL ANIMALS
alone was performed in 2 of the 13 cats that underwent
surgery, and resection and anastomosis were performed
in the remaining 11. Reasons for intestinal resection
and anastomosis included an inability to reduce the in-
tussusception (4), intestinal mass or mural thickening
(3), vascular compromise (2), and intestinal wall defect
(1). The reason for resection and anastomosis was not
recorded in 2 cats. Enteroplication was performed in 3
cats. Additional intraoperative findings included mes-
enteric lymphadenopathy (5 cats), a hepatic mass (1),
hepatomegaly (1), and a darkened liver with multifocal
discoloration (1).
The intussusception was jejuno-jejunal in 8 of the
20 cats, ileo-colic in 5, ileo-ileal in 2, ileo-cecal in 2,
and jejuno-ileal, jejuno-ileo-colic, and duodeno-jejunal
in 1 cat each. None of the cats had gastroesophageal in-
tussusception. Overall, therefore, 12 of the 20 cats had
an enteroenteric intussusception, and 8 had an entero-
colic intussusception. Length of the intussusception
ranged from 2 to 15 cm (median, 6.8 cm). None of the
cats had an intestinal foreign body or gross evidence of
parasitism.
In 8 of the 10 cats that were < 1 year old and 8
of the 9 cats that were ≥ 6 years old, a portion of the
affected intestine had been submitted for histologic ex-
amination. Histologic findings included lymphoma (5
cats) and changes consistent with IBD (3). Intussus-
ceptions in the remaining 8 cats were considered idio-
pathic because histologic examination revealed either
normal intestinal morphology or inflammatory change
considered secondary to the intussusception. This in-
cluded 5 cats with enteroenteric intussusception and 3
cats with enterocolic intussusception. Intussusceptions
were considered idiopathic in 7 of the 8 cats that were
< 1 year old and secondary to lymphoma in 1. Four
of the 8 cats that were ≥ 6 years old had alimentary
Figure 1—Ultrasonographic transverse view of gastrointestinal
tract intussusception in a cat.
 lymphoma, 3 had IBD, and only 1 had an idiopathic in-
SMALL ANIMALS
tussusception. Intussusceptions were enteroenteric in 2
of the cats with lymphoma and enterocolic in 3; intus-
susceptions were enteroenteric in 2 of the cats with IBD
and enterocolic in 1.
Of the 8 cats with idiopathic intussusception, 5 had
conditions that may have predisposed to intussuscep-
tion. Two cats were lactating, having queened within
the previous 2 months; 1 cat had multiorgan thrombo-
sis and infarctions; 1 cat had severe pneumonia with
pulmonary abscesses; and 1 cat was being treated orally
with griseofulvin and trimethoprim-sulfonamide be-
cause of dermatophytosis and a nasal discharge and
was found to have bilateral otitis media at necropsy. No
plausible predisposing historical or physical conditions
could be identified in the remaining 3 cats with idio-
pathic intussusceptions.
Twelve of the 13 cats that underwent surgery sur-
vived through the immediate postoperative period. The
remaining cat was euthanized at the time of surgery be-
cause of diffuse thickening of the intestines. Two of the
3 cats in which enteroplication was performed devel-
oped severe, generalized ileus, as determined by means
of abdominal radiography and ultrasonography, after
surgery. One of these cats died 4 days after surgery, and
the other was euthanized 6 days after surgery. Neither
of these 2 cats underwent a necropsy, and the cause of
the ileus was not identified in either cat. None of the
remaining 10 cats that survived the immediate post-
operative period developed clinical evidence of ileus,
and all 10 were discharged from the hospital. Five of
the cats that were discharged reportedly did not have a
recurrence of intussusception; the other 5 were lost to
follow-up.
Discussion
The age distribution of cats in the present study was bi-
modal. In contrast, in most previous reports,2,17,19–22,25–28,30,31
cats with intussusception were primarily young, often < 1
year of age. Older cats with intussusception may have been
underreported previously because they were euthanized
owing to advancing age or an anticipated poor prognosis.
Alternatively, the fact that our study population consisted
of cases from a referral center may have skewed the age
distribution in the present study. In 3 previous reports,2,5,31
Siamese cats were the most common breed of cat affected,
whereas in other studies,17,19,28 Burmese cats were most
common. We did not identify a breed predisposition in the
present study, but our study population was small.
The most common owner complaints in the pres-
ent study were largely consistent with those in other re-
ports. Together, these findings suggest that cats with in-
tussusception may have diarrhea less often than dogs.2
Other than hypothermia, physical examination findings
in the present study were also consistent with findings
in previous reports17,19–22 and generally were consistent
with the pathophysiology of intussusception. Previous
reports20,22 have reported fever more frequently than
hypothermia, but cats in the present study may have
been sicker than those described in previous reports
because the veterinary teaching hospital is a referral
center. Hypothermia in some cats in the present study
774 Scientific Reports JAVMA, Vol 234, No. 6, March 15, 2009
may have been due to disease severity, shock, or sep-
sis.39 There was no clear relationship between rectal
temperature and age or between rectal temperature and
underlying disease process.
The ultrasonographic appearance of intestinal in-
tussusception in dogs and cats has been described,1,8,37
and intussusception was evident on ultrasound images
from all 7 cats in the present study for which such im-
ages were available for review. Consistent with findings
in previous reports,2,17 abdominal radiography was use-
ful in recognizing intestinal obstruction in cats in the
present study. However, intussusception could not be
definitively diagnosed on survey radiographs from any
of the 10 cats in which it was performed, and results of
contrast radiography were specific for intussusception
in only 1 of 3 cats. Therefore, abdominal ultrasonogra-
phy appeared more likely than radiography to provide
a specific diagnosis of intussusception.
Twelve of the 20 cats in the present study had en-
teroenteric intussusceptions. This finding was in con-
trast to findings in most previous reports,2,17,31,37 which
indicated that ileocolic intussusception was the most
common. A previous study5 suggested that idiopathic
intussusceptions were ileocolic, whereas intussuscep-
tions with an identified underlying cause were more
likely to be enteroenteric. In the present study, howev-
er, there was no clear relationship between underlying
cause and anatomic site of intussusception.
No intussusceptions involving the stomach or esoph-
agus were identified in the present study. A search of the
PubMed database performed in January 2008 for the term
cat or feline paired with intussusception yielded a total
of 65 cases reported prior to the present study, 5 (8%) of
which involved cats with intussusceptions proximal to the
duodenum.18,27,33,34,38 Therefore, gastroesophageal intus-
susception appears to be uncommon in this species. Al-
though there have been reports of intussusception proxi-
mal to the duodenum in dogs,40–45 a proximal location is
reportedly uncommon in dogs as well.2,5
Only 8 of the 16 cats for which histologic data were
available in the present study were considered to have
idiopathic intestinal intussusception. Seven of the 8 cats
with idiopathic intussusceptions were < 1 year old, where-
as 7 of the 8 cats ≥ 6 years old had IBD or alimentary lym-
phoma, suggesting that as is the case in dogs, young cats
may be more likely to have idiopathic intussusception,
and older cats with intussusception may be more likely to
have primary gastrointestinal tract disease.
Five of the 8 cats with idiopathic intussusception
in the present study had physical or medical conditions
that may have predisposed them to intussusception. De-
velopment of intussusception in cats with severe non-
gastrointestinal tract disease is consistent with previous
reports2,3,5,6 of intussusception in dogs associated with
systemic disease or recent extra-abdominal surgery. As
was the case for 2 cats in the present study, intussus-
ception has been reported previously in cats within 2
months after parturition.26 Possibly lactation and wean-
ing predispose to endocrine-mediated changes in gas-
trointestinal tract motility, which may predispose to
intussusception.
Ten of the 13 cats that underwent surgery in the
present study were discharged from the hospital, and
this short-term survival rate was similar to the rate
(80%) reported in a previous study.17 Owing to the time
period of the present study, obtaining long-term fol-
low-up information was difficult. Recurrence rate was
difficult to assess because 5 of the 10 cats that were dis-
charged were lost to follow-up. However, none of the 5
cats for which follow-up information was available had
a recurrence of intussusception. Others have reported
low recurrence rates in cats,2 but recurrence rates as
high as 20% have also been reported.17
The role of enteroplication in the surgical man-
agement of cats with intussusception is poorly charac-
terized.2 In the present study, the only 2 cats that died
in the immediate postoperative period had undergone
enteroplication and developed severe ileus, whereas
all 9 cats without enteroplication survived to the time
of discharge. The 2 cats that didn’t survive were in dif-
ferent age groups, and neither cat had any confirmed
predisposing cause for the intussusception. Whether
enteroplication predisposes cats to ileus is unknown,
and because diagnostic imaging was not performed
in cats without postoperative complications, we do
not know whether ileus occurred in those cats that
did not undergo enteroplication. Owing to the small
number of cats in the present study that underwent
enteroplication, it is impossible to draw any conclu-
sions regarding this technique in cats. Others have re-
ported complications associated with enteroplication
in cats.28
Major limitations of the present study were the
lack of fecal parasite examinations in most cats and the
fact that fecal samples were not submitted for bacte-
rial culture. Previous studies2,17,19 have found intestinal
infection or infestation associated with intussuscep-
tion in dogs and cats. However, no gross or histologic
evidence of infection was reported in any of the 16 cats
in which biopsy samples were submitted for histologic
examination. An additional limitation was the require-
ment that the diagnosis had to have been confirmed
at surgery or necropsy for cats to be included in the
study. Spontaneous reduction has been reported in dogs
with intussusception,46 and cats with intermittent in-
tussusception may have been excluded from the pres-
ent study. The referral nature of the veterinary teaching
hospital may also have skewed the study population
toward more severely affected cats, and the postopera-
tive survival rate may have been exaggerated owing to
the availability of 24-hour intensive care. Furthermore,
because of the small sample size, the investigation had
insufficient statistical power to make meaningful state-
ments about statistical associations between risk factors
and outcome in cats with intussusception.
In conclusion, results of the present study suggest-
ed that cats with intussusception may have a bimodal
age distribution and that IBD or alimentary lymphoma
may be an important underlying cause in older cats with
intussusception. Further investigation into the role of
nongastrointestinal tract diseases and metabolically
stressful events in the development of intussusception
in cats is warranted. The most common site of intus-
susception in cats remains unclear, although intussus-
ceptions proximal to the duodenum appear uncommon
in this species. Abdominal ultrasonography is likely the
JAVMA, Vol 234, No. 6, March 15, 2009 Scientific Reports 775
most accurate presurgical method for the diagnosis of
SMALL ANIMALS
intussusception in cats.
a. Aloka 650, 5.0-MHz convey array, 7.5-MHz mechanical array,
Aloka Co Ltd, Wallingford, Conn.
b. ATL Ultramark 9 HDI, C7-4 curved array, L10-5 linear array,
Advanced Technology Laboratories Inc, Bothell, Wash.
References
1. Lamb CR, Mantis P. Ultrasonographic features of intestinal in-
tussusception in 10 dogs. J Small Anim Pract 1998;39:437–441.
2. Levitt L, Bauer MS. Intussusception in dogs and cats: a review of
thirty-six cases. Can Vet J 1992;33:660–664.
3. Oakes MG, Lewis DD, Hosgood G, et al. Enteroplication for
the prevention of intussusception recurrence in dogs: 31 cases
(1978–1992). J Am Vet Med Assoc 1994;205:72–75.
4. Weaver AD. Canine intestinal intussusception. Vet Rec 1977;100:
524–527.
5. Wilson GP, Burt JK. Intussusception in the dog and cat: a review
of 45 cases. J Am Vet Med Assoc 1974;164:515–518.
6. Applewhite AA, Hawthorne JC, Cornell KK. Complications
of enteroplication for the prevention of intussusception re-
currence in dogs: 35 cases (1989–1999). J Am Vet Med Assoc
2001;219:1415–1418.
7. Rallis TS, Papazoglou LG, Adamama-Moraitou KK, et al. Acute
enteritis or gastroenteritis in young dogs as a predisposing fac-
tor for intestinal intussusception: a retrospective study. J Vet Med
A Physiol Pathol Clin Med 2000;47:507–511.
8. Patsikas MN, Jakovljevic S, Moustardas N, et al. Ultrasonographic signs
of intestinal intussusception associated with acute enteritis or gastroen-
teritis in 19 young dogs. J Am Anim Hosp Assoc 2003;39:57–66.
9. Du Toit DF, Homan WP, Reece-Smith H, et al. Canine intestinal
intussusception following renal and pancreatic transplantation.
Vet Rec 1981;108:34–35.
10. Colon JA, Maritato KC, Ryan KA. What is your diagnosis? Ileo-
colic intussusception. J Am Vet Med Assoc 2007;230:823–824.
11. Gal A, Harrus S, Arcoh I, et al. Coinfection with multiple tick-
borne and intestinal parasites in a 6-week-old dog. Can Vet J
2007;48:619–622.
12. Okewole PA, Odeyemi PS, Cole T, et al. Double intussuscep-
tion fatally complicated by clostridial infection in a dog (a case
report). Br Vet J 1989;145:291–292.
13. Evermann JF, Abbott JR, Han S. Canine coronavirus-associated
puppy mortality without evidence of concurrent canine parvo-
virus infection. J Vet Diagn Invest 2005;17:610–614.
14. Eckerlin RH. Ileal polypoid leiomyoma in a dog. J Am Vet Med
Assoc 1975;167:70–71.
15. Runyon CL, Merkley DF, Hagemoser WA. Intussusception as-
sociated with a paracolonic enterocyst in a dog. J Am Vet Med
Assoc 1984;185:443.
16. Halfacree ZJ, Beck AL, Lee KC, et al. Torsion and volvulus of
the transverse and descending colon in a German shepherd dog.
J Small Anim Pract 2006;47:468–470.
17. Bellenger CR, Beck JA. Intussusception in 12 cats. J Small Anim
Pract 1994;35:295–298.
18. Martinez NI, Cook W, Troy GC, et al. Intermittent gastroesoph-
ageal intussusception in a cat with idiopathic megaesophagus.
J Am Anim Hosp Assoc 2001;37:234–237.
19. Bellenger CR, Middleton DJ, Ilkiw JE, et al. Double intus-
susception followed by reintussusception in a kitten. Vet Rec
1982;110:323–324.
20. Bennett D. Intussusception of the jejunum in a young cat. Vet
Rec 1973;92:231.
21. Lansdown AB, Fox EA. Colorectal intussusception in a young
cat. Vet Rec 1991;129:429–430.
22. Wolfe DA. Compound intussusception in a kitten (a case re-
port). Vet Med Small Anim Clin 1978;73:455, 458–459.
23. Prier J, Prier S. Intestinal granuloma in a cat with intussuscep-
tion and prolapse. Calif Veterinarian 1980;5:17.
24. Demetriou JL, Welsh EM. Rectal prolapse of an ileocaecal neo-
plasm associated with intussusception in a cat. J Feline Med Surg
1999;1:253–256.
 25. Hunter FS. Intussusception at the ileocaecocolic junction in kit- nographic findings of intestinal intussusception in seven cats.
tens. Vet Rec 2001;148:252. J Feline Med Surg 2003;5:335–343.
SMALL ANIMALS

26. Doherty D, Welsh EM, Kirby BM. Intestinal intussusception in
five postparturient queens. Vet Rec 2000;146:614–616.
27. Van Camp S, Love NE, Kumaresan S. Radiographic diagnosis—
gastroesophageal intussusception in a cat. Vet Radiol Ultrasound
1998;39:190–192.
28. Culvenor JA. Peritonitis following intestinal anastomosis and
enteroplication in a kitten with intussusception. Aust Vet J 1997;
75:175–177.
29. Williams J, Reichle J. What is your diagnosis? Ileocecocolic in-
tussusception. J Am Vet Med Assoc 1993;203:1671–1672.
30. Davies TD. Intussusception in the cat. Vet Rec 1985;117:191.
31. Kavanagh MF. Intussusception in Siamese cats. Vet Rec 1981;109:
165.
32. Orton RG. Intussusception of the jejunum in the cat. Vet Rec
1973;92:301.
33. van Geffen C, Saunders JH, Vandevelde B, et al. Idiopathic
megaoesophagus and intermittent gastro-oesophageal intussus-
ception in a cat. J Small Anim Pract 2006;47:471–475.
34. Owen MC, Morris PJ, Bateman RS. Concurrent gastro-oesopha-
geal intussusception, trichobezoar and hiatal hernia in a cat.
N Z Vet J 2005;53:371–374.
35. Harris ME. Intussusception in the cat. Vet Rec 1968;83:597–598.
36. Kolata RJ, Wright JH. Inflammation and inversion of the cecum
in a cat. J Am Vet Med Assoc 1973;162:958.
37. Patsikas MN, Papazoglou LG, Papaioannou NG, et al. Ultraso-
38. Crowe DT Jr. Use of a nasogastric tube for gastric and esoph-
ageal decompression in the dog and cat. J Am Vet Med Assoc
1986;188:1178–1182.
39. Brady CA, Otto CM, Van Winkle TJ, et al. Severe sepsis in cats:
29 cases (1986–1998). J Am Vet Med Assoc 2000;217:531–535.
40. Applewhite AA, Cornell KK, Selcer BA. Pylorogastric intussus-
ception in the dog: a case report and literature review. J Am Anim
Hosp Assoc 2001;37:238–243.
41. Graham KL, Buss MS, Dhein CR, et al. Gastroesophageal intus-
susception in a Labrador retriever. Can Vet J 1998;39:709–711.
42. Masloski A, Besso J. What is your diagnosis? Gastroesophageal
intussusception with megaesophagus in a dog. J Am Vet Med Assoc
1998;212:23–24.
43. Roach W, Hecht S. What is your diagnosis? Gastroesophageal
intussusception. J Am Vet Med Assoc 2007;231:381–382.
44. Pietra M, Gentilini F, Pinna S, et al. Intermittent gastroesopha-
geal intussusception in a dog: clinical features, radiographic and
endoscopic findings, and surgical management. Vet Res Commun
2003;27(suppl 1):783–786.
45. Greenfield CL, Quinn MK, Coolman BR. Bilateral incisional gas-
tropexies for treatment of intermittent gastroesophageal intus-
susception in a puppy. J Am Vet Med Assoc 1997;211:728–730.
46. Patsikas MN, Papazoglou LG, Adamama-Moraitou KK. Spon-
taneous reduction of intestinal intussusception in five young
dogs. J Am Anim Hosp Assoc 2008;44:41–47.

Selected abstract for JAVMA readers from the

American Journal of Veterinary Research
Effect of long-term dietary supplementation with clinoptilolite on performance
and selected serum biochemical values in dairy goats
Panagiotis D. Katsoulos et al

Objective—To determine the effect of dietary supplementation with clinoptilolite on health and
production as well as serum concentrations of fat-soluble vitamins, macroelements and trace ele- March 2009
ments, and activities of hepatic enzymes in dairy goats.
Animals—72 Saanen-cross dairy goats.
See the midmonth issues
Procedures—Goats were randomly assigned to 1 of 2 groups. The clinoptilolite group (n = 36)
received concentrate feed, of which 2.5% contained clinoptilolite; the control group (36) received of JAVMA
unsupplemented feed. The experiment began 8 weeks before parturition and continued to the be-
ginning of the next nonlactating period (280 days of lactation). At the day of parturition, kids were for the expanded
weighed. Milk yields were recorded at day 60 of lactation and thereafter at monthly intervals. Milk
percentages of fat, protein, and lactose and somatic cell count (SCC) were evaluated at the same
points. Blood samples were obtained at the beginning of the experiment, the day of parturition, and table of contents
thereafter at monthly intervals to measure serum concentrations of fat-soluble vitamins, macroele-
ments and trace elements, and activities of hepatic enzymes. for the AJVR
Results—Birth weights of triplets and quadruplets were significantly higher in clinoptilolite-treated
goats versus control goats. Milk fat percentage was significantly higher and SCC was significantly
lower in clinoptilolite-treated goats, compared with respective values in control goats. However, no
or log on to
changes in serum concentrations of any variable were detected.
Conclusions and Clinical Relevance—In the context of this experiment, clinoptilolite supple- avmajournals.avma.org
mentation of concentrate feed at 2.5% improved milk fat percentage in dairy goats, without ad-
verse effects on the serum variables evaluated. Furthermore, the reduction of SCC achieved with for access
clinoptilolite supplementation provided some evidence of improved milk hygiene. (Am J Vet Res
2009;270:346–352)
to all the abstracts.

776 Scientific Reports JAVMA, Vol 234, No. 6, March 15, 2009
Esophagitis and esophageal strictures.

Glazer A, Walters P.

Compend Contin Educ Vet. 2008 May;30(5):281-92.

¿Cómo pasa el bolo alimenticio a través del esófago?

¿Qué drogas anestésicas incrementan el riesgo de reflujo por disminuir lel tono del LES?

¿Qué otras drogas pueden producir estenosis?

Indica cómo varía la capa muscular del esófago dependiendo si se trata de un perro o un
gato.

¿Cómo puede influir el ayuno en el reflujo gástrico durante la anestesia?¿Cuánto tiempo

recomiendan los autores?

¿Cuáles son los síntomas más típicos de la enfermedad esofágica?¿Por qué puede haber
síntomas respiratorios?

¿Es interesante la administración de córticos en las estenosis esofágica?

Cuando hay una estenosis esofágica, ¿Qué capas del esófago están afectadas?

¿Cuál es la causa más frecuente de esa estenosis esofágica?

Define los esfínters esofágicos que conoces, e indica por quién están formados?

Explica los objetivos que persigue el tratamiento médico de la esofagitis.

¿Por qué es mejor el tratamiento de la esofagitis con omeprazol que con ranitidina?

¿Qué complicaciones puede tener la dilatación con bujías?

¿Qué porcentaje de éxitos podemos insinuarle al propietario?

 CE Article #2

Esophagitis and Esophageal

Strictures
Alan Glazer, DVM, DACVIMa
Patricia Walters, VMD, DACVIM, DACVECC
New England Animal Medical Center
West Bridgewater, Massachusetts

ABSTRACT: Esophagitis and esophageal strictures are relatively uncommon but significant diseases
in companion animals. Often, an esophageal disorder is suspected based on the animal’s medical
history and clinical signs. Esophagitis and acquired esophageal strictures are caused by prolonged
contact of caustic substances or foreign bodies with the esophageal lining, leading to mucosal injury.
In cases of stricture, damage extends into the submucosal and muscular layers.Timely detection and
appropriate management of esophagitis and esophageal strictures significantly improve nutritional
status, dysphagia, and pain and often return the animal to a normal quality of life.This article reviews
the current literature and focuses on the diagnosis and treatment of esophagitis and esophageal
strictures caused by fibrosis secondary to esophageal inflammation.

E
sophageal diseases cause a range of clinical
signs, including regurgitation, weight loss,
and respiratory distress. The diagnosis of
esophagitis is challenging and often requires
specialized procedures such as endoscopy. If
inflammation damages the submucosa and
muscularis, a cicatrix may develop, resulting in
obstruction of the esophageal lumen and more
serious illness. However, significant advances
have been made in the treatment of esophagitis
and esophageal strictures. With appropriate
management of esophageal disease, veterinary
patients can have considerable improvement of
clinical signs and return to normal lives.
NORMAL ANATOMY
AND PHYSIOLOGY
• Take CE tests The esophagus is made up of
• See full-text articles three layers: mucosa, submu-
a Dr.Glazer discloses that he
CompendiumVet.com owns shares in Pfizer Inc.
cosa, and muscle. The mucosa is lined by squa-
mous epithelium and overlies the submucosa. In
dogs, the muscle layer is composed entirely of
skeletal muscle; in cats, the distal third is smooth
muscle. The esophagus does not have a serosal
layer; instead, it is covered by adventitia (Figure 1).
The esophagus has upper and lower sphincters.
The upper esophageal sphincter is composed of the
cricopharyngeus and thyropharyngeus muscles.
The lower esophageal sphincter (LES) is made
up of muscle layers around the esophagus and
diaphragmatic crura (Figure 2). These layers are
thought to create a pressure barrier that prevents
reflux of gastric contents into the esophagus. The
LES relaxes during swallowing to allow ingesta to
pass into the stomach. It has been suggested that
the location of the LES could play a role in the
occurrence of reflux. In theory, an intraabdominal
LES prevents reflux because the positive pressure
in the abdomen puts more force on the esopha-
gus relative to the stomach and increases barrier

May 2008 281 COMPENDIUM

282 CE Esophagitis and Esophageal Strictures
Figure 1. Cross-section of the esophagus.
pressure. Consequently, some humans who do not have an
abdominal esophageal component are more prone to pri-
mary gastroesophageal reflux disease. However, a recent
study of greyhounds and beagles indicated that dogs vary
with respect to whether the position of the gastroe-
sophageal junction is intrathoracic or intraabdominal. This
Patients with recurrent respiratory signs should be evaluated for esophageal disease,
as should patients that present with regurgitation and gastrointestinal disturbances.
finding implies that an intraabdominal LES may not be
essential to prevent reflux in dogs.1
When a bolus of ingesta reaches the caudal pharynx,
afferent sensory fibers stimulate the swallowing center
in the brain. Respiration is temporarily inhibited while
efferent motor fibers stimulate the esophagus via the
vagus nerve, causing primary peristalsis to transport the
ingesta aborally. Secondary peristalsis is similar to pri-
mary peristalsis except that the impulse is initiated by
esophageal distention. As food approaches the stomach,
transmission of sensory information results in relaxation
of the LES. Innervation of the esophagus is mainly
parasympathetic from the vagus nerve.
COMPENDIUM
PATHOPHYSIOLOGY
The normal physiologic defenses against esophageal
inflammation are the LES, the esophageal mucosal lin-
ing, clearance of the esophagus via peristalsis, the neu-
tralizing effect of alkaline saliva, and esophageal cell
turnover. Esophagitis is defined as inflammation and dis-
ruption of the esophageal mucosa with resultant expo-
sure of the esophageal submucosa. Causes of esophagitis
include gastroesophageal reflux, vomiting, and ingestion
of foreign bodies, caustic substances, or medications.
Anesthesia-induced gastroesophageal reflux is the most
commonly reported cause in the veterinary literature.2–6
The factors that affect the likelihood that a refluxate
will cause esophageal damage are the content of the
refluxate, the contact time, and the effectiveness of nor-
mal esophageal defense mechanisms. Studies have
shown that a refluxate with a pH less than 4 is most
likely to cause damage. The presence of pepsin and bile
acids in refluxate has also been shown to damage the
esophageal lining.7–11 Increased damage is correlated
with prolonged contact of these substances with the
esophageal mucosa. Normally, the esophagus clears most
refluxate with primary and secondary peristaltic waves,
and the bicarbonate present in salivary secretions neutral-
izes any residual refluxate. In animals, esophageal inflam-
mation has been shown to decrease LES tone, which
leads to further reflux, thus creating a vicious cycle.7,11–13
The LES normally relaxes only during swallowing.
However, in humans, transient lower esophageal relax-
ations have been reported that do not seem to be related
to swallowing but have been correlated with reflux
events.7 Primary gastroesophageal reflux disease is rare
in animals but has been reported in cats.14 Gastric dis-
tention and certain anesthetic drugs decrease LES tone,
increasing the likelihood of reflux events. In animals,
morphine, thiopentone, propofol, xylazine, and atropine
all decrease LES tone or increase the likelihood of
reflux.15–17 One study in animals suggests that fasting for
longer than 24 hours before surgery is more likely to
cause reflux under anesthesia than fasting less than 4
hours. The ideal fasting interval suggested by the authors
of this study is 8 to 12 hours.17
May 2008

Figure 2. Normal anatomy of the canine and feline esophagus.
Body position during anesthesia is not associated with
an increase in reflux despite the finding that LES barrier
pressure is decreased in dogs positioned in sternal
recumbency.18,19 Intraabdominal surgical procedures are
more likely to cause gastroesophageal reflux than other
types of procedures. Ovariohysterectomy is the proce-
dure most commonly associated with increased reflux.18
However, any anesthetic event increases the likelihood
of gastroesophageal reflux.
In humans, some oral medications—tetracycline,
May 2008
Esophagitis and Esophageal Strictures CE 283
doxycycline, NSAIDs, potassium chloride, and quini-
dine—have been shown to induce severe esophagitis and
esophageal strictures.20 In cats, tetracyclines are most
frequently associated with esophagitis.21–23 Tetracycline
formulations tend to be very acidic, and prolonged expo-
sure to them results in inflammation of the esophageal
mucosa that may progress to formation of a stricture.
Esophageal stricture formation results from extensive
damage to the esophageal lining. Esophageal inflamma-
tion that extends through the mucosa into the submu-
COMPENDIUM
286 CE Esophagitis and Esophageal Strictures
cosa and muscularis leads to collagen deposition and
scarring. If the scarring is severe enough, an esophageal
stricture develops. Other causes of esophageal stricture
include congenital strictures, persistent right aortic arch,
and extramural esophageal compression secondary to a
mass. These causes are beyond the scope of this article.
HISTORY AND CLINICAL SIGNS
Animals with esophageal disease often have a variety
of clinical signs, including ptyalism, regurgitation, dys-
phagia, repetitive swallowing, odynophagia (painful
swallowing), and weight loss. Events of particular inter-
est in the medical history include exposure to caustic
substances, recent medications, and surgeries. It is
important to differentiate regurgitation from vomiting
and to recognize that esophageal disease and regurgita-
tion may be part of a more complex disorder such as
foreign body ingestion or may be secondary to an
underlying disease causing chronic vomiting. Timing of
events with regard to eating may be helpful in distin-
The most common cause of stricture formation in animals is
gastroesophageal regurgitation secondary to anesthesia.
guishing between regurgitation and vomiting because
regurgitation most often occurs shortly after ingestion.
However, animals with distal esophageal disease or
esophageal hypomotility may not regurgitate until hours
after eating. Unless odynophagia is present, these ani-
mals often present with a history of ravenous appetite.
Animals with esophageal obstructions or strictures may
tolerate liquids better than solids, whereas animals with
motility disorders are likely to have problems with liq-
uids as well as solids. Weight loss is common.
Animals with esophageal disease may present with
signs that are not immediately suggestive of alimentary
tract disease. For example, respiratory signs (e.g., nasal
discharge, coughing) may be present because regurgita-
tion can cause nasal inflammation and aspiration. Any
animal with recurrent pneumonia and respiratory signs
without an obvious cause (e.g., neoplasia, immunosup-
pression) should be evaluated for esophageal disease.
DIAGNOSTIC TESTING
Observation of the animal while it is swallowing food
can help localize disease to the pharynx and esophagus.
COMPENDIUM
In animals with suspected esophageal disease, results of
the following should be obtained: complete blood count,
serum chemistry profile, urinalysis, and thoracic and
neck radiography. Systemic disorders that cause similar
signs of increased appetite with weight loss, such as dia-
betes mellitus and hyperthyroidism, should be ruled out.
Survey thoracic radiographs can disclose the cause of
esophageal disease in cases of neoplasia, megaesophagus,
or foreign body ingestion and should also be evaluated
for the presence of aspiration pneumonia.
Survey thoracic radiographs are insensitive for the
detection of esophagitis or esophageal stricture. A positive
contrast barium esophagogram is more useful for deter-
mining the presence of strictures and evaluating
esophageal motility. However, administration of barium to
patients with esophageal disease carries the risk of aspira-
tion. If fluoroscopy is available, it is a valuable adjunct to
barium administration to evaluate more specifically for the
presence of pharyngeal disorders, more fully assess
esophageal motility, and possibly observe reflux episodes.
Esophagoscopy is necessary to definitively diagnose
esophagitis and esophageal stricture as well as to obtain
biopsy samples from esophageal masses. It may be useful
to obtain a barium esophagogram before esophagoscopy
to identify the length and number of strictures present
because the endoscope may not be able to pass beyond a
proximal stricture site. However, barium administration
must be separated from esophagoscopy because barium
obscures visualization through the endoscope. Our prefer-
ence is to wait 24 hours between obtaining a barium
esophagogram and performing esophagoscopy. Esopha-
goscopy should be performed slowly and carefully to iden-
tify lesions and avoid iatrogenic damage. Esophagitis
appears as mucosal hyperemia, mucosal edema, ulceration,
and bleeding (Figure 3). Lesion characteristics and loca-
tions should be carefully noted; the length of the endo-
scope can be used to record the depth at which a lesion
was identified. These records can then be used during fol-
low-up evaluation to identify any response to treatment
and newly formed strictures.
Ideally, biopsy samples of mass and proliferative
lesions should be obtained for definitive diagnosis.
May 2008
 Esophagitis and Esophageal Strictures CE 287

However, performing a biopsy of the esophagus is diffi-

cult because most endoscopic biopsy instruments need
to be perpendicular to the tissue being sampled in order
to properly grasp and cut the tissue and obtain an ade-
quate sample. Biopsy cups with spikes or suction biopsy
instruments can allow esophageal biopsy specimens to
be obtained more easily.
The endoscope should be passed into the stomach
and duodenum to evaluate for the presence of other
upper gastrointestinal disease because esophageal dis-
ease may represent only one part of a more complex dis-
ease process.

TREATMENT
Medical Management
Treatment of esophagitis is directed at healing inflam-
Figure 3. Endoscopic appearance of esophagitis with
mation and preventing further injury while supporting
partial stricture (arrow) formation. (Courtesy of Dr. Allyson
the animal’s nutritional needs. Esophageal healing is pro- Berent, Matthew J. Ryan Veterinary Hospital of the University of
moted by decreasing mechanical trauma to the esophagus Pennsylvania)
through feeding soft or blenderized food or placing a gas-
trostomy tube. Sucralfate may assist healing of the
mucosal surface through stimulation of prostaglandins. frequent administration, which often makes client com-
This drug has been shown to relieve clinical signs in pliance poor. H2-Blockers and proton-pump inhibitors
humans, but results of clinical trials vary as to whether have been used successfully (Table 1). Studies in human
sucralfate is capable of healing esophagitis as a sole medicine have proven omeprazole superior to ranitidine
agent.24,25 Sucralfate requires administration as a slurry for the healing and prevention of ulcers secondary to
three to four times per day, ideally separate from food and gastroesophageal reflux disease.20,28,29 Omeprazole also
other oral medications. Administration of sucralfate with has the advantage of less-frequent dosing and is available
food inhibits its ability to adhere to denuded mucosa. as an over-the-counter medication. Unfortunately,
Administration with other medications can decrease omeprazole is not available in a liquid form, making it
absorption of the other medica-
tions. In veterinary medicine, clin-
ical opinion varies as to the Table 1. Oral Dosages for Drugs Commonly
function of sucralfate in the Used to Treat Esophagitis32
nonacidic environment of the Medication Dogs Cats
esophagus. The recommendation
Mucosal protectant
for esophagitis, in humans and
Sucralfate 0.5–1 g PO q8h 0.25–0.5 g PO q8h
animals, is to use sucralfate in
combination (but not simultane- H2-Blockers
ously) with other medications and Cimetidine 5–10 mg/kg PO q6–8h 5–10 mg/kg PO q6–8h
not as a sole agent.20,26,27 Famotidine 0.5–1 mg/kg PO q12h 0.5 mg/kg PO q12h
Further injury to the esophagus Ranitidine 1–2 mg/kg PO q12h 3.5 mg/kg PO q12h
can be prevented by reducing the
acidity of gastric secretions and Proton-pump inhibitor
increasing LES tone. Antacids Omeprazole 0.7–1 mg/kg PO q24h 0.7–1.5 mg/kg PO q12–24h
(e.g., calcium carbonate), H 2 -
blockers, and proton-pump Prokinetics
Cisapride 0.25–0.5 mg/kg PO q8–12h 1.25–2.5 mg/cat PO q8–12h
inhibitors are all used to lower
Metoclopramide 0.2–0.4 mg/kg PO q8h 0.2–0.4 mg/kg PO q8h
gastric acidity. Antacids require

May 2008 COMPENDIUM

288 CE Esophagitis and Esophageal Strictures
Figure 4. Balloon dilation equipment.
Alliance II Integrated Inflation/Litho Handle with syringe and
pressure gauge.
Dilated balloon. (Microvasive, Boston Scientific, Natick, MA)
difficult to use in smaller animals and animals requiring
a feeding tube. Injectable proton-pump inhibitors can be
prohibitively expensive.
The prokinetics metoclopramide and cisapride are used
to increase LES tone and increase gastric emptying. Cis-
apride is considered superior to metoclopramide.26,27,30
Metoclopramide has a limited effect on esophageal
motility. In cases of megaesophagus that are not second-
ary to esophagitis, increasing LES tone can further
decrease esophageal emptying and increase regurgitation.
Cisapride may improve lower esophageal smooth muscle
motility in cats.31 Cisapride is no longer available at tradi-
tional pharmacies because of its association with cardiac
arrhythmias in humans, but it is available through com-
pounding pharmacies.26 Side effects appear to be minimal
in animals; gastrointestinal disturbances such as cramping
and diarrhea have been reported. 26,32 Ranitidine and
erythromycin also speed gastric emptying and subse-
quently reduce the amount of gastroesophageal reflux.31
If oral antibiotics are required, liquid formulations are
preferred because they are less likely to be retained in
the esophagus. If a tablet or pill is to be administered,
COMPENDIUM
following the pill with an oral water bolus has been
shown to markedly improve esophageal transit time.33
Many animals with esophagitis regurgitate or have
pain when swallowing, which leads to a chronic decrease
in caloric intake. Restoration and maintenance of ade-
quate nutrition is of utmost importance. If the animal is
willing to eat, feeding blenderized foods from an ele-
vated position may be all that is needed. If necessary,
nutrition can be maintained through placement of a gas-
trostomy tube. The prescribed diet should be nutrition-
ally complete with adequate protein and calories. Fat in
the diet delays gastric emptying, but higher calorie con-
tent, often provided as a higher proportion of calories in
the form of fat, is often necessary to minimize the vol-
ume fed. If an animal has initial difficulty with a high-fat
diet, a change to a low-fat diet may be effective.
Esophageal Stricture Dilation
Esophageal strictures generally require dilation to effec-
tively improve the animal’s clinical signs. Occasionally,
mild strictures may be manageable with a blenderized
diet and elevated feedings alone. The two nonsurgical
techniques for esophageal stricture dilation are bougie-
nage and balloon dilation (see the box on page 289).
Bougienage involves the use of a long, narrow, rigid
instrument (a bougie) that is gently pushed through the
stricture to progressively break down and stretch the scar
tissue. This technique has been described using an endo-
scope as a bougie or using specifically designed bougie-
nage instruments.20 Many types of bougies are available;
in general, they are rounded, oblong instruments that are
serially passed through the stricture. Once one size is
passed easily, the next larger diameter instrument is
selected. The goal is to gradually increase the diameter of
the esophagus at the stricture site. Fluoroscopy is useful
for this technique when a guidewire is used. Bougienage
has also been described using measured guidewires or
endoscopic guidance.
The procedure of esophageal balloon dilation involves
passing an inflatable balloon into the stricture under
endoscopic or fluoroscopic guidance. The balloon is
expanded with saline or a dilute contrast agent (if using
fluoroscopy) to a preset diameter and pressure to gradu-
ally stretch the stricture (Figure 4).
There have been many debates over the relative safety
and effectiveness of bougienage versus balloon dilation. In
theory, the balloon method applies an even radial force,
whereas bougies apply both a radial and a shear force.
The absence of a shear force has been suggested to make
May 2008

Overview of Bougienage and Balloon Dilation
For either procedure, start with the bougie or balloon
that is closest to the stricture in size. The stricture diameter
may be estimated by comparing it with the endoscope
width or by passing a Foley catheter into the site. For
bougienage, use slow, steady pressure to dilate the stricture.
Although no specific guidelines for bougienage have been
published in the veterinary literature, the recommendation
in human medicine is to follow the “rule of three.”a This
states that the clinician should dilate only three sizes (or 3
mm) beyond the first setting for which resistance is felt.
This guideline may be useful in veterinary patients but
should not supersede clinician assessment.
For the technique of balloon dilation, place the balloon
within the stricture, leaving a small part of the balloon
visible proximal to the stricture. Inflate the balloon to the
pressure on the manometer that correlates with the
aEsophageal dilation. American Society for Gastrointestinal
Endoscopy. Gastrointest Endosc 1998;48(6):702-704.
Figure A. Balloon dilation of a stricture. (Courtesy of Dr. Berent)
An esophageal stricture. Insertion of the balloon through the
stricture site.The arrow indicates the
balloon dilator.
balloon dilation safer. Some authors cite personal anec-
dotes of improved efficacy with fewer complications
when using the balloon method; however, retrospective
studies have shown no significant difference.34–36 Factors
that may make one method preferable to the other
include the cost of equipment and the type of diagnostic
imaging available. Bougies tend to be less expensive and
are reusable. Balloons are intended for single use,
although many clinicians reuse them as long as they
remain intact. Endoscopic guidance is required for bal-
loon dilation, while either fluoroscopy or endoscopy may
be used with bougienage. With either method, a
guidewire may be necessary to safely traverse a long, tor-
May 2008
Esophagitis and Esophageal Strictures CE 289
appropriate balloon diameter. Hold this pressure for 60 to
90 seconds. Deflate the balloon and reassess the stricture
site. Balloon dilation lessens the resistance that can be felt,
so direct visualization of the stricture site is necessary to
assess for adequate dilation and potential complications
such as bleeding or tears (Figure A). Mild bleeding is
expected, but if the bleeding appears excessive, discontinue
further dilation and assess for esophageal tears. If the
stricture diameter is not sufficiently increased, repeat
with the same pressure. If the diameter has increased
approximately to the chosen balloon diameter, increase to
the next size. Dilation can be repeated until an adequate
diameter has been achieved or the clinician feels that
further trauma is unacceptable.37,40 Repeat procedures are
usually required at 1- to 3-week intervals for an average of
two to four dilations per patient to achieve an adequate
clinical response as assessed by improvement in clinical
signs and tolerance to food.4,40,41
The stricture site after the dilation
procedure. Note the mild bleeding
associated with the dilation procedure.
tuous stricture. The choice of method used for esophageal
dilation should be based on available equipment and the
practitioner’s level of comfort with the technique.
Potential complications of bougienage or balloon dila-
tion include bleeding, esophageal tear, esophageal diver-
ticulum formation, infection, aspiration, and pain. Mild
bleeding is usually self-limiting. Patients with coagula-
tion disorders, recent esophageal surgery, esophageal
tears, or respiratory disease should be treated with more
gradual dilation to prevent complications. The reported
perforation rate is low (0% to 3.9%). Higher perforation
rates occur with blind bougienage techniques. 34,37–39
Overall successful outcome, defined as moderate to
COMPENDIUM
290 CE Esophagitis and Esophageal Strictures
complete resolution of clinical signs, has been reported
in 74% to 88% of animal patients.6,37,40,41
Steroids
Theoretically, corticosteroids could prevent stricture
recurrence after dilation because steroids reduce fibrosis
and collagen formation. However, in a controlled study
of children with esophagitis induced by caustic substance
ingestion, oral steroids were not shown to be beneficial.42
No controlled studies in animals have evaluated the use
of systemic steroids after esophageal stricture dilation.
Interest has turned from systemic steroid therapy to
local injection of steroids into the stricture using endo-
scopic guidance. In keloids and dermal scars, intrale-
sional steroid injections have been shown to reduce scar
formation. The procedure involves the use of an endo-
scopic sclerotherapy needle to inject triamcinolone ace-
tonide or dexamethasone at three or four sites around
the stricture before or immediately after the dilation
procedure. In humans, studies have shown a significant
reduction in the number of repeat dilation procedures
needed after the use of local steroid injection.43–46
Surgical Management
Surgery of the esophagus is difficult. Most of the
esophagus resides within the thoracic cavity, making
surgery a very invasive procedure. The lack of serosa and
the longitudinal orientation of the musculature make
secure surgical closure of the esophagus challenging. In
human medicine, the most common indication for
esophageal surgery is resection of an esophageal tumor.
Other indications include esophageal strictures unre-
sponsive to medical therapy and dilation and esophageal
perforations. The most commonly reported complica-
tions of esophageal surgery are anastomotic leak, ischemia
and necrosis, and stricture formation.47,48 Very small
leaks can respond to conservative therapy such as
esophageal rest, which involves placement of a gastros-
tomy tube, antibiotics, wound management (if in the
neck), and possibly chest drainage. More severe compli-
cations are likely to require additional surgery. Strictures
that form after surgical healing are often manageable
with dilation. Fortunately, the high success rate with
dilation techniques has made surgical resection for
benign strictures largely unnecessary.
CONCLUSION
Although primary esophageal disease is a relatively
infrequent presentation in companion animals, it is
COMPENDIUM
associated with significant morbidity. Many advances in
the therapy of esophagitis and esophageal strictures have
enabled most veterinary patients to be effectively treated
and lead normal lives.
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8. Galmiche JP, Janssens J. The pathophysiology of gastro-oesophageal reflux
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9. Vantrappen G, Tack J, Huyberechts G, et al. Studies on the relationship
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10. Szentpali K, Eros G, Kaszaki J, et al. Microcirculatory changes in the canine
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11. Zawie DA. Medical diseases of the esophagus. Compend Contin Educ Pract
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12. Zhang X, Geboes K, Depoortere I, et al. Effect of repeated cycles of acute
esophagitis and healing on esophageal peristalsis, tone, and length. Am J Phys-
iol Gastrointest Liver Physiol 2005;288(6):G1339-G1346.
13. Poorkhalkali N, Rich HG, Jacobsen I, et al. Chronic oesophagitis in the cat.
Scand J Gastroenterol 2001;36(9):904-909.
14. Han E, Broussard J, Baer KE. Feline esophagitis secondary to gastro-
esophageal reflux disease: clinical signs and radiographic, endoscopic, and
histopathologic findings. JAAHA 2003;39(2):161-167.
15. Wilson DV, Evans AT, Miller R. Effects of preanesthetic administration of
morphine on gastroesophageal reflux and regurgitation during anesthesia in
dogs. Am J Vet Res 2005;66(3):386-390.
16. Galatos AD, Savas L, Prassinos NN, Raptopoulos D. Gastro-oesophageal
reflux during thiopentone or propofol anaesthesia in the cat. J Vet Med A
Physiol Pathol Clin Med 2001;48(5):287-294.
17. Galatos AD, Raptopoulos D. Gastro-oesophageal reflux during anaesthesia
in the dog: the effect of preoperative fasting and premedication. Vet Rec
1995;137(19):479-483.
18. Galatos AD, Raptopoulos D. Gastro-oesophageal reflux during anaesthesia
in the dog: the effect of age, positioning and type of surgical procedure. Vet
Rec 1995;137(20):513-516.
19. Pratschke KM, Bellenger CR, McAllister H, Campion D. Barrier pressure at
the gastroesophageal junction in anesthetized dogs. Am J Vet Res
2001;62(7):1068-1072.
20. Wo JM, Waring JP. Medical therapy of gastroesophageal reflux and manage-
ment of esophageal strictures. Surg Clin North Am 1997;77(5):1041-1062.
21. German AJ, Cannon MJ, Dye C, et al. Oesophageal strictures in cats associ-
ated with doxycycline therapy. J Feline Med Surg 2005;7(1):33-41.
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22. McGrotty YL, Knottenbelt CM. Oesophageal stricture in a cat due to oral following balloon dilatation of anastomotic stricture after esophagogastros-
administration of tetracyclines. J Small Anim Pract 2002;43(5):221-223. tomy. Am J Surg 1997;174:442-444.
23. Melendez LD, Twedt DC, Wright M. Suspected doxycyline-induced 46. Altintas E, Kacar S, Tunc B, et al. Intralesional steroid injection in benign
esophagitis with esophageal stricture formation in three cats. Fel Pract esophageal strictures resistant to bougie dilation. J Gastroenterol Hepatol
2000;28(2):10-12. 2004;19:1388-1391.
24. Tytgat GNJ, Koelz HR, Vosmaer GDC. Sucralfate maintenance therapy in 47. Cassivi SD. Leaks, strictures, and necrosis: a review of anastomotic complica-
reflux esophagitis. Am J Gastroenterol 1995;90(8):1233-1237. tions following esophagectomy. Semin Thorac Cardiovasc Surg 2004;16(2):
25. Carling L, Cronstedt J, Engqvist A, et al. Sucralfate versus placebo in reflux 124-132.
esophagitis: a double-blind multicenter study. Scand J Gastroenterol 48. Briel JW, Tamhankar AP, Hagen JA, et al. Prevalence and risk factors for
1988;23(9):1117-1124. ischemic, leak, and stricture of esophageal anastomosis: gastric pull-up versus
26. Han E. Diagnosis and management of reflux esophagitis. Clin Tech Small colon interposition. J Am Coll Surg 2004;198(4):536-541.
Anim Pract 2003;18(4):231-238.
27. Sellon RK, Willard MD. Esophagitis and esophageal strictures. Vet Clin
North Am Small Animal Pract 2003;33(5):945-967.
ARTICLE #2 CE TEST
28. Smith PM, Kerr GD, Cockel R, et al. A comparison of omeprazole and rani-
tidine in the prevention of recurrence of benign esophageal stricture. Gas- This article qualifies for 2 contact hours of continuing CE
troenterology 1994;107:1312-1318. education credit from the Auburn University College
29. Marks RD, Richter JE, Rizzo J, et al. Omeprazole versus H2-receptor antago- of Veterinary Medicine. Subscribers may take
nists in treating patients with peptic stricture and esophagitis. Gastroenterol- individual CE tests or sign up for our annual
ogy 1994;106:907-915.
CE program. Those who wish to apply this credit to
30. Willard MD. Recognizing and treating esophageal disorders in dogs and
cats. Vet Med 2004;99(5):448-454.
fulfill state relicensure requirements should consult their
respective state authorities regarding the applicability
31. Washabau RJ, Hall JA. Diagnosis and management of gastrointestinal motil-
ity disorders in dogs and cats. Compend Contin Educ Pract Vet 1997;19(6): of this program. CE subscribers can take CE tests online
721-736. and get real-time scores at CompendiumVet.com.
32. Plumb DC. Plumb’s Veterinary Drug Handbook. 5th ed. Stockholm, Wiscon-
sin: PharmaVet Inc; 2005.
1. Which type of tissue is not a part of normal
33. Westfall DS, Twedt DC, Steyn PF, et al. Evaluation of esophageal transit of
tablets and capsules in 30 cats. J Vet Intern Med 2001;15(5):467-470. canine esophageal anatomy?
34. Scolapio JS, Pasha TM, Gostout CJ, et al. A randomized prospective study a. squamous epithelium c. smooth muscle
comparing rigid to balloon dilators for benign esophageal strictures and rings. b. adventitia d. submucosa
Gastrointest Endosc 1999;50(1):13-17.
35. Saeed ZA, Winchester CB, Ferro PS, et al. Prospective randomized compari-
2. Secondary peristalsis is initiated by
son of polyvinyl bougies and through-the-scope balloons for dilation of pep-
tic strictures of the esophagus. Gastrointest Endosc 1995;41(3):189-195. a. food in the caudal oropharynx.
36. Cox JG, Winter RK, Maslin SC, et al. Balloon or bougie for dilatation of b. conscious perception.
benign esophageal stricture? Dig Dis Sci 1994;39(4):776-781. c. the chemoreceptor trigger zone.
37. Harai BH, Johnson SE, Sherding RG. Endoscopically guided balloon dila- d. esophageal distention.
tion of benign esophageal strictures in 6 cats and 7 dogs. J Vet Intern Med
1995;9:332-335.
38. Hernandez LV, Jacobsen JW, Harris MS. Comparison among the perforation
3. In veterinary medicine, the most common cause
rates of Maloney, balloon, and Savary dilation of esophageal strictures. Gas- of esophagitis is
trointest Endosc 2000;51(4):460-462. a. gastroesophageal reflux secondary to anesthesia.
39. Said M, Mekki M, Golli M, et al. Balloon dilation of anastomotic strictures b. foreign body ingestion.
secondary to surgical repair of oesophageal atresia. Br J Radiol
2003;76(901):26-31.
c. chronic vomiting.
40. Leib MS, Dinnel H, Ward DL, et al. Endoscopic balloon dilation of benign
d. ingestion of caustic substances.
esophageal strictures in dogs and cats. J Vet Intern Med 2001;15(6):547-552.
41. Chiu YC, Hsu CC, Chiu KW, et al. Factors influencing clinical applications 4. Which drug decreases LES tone or increases the
of endoscopic balloon dilation for benign esophageal strictures. Endoscopy likelihood of reflux?
2004;36(7):595-600.
a. morphine c. propofol
42. Anderson KD, Rouse TM, Randolph JG. A controlled trial of corticosteroids
in children with corrosive injury of the esophagus. N Engl J Med
b. atropine d. all of the above
1990;323(10):637-640.
43. Kochhar R, Makharia GK. Usefulness of intralesional triamcinolone in treat- 5. Which factor does not worsen esophageal
ment of benign esophageal strictures. Gastrointest Endosc 2002;56(6):829- inflammation secondary to reflux?
834.
a. prolonged contact time
44. Kochhar R, Ray JD, Sriram PV, et al. Intralesional steroids augment the
effects of endoscopic dilation in corrosive esophageal strictures. Gastrointest b. bicarbonate
Endosc 1999;49(4):509-513. c. refluxate pH less than 4
45. Miyashita M, Onda M, Okawa K, et al. Endoscopic dexamethasone injection d. pepsins

May 2008 COMPENDIUM

292 CE Esophagitis and Esophageal Strictures

6. Which clinical sign is not associated with

esophageal strictures?
a. odynophagia
b. recurrent pneumonia
c. weight loss
d. difficulty in ingesting liquids but not solid foods

7. In humans, _______ has been proven superior for

treating esophageal ulcers.
a. omeprazole
b. ranitidine
c. sucralfate
d. calcium carbonate

8. Which statement is not an important nutritional

guideline for animals with esophagitis?
a. A gastrostomy tube should be placed if an animal is
unwilling or unable to eat.
b. Elevated feedings and blenderized food may help pre-
vent regurgitation.
c. Fat may be useful in the diet because it speeds gastric
emptying.
d. The diet should be complete with adequate protein
and calories.

9. Which statement regarding treatment of stric-

tures is false?
a. Balloon dilation applies only radial forces and
bougienage applies radial and shear forces; however,
no evidence shows increased complications with one
versus the other.
b. Surgery is indicated in cases of esophageal neoplasia,
esophageal perforations, or strictures that are unre-
sponsive to medical therapy.
c. The rate of a successful outcome with balloon dila-
tion is greater than 80%.
d. Systemic steroid use has been shown to reduce
esophageal scar tissue and improve outcome.

10. The “rule of three” states that

a. if a stricture requires more than three dilation proce-
dures, surgery should be considered.
b. the practitioner should dilate only three sizes (or 3
mm) beyond the first setting at which resistance is felt.
c. repeating procedures at 3-week intervals reduces the
complication rate to less than 3%.
d. animals should receive “triple” therapy consisting of
sucralfate, an acid reducer such as omeprazole, and a
prokinetic agent.

COMPENDIUM May 2008

 Caso clínico 5
Última parte

“LUCAS”
Cocker Spaniel
Macho no castrado, 12 kg

Plan postoperatorio
Tratamiento postquirúrgico 24h
•  Analgesia
•  Buprenorfina 20 µg/kg IV q 6 horas
•  Lidocaína 25 µg/kg/min
•  Antibioterapia
•  Cefazolina 25 mg/kg IV q 8h
•  Fluidoterapia
•  Glucosalino + 20 mEq/L de KCl a ½ x Vol de
Mantenimiento
•  Anti-H2
•  Ranitidina 2 mg/kg q 12 IV lento
•  NPO 12 horas
•  Inicio agua poca cantidad en 12h
•  Inicio dieta intestinal en 24 – 36 horas si tolera agua
§  Si vomita, parar el agua y la alimentación
y continuar con fluidoterapia.
§  Maropitant
§  Control ecográfico diario.
§  La dehiscencia de la sutura ocurre en el
cuarto día y se demuestra por la presencia
de líquido libre dentro del abdomen
§  Ya llevas unos cuantos casos revisados
§  ¿Qué te parece el sistema?
§  ¿Lo encuentras útil?
§  DANOS TU OPINIÓN

§  Ya sé que los artículos están en inglés,

pero es la única posibilidad de avanzar
Oesophageal and gastric endoscopic foreign body removal:
complications and follow-up of 102 dogs

P. GIANELLA, N. S. PFAMMATTER AND I. A. BURGENER

Journal of Small Animal Practice (2009) 50, (12) 649–654

PREGUNTAS

¿Dónde se alojan los cuerpos extraños esofágicos?

¿Cuándo practicaremos una esofagotomía ante la presencia de un cuerpo extraño?

¿Cuál es la raza más afectada por la presencia de cuerpos extraños esofágicos?

¿Cuál es la complicación más frecuente ante la presencia de un cuerpo extraño

esofágico y qué sintomatología tiene asociada?

Indica los tres factores de riesgo que dificultan la extracción de un cuerpo extraño
esofágico

¿Qué tipo de cuerpo extraño esofágico es especialmente difícil de poder ser

extraido por la boca y debe ser empujado al estómago y por qué?

¿Qué porcentaje de éxito obtienen los autores en la extracción de cuerpos

extraños?¿Es comparable con otros estudios?

¿Cómo trata pequeñas perforaciones esofágicas?

¿Las estenosis esofágicas son frecuentes tras la extracción de un cuerpo extraño?

PAPER
Oesophageal and gastric endoscopic
foreign body removal: complications
and follow-up of 102 dogs
OBJECTIVES: To assess complication rate, risk factors for complica-
tions and outcome in dogs with oesophageal and gastric endoscop-
ic foreign body (FB) removal.
METHODS: Medical records of 102 dogs undergoing endoscopic
removal of oesophageal and/or gastric FBs from March 2001 to
November 2006 were retrospectively reviewed. All owners were
contacted by telephone to provide follow-up information.
RESULTS: West Highland white terriers, Yorkshire terriers and Ber-
nese mountain dogs were over-represented compared to the hos-
pital population. Endoscopy alone was successful in 92/102 dogs
(90·2 per cent), whereas gastrotomy (but no oesophagotomy) was
required in 10 dogs (9·8 per cent). Complications in 13/102 dogs
(12·7 per cent) were perforation (8), oesophageal stricture (1),
oesophageal diverticula (1), perioesophageal abscess (1), pneu-
mothorax and pleural effusion (1) and respiratory arrest (1). Six
dogs (all weighing <10 kg) had complications resulting in death or
euthanasia. Bone FBs, bodyweight of less than 10 kg, and oesoph-
ageal or gastric FB in place for more than three days were signifi-
cant risk factors for complications. Of the dogs available for follow-
up (75/96), 92 per cent had no complications after discharge.
CLINICAL SIGNIFICANCE: Endoscopic FB removal is associated with a
low overall complication rate with bone FBs and bodyweight of less
than 10 kg as significant risk factors.
P. GIANELLA, N. S. PFAMMATTER AND
I. A. BURGENER
Journal of Small Animal Practice (2009)
50, 649–654
DOI: 10.1111/j.1748-5827.2009.00845.x
Accepted: 28 July 2009
Department of Clinical Veterinary Medicine,
Division of Small Animal Internal Medicine, Vet-
suisse Faculty of the University of Bern, 3001
Bern, Switzerland
Journal of Small Animal Practice • Vol 50 • December 2009
INTRODUCTION
Gastrointestinal foreign bodies (FBs) are
relatively common in both canine and
feline practice. Due to their slightly indis-
criminate eating habits, swallowing of
incompletely masticated food, and expo-
sure to toys and dental chews, dogs are
more likely to be presented with gastroin-
testinal FBs than cats. If unresolved, these
FBs can become life threatening. Bone or
cartilage material, fishhooks, needles, chew
treats, balls and toys are reported FBs in
dogs (Spielman and others 1992, Michels
• © 2009 British Small Animal Veterinary Association
and others 1995, Sale and Williams 2006,
Leib and Sartor 2008). Depending on the
localisation, common clinical signs are
salivation, retching, gagging, vomiting,
regurgitation, anorexia, pain, respiratory
distress and restlessness (Gualtieri 2001,
Tams 2003, Willard 2004). The severity
of the clinical signs depends on the type
and size of FB, its location, the dura-
tion of obstruction, and the presence or
absence of a stricture or a wall perfora-
tion with subsequent abscessation, pleu-
ritis, mediastinitis, pneumomediastinum,
pneumothorax, peritonitis and pneumo-
peritoneum (King 2001, Seiler and others
2001). Occasionally, dogs show no clinical
signs. The duration of FB impaction can
vary from hours to days or weeks before
presentation and diagnosis. Oesopha-
geal and gastric FBs can be visualised on
lateral chest or abdominal radiographs.
However, small and non-radiopaque FBs,
especially in the stomach, are sometimes
difficult to see on survey radiographs and
may require positive contrast radiography.
In the oesophagus, FBs tend to lodge in
the narrowest points: the thoracic inlet,
the heart base and just cranial to the lower
oesophageal sphincter. Given the possible
complications, oesophageal FBs should
be promptly removed or gently pushed
into the stomach for dissolution or gas-
trotomy. This can be achieved using rigid
and flexible endoscopes (Houlton and
others 1985, Spielman and others 1992,
Michels and others 1995, Leib and Sar-
tor 2008), fluoroscopic guidance (Moore
2001), thoracoscopy/laparoscopy or sur-
gery (Michels and others 1995, Sale and
Williams 2006). The latter, although
more aggressive, appears to be a necessary
approach if endoscopic removal fails or if
oesophageal or gastric perforation is pres-
ent (Parker and others 1989).
Although reports of endoscopic, fluo-
roscopic or surgical removal of FBs have
been published, there is little information
in recent literature regarding complica-
tions and long-term follow-up of endo-
scopic FB removal in a large case series.
The purpose of this study was to assess the
649

complication rate, risk factors for compli-
cations and outcome in dogs with oesoph-
ageal and gastric endoscopic FB removal.
MATERIALS AND METHODS
Case selection
Medical records of dogs with gastroin-
testinal FBs that underwent endoscopic
removal in the Small Animal Clinic of the
University of Bern, Switzerland, between
March 2001 and November 2006 were
reviewed. Data retrieved included signal-
ment, clinical signs at presentation, dura-
tion of clinical signs, type and location of
FB, degree of macroscopic mucosal dam-
age, technique of FB removal, short-term
complications and length of hospitalisa-
tion. All canine patients entering the hos-
pital during the study period were used as
a control population.
Follow-up
During medical records review, owners
were contacted by telephone to provide
follow-up information. A single investiga-
tor (NSP) interviewed the owners with a
standard questionnaire to ensure that all
owners were asked the same questions.
They were asked if clinical signs related to
the FB removal (vomiting, regurgitation,
respiratory distress, apathy, pain) or diffi-
culties in eating were observed after hos-
pital discharge. Furthermore, information
was gathered about further medical care
sought and, in the case of death, the cause
of death if known.
Statistical analysis
Statistical analyses were performed with
NCSS (Kaysville, Utah, USA). Successful
Table 1. Comparison of breeds between the study (n=102) and the hospital population (n=15147). Only the breeds with at
least 3 cases were included in the calculation
Breed
(n = 102)
West Highland white terrier
Yorkshire terrier
Bernese mountain dog
Labrador retriever
Golden retriever
German shepherd dog
CI = confidence interval.
650
P. Gianella and others
endoscopic FB removal was defined as
removal without gastrotomy or oesoph-
agotomy and did not necessarily implicate
successful outcome. The results were sum-
marised in contingency tables. The impact
of bodyweight, the duration of a FB in
place, as well as type and location of the
FB on complications and death/euthana-
sia was examined with Fisher’s exact test
(P-value of <0·05 considered significant)
and odds ratios with 95 per cent confi-
dence interval (odds ratios with confi-
dence intervals not including 1 considered
significant).
RESULTS
Study population
During the study period 102 dogs under-
went gastrointestinal endoscopic FB
removal (102/15147, this represents a
prevalence of 0·67 per cent of the canine
hospital population). The FB was located
in the oesophagus (n = 57), in the stomach
(n = 36) or both (n = 9). The study popu-
lation consisted of dogs from 50 different
breeds and 10 mixed-breed dogs. Only six
breeds showed at least three cases, with
West Highland white terrier, Yorkshire
terrier and Bernese mountain dog over-
represented compared to the hospital pop-
ulation during the study period (Table 1).
Fifty-two dogs were males (21 neutered)
and 50 were females (29 spayed). The
median age was 4 years, with a range of 3
months to 17 years. Seventeen dogs were
less than 1 year old at presentation, 45
dogs were aged between 1 and 5 years, 32
dogs between 5 and 10 years, and 8 dogs
were more than 10 years old. The median
body weight was 18·9 kg with a range from
Cases Controls
(n = 15, 147)
11 201
9 451
9 508
7 1040
5 629
3 1016
Journal of Small Animal Practice • Vol 50
1·3 to 47·3 kg. Forty-six dogs weighed less
than 10 kg, 14 between 10 and 20 kg, 12
between 20 and 30 kg and 29 less than
30 kg. For one dog, bodyweight was not
recorded.
Patient history and clinical signs
Clinical signs described by the owner
or noted during physical examination
included retching/gagging (31/102; 25/57
with oesophageal FB, 5/9 with oesopha-
geal and gastric FB, 1/36 with gastric
FB), vomiting (27/102; 0/0/27), cough/
dyspnea (19/102; 17/2/0), anorexia
(15/102; 9/1/5), regurgitation (14/102;
10/4/0), lethargy (11/102; 7/0/4), rest-
lessness (8/102; 5/2/1), hematemesis
(6/102; 1/0/5), hypersalivation (5/102;
4/1/0), weight loss and pain (4/102 each;
0/0/4) and fever (2/102; 1/0/1). No clini-
cal signs were reported by the owner or
were observed during physical examina-
tion in 18/102 dogs. These dogs had been
observed to have ingested foreign material
(7 oesophageal and 11 gastric FBs) right
before the hospital admission. In the 84
patients with FB-related clinical signs, the
duration of the clinical signs before pre-
sentation ranged from 2 hours to 40 days.
The duration was less than one day in 38
dogs, one to three days in 18 dogs, and
greater than three days in 28 dogs.
Location and type of FB
A single lateral thoracic radiograph was
diagnostic for oesophageal FB in all 63
cases performed, whereas three of the
patients observed to have ingested for-
eign material underwent direct endo-
scopic evaluation without radiographs.
Abdominal radiographs (two standard
views) were diagnostic for gastric FB in all
Odds ratio 95% CI P-value
8.93 5.25-15.17 <0.001
3.13 1.63-6.03 0.004
2.77 1.43-5.36 0.008
0.99 0.46-2.14 1.000
1.18 0.48-2.91 0.619
0.42 0.14-1.28 0.162
• December 2009 • © 2009 British Small Animal Veterinary Association

but two cases (43/45), in which the defini-
tive diagnosis was only made at endoscopy
(1 wood, 1 organic material). A concur-
rent presence of oesophageal and gastric
FBs was found in nine dogs, where the
same material was removed from oesopha-
gus and stomach. The location and type of
FB is summarised in Table 2.
Removal
Flexible oesophagoscopy and gastroscopy
were performed within two hours after
radiographs were taken (GIF-XP160
or GIF-Q165, Olympus, Volketswil,
Switzerland). A retrieval using a large rigid
grasping forceps (85 cm, Eickemeyer,
Tuttlingen, Germany) alongside the
endoscope was attempted in most cases,
whereas endoscopic grasping forceps or
baskets (Olympus) were used for smaller
FBs. Endoscopy alone was successful in
92/102 dogs: in 83 dogs, the FB was orally
removed, whereas in nine, the oesophageal
FB was pushed into the stomach for dis-
solution without gastrotomy required
(6× bone, 3× organic material). Gas-
trotomy was necessary only in 10 dogs
with primary gastric FB for definitive FB
removal after an unsuccessful endoscopic
event. Oesophagotomy was not required
in any case.
In 22/57 cases with oesophageal FBs,
oesophagitis was subjectively considered
mild to moderate, with generalised hyper-
emia and single or confluent erosions,
whereas in 23/57 animals, oesophagitis
was judged to be severe with ulcerations
and focal necrosis. In 12/57 cases treated
during emergency duties, this information
Table 2. Site of lodgement of FB and type of material
Localisation Bone Plastic
Oesophagus
thoracic inlet 4 –
heart base 12 1 –
distal 25
not reported 3 –
Stomach 2 15
Oesophagus and 4 1
stomach
Total 50 17
For the nine dogs with FBs in the oesophagus and the stomach, the material retrieved was the same in both localisations. The sharp objects include five fishhooks, two pieces of aluminium,
and two needles, whereas the organic material includes dried pig’s ears, chestnuts, nuts, and fruits.
Journal of Small Animal Practice • Vol 50 • December 2009
Endoscopic foreign body removal
was missing. Superficial erosions and
small ulcerations of the gastric mucosa
were noted in only five dogs with gastric
FBs. In the remaining animals, the gastric
mucosa was either judged to be normal or
not completely evaluated because of gas-
tric repletion.
Post-procedural thoracic radiographs
were obtained in 46 dogs with an oesoph-
ageal FB. Patients with a smooth FB
lodged in the oesophagus only for a few
hours and patients without any visible
mucosal damage and a fast and uneventful
retrieval were not always radiographically
evaluated.
Complications
Overall, a total of 13 dogs suffered compli-
cations as summarised in Table 3. Of these,
eight had perforations. In 2/5 oesophageal
perforations, pneumomediastinum was
only evident after endoscopy, whereas
only 1/5 perforation was visible at endos-
copy. Two of the three gastric perforations
were identified at laparotomy, whereas a
pneumoperitoneum was clearly identified
on abdominal radiographs before laparot-
omy in the third. All five oesophageal per-
forations were associated with oesophageal
FBs and not with retrieval of gastric FBs.
In 75 per cent (6/8) of the dogs with per-
foration, the FB was a bone.
One dog with aspiration pneumonia
diagnosed on initial presentation devel-
oped a perioesophageal abscess after the
FB removal. In this dog, the oesopha-
geal FB was pushed into the stomach
and removed by gastrotomy. No signs of
perforation were detected either during
Sharp Chew Tissue Wood
objects treats
3 – – –
2 – – –
– 3 – –
– – – –
6 – 4 3
– 3 – –
9 8 4 3
• © 2009 British Small Animal Veterinary Association
endoscopy or on radiographs thereafter.
A soft-tissue opacity in the caudal medi-
astinum was suspected at presentation, but
only confirmed after radiographic signs of
aspiration pneumonia had resolved two
weeks later. An endoscopic ultrasonogra-
phy of the caudal mediastinum was per-
formed to better define this opacity in the
region of the caudal oesophagus. Due to
the suspicion of a perioesophageal abscess,
a thoracotomy was performed and the
abscess removed.
Six dogs had complications resulting in
death (four) or euthanasia (two). The first
dog had a respiratory arrest after oesopha-
goscopy was initiated and died. Blood was
recovered from the tracheal tube and a
traumatic tracheal rupture was suspected
secondary to the bone itself and its removal.
The second dog with a severe oesophagitis
and multiple diverticula suddenly died at
home two days after discharge. Dogs 3
and 4 had an oesophageal perforation and
died due to cardiac arrest and pneumo-
thorax following FB removal. Dogs 5 and
6 were euthanased upon owner request.
Dog 5 had an oesophageal perforation,
pleural effusion and mediastinitis and was
euthanased after endoscopy, whereas dog
6 developed pneumothorax and pleural
effusion one week after the initial oesoph-
agoscopy. Unfortunately, necropsy was not
available for any of the six dogs.
Endoscopic oesophageal re-evaluation
due to regurgitation was deemed necessary
in only one dog seven days after discharge.
An oesophageal stricture was identified
and endoscopic balloon dilation was suc-
cessfully performed.
Stones Organic Unknown Total
material
– – – 7
– – 15
– 4 – 32
– – – 3
1 2 3 36
– 1 – 9
1 7 3 102
651
 P. Gianella and others

Table 3. Data from 13 dogs with complications (10 with oesophageal FB, 3 with gastric FB, none with FB in both localisations)
Dog number FB type FB localisation Duration of Type of complication Length of Death or
clinical signs hospitalisation euthanasia
1 Plastic Stomach >3 days Perforation/pneumoperitoneum >3 days –
2 Bone Oesophagus heart base >3 days Perioesophageal abscess >3 days –
3 Bone Distal oesophagus >3 days Stricture >3 days –
4 Bone Distal oesophagus >3 days Perforation/pleural effusion /mediastini- – Euthanasia
tis/pneumomediastinum
5 Fishhook Stomach <1 day Perforation 1–3 days –
6 Bone Stomach >3 days Perforation >3 days –
7 Bone Distal oesophagus >3 days Perforation/pneumothorax/cardiac arrest – Death
8 Bone Distal oesophagus Unknown Severe oesophagitis/diverticula – Death
9 Bone Oesophagus thoracic <1 day Perforation / pneumomediastinum >3 days –
inlet
10 Bone Distal oesophagus >3 days Perforation / pneumothorax/cardiac arrest -– Death
11 Bone Oesophagus heart base 1 day Respiratory arrest /traumatic tracheal – Death
rupture
12 Bone Distal oesophagus Unknown Perforation / pneumothorax / pneumome- >3 days –
diastinum
13 Chew treat Oesophagus heart base >3 days pneumothorax / pleural effusion – Euthanasia
after one
week

Of the 96 dogs that survived, 62 were
hospitalised less than one day, 18 between
one and three days, and 16 for more than
three days. Of the seven surviving patients
with complications, all but one were hos-
pitalised for more than three days.
Risk factors for complications
All six dogs that died or were euthanased
weighed less than 10 kg and only one dog
with greater than 20 kg showed complica-
tions. Besides the increased risk for death/
euthanasia (P = 0·007), dogs weighing less
than 10 kg had a significantly increased
risk for complications (P = 0·018; OR
4·82, 95 per cent CI 1·35 to 17·18). An
oesophageal or gastric FB in place for
more than three days was also associated
with a significantly increased risk for com-
plications (P = 0·006; OR 5·52, 95 per
cent CI 1·69 to 17·93) and death/eutha-
nasia (P = 0·047; OR 6·00, 95 per cent CI
1·19 to 29·74), whereas a FB in place for
less than one day yielded a reduced risk
for complications (P = 0·015; OR 0·20,
95 per cent CI 0·06 to 0·74). Five of the
six dogs that died or were euthanased
and 10/13 that developed complications
had a bone FB. Even though bone FBs
yielded significantly more complications
(P = 0·039; OR 3·83, 95 per cent CI 1·05
to 13·78) than other types of foreign
material, there was no statistically signifi-
cant association observed between bone
FB and death/euthanasia (P = 0·107).
Finally, the localisation of the FB was not
a risk factor neither for complications nor
for death/euthanasia, even though all six
dogs that died or were euthanased only
had oesophageal FBs (two heart base, four
distal oesophagus).
Follow-up
A follow-up was available for 75/96 dogs
discharged from the hospital after the
procedure (41/57 oesophageal, 28/36
gastric and 6/9 gastric and oesophageal
FBs). Of these, 69 recovered unevent-
fully (eight died of unrelated cause), four
with oesophageal FB suffered coughing
or retching only for a few days after dis-
charge, and two with oesophageal FB were
presented for a second oesophageal FB 1
to 2 months later (second endoscopic FB
removal without complications).
DISCUSSION
The value of endoscopic FB removal has
been emphasised in several studies (Houl-
ton and others 1985, Spielman and others
1992, Kaiser and others 2003), where suc-
cessful endoscopic removal ranged from
26 to 63 per cent. In the study presented
here, endoscopic removal of oesophageal
FBs was successful in 86 per cent (57/66),
with only 14 per cent of FBs pushed
into the stomach compared with 29 to
52 per cent in the aforementioned stud-
ies. In a recent study about oesophageal
obstruction caused by dental chew treats
(Leib and Sartor 2008), oral removal was
uncommon (26 per cent) and most of the
FBs were pushed into the stomach. How-
ever, it was speculated by the authors, that
the low oral retrieval rate could be likely
attributable to the smooth surfaces that
do not easily lend themselves to grasping
instruments. However, there is no proof in
literature that endoscopic removal is supe-
rior to pushing the FB into the stomach.
Thoracic and abdominal radiographs
were diagnostic or highly suggestive for
oesophageal and gastric FBs in 100 and
95·6 per cent, respectively. For oesopha-
geal FBs, similar rates have been found
before ranging from 75·9 to 100 per cent
(Spielman and others 1992, Sale and
Williams 2006, Rousseau and others 2007,
Leib and Sartor 2008). However, there is
no data available for gastric FBs.
The complication rate of oesophageal
FB removal varies between authors and
methods of retrieval from 8 to 38 per cent
in the aforementioned studies, but no

652 Journal of Small Animal Practice • Vol 50 • December 2009 • © 2009 British Small Animal Veterinary Association

studies on complication rates of gastric FB
removal were found. This study revealed
an overall complication rate of 12·7 per
cent (13/102), with 10/66 (15·2 per cent)
and 3/45 (6·7 per cent) dogs revealing
complications with oesophageal or gas-
tric FBs, respectively. The most common
complication was oesophageal or gastric
perforation (6/8 with bone FB). Second-
ary pneumomediastinum, pneumothorax
or pneumoperitoneum were only visible
in 4/8 dogs with perforation before endos-
copy or gastrotomy, which underscores
the importance of post-procedural radio-
graphs. Two small oesophageal perfora-
tions (only one visible at endoscopy) were
allowed to close spontaneously with good
success according to previous literature
(Ryan and Greene 1975, Parker and oth-
ers 1989). Due to the nature of the gastric
FBs (fishhook, plastic and bone) and/or
the presence of pneumoperitoneum, the
gastric perforations could potentially be
attributed to the FB itself and not to the
endoscopic removal.
Six dogs had complications resulting
in death (four) or euthanasia (two). In
three of these, oesophagoscopy was fol-
lowed by cardiac or respiratory arrest. For
the remaining three, one died suddenly
two days after the FB removal and the
other two were euthanased upon owner’s
request. It therefore seems that the most
serious complications result from oesoph-
ageal perforation or secondary to efforts
associated with FB removal.
Benign oesophageal strictures in dogs
are complications of severe oesophagi-
tis and are usually associated with gas-
tric reflux during anaesthesia, vomiting
of gastric content, ingestion of a caustic
substance and FB trauma (Sellon and
Willard 2003). In this study, only one
dog presented with an obvious oesopha-
geal stricture. Strictures are more com-
mon secondary to oesophageal impaction
with dental chew treats (Leib and Sartor
2008). The reason for this is unclear, and
the authors only speculated about the
unique characteristics of the dental chew
treats causing severe diffuse oesophageal
damage.
Overall, this study revealed a signifi-
cant association between complications
and bone FBs, bodyweight less than 10
kg, and duration of FB presence. Bones
Journal of Small Animal Practice • Vol 50
Endoscopic foreign body removal
are the most common cause of oesopha-
geal obstruction with reported incidences
as high as 94 per cent (Houlton and others
1985). The lower incidence of 49 per cent
reported here may reflect a wider range of
chewable objects encountered nowadays,
or the increased awareness of the owners
about possible complications with bones.
In a smaller study performed in the same
hospital between 1992 and 1997 (Lüthi
and Neiger 1998), the percentage of bones
was still much higher with 77 per cent.
Dental chew treats, another commonly
reported cause of oesophageal obstruction
(Leib and Sartor 2008), were rarely found
in our patients.
In regard to bodyweight, all six dogs
that died or were euthanased weighed less
than 10 kg. This association has not been
clearly documented, but could be extrap-
olated from previous studies considering
that most of the dogs were of small breed.
Part of this could be explained by the size
of the FBs compared to the body size (that
is, the same piece of FB is potentially more
dangerous for smaller dogs). Nevertheless,
not only small breeds such as West High-
land white terrier and Yorkshire terrier
were over-represented in our study, but
also Bernese mountain dogs. No previous
report indicated an increased risk for large
breed dogs, but unlike the terriers, none of
the Bernese mountain dogs showed com-
plications after FB removal.
A negative correlation between dura-
tion of clinical signs and complications
has been reported elsewhere (Rousseau
and others 2007). Similarly, this study
revealed a significant association between
FB of more than three days duration and
complications. The present study also
confirmed that the majority of oesopha-
geal FBs are found in the caudal portion
of the oesophagus (Houlton and others
1985, Parker and others 1989, Moore
2001, Leib and Sartor 2008).
It should be reminded that this study
has some limitations due to its retrospec-
tive character. Particularly, the degree
of mucosal damage was not objectively
evaluated in all cases (not all emergency
endoscopies fully documented). Further-
more, no attempt was made to relate the
therapy after FB removal to the outcome.
Another limitation was the different level
of experience of the clinicians performing
• December 2009 • © 2009 British Small Animal Veterinary Association
the endoscopies, and its possible effect on
the outcome. It should be noted, how-
ever, that only faculty members or senior
residents were allowed to performed the
FB removals. Unfortunately, 21 patients
were lost to follow-up, which could have
impacted the follow-up results.
In conclusion, the present study docu-
ments that oesophageal and gastric FBs are
still a common cause of referral to teach-
ing hospitals. Even though the overall
complication rate is low, potentially life-
threatening complications may develop
especially in small breed dogs and dogs
with bone FBs. The risk for complications,
and especially perforation, increases when
the FB has been in place for more than
three days. The overall outcome appears
to be very good.
Acknowledgements
The authors would like to thank all cli-
nicians from the Small Animal Hospital
of the University of Bern involved in the
patient management of the cases described
herein.
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Journal of Small Animal Practice • Vol 50 • December 2009
TAMS, T. R. (2003) Disease of the esophagus. In:
Handbook of Small Animal Gastroenterology. 2nd
edn. Ed T. R. Tams. W.B.Saunders, Philadelphia,
PA, USA. pp 151-155
WILLARD, M. D. (2004) Recognizing and treating esoph-
ageal disorders in dogs and cats. Veterinary Medi-
cine 99, 448-454
• © 2009 British Small Animal Veterinary Association
 Caso clínico 5
XIV parte

“LUCAS”
Cocker Spaniel
Macho no castrado, 12 kg

Cierre de la enterotomía
Félix García

•  Monofilamento reabsorbible 3/0

•  Punta redonda
•  Incluyendo todas las capas
 Félix García

•  Monofilamento reabsorbible, nunca multifilamento

ya que la capilaridad permitiría que las bacterias de
la luz intestinal, saliesen a la cavidad abdominal
Gliconato Monosyn 3/0 mantiene la resistencia
media 3 semanas, Polidioxanona Monoplus3/0
mantiene la resistencia media 6 semanas
•  Punta redonda
•  Incluyendo todas las capas, esto asegura coger la
submucosa, que será la que dé la consistencia
Prueba de estanqueidad

Félix García
 Parche de omento Dilatación del yeyuno craneal
a la obstrucción

Félix García
Plantea el postoperatorio
 Caso clínico 5
XII parte

“LUCAS”
Cocker Spaniel
Macho no castrado, 12 kg

Plan anestésico
Parece que el hígado de lucas no funciona del todo bien.
El siguiente paso para el diagnóstico, sería la biopsia o la citología,
pero los propietarios prefieren no hacer más pruebas.

¿Qué fármacos no usarías en la anestesia de Lucas teniendo en

cuenta el hígado?

Los que tienen metabolismo y excreción hepática:

TIOPENTAL y BENZODIACEPINAS

¿Qué fármacos no usarías en la anestesia de Lucas teniendo en

cuenta el soplo?

Los fármacos que producen hipotensión:

ACEPROMACINA, MEDETOMIDINA, PROPOFOL
PROTOCOLO ANESTÉSICO

PREOXIGENAR SIEMPRE
(mascarilla si la tolera)

Etomidato 1 mg/kg IV lento

(repetir bolo 1 mg/kg de etomidato en función de la necesidad)
Usar diacepam/midazolam por temblores

ISOFLORANO 1.5 – 2%
SEVOFLUORANE 2,5-3%

ANALGESIA PRE y POSTOPERATORIA

Buprenorfina 20 µg/kg IV q 6 horas
Lidocaína 25 µg/kg/min

¿A qué velocidad instaurarías la fluidoterapia?

PROTOCOLO ANESTÉSICO

PREOXIGENAR SIEMPRE
(mascarilla si la tolera)

Etomidato 1 mg/kg IV lento

(repetir bolo 1 mg/kg de etomidato en función
de la necesidad)
Usar diacepam/midazolam por temblores

ISOFLORANO 1.5 – 2%
SEVOFLUORANE 2,5-3%

ANALGESIA PRE y POSTOPERATORIA

Buprenorfina 20 µg/kg IV q 6 horas
Lidocaína 25 µg/kg/min

¿A qué velocidad instaurarías la fluidoterapia?

¿Qué nivel de monitorización necesita nuestro paciente?

 Consulta este libro:
Veterinary Anaesthesia 11 Ed. K. W. Clarke &C. M. Trim
Cap 2.

§  http://
www.sciencedirect.com.are.uab.
cat/science/book/9780702027932

¿Qué parámetros debes controlar y cómo?

 Chapter
Patient monitoring and clinical measurement
Introduction 19
General considerations relating Hypothermia 56
to monitoring 20
Clinical assessment of the patient 21
Monitoring the central nervous system 21
Eye position and reflexes 23
Anaesthetic gas analysers 24
EEG and Bispectral index 25
Monitoring the circulation 26
Pulse rate and rhythm 26
Heart rate monitors 27
Tissue perfusion 29
Arterial blood pressure 30
Central venous pressure 38
Left atrial pressure (pulmonary artery
wedge pressure) 39
Cardiac output 39
Blood loss 42
Monitoring the respiratory system 42
Rate monitors and apnoea alarms 42
Tidal and minute volume monitors 43
Blood gas analysis 43
Pulse oximetry 47
Capnography 49
Transcutaneous CO2 analysis 53
Acid–base analysis 53
Blood gas and acid base values 53
Interpretation of acid base abnormalities 55
©2014 Elsevier Ltd
2 
Monitoring body temperature 56
Hyperthermia 57
Malignant hyperthermia 57
Monitoring urine volume 58
Monitoring blood glucose 58
Monitoring neuromuscular blockade 58
INTRODUCTION
From the earliest days of anaesthesia, the anaesthetist has
monitored the patient’s pulse rate, pattern of breathing
and general condition. Advances in electronic technology
have made reasonably reliable, easily attached, non-
invasive monitoring devices available for clinical practice.
Observations and measurements of certain parameters
before, during, and after anaesthesia provide important
data to support the clinical assessment of the animal’s
condition and improve the chances of survival of the very
ill by indicating what treatment is needed, as well as the
response to treatment already given.
It is necessary to know what to measure as well as how
to measure it and not all anaesthetists may agree on the
priority ranking of the monitoring devices available.
However, for major surgery, for anaesthesia and surgery of
poor-risk patients, and for equine anaesthesia, it would be
difficult to defend the failure to use monitoring equip-
ment, especially if it were available. Recommendations for
monitoring of anaesthetized patients are available on the
19
Section 1 Principles and procedures
web sites for the Association of Veterinary Anaesthetists,
American College of Veterinary Anesthesia and Analgesia,
and the American Animal Hospital Association.
GENERAL CONSIDERATIONS
RELATING TO MONITORING
Complications, including death, may occur in healthy
patients at all stages of anaesthesia and monitors provide
early warning of life-threatening developments. Anaes-
thetic mishaps may be caused by mechanical malfunction,
disconnection of equipment, or human error. Judgemen-
tal error frequently occurs when the anaesthetist is in a
hurry and circumvents basic practices and procedures, or
when a decision must be made in an emergency. The
prevalence of complications may also be associated with
inadequate training or experience of the anaesthetist.
Knowledge and experience are a function of the nature
of the training received and the years of practice, but
proper vigilance at all times can only be generated by
self-motivation.
Routines should be developed to ensure that each aspect
of apparatus function is checked before use. Failure to
follow a simple checklist in every case features high on the
list of causes of anaesthetic disasters. All anaesthetic equip-
ment, including monitoring devices, should be main-
tained in good functioning order. It should be a matter of
course to maintain monitors with a battery back up fully
charged in case of need in an area without a convenient
electricity outlet nearby, failure of electricity supply, or the
need to disconnect from the main supply to minimize
electrical interference with other monitoring equipment.
Proficiency with methods of electronic surveillance
must be acquired during minor procedures so that they
can be applied properly in circumstances where their use
is mandatory (e.g. during major surgery or a cardiovascular
crisis). Routine use ensures that probes, sensors, elec-
trodes, etc. can be applied quickly to the animal and
increases the likelihood that the information obtained is
reliable.
Although current practice is to establish monitoring
only after the animal has been anaesthetized, it must
be recognized that many complications occur during
induction of anaesthesia. Ideally, especially for poor-risk
patients, monitoring should begin when the drugs for
premedication are administered. Dogs and cats may vomit
after administration of an opioid and the quantity and
content of the vomit may warn that the animal was fed
recently and so may be at risk for regurgitation and pul-
monary aspiration of gastric material. Brachycephalic
breeds and animals with respiratory problems should
always be observed after administration of preanaesthetic
drugs because sedation may cause partial or complete
airway obstruction or serious respiratory depression and
20
hypoxaemia. In any animal, evaluation of the degree of
sedation produced by premedicant drugs may indicate
that the anaesthetic plan should be reassessed and either
drug doses reduced or additional agents included.
Careful observation of the patient during induction of
anaesthesia may allow precise titration of drugs to achieve
the desired depth of anaesthesia and ensure early recogni-
tion of a complication that requires immediate specific
treatment, such as cyanosis, anaphylaxis, or cardiac arrest.
Where possible, patients at risk for complications may be
attached to specific monitoring equipment before induc-
tion of anaesthesia. Appropriate equipment for this would
be the electrocardiograph (ECG), a device for measure-
ment of blood pressure, or a pulse oximeter.
Recording drugs, dosages and responses for each patient
is essential and provides valuable information for any
subsequent time that anaesthesia may be needed. Noting
all measurements on an anaesthetic record provides a pic-
torial description of changes that can be used to predict
complications and plan treatment (Fig. 2.1). Retrospective
evaluation of difficult cases and of series of records,
perhaps of patients with similar surgical procedures, or to
compare different anaesthetic protocols, can be used to
monitor the anaesthetist’s performance and identify dif-
ficult situations that require further thought and improved
management. For research purposes, data can be acquired
into a computer for accurate data summaries.
Monitoring animals during anaesthesia must include
observation of behaviour and reflexes and measurement
of various physiological parameters at regular intervals to
accomplish two objectives. The first objective is to ensure
that the animal survives anaesthesia and surgery. The
second objective is to obtain information that can be used
to adjust anaesthetic administration and management to
minimize physiological abnormalities, which is especially
important for animals that have already compromised
organ systems. The goal is to prevent development of pre-
ventable adverse consequences 1 hour, 12 hours, or even
3 days after anaesthesia.
Monitoring should continue into the recovery period to
determine the need for additional analgesic drugs, ade-
quacy of ventilation, and to record serious deviations in
body temperature. Mucous membrane colour should be
checked for at least 20 minutes after the animal has been
disconnected from oxygen as it may take that long for
hypoxaemia to develop in animals that are moderately
hypoventilating and breathing air.
A variety of methods using inexpensive or expensive
equipment can be used to monitor parameters determined
by the species of animal to be anaesthetized and by the
abnormalities already present in the patient. Not all moni-
toring techniques need to be applied to every patient. A
recommendation for three levels of monitoring is pre-
sented in Table 2.1; level 1 monitoring information should
be obtained from all anaesthetized animals, level 2 moni-
tors are affordable and recommended for routine use in
 Patient monitoring and clinical measurement Chapter 2

Abbreviations AG 1 2 3 4 AE

TIME 0 15 30 45 0 15 30 45 0 15 30

O2 flow L/min 2
End tidal CO2 37 32 38 38 38
Vaporizer % 2 1.75 2 1.5

HR
180 180
Arterial pressure:
160 160
V
V Systolic
Diastolic 140 V V 140
X Mean V V V
120 V V V 120
Ventilation: V V V V
V V V V
VV V V V V V V V V V V V
Spontaneous 100 100
S
V VV V V XX X
V X X X
80 80
X XX V V V V XXXXX XX
Controlled XXX V
XXX V V X V V V V V
60 V
C VV V V V V V V V V V V 60
V
40 40
AI Anes. induction S S
AG Begin inhalant 20 S 20
AE End anes.
SS Surgery start 10 10
SE Surgery end
E Extubation 0 0
Temperature 103.1 101.6 101.6 99.9 98.8 98.6 98.1 97.5 97.2 96.6 96.1 96.5
Fluids (ml) LRS 175 350 550 850 1050 1430 2050 2200 2530 2650 2725
Other

DETAILED COMMENTS:
1. Oxymorphone 4.5mg slowly IV
2. Move to O.R. 1200mg Cefotetan IV
3. Change from indirect to direct arterial BP monitoring
4. Morphine 30mg IM
Figure 2.1  Anaesthetic record of a 61 kg, 6-year-old female Great Dane anaesthetized for exploratory laparotomy because of
torsion of the spleen. Anaesthesia was induced by intravenous administration of ketamine, 200 mg, and diazepam, 10 mg,
and maintained with isoflurane. Heart rate, blood pressure and respiratory rate were recorded at regular intervals to facilitate
early recognition of adverse trends.

some groups of patients, and level 3 monitors individually CLINICAL ASSESSMENT  

offer improved monitoring for patients with specific
problems. OF THE PATIENT
This chapter will describe the techniques of monitor-
ing using a systems approach, and offer guidelines for Monitoring the central  
interpretation of the information obtained. Further
nervous system
recommendations are given in the chapters devoted to
species anaesthesia and the chapter on management of Monitoring the depth of anaesthesia is not easy (see
complications. Chapter 1). An early attempt at definition through

21
Section 1 Principles and procedures

Table 2.1  Prioritization of monitoring

Monitor Information obtained Specific use

Level 1 (Basic monitoring)

Palpebral and pedal reflexes, eye position Depth of anaesthesia All anaesthetized animals

Respiratory rate and depth of chest or bag Adequacy of ventilation All anaesthetized animals
excursion

Oral mucous membrane colour Oxygenation All anaesthetized animals

Heart rate, rhythm, pulse strength, capillary Assessment of circulation All anaesthetized animals
refill time

Temperature Temperature Dogs and cats anaesthesia greater than

30 min; all inhalation anaesthesia

Level 2 (Routine use recommended for some patients)

Arterial blood pressure measurement Blood pressure; pulse pressure variation All inhalation anaesthesia; cardiovascular
(indirect or direct methods) disease or depression

Blood glucose Blood glucose Paediatric patients; diabetics; septicaemia;

insulinoma

Electrocardiography Cardiac rate and rhythm; diagnosis of All inhalation anaesthesia; thoracic
arrhythmia or cardiac arrest trauma or cardiac disease

Pulse oximetry Haemoglobin oxygen saturation; pulse rate Animals breathing air during anaesthesia;
recovery from anaesthesia; thoracic
trauma or pulmonary disease;
septicaemia/endotoxaemia

Capnography End-tidal carbon dioxide concentration; estimate All inhalation anaesthesia; patients at risk
of adequacy of ventilation; warning of circuit for complications
disconnect/malfunction or cardiac arrest

Urine output, either by expression of urinary Urine volume produced during anaesthesia Dogs and cats; renal disease; some
bladder or by urethral catheterization urinary tract surgery; multiorgan failure

Level 3 (Use for specific patients or problems)

Anaesthetic gas analyser Inspired and end-tidal anaesthetic agent Any patient on inhalation anaesthesia
concentration; evaluation of depth of
inhalation anaesthesia

Blood gases and pH PaCO2, PaO2, pH, HCO3, base excess/deficit Suspected hypoventilation or hypoxaemia;
measurement of metabolic status

Cardiac output measurement Cardiac output Sick animals with decreased perfusion;
complicated surgeries

Central venous pressure Indicator of central blood volume Dehydrated/hypovolaemic patients

Packed cell volume and total protein Haemodilution and protein concentration Haemorrhage; large volume infusion of
crystalloid solution

Peripheral nerve stimulator Neuromuscular transmission Use of neuromuscular blocking agents

observation of changes in reflexes, muscle tone, and respi-
ration with administration of increased concentration of
ether resulted in classification of anaesthesia into four
stages (Fig. 2.2). The animal was said to make the transi-
tion from consciousness to deep anaesthesia by passing
sequentially through Stage I (in which voluntary
excitement might be observed), Stage II (when the animal
appeared to be unconscious but exhibited involuntary
muscle movement, such as limb paddling, and vocaliza-
tion), Stage III (surgical anaesthesia), and Stage IV (anaes-
thetic overdose immediately prior to death). Stage III was
further divided into Plane 1 (light anaesthesia sufficient

22
 Patient monitoring and clinical measurement Chapter 2

VENTILATION

Intercostal Diaphragm Pattern Pupil Eyeball Eye Lacrimation Response to

position reflexes surgical stim.

Irregular
Awake panting

Irregular
Stage II breath- Palpebral
holding

Stage III
LIGHT Regular
Plane 1

MEDIUM Regular
Plane 2 shallow

DEEP Jerky
Plane 3
Corneal

Stage IV

Figure 2.2  Changes in ventilation and eye signs follow recognized patterns with different stages of inhalation anaesthesia.
The progression of these changes will be influenced by inclusion of injectable anaesthetic agents.
Adapted from Soma, 1971.

only for non-painful procedures), Plane 2 (medium depth

anaesthesia employed for most surgical procedures), Plane
3 (deep anaesthesia), and Plane 4 (excessively deep anaes-
thesia). Although the progression of changes described in
Fig. 2.2 are generally accurate representations of the transi-
tion from light to deep anaesthesia, the rate of changes are
altered by concurrent administration of injectable drugs.
Thus, in clinical practice, depth of anaesthesia is judged
by a number of methods, including altered somatic and
autonomic reflexes in response to nociceptive stimulation
and by knowledge of the amount of anaesthetic and anal-
gesic agents administered.

Eye position and reflexes

Eye movements are similar with thiopental, propofol, eto-
midate, alfaxalone, and inhalant anaesthetics in that the
eyeball rotates rostroventrally during light and moderate
depths of surgical anaesthesia, returning to a central posi-
tion during deep anaesthesia (Fig. 2.3). Muscle tone is Figure 2.3  The rostroventral rotation of the eye in this dog
retained during ketamine anaesthesia and the eye remains is consistent with light and medium planes of isoflurane or
centrally placed in the orbit in dogs and cats (Fig. 2.4), sevoflurane anaesthesia.

23
Section 1 Principles and procedures
Figure 2.4  The central position of the eye, with a brisk
palpebral reflex and pupillary dilation, is observed typically
during ketamine anaesthesia in cats.
and only slightly rotated in horses and ruminants. Fine
nystagmus may be present in horses anaesthetized with
ketamine (see Chapter 11). The palpebral reflex, which is
partial or complete closure of the eyelids (a blink) elicited
by a gentle tap at the lateral canthus of the eye or gentle
stroking of the eyelashes, is frequently a useful guide to
depth of anaesthesia. At a plane of anaesthesia satisfactory
for surgery, the palpebral reflex is present but weak and
nystagmus is absent. A brisk palpebral reflex develops
when anaesthesia lightens. Ketamine anaesthesia is associ-
ated with a brisk palpebral reflex.
A corneal reflex is a similar lid response elicited by
gentle pressure on the cornea. The presence of a corneal
reflex is no indicator of depth of anaesthesia and may
still be present for a short time after cardiac arrest has
occurred.
The pedal reflex is frequently tested in dogs, cats and
small laboratory animals to determine if depth of anaes-
thesia is adequate for the start of surgery. Pinching the web
between the toes or firm pressure applied to a nail bed will
be followed by withdrawal of the limb if analgesia is inad-
equate. Other species-specific reflexes that have been
found useful include the whisker reflex in cats, where
pinching of the pinna elicits a twitch of the whiskers, and
tickling the inside of a pig’s ear, where a shake of the
head indicates inadequate anaesthesia for surgery. It must
be remembered that administration of neuromuscular
blocking agents blocks somatic reflexes and respiratory
responses, and that the eye position will be central.
Increasing the depth of anaesthesia by increasing
administration of an anaesthetic agent in most cases pro-
duces increased respiratory and cardiovascular depression.
However, more than one anaesthetic or preanaesthetic
agent is generally administered and the cardiopulmonary
effects are determined by the combination of agents used
and their dose rates. Thus measurements of respiratory
24
Table 2.2  Approximate MAC* values for isoflurane
and sevoflurane in several species
Anaesthetic agent Dogs Cats Horses
Isoflurane 1.4 1.6 1.3
Sevoflurane 2.4 2.6 2.3
*MAC: minimum alveolar concentration of anaesthetic agent
required to prevent purposeful movement in 50% of animals in
response to a standard painful stimulus; see species chapters for
ranges of values.
rates, heart rates, and blood pressure are not reliable
guides to depth of anaesthesia. It is not uncommon for an
unstimulated dog or horse anaesthetized with an inhala-
tion agent to have a low arterial blood pressure and yet in
the next minute start moving its legs in response to a skin
incision, all accompanied by a dramatic increase in blood
pressure. Nevertheless, significant increases in heart rate
and/or arterial blood pressure in response to surgical stim-
ulation are an indication of inadequate analgesia. In
certain circumstances, surgical pain can induce a vaso-
vagal response resulting in bradycardia, decreased periph-
eral perfusion and pale mucous membranes. An example
is traction on the ovarian ligament during ovariohysterec-
tomy in a bitch. Preanaesthetic administration of an anti-
cholinergic may prevent bradycardia but may also obscure
heart rate responses to painful stimuli.
Anaesthetic gas analysers
The anaesthetic gas analyser measures the concentration
of inhalation anaesthetic agent in inspired and expired
gases (Fig. 2.5). The gases are sampled at the junction of
the endotracheal tube and breathing circuit by continuous
aspiration of gases at a rate of 150 mL/min to a monitor
placed at some distance from the patient. To assess the
depth of anaesthesia, the end-tidal concentration of inha-
lation agent is measured (alveolar concentration is meas-
ured at the end of exhalation) and compared with the
Minimum Alveolar Concentration (MAC) value for that
inhalant anaesthetic and species (Table 2.2). Using MAC
for monitoring depth of anaesthesia is not precise as MAC
is only an approximation of the predicted response in 50%
of a population and MAC is decreased in very young and
in old patients. Higher than MAC values will be required
to prevent movement in all patients, and to block auto-
nomic responses and increases in cortical electrical activity
in response to a painful stimulus (March & Muir, 2003a),
usually 1.2–1.5 times MAC, when anaesthesia is main-
tained almost entirely by inhalation agent. Less than MAC
value may be sufficient when the patient is receiving con-
tinuous or intermittent administration of an adjunct
agent(s) such as an opioid, lidocaine, ketamine, propofol,
 Patient monitoring and clinical measurement Chapter 2

Figure 2.5  This gas analyser (Capnomac UltimaTM, Datex-Engstrom Inc., Tewksbury, Maryland, USA) is monitoring a 27 kg
female English Bulldog that was premedicated with glycopyrrolate and butorphanol and anaesthesia induced with propofol.
She has been breathing oxygen and isoflurane at a vaporizer setting of 2.5% for 5 minutes. The monitor indicates that the
inspired (Fi) isoflurane concentration is less than the vaporizer setting and that the end-tidal (ET) isoflurane concentration is
less than MAC value.

or medetomidine/dexmedetomidine. For these animals, EEG and Bispectral index

the anaesthetic administration must be adjusted according
to observation of reflexes and lack of significant cardiovas-
cular response to surgical stimulus.
It should be noted that the gas analyser also accurately
measures inspired anaesthetic concentration, which may
be substantially lower than the vaporizer setting in
rebreathing systems during anaesthesia in large dogs,
horses and ruminants (see Fig. 2.5). A situation may arise
where administration of an anaesthetic agent may be inad-
equate despite an apparently adequate vaporizer setting.
In a retrospective study of equine anaesthesia, it was found
that horses were four times more likely to move during
anaesthesia when an anaesthetic agent analyser was not
used (Parviainen & Trim, 2000).
Some monitors using the principles of infrared absorp-
tion spectrometry cannot be used for horses or ruminants
as they will measure exhaled methane and record the con-
centration as halothane, for example the Datex Capnomac/
Normac (Taylor, 1990). There may be minimal effect with
isoflurane but negligible with sevoflurane and desflurane.
Analysers that use higher wavelengths of infrared light
should be unaffected by methane (Moens et al., 1991).
The subject of encephalogram (EEG) guidance to depth of
anaesthesia has been discussed in Chapter 1 and Murrell
and Johnson (2006) have published a review of the tech-
niques using bispectral index and somatosensory evoked
potentials for assessment of pain in animals.
Intraoperative awareness occurs when a patient becomes
conscious during general anaesthesia. Significant psycho-
logical effects have been identified in humans after epi-
sodes of awareness that later are associated with changed
behaviour (Apfelbaum et al., 2006). The American Society
of Anesthesiologists (ASA) task force identified certain
procedures and anaesthetic techniques during anaesthesia
of human patients that may be associated with intraopera-
tive awareness and these included caesarian section,
cardiac surgery, trauma surgery, rapid-sequence induction,
total intravenous anaesthesia, and use of reduced anaes-
thetic drug dosages with or without neuromuscular paraly-
sis. Awareness has been reported in the absence of
tachycardia or hypertension. Nonetheless, clinical tech-
niques such as observation for lack of movement, the
palpebral reflex, and other monitors are useful to assess
anaesthetic unconsciousness.

25
Section 1 Principles and procedures
Monitoring of brain electrical activity has clinical appli-
cation and a number of monitors have been developed.
Various signal processing algorithms can be applied to the
frequency, amplitude, and latency of the EEG to generate
a number. This number, or ‘index’, is scaled 0 to 100 with
a value of 100 associated with wakefulness and 0 referring
to an isoelectric EEG. One monitor, the Bispectral Index
(BIS) has become the one most used. BIS is a proprietary
algorithm based on a large number of EEG recordings
taken during human anaesthesia that converts a single
channel frontal EEG to an index 0 to 100, of which a range
of 40 to 60 is reported to be associated with anaesthesia
without awareness or decreased incidence of awareness
when compared with anaesthesia monitored by other
means. It has also been proposed that targeting a specific
BIS index range may avoid excessive depth of anaesthesia
such that the patients enter recovery at a lighter plane of
anaesthesia with less respiratory depression and experi-
ence shorter recovery times. Concerns are that the numeric
value may be influenced by other factors such as bolus
administration of anaesthetic drugs, electrocautery, or cer-
ebral hypoxia, and may not accurately reflect the depth of
anaesthesia and initiate an inappropriate change in anaes-
thetic administration. Further, that use of a brain function
monitor may result in excessively deep anaesthesia to the
detriment of organ blood flow and function. Several pro-
spective multicentre controlled trials involving human
patients have evaluated the role of BIS monitoring in
determining depth of anaesthesia and reliability for pre-
vention of awareness during intravenous or inhalant
general anaesthesia (Bruhn et al., 2005; Avidan et al.,
2008; Ellerkmann et al., 2010; Kertai et al., 2011). The
results thus far have not supported a unified view, however,
it appears that BIS monitoring may have an impact on
incidence of awareness but not influence the amount of
anaesthetic agents administered or influence postoperative
mortality.
The use of BIS monitoring is being investigated in
animals. Electrodes manufactured for human patients
may require modification and reconfiguration to adjust
to the differences in shape and nature of animals’
heads. Decreasing BIS values have been recorded with
increasing concentrations of isoflurane and sevoflurane
in dogs and cats (March & Muir, 2003b; Lamont et  al.,
2004; Campagnol et  al., 2007). Burst suppression of the
EEG, characterized by periods of low amplitude waves
interspersed with bursts of high amplitude waves, occurs
during deep anaesthesia (2.0 MAC) resulting in paradoxi-
cal increases in BIS values (Lamont et  al., 2004; Henao-
Guerrero et  al., 2009). Concern has been expressed that
the BIS range for animals may not be the same as the
accepted range for anaesthesia in humans. A study in
experimental cats found that pedal and palpebral reflexes
were lost at BIS values 66 to 67, however, these values
may not be associated with a surgical depth of anaesthesia
(March & Muir, 2003b). BIS values increased significantly
26
in anaesthetized cats in response to a noxious stimulus
(March & Muir, 2003a). The relationship between BIS
and clinically evaluated anaesthetic depth in dogs was
found to be unsatisfactory (Bleijenberg et  al., 2011).
Although BIS decreased significantly between sedation
and anaesthesia, BIS values overlapped significantly
between light and deep anaesthesia. Similarly, in horses
anaesthetized with isoflurane, BIS monitoring was not
found to be a useful predictor of depth of anaesthesia
or warning of patient movement (Haga & Dolvik, 2002).
In another investigation in horses anaesthetized with
sevoflurane and undergoing a variety of surgical proce-
dures, the mean BIS value was >60 and changes in BIS
values were not detected in all horses that moved during
anaesthesia (Belda et  al., 2010). Further investigations are
needed to define the recommendations for BIS monitor-
ing in veterinary medicine.
Another monitor used in human anaesthesia is the
cerebral state index (CSI) monitor. The CSI is not depend-
ent on algorithms derived from human patients (see
Chapter 1) and, consequently, was hoped to be more reli-
able in domestic species. However, Ribeiro et al. (2009)
investigating induction of anaesthesia with propofol in
dogs concluded that CSI monitoring was not consistent
with the clinical observations observed in different stages
of depth of anaesthesia.
Monitoring the circulation
The heart rate, pulse rate and rhythm, tissue perfusion, and
blood pressure of all anaesthetized animals should be
assessed at frequent regular intervals (Table 2.3).
Pulse rate and rhythm
The peripheral pulse rate and rhythm may be counted by
palpation of a peripheral arterial pulse, such as the femoral
artery in dogs and cats, lingual artery in dogs (Fig. 2.6),
facial, median or metatarsal arteries in horses (Fig. 2.7),
and femoral, median, or auricular arteries in ruminants
and pigs. The pulse rate and rhythm can also be deter-
mined from the audible sound of blood flow from a
Doppler ultrasound probe (see later) and as a digital
number and waveform generated by a pulse oximeter. The
physiological relationship between the heart sounds, ECG,
and arterial pulse is depicted in Figure 2.8. Pulse deficits
are identified by palpation of a peripheral pulse that has
an irregular rhythm, pauses, or a pulse rate that is less than
the heart rate determined by auscultation of the heart
using a stethoscope. Pulse deficits may be associated with
any of several cardiac dysrhythmias, such as sinoatrial
heart block, atrioventricular heart block, premature ven-
tricular depolarizations, or atrial fibrillation, and will
require an ECG for diagnosis.
 Patient monitoring and clinical measurement Chapter 2

Table 2.3  Methods of assessing cardiovascular

function in anaesthetized clinical patients

Heart rate and rhythm

Transverse
Palpation of arterial pulse
Oesophageal stethoscope
facial artery
Electrocardiogram
Blood pressure monitor
Pulse oximeter

Tissue perfusion
Mucous membrane colour
Capillary refill time
Blood pressure
Bleeding at operative site
Observation of intestine colour
Urine output

Arterial blood pressure

Palpation of arterial pulse
Facial artery
Doppler ultrasound method
Oscillometric method
Arterial catheterization Lateral
nasal artery
Blood volume
Figure 2.7  Sites for palpation of arterial pulse or catheter
Pulse pressure variation placement for blood pressure measurement in horses.
Central venous pressure
Assess blood loss
Aortic Aortic
valve valve
opens closes
AA

Aortic Aortic
valve valve
closes R opens

P T
BB
Q
S
1st 2nd 3rd
CC

Systole Diastole Systole

Figure 2.8  Relationship between aortic pulse (A), ECG (B),
and heart sounds as auscultated with a stethoscope (C).
Modified from Guyton, 1986.

Heart rate monitors

Figure 2.6  The lingual artery is easily palpated in dogs
midline on the ventral surface of the tongue, adjacent to the
nerve and between the lingual veins. The arrow in the
photograph points to a line drawn adjacent to the lingual
artery.
Heart rates measured before anaesthesia are greatly influ-
enced by the environment. Means (standard deviations,
range) of heart rates obtained by palpation from healthy
cats at home were 118 mean (SD 11, range 80–160) beats
per minute compared with mean 182 (SD 20, range 142–
222) when obtained by electrocardiography in the veteri-
nary hospital (Sawyer et al., 1991).
The lowest acceptable heart rates during anaesthesia are
controversial, but reasonable guidelines are 55 beats/min

27
Section 1 Principles and procedures
Figure 2.9  The oesophageal stethoscope. It may be used with a single earpiece or with a conventional stethoscope
headpiece. This is a simple and inexpensive monitoring device for heart beat and respiratory activity.
for large dogs, 65 beats/min for adult cats, 26 beats/min
for horses, and 50 beats/min for cattle. Heart rates should
be higher in small breed dogs and much higher in imma-
ture animals. Heart rates may be less than these values
when medetomidine/dexmedetomidine has been admin-
istered. It should be remembered that heart rate is a major
determinant of cardiac output, consequently, bradycardia
should be treated if blood pressure and peripheral per-
fusion are also decreased.
Oesophageal stethoscope
The oesophageal stethoscope (Fig. 2.9) is a simple method
of monitoring heart rate in dogs and cats. This monitor
consists of a tube with a balloon on the end which is
passed dorsal to the endotracheal tube and into the
oesophagus until the tip is level with the heart. The open
end of the tube is connected to an ordinary stethoscope
headpiece, to a single earpiece that can be worn by the
anaesthetist or surgeon, or connected to an amplifier that
makes the heart sounds audible throughout the room.
This monitor provides only information about heart rate
and rhythm; the intensity of sound is not reliably associ-
ated with changes in blood pressure or cardiac output.
Other electronic oesophageal probes are available to
provide heart rate, and some also may produce an ECG
and oesophageal temperature.
28
Electrocardiography
Heart rate and rhythm can be obtained from an ECG using
standard limb leads in small animals, clip electrodes and
ECG paste or gel, and selecting ECG Lead II on the oscil-
loscope (Fig. 2.10A). Poor contact of the electrodes to the
skin from hair bunched in the clips, or close proximity to
another electrical apparatus, such as the hot water circulat-
ing pad, can result in electrical interference that obscures
the ECG. The leads should not be placed over the thorax
as breathing will move the electrodes and result in a wan-
dering ECG baseline (Fig. 2.10B).
A frequently used monitor lead in equine anaesthesia is
the ‘base-apex’ lead. The right arm electrode is clipped on
the neck in the right jugular furrow and the left arm elec-
trode is passed between the forelimbs and clipped at the
apex of the heart over the left fifth intercostal space several
inches from the midline. The left leg electrode is clipped
on the neck or on the shoulder. Good electrical contact is
achieved with alcohol or electrode paste. Lead I is selected
on the electrocardiograph and the normal configuration
includes a negative R wave (see Fig. 2.10C). A bifid P wave
is frequently observed in the normal equine ECG. Sinus
arrhythmia in dogs and cats is abolished when atropine
or glycopyrrolate has been administered. Other arrhyth-
mias, for example second degree atrioventricular heart
block and ventricular premature depolarizations (VPD) or
 Patient monitoring and clinical measurement Chapter 2

Figure 2.10  (A) Normal lead II ECG from a Labrador during inhalation anaesthesia. (B) ECG with a wandering baseline
induced by movement of leads as the dog breathes. The bottom trace is arterial blood pressure. This dog has a heart rate of
114 beats per minute, systolic arterial pressure of 96 mmHg, diastolic pressure of 46 mmHg, and mean pressure of 61 mmHg.
(C) Normal base apex ECG and blood pressure recorded from a horse anaesthetized with isoflurane.

premature ventricular complexes (PVC), may or may not

require specific treatment (see Chapter 21).
There is a high incidence of sinus arrhythmia and first
and second degree atrioventricular (AV) heart block in
conscious unsedated horses (Robertson, 1990). In con-
trast, AV block during anaesthesia is uncommon except
when the horse has been premedicated with detomidine,
or supplemental intravenous injections of xylazine are
given during anaesthesia. The appearance of this arrhyth-
mia during anaesthesia on any other occasion is cause for
concern as this rhythm may progress within a few minutes
to advanced heart block (P waves only, no ventricular
complexes) and cardiac arrest. Atrial fibrillation and PVCs
occur rarely in horses but may require specific treatment
if associated with hypotension.
Tissue perfusion
Evaluation of tissue perfusion can be done by considering
gum or lip mucous membrane colour, the capillary refill
time, and the blood pressure. High mean arterial pressure
does not guarantee adequate tissue perfusion. For example,
when blood pressure increases during anaesthesia in
response to a surgical stimulus, cardiac output may be
decreased due to increased afterload from peripheral
vasoconstriction.
Tissue perfusion is usually decreased when the gums are
pale, rather than pink, sometimes when very pink, and the
capillary refill time (CRT) exceeds 1.5 seconds, or the
mean arterial pressure (MAP) is less than 60 mmHg.
When MAP is above 60 mmHg, palpation of the strength

29
Section 1 Principles and procedures
Abbreviations
NIBP Non-invasive blood pressure
IBP Invasive blood pressure
SAP Systolic arterial pressure
DAP Diastolic blood pressure
MAP Mean arterial pressure
CVP Central venous pressure
CO Cardiac output
of the peripheral pulse and observation of oral membrane
colour and CRT should be used to assess adequacy of
peripheral perfusion and cardiac output. During laparot-
omy, intestinal colour should be bright pink and intestines
that are pale pink, white, or grey may be an indicator of
inadequate tissue perfusion. Measurement of central
venous O2 saturation may provide further information in
sick patients, as described later.
Arterial blood pressure
Systolic (SAP), mean (MAP), and diastolic (DAP) arterial
pressures in awake healthy animals are approximately
125–160 mmHg, 90–110 mmHg, and 75–95 mmHg,
respectively. Excepting when premedication has included
detomidine or medetomidine or when anaesthesia was
induced with ketamine or tiletamine, arterial blood pres-
sure is decreased from the awake value during anaesthesia.
Arterial blood pressure is lower in paediatric patients than
in mature animals. For example, healthy 5- or 6-day-old
foals anaesthetized with isoflurane had an average MAP of
58 mmHg. When the same foals were reanaesthetized 4–5
weeks later, the average MAP had increased to 80 mmHg,
with a corresponding decrease in cardiac index (Hodgson
et al., 1990).
Hypotension may be defined as MAP less than 65 mmHg
in mature animals. A MAP as low as 60 mmHg may be
allowed in dogs and cats provided that the mucous mem-
brane colour is pink and CRT is 1 second. This combina-
tion of values may occur during inhalation anaesthesia at
the time of minimal stimulation during preparation of the
operative site and before the onset of surgery. MAP is
not usually allowed to fall below 65–70 mmHg for any
length of time in anaesthetized horses because of the
increased risk for postanaesthetic myopathy. When hypo-
tension is documented, appropriate treatment can be
instituted, such as decreasing anaesthetic depth or com-
mencing or increasing the intravenous administration of
fluids or administration of a vasoactive drug such as
dopamine, dobutamine, or ephedrine. The outcome of
untreated severe or prolonged hypotension may be unex-
pected cardiac arrest during anaesthesia or neurological
deficits, blindness or renal failure after recovery from
anaesthesia.
30
Myths about blood pressure in anaesthetized
animals
If you can feel a strong pulse the blood pressure is
adequate
Heart rate will increase during hypotension
An approximate estimate of blood pressure can be made
from palpation of a peripheral artery. However, strength
of a palpated pulse is determined by the pulse pressure
(difference between systolic and diastolic pressures) and,
in states associated with vasodilatation, a peripheral pulse
can be palpated at MAP as low as 40 mmHg so that, in
some cases, palpation alone does not suggest the urgency
for treatment. The turgidity of the artery will provide
further information because pressure is likely to be low if
the artery is soft or collapsible rather than solid like a
pencil. Bear in mind that it is not uncommon for heart
rates to be within an accepted normal range while blood
pressure is low or decreasing (Fig. 2.11).
Measurement of blood pressure can be made easily;
equipment cost varies. The investment in time and money
is worthwhile in animals at risk for hypotension, such as
small animals and horses anaesthetized with inhalation
agents, and in animals with abnormalities likely to give
rise to complications during anaesthesia. The least expen-
sive techniques are the Doppler ultrasound technique in
dogs and cats, and direct blood pressure measurement
using an anaeroid manometer in horses, however, pur-
chase of a unit that monitors more than one parameter,
for example, ECG, blood pressure, and temperature, is
more economical than acquiring monitors individually.
Doppler ultrasound for indirect measurement
of blood pressure
Hair is first clipped from the skin on the palmar surface
of the paw of dogs and cats (Fig. 2.12). A probe covered
with contact gel is placed over the artery and taped in place
with the electrical lead pointing down towards the toes
(Fig. 2.13). Ultrasound waves emitted from one of the two
piezoelectric crystals embedded in the probe pass through
the skin and deeper tissues. A structure that is stationary
will reflect sound back to the second crystal without any
frequency change (Stegall et al., 1968). Moving objects,
such as erythrocytes and the artery wall, will reflect some
of the sound at a different frequency (Doppler-shift). The
change in frequency can be heard through a loudspeaker
as an audible swooshing sound with each pulse.
A cuff is wrapped snugly around the extremity proximal
to the probe, in dogs and cats with the centre of the inflat-
able part of the cuff, or an arrow or dot, on the medial
aspect of the limb and the air tube positioned on the distal
end of the cuff. The cuff is connected to an anaeroid
 Patient monitoring and clinical measurement Chapter 2

TIME 135 150 165 180 195 210 225

O2 L/min 1
Vaporizer 2.2 0 1.5 1
Inspired Iso
End tidal Iso 1.6 1.0
End tidal CO2 28
32
SpO2 98
140

120 1

100

80

60
Systolic
40
Heart rate 2
20
C C S
Resp rate
10

Figure 2.11  Blood pressure (Doppler systolic) decreased without a change in heart rate after this hound was turned over
(Arrow 1) during anaesthesia. Blood pressure continued to decrease after isoflurane was discontinued. Infusion of dobutamine
(Arrow 2) produced a rise in blood pressure.

A B
3
1 Figure 2.13  Doppler-shift pulse detector. One piezoelectric
4
2 crystal emits incident ultrasound signal while the other
5 receives the reflected signal from cells in flowing blood. The
6 frequency shift between the incident and reflected sound is
converted to audible sound.

manometer and a bulb for manual inflation of the cuff

Figure 2.12  Sites for application of the Doppler probe for
indirect measurement of arterial blood pressure in dogs. 1 & 2:
Ulnar artery on the caudal surface of the forelimb, above
and below the carpal pad; 3: cranial tibial artery on the
craniolateral surface of the hindlimb; 4 & 5: saphenous artery
on the medial surface of the flexor tendons and on the plantar
surface of the paw proximal to the foot pad; 6: dorsal pedal
artery; 7: coccygeal artery on the ventral surface of the tail.
with air (Fig. 2.14). In horses, the cuff is wrapped around
the base of the tail with the cuff air bladder centred over
the ventral surface of the tail. The probe is taped distal
to the cuff over the coccygeal artery in the ventral midline
groove. The coccygeal artery can be used for this technique
in adult cattle but the results are not reliable. In foals, the
probe and cuff are commonly attached to the tail. In foals

31
Section 1 Principles and procedures
Figure 2.14  Measurement of arterial pressure in a dog by
taping a Doppler probe over an artery distal to the carpal
pad so that audible sounds of arterial pulses are emitted
from the box. A blood pressure cuff is applied higher up the
limb and the anaeroid manometer attached to the cuff is
used to identify systolic and diastolic pressures.
and small ruminants in lateral recumbency, the probe can
be taped over the metatarsal artery on the lateral surface
of the hind limb or the common digital artery on the
medial side of the forelimb distal to the carpus. The cuff
is secured around the limb above the hock or carpus and
positioned level with the sternum. In pigs, the probe is
most reliable when taped over the common digital artery
on the caudomedial aspect of the forelimb. The cuff
should be placed between the carpus and the elbow but,
because of the triangular shape of the forearm, it may be
unable to occlude blood flow when inflation of the cuff
causes it to slip down over the carpus. For all animals, the
width of the air bladder within the cuff is important for
accuracy; a bladder that is too narrow will overestimate
blood pressure and one that is too wide will underesti-
mate it. The cuff (air bladder) width should be 40% of the
circumference of the extremity and the leg positioned so
32
that the cuff is level with the manubrium. Furthermore, a
cuff that is attached too loosely or slips down the extrem-
ity and becomes loose, or situated over a joint such as the
carpus will result in an erroneously high value.
To measure blood pressure, the cuff is inflated to above
systolic pressure to occlude the artery and no sound is
heard. The pressure in the cuff is gradually released until
the first sounds of blood flow are detected at systolic pres-
sure. As additional pressure is released from the cuff,
diastolic pressure is heard as a change in character of
sound from a one or two beat sound to a multiple beat
sound, to a muffling of sound, or to a growl. This will
occur 15–40 mmHg below systolic pressure. The sounds
associated with diastolic pressure are well defined in some
animals but not at all clear in others. In some animals, a
first muffling of beat signals may occur 10–15 mmHg
above the true diastolic pressure. In this event, the second
change in beat signal will be more abrupt or distinct. Mean
pressure can be calculated as one third of the pulse pres-
sure (systolic−diastolic) plus diastolic pressure.
A decrease in intensity of the pulsing sound, when the
attachment and setting have been unchanged, is a reliable
indication of decreased blood flow. Furthermore, changes
in cardiac rhythm are easily detected by listening to this
monitor.
The Doppler ultrasonic method was observed to provide
both overestimated and underestimated values over a wide
range of systolic pressures in conscious and anaesthetized
dogs, with a tendency for overestimation when MAP
<80 mmHg and underestimation at high pressures
(Haberman et al., 2006; Bosiack et al., 2010). An investiga-
tion in cats comparing the Doppler ultrasonic method,
using a cuff placed halfway between the carpus and the
elbow, with measurements obtained from a femoral artery
catheter revealed that the indirect method consistently
underestimated systolic pressure by an average of
14 mmHg (Grandy et al., 1992). Caulkett et al. (1998)
also determined that the Doppler method both overesti-
mated and underestimated systolic blood pressure in
anaesthetized cats but that it proved to be an accurate
predictor of MAP. Using this technique of measuring
blood pressure in mature horses using a cuff width 48%
of the circumference of the tail (bladder width 10.4 cm)
systolic pressure was underestimated and diastolic pres-
sure overestimated by approximately 9% (Parry et al.,
1982). In another investigation, measurements of systolic
arterial pressure in horses anaesthetized in dorsal recum-
bency with halothane using a cuff 41% of the tail circum-
ference was reasonably accurate but, in 5% of the horses,
this technique had an error range of ±20 mmHg (Bailey
et al., 1994).
Oscillometry for indirect measurement
of blood pressure
Devices that non-invasively measure peripheral blood
pressure using the oscillometric method operate by
 Patient monitoring and clinical measurement Chapter 2

Figure 2.15  Non-invasive measurement of blood pressure by oscillometry. The cuff should be positioned level with the
manubrium or sternum, and for big dogs it may be necessary to hold the limb elevated during measurement to achieve
alignment. A Doppler ultrasound probe is also attached to the limb of this dog for audible recognition of blood flow.

automatically inflating a cuff placed around an extremity,
either above or below the carpus, above or below the hock,
or the tail (Fig 2.15). The monitor measures and records
the amplitude of pressure changes in the cuff caused by
pulses in underlying arteries. The cuff is inflated to above
systolic pressure and deflated slowly. The pressure oscilla-
tions in the cuff start small and increase to a maximum
value (corresponding with MAP) and then decrease. Each
monitor uses fixed or variable parameter identification
points based on the MAP value to calculate electronically
systolic and diastolic pressures. The algorithm determin-
ing systolic and diastolic pressures varies between models
and thus measurement results are not the same for all
models. There is a also small difference in the recorded
MAP and MAP calculated from the systolic and diastolic
pressures using the formula MAP = diastolic pressure +
0.33 (systolic − diastolic) and this value is dependent on
the measurement device (Kiers et al., 2008). Values for
SAP, DAP, MAP, and heart rate are digitally displayed and
the monitor can be programmed to measure automatically
at a specified time interval. The cuff should be situated
approximately level with the heart (manubrium or
sternum if in lateral recumbency) for accurate measure-
ment. Artefactual pressure changes induced in the cuff by
movement of the extremity, for example, during prepara-
tion of the surgical site, will either induce abnormal read-
ings or prevent the monitor from obtaining a measurement
(Haberman et al., 2006; Bosiack et al., 2010). Closest cor-
relations between direct and indirect measurements have
been measured using cuff widths of 40% of the circumfer-
ence of the animal’s leg or tail.
By far the highest number of published articles compar-
ing NIBP and IBP measurements have been in dogs. Not
all investigations have produced similar results, in part
influenced by use of different models from several manu-
facturers, measurement in awake versus anaesthetized
animals, increased variability attributed to haemodynamic
alterations imposed by disease, differences in size and
gender, sites of measurement, patient body position, phar-
macological methods used to alter blood pressure, and the
investigators varied definitions of hypotension or hyper-
tension. The ‘take home’ message is that NIBP does not
accurately predict IBP all of the time and that no treatment
decision should be made based solely on one measure-
ment. Investigations of specific models have employed
the average of three to six consecutive readings taken
30–60 seconds apart to increase accuracy. Frequently
during anaesthesia, the site of surgery and accessibility
dictates the site for application of the cuff. Different sites
have been investigated with the result that the forelimb
in dogs was determined to be more accurate when com-
pared with lingual artery pressure and the hind limb
more accurate when compared with dorsal pedal artery
pressure (McMurphy et al., 2006), no difference between

33
Section 1 Principles and procedures
measurements was recorded between the fore and hind
limbs (Sawyer et al., 1991), or that the tibial or coccygeal
arteries provided better correlation than the metacarpal
artery when compared with aortic or anterior tibial artery
pressure (Sawyer et al., 2004; Haberman et al., 2006).
Most oscillometric monitors provide a reasonable approx-
imation of MAP in normotensive animals.
The greatest concern during most anaesthetic episodes
is the accurate identification of hypotension to avoid
cardiac arrest or postoperative organ malfunction. The
Surgivet V60046, with the cuff placed distal to the hock,
provided accurate information for MAP in normotensive
and hypotensive dogs, with 90.6% of the dogs with MAP
<70 mmHg being accurately diagnosed as hypotensive
(Deflandre & Hellebrekers, 2007). The monitor was less
accurate at high pressures. The Cardell 9401, DINAMAP
(Device for Indirect Noninvasive Automatic Mean Arterial
Pressure) 8100, DINAMAP 8300 and PetMAP overesti-
mated pressures during hypotension (Sawyer et al., 1991;
Meurs et al., 1996; Bosiack et al., 2010; Shih et al., 2010),
and did not reliably predict the severity of hypotension in
animals with acute haemorrhage or in critically-ill patients
in the ICU. Wernick et al. (2010) compared measurements
in anaesthetized dogs between pressures recorded from
the dorsal pedal artery and from a cuff around the ante-
brachium using the DINAMAP 8300. The DINAMAP
slightly underestimated SAP and DAP and overestimated
MAP; comparisons that fell just short of the validation
requirement proposed by the American College of Veteri-
nary Internal Medicine (Brown et al., 2007). In contrast,
the DINAMAP 8300 underestimated all BP parameters in
awake experimental Beagles, and to a greater extent at high
pressures generated by administration of phenylephrine
(Haberman et al., 2006). Comparisons with the Cardio-
cap II in clinical canine patients using premedication to
alter blood pressure (acepromazine or medetomidine)
generated a smaller bias than previously reported (Sawyer
et al., 2004; McMurphy et al., 2006) but greater limits of
agreement (variability) that was attributed to variation in
clinical population (MacFarlane et al., 2010).
In clinical practice, it may be necessary to identify hyper-
tension before anaesthesia and to measure accurately high
pressures during anaesthesia in patients at risk, such as
phaeochromocytoma, renal or endocrine disease. Oscil-
lometric methods tend to underestimate systolic blood
pressures during hypertension (Haberman et al., 2006;
McMurphy et al., 2006; Deflandre & Hellebrekers, 2007;
Bosiack et al., 2010), consistently underestimate MAP or
DAP (Haberman et al., 2006), overestimated MAP or DAP
(Bosiack et al., 2010), or underestimated SAP and DAP
with close agreement with MAP (McMurphy et al., 2006).
The Cardell 9301V with 2.5 cm-wide neonatal pressure
cuff placed around the forelimb above the carpus, with the
monitor set at ‘small cuff’ mode has been evaluated in cats
(Pedersen et al., 2002). Low pressure MAP <60 mmHg
was achieved by increasing depth of anaesthesia with
34
isoflurane and high pressures MAP >140 mmHg were
created by administration of medetomidine. Mean differ-
ences between NIBP and IBP were <5 mmHg for MAP and
DAP in all pressure ranges; SAP differences increased
as pressure increased from hypotension to hypertension
resulting in underestimation of SAP. The DINAMAP had
good correlation with IBP systolic pressure in anaesthe-
tized cats (Caulkett et al., 1998), however, the Datascope
Passport did not accurately estimate direct blood pressure
in cats (Branson et al., 1997).
In horses, the oscillometric method of blood pressure
measurement is used when direct measurement of arterial
pressure is not possible, for total intravenous anaesthesia,
and for awake animals. The cuff is wrapped around the tail
of mature horses and foals or around the hind limb near the
metatarsal artery in foals. The cuff should not be wrapped
tightly. Some investigators have recommended that the tail
cuff be placed close to the base of the tail but, in this
author’s opinion, more accurate readings are obtained with
the cuff applied approximately 10 cm from the base of the
tail, where the tail diameter is constant for the length of the
cuff. In standing horses, cuff placement may be higher than
the atrium, resulting in a measurement that is lower than
the actual pressure. Early investigations of the DINAMAP
confirmed accurate and clinically useful values for arterial
pressure using a cuff width 24% of the tail circumference in
ponies (Geddes et al., 1977) and 25–35% in horses
(Latshaw et al., 1979; Muir et al., 1983). However, meas-
urements were inaccurate at heart rates of less than 25
beats/minute. Our experience using a Model 8300
DINAMAP and a cuff width 35–40% of the tail circumfer-
ence ratio (child or small adult cuff for a mature horse
depending on tail thickness and the amount of hair) has
been that MAP value obtained from this monitor is usually
the same as that obtained by direct blood pressure measure-
ment. Occasionally, the DINAMAP recorded pressures
10–20 mmHg higher than the true MAP. An evaluation of
the Cardell Model 9402 and the DINAMAP Pro 100 in
anaesthetized foals of less than 7 days of age using cuff sizes
recommended by the manufacturers revealed that both
monitors had similar performance (Giguère et al., 2005b).
Analysis of MAP values confirmed acceptable accuracy with
the cuffs on the tail or metatarsus for conditions of normo-
tension and hypotension, although the Cardell was most
accurate over the coccygeal artery and the DINAMAP over
the metatarsal artery. Cuffs placed over the median artery
produced less accurate values and wider variability. This
study also confirmed that blood pressure did not correlate
well with cardiac output, i.e. a good MAP does not guaran-
tee that cardiac output is also acceptable. In summary,
indirect method of measurement of blood pressure pro-
vides useful information in most horses, but may produce
erroneous values in a small number. Consequently, blood
pressure should be measured by direct means whenever
possible in horses at risk of developing low blood pressure,
for example, during inhalation anaesthesia.
 Patient monitoring and clinical measurement
Standards have been set for automated sphygmoma-
nometers in human medicine by several organizations,
including the British Hypertension Society, the Associa-
tion for the Advancement of Medical Instrumentation
(AAMI) and the American National Standards Institute,
Inc. (ANSI). Devices validated for use in humans must
have a correlation of ≥0.9 across a range of measurements
with specific % of readings to be within 5, 10, or 15 mmHg
of the standard measurement. Requirements for validation
were tightened in 2011. These standards have been met for
MAP at low and normal pressures in dogs with the Surgivet
V60046 (Deflandre & Hellebrekers, 2007), for MAP and
DAP in cats with the Cardell 9301V (Pedersen et al., 2002),
and for MAP in foals using the Cardell 9402 and DINAMAP
Pro 100 (Giguère et al., 2005b). For the most part, oscil-
lometric blood pressure monitors provide useful informa-
tion for management of the clinical patient. Trends in
pressures can be used to direct management of anaesthesia
and, although hypotension may not be accurately diag-
nosed, a decrease in measurements to low values should
be a warning that action should be taken. A single abnor-
mal measurement should be confirmed by taking two
more readings. Failure of the monitor to achieve a reading
(‘timed out’) when it had just previously been recording
may indicate a change in peripheral blood flow. It must
be remembered that although on average there is reason-
able correlation between direct and indirect pressure
measurements, in individual patients the difference in
readings can be up to 20 mmHg and a patient may not be
identified as having a MAP outside an accepted range.
Therefore, NIBP readings must be assessed together with
other observations of cardiovascular performance and
depth of anaesthesia.
High-definition oscillometry
In contrast to previously described oscillometric tech-
niques, high-definition oscillometric (HDO) technology
discriminates between pressure waveform changes that are
characteristic for systolic, mean, and diastolic pressures.
The technology allows much more rapid assessments that
minimize the impact of outside factors, and is able to
accommodate fast heart rates and weak pulse signals. The
expectation is for increased accuracy at high and low
blood pressures and increased reliability for use in ill
patients. In anaesthetized dogs, comparison between IBP
measured at the dorsal pedal artery and a high-definition
oscillometric device, Memodiagnostic MD_15/90 Pro,
revealed that values for SAP, MAP, and DAP were all over-
estimated by HDO and the overestimation increased for
SAP and DAP with increasing pressures (Wernick et al.,
2010). The precision exceeded the 15 mmHg limit required
for validation and only 50–60% of readings were within
10 mmHg. In a group of conscious experimental Beagles
with implanted aortic devices for telemetry of blood pres-
sures, measurement of pressures from a cuff around the
base of the tail using HDO revealed that MAP most closely
Chapter 2
paralleled the telemetered pressures (Meyer et al., 2010).
The standards set by AAMI were not met in this study. The
authors noted that the mean standard deviations were
substantially decreased by use of six averaged measure-
ments at any time point compared with a single
measurement.
Direct measurement of blood pressure
Measurement of arterial blood pressure directly is accom-
plished by insertion of a 20 gauge, 22 gauge or, in very
small animals, a 24 gauge catheter aseptically into a
peripheral artery; the dorsal pedal, anterior tibial, femoral,
coccygeal, metacarpal, auricular or lingual artery in dogs
(Fig. 2.16), the dorsal pedal, femoral or coccygeal artery
in cats, the lateral nasal, facial, transverse facial, or meta-
tarsal artery in horses (see Fig. 2.7), or an auricular artery
in ruminants, pigs and rabbits (Fig. 2.17). Placement of a
catheter in an artery in most animals is not difficult with
experience. Complications are rare provided there is strict
attention to asepsis during insertion, wrapping to main-
tain cleanliness, use of sterile solutions for flushing, and
appropriate pressure on the artery when the catheter is
removed to avoid a haematoma. The cap or extension
must be secured firmly to the arterial catheter to prevent
accidental disconnection and blood loss. The catheter is
connected by saline-filled tubing to either an anaeroid
manometer (Fig. 2.18) or an electrical pressure transducer
(Fig. 2.19) for measurement of arterial pressure. Either an
air gap or a connector containing a latex diaphragm
Cranial
tibial artery
Dorsal
pedal artery
Figure 2.16  Sites for insertion of arterial catheters on the
cranial aspect of the right hind limb of a dog.
35
Section 1 Principles and procedures

should be maintained next to the anaeroid manometer to

prevent saline entering the manometer and to maintain Fine nylon
sterility. An optional addition to the electrical transducer Anaeroid catheter or
is a continuous flushing device (Fig. 2.20) that can be manometer needle in artery
inserted between the transducer and the artery. This device
is connected to a bag of saline that has been pressurized
to 200 mmHg and will deliver 2–4 mL saline/hour to help Three-way tap
prevent clotting of blood in the catheter. Extension tubing

Plastic tube
6-8 cm long

Drip extension tube

Male Luer
conection
Three-way
taps

20 ml syringe

Drip extension tube

Figure 2.18  Inexpensive apparatus for the direct
Figure 2.17  Ink lines have been drawn over the auricular measurement of mean arterial blood pressure.
arteries in this goat.

Figure 2.19  Direct measurement of blood pressure in a horse using a catheter in the facial artery connected by saline-filled
tubing to an electrical transducer.

36
 Patient monitoring and clinical measurement
Figure 2.20  Continuous infusion valve (c) for attachment to a pressure transducer (b). A pressurized bag of intravenous fluid
(d) is connected to the device to give a continuous infusion of 3 mL per hour. With this particular version, rapid flushing of
the saline-filled tubing (a) to the arterial catheter is achieved by squeezing the tabs (arrow) around the valve.
sold specifically for arterial pressure measurement is non-
distensible to preserve an accurate waveform.
For accurate measurement, the electrical transducer, or
the air–saline junction in the tubing connected to the
manometer, are zero reference points and should be
placed level with the right atrium that approximately cor-
responds to the manubrium; the point of the shoulder or
thoracic inlet when the animal is in dorsal recumbency
or level with the sternum or spine when in lateral
recumbency.
The anaeroid manometer costs very little but provides
only MAP. The needle of the anaeroid manometer deflects
slightly with each beat and the value at the upper deflec-
tion of the needle is slightly less than the MAP value
obtained by direct measurement (Riebold & Evans, 1985).
The electrical transducer provides values for SAP, MAP and
DAP, heart rate, and a waveform that can be observed on
the oscilloscope or paper printout (Fig. 2.21). Values may
be slightly different when recorded from different sites, for
example comparison of lingual artery and dorsal pedal
artery pressures in dogs revealed that systolic pressure was
higher and the diastolic pressure was lower in the pedal
artery (McMurphy et al., 2006). Mean pressures should be
similar in most arteries but systolic pressure increases by
up to 30% and diastolic pressure decreases by 10–15%
with increasing distance of measurement site from the
heart due to enhancement of the peripheral pulse pressure
(Guyton, 1986).
Important advantages of direct measurement of blood
pressure are the reliability of measurement compared with
NIBP, independence from observer error, and the ability
continuously to observe the pressure and immediately
detect an abnormality (Fig. 2.22). Systolic pressure varia-
tion (pulse pressure variation, ‘cycling’) caused by control-
led ventilation is an indication of decreased cardiovascular
function (Fig. 2.23). Artificial ventilation is key to induc-
ing cycling in that the increase in thoracic pressure during
inspiration causes a significant decrease in stroke volume
in situations of decreased venous return to the heart. A
Chapter 2
mmHg
120
80
A B
mmHg dP/dt
120
80
C D
Figure 2.21  Waveforms from direct measurement of the
arterial pressure. (A) Good trace. (B) Recording of the same
pressure but with excessive damping, systolic pressure low,
diastolic pressure high, mean arterial pressure unchanged.
(C) Recording of same pressures but with resonance, systolic
pressure apparently increased while diastolic pressure
reduced, mean pressure unchanged. (D) Illustration of how
left ventricular contractility may be estimated from the rate
of rise of pressure during early systole (dP/dt) while the
shaded area gives an index of stroke volume.
significant relationship has been documented between
pulse pressure variation and volume loss and measure-
ment of pulse pressure variation has been used to predict
responsiveness of a patient by increased cardiac output to
volume loading with IV crystalloid and/or colloid fluid
(Durga et al., 2008; Pizov et al., 2010; Cannesson et al.,
2011). One multicentre study of human patients noted
that approximately 25% of patients with small pulse pres-
sure variation still experienced a clinically significant
increase in cardiac output in response to fluid loading
(Cannesson et al., 2011). Pulse pressure variation has been
determined to be better than measurement of central
37
Section 1 Principles and procedures

1 second 1 minute 1 second

Arterial B.P.
150 mmHg 150 mmHg

0 0

ECG

Figure 2.22  Top: pressure trace from a dog’s femoral artery. Bottom: Lead II electrocardiogram. Circulatory failure from an
overdose of pentobarbital. Note that while the pressure trace shows the circulation to be ineffective, the ECG trace is little
different from normal – heart rate monitors relying on the QRS complex for detection of the heart beat would, under these
circumstances, show an unchanged heart rate and, in the absence of a blood pressure record, encourage the erroneous belief
that all was well with the circulatory system.

A B

Figure 2.23  (A) Variations in the height of systolic arterial pressure and pulse pressures corresponding to positive pressure
ventilation as seen in this arterial waveform of a dog anaesthetized with isoflurane are predictive of decreased preload or
hypovolaemia. Note that hypovolaemia was present even when the arterial pressures were within accepted ranges. (B)
Expansion of blood volume using an IV fluid bolus resulted in improvement in cardiovascular function as demonstrated by
disappearance of systolic pressure and pulse pressure variations increased blood pressure, and decreased heart rate.

venous pressure for optimizing fluid therapy. Not all
animals with hypovolaemia may show systolic pressure or
pulse pressure variations. Each patient with obvious pulse
pressure variation should be evaluated for the potential
adverse effect of volume loading before administration of
IV fluids. It must be remembered that cycling will not be
observed in animals that are spontaneously breathing or
are ventilated with small (6 mL/kg) tidal volumes.
Central venous pressure
The apparatus for measurement of central venous pressure
(CVP) can include a commercially available plastic venous
manometer set or be constructed from venous extension
tubes and a centimetre ruler (Fig. 2.24). A catheter of suf-
ficient length is introduced into the jugular vein and
advanced until its tip lies in the cranial vena cava. The
distance the catheter tip has to be introduced is, initially,
estimated by measurement of length from the jugular vein
to the third rib and, once the catheter is connected to the
manometer, its position may be adjusted until the level of
fluid in the manometer tube moves in time with the ani-
mal’s respiratory movements. In dogs and cats, the intro-
duction of a catheter into the jugular vein is often greatly
facilitated by laying the animal on its side and extending
its head and neck over a rolled up towel or sandbag. Care

38
 Patient monitoring and clinical measurement
Balanced electrolyte
solution with
administration set
Fluid-filled
manometer
calibrated
in cm
3–way stopcock
Manometer connected Zero on scale
to jugular catheter corresponds with
(covered by bandage thoracic inlet
around neck)
Figure 2.24  Schematic diagram of the apparatus for
measurement of central venous pressure.
must be taken to avoid entrainment of air during insertion
of the catheter. Air embolism will occur through an open-
ended catheter that is inserted with the animal in sternal
or standing position or during inspiration in a recumbent
animal. If the catheter is to be left in position for a long
time, it is kept patent with a drip infusion or the catheter
is kept filled with heparin–saline solution (10 units/mL)
between measurements. Readings may be taken at any
time. If an intravenous drip is used, it is turned full on and
the stopcock manipulated first to fill the manometer tube
from the bag or bottle and then to connect the manometer
tube to the catheter. The fall of fluid in the manometer is
observed and should be ‘step-like’ in response to respira-
tory pressure changes. The CVP is read off when fluid fall
ceases.
Central venous pressure may also be measured by
attaching an electrical transducer to the jugular catheter.
Venous pressures being low, the margin of error intro-
duced by inaccuracies in obtaining a suitable reference
point to represent zero pressure may be clinically signifi-
cant. Whatever apparatus is used, the zero of the scale
should be carefully located, either by placing the patient
Chapter 2
and manometer in close proximity or by using a spirit level
to ensure accuracy. The ideal reference point is the mean
pressure in the right atrium but, for practical purposes, the
most appropriate is the sternal manubrium which is easily
located and is related to the position of the right atrium
in all animals, irrespective of body position. Measure-
ments of CVP are not significantly affected by positioning
the animal in right or left recumbency or by catheter size,
although oscillations are more easily observed with a 16
gauge catheter (Oakley et al., 1997).
CVP is used in the evaluation of adequacy of blood
volume, with the normal range being 0–5 cmH2O or
0–4 mmHg in small animals. Hypovolaemia is indicated
when the CVP is less than 0 cmH2O. An increase in pres-
sure above 12 cmH2O or 9 mmHg may be caused by fluid
overload or cardiac failure. A recent study measured mean
CVP of 9.4 ± 3.6 cmH2O in standing horses with their
heads in a neutral position (Norton et al., 2011). Head
height exerted a significant effect on CVP in that the CVP
decreased by 2.0 ± 6.5 cmH2O when the horses’ heads
were elevated and increased by 3.7 ± 5.5 cmH2O when the
heads were lowered to the ground. The authors suggested
to increase accuracy of comparison of measurements to be
made over several hours that the zero reference point be
identified by a small line of clipped hair.
Left atrial pressure (pulmonary arterial
occlusion pressure)
Left heart failure may precede that of the right side and
precipitate pulmonary oedema without a rise in central
venous pressure. The pulmonary arterial occlusion pres-
sure (PAOP) is used as a measure of the left atrial filling
pressure. A balloon-tip catheter is introduced into the
jugular vein and its tip advanced into the heart. Inflation
of the balloon with 0.5 mL air facilitates floating the cath-
eter in the bloodstream into the pulmonary artery and
then the catheter can be advanced until the tip is wedged
in a small pulmonary vessel. The measurement is made
using the same apparatus as is used for the measurement
of central venous pressure or using an electrical pressure
transducer. Care must be taken to ensure that vessel occlu-
sion is not maintained between measurements or pulmo-
nary infarction may occur. If a balloon catheter is used,
the balloon should only be inflated while measurements
are made and, if a simple catheter is used, it should be
slightly withdrawn from the wedged position between
measurements.
Cardiac output
The measurement of cardiac output is not one that has
been routinely carried out in clinical veterinary anaesthe-
sia. Invasive methods are commonly employed in research
and there are minimally invasive and non-invasive
methods available for use in research and clinical patients.
39
Section 1 Principles and procedures
The cost of the equipment, as always, is a limiting factor.
Various sources of inaccuracy are likely to influence results
of cardiac output measurements and personnel using
these techniques should first read relevant literature.
Fick method
The Fick method was one of the earliest methods to be
used to calculate cardiac output (CO) and utilized oxygen
as the indicator. The method used the formula CO = O2
consumption per minute/(arterial O2 content − mixed
venous O2 content) × 100 because the size of a fluid stream
can be calculated when the amount of a substance enter-
ing the stream and the concentration difference between
entry and removal are known (Lake, 1990). This method
has a number of technical difficulties and, more recently,
a non-invasive technique using CO2 has been used in
clinical patients. The non-invasive cardiac output (NICO)
method employs a differential Fick partial rebreathing
technique that eliminates the need to measure mixed
venous CO2 by assuming that the value remains constant
(Jaffe, 1999). A combined mainstream capnometer and
fixed orifice differential pressure pneumotachometer (to
measure flow) adapter is inserted next to the endotracheal
tube adapter (Fig. 2.25). An adjustable (rebreathing) loop
of tubing with an automatic valve is then attached before
connecting the patient to the circle anaesthesia system.
The animal must be on controlled ventilation and the
rebreathing loop is expanded or contracted so that the
volume of the loop matches 35–70% of the ventilator’s
tidal volume setting. The NICO has a 3-minute cycle
within which the rebreathing valve is activated for 35
seconds so that the animal’s breathing is rerouted from
the anaesthesia circle into the rebreathing loop. Typically,
A B
Figure 2.25  (A) Rebreathing circuit of the NICO™ (Novametrix Medical Systems, Inc. Wallingford, CT, USA). (B) NICO™
monitor measuring cardiac output in an anaesthetized dog.
40
the patient’s PaCO2 increases up to 5 mmHg during
rebreathing. Concurrent input from the pulse oximeter
allows the NICO to calculate stroke volume and manual
entry of the patient’s weight produces CO in mL/kg. Accu-
racy of the NICO is unsatisfactory in patients <18 kg
bodyweight (Yamashita et al., 2007). This technique is
contraindicated in any animal for which a small increase
in PaCO2 would be deleterious, such as conditions at risk
for increased intracranial pressure. Cardiac output meas-
urements obtained by NICO are useful to assess trends but
should not be considered as absolute values (Giguère
et al., 2005a).
Indicator dilution method
The principle involves injection of an indicator substance
into a central or peripheral vein and blood is withdrawn
from an artery continuously with a pump and directed
through an electrical cuvette densitometer where the con-
centration of the indicator is measured. This blood is then
delivered back to the patient. The electrical input from the
densitometer is proportional to the indicator concentra-
tion and the monitor generates an indicator–dilution
curve that is plotted against time. The area under the curve,
with some modifications, is proportional to the cardiac
output. The original technique used indocyanine green, a
non-toxic dye, but this technique is complicated by a
gradual increase in baseline due to recycling. Thermodilu-
tion cardiac output measurement (TDCO) is an indicator
dilution method that has replaced dye dilution and is the
technique that is used for comparing all new methods of
cardiac output measurement. A multilumen catheter with
a thermistor approximately 4 cm from the tip (Swan–
Ganz catheter) is inserted into the jugular vein and
 Patient monitoring and clinical measurement
advanced through the heart until the tip lies in the pul-
monary artery. Correct placement of the catheter is con-
firmed by connecting a pressure transducer to the lumen
that exits at the tip of the catheter and observation of the
distinctive pressures and waveforms as the catheter passes
through the atrium, ventricle and pulmonary artery. The
catheter is designed such that one lumen of the catheter
exits in the right atrium and that port is used for injection
of cooled saline or 5% dextrose. The time of injection and
temperature of injectate is recorded by the monitor, the
temperature changes in the pulmonary artery are detected,
and the time lapse from injection to measured tempera-
ture change allow calculation of cardiac output. Different
lengths of catheter and varying volumes of injectate are
chosen to accommodate various sizes of animals, from
cats to horses. Either the ventilator is temporarily shut off
or each injection is made at the same time in the respira-
tory cycle and two to three measurements are performed
in quick succession and averaged to improve accuracy.
Problems associated with insertion of a Swan–Ganz cath-
eter include prolongation of anaesthesia time, initiation
of premature ventricular depolarizations, and potential
complications of laceration of a blood vessel, knotting of
the catheter, and infection.
Lithium dilution cardiac output (LiDCO™) technique
mimics the dye dilution technique by injection of lithium
chloride into a central or peripheral vein and a pump
withdraws blood from an artery pulling it through a
lithium sensor to measure blood concentration. Advan-
tages of this system include no major invasive catheteriza-
tion and a small volume of injectate that is easily injected
by hand and which causes minimal haemodynamic effect.
The patient’s haemoglobin and sodium concentrations
must be entered into the monitor because lithium is dis-
tributed only in plasma. Some blood loss may occur even
though the sampled blood is returned to the patient. A
close correlation between the LiDCO and thermodilution
techniques has been verified in several animal species
(Linton et al., 2000; Mason et al., 2001; Beaulieu et al.,
2005). One experimental study in anaesthetized neonatal
foals discovered that the LiDCO technique overestimated
TDCO measurements when CO <10 L/min and that the
correlations changed over time, however, the authors con-
cluded that LiDCO was an acceptable alternative to TDCO
(Corley et al., 2002).
In anaesthetized healthy experimental dogs weighing
22–25.4 kg ventilated with tidal volumes of 10–15 mL/kg,
cardiac outputs ranged from 50 to 303 mL/kg/min and the
average difference between the LiDCO and NICO was
9.3 mL/kg/min, indicating that NICO would be accepta-
ble for clinical use (Gunkel et al., 2004). Comparison of
the NICO and LiDCO techniques in foals 1–6 days old
and weighing 32–61 kg identified a good correlation for
CO measurements between the two techniques over a
wide range of values (Valverde et al., 2007). The NICO
technique tended to overestimate the LiDCO values at low
Chapter 2
cardiac outputs but have a closer agreement at higher
values.
Pulse contour method
Monitors have been developed for assessing changes in
cardiac output by analysis of the arterial pulse waveform.
The LiDCO™plus monitor includes the PulseCO™ system
that analyses the arterial waveform following initial calibra-
tion by measuring cardiac output by lithium dilution and
calculates stroke volume and CO. The PiCCO™ system’s
initial calibration uses transpulmonary thermal dilution
and requires cardiac catheterization. The FloTrac™/Vigileo™
is ‘self-calibrated’ based on an algorithm derived from
measurements in humans. These systems have been increas-
ingly used for tracking the haemodynamic status of human
patients in the ICU or postoperative recovery areas. Studies
in human patients have determined that the monitors lose
accuracy with time and require recalibration, particularly
when major changes in cardiovascular status have occurred,
and that values obtained by one monitor differ from
values obtained from a monitor from a different manufac-
turer. Although good agreement was obtained between
LiDCO™ and PulseCO™, cardiac output measurements in
dogs anaesthetized with fentanyl and pentobarbital, the
PulseCO™ was unable to measure accurately the decrease
in CO after severe haemorrhage and the authors concluded
that recalibration was necessary after any major alteration
in haemodynamic status (Cooper & Muir, 2007). Investiga-
tions of the PulseCO™ in dogs with systemic inflammatory
response syndrome (SIRS) (Duffy et al., 2009) and in
horses using inotropes to change cardiovascular dynamics
(Schauvliege et al., 2009) revealed failure of accuracy when
compared with LiDCO™ and the need for frequent recali-
bration. In anaesthetized neonatal foals, values for CO
recorded using PulseCO™ agreed significantly better
with values from LiDCO™ than measurements using the
PiCCO™ method (Shih et al., 2009). Comparison of the
FloTrac™/Vigileo™ with TDCO in experimental dogs docu-
mented overestimations, sometimes excessive, influenced
by MAP which led to the conclusion that FloTrac™/Vigileo™
was not suitable for CO measurement in dogs (Bektas
et al., 2012).
Flow method
Transoesophageal Doppler echocardiography cardiac
output (TEECO) is increasingly used as a cardiovascular
monitor in anaesthetized human patients. The technique
involves insertion of a probe into the oesophagus to the
level of the left ventricular outflow tract. The pulsed-wave
Doppler crystal emits an ultrasound wave and moving
objects (red blood cells) change the frequency resulting in
a curved waveform. Cardiac output is calculated from the
velocity-time integral (VTI, area under the curve) of the
ascending aorta × aortic cross-sectional area × heart rate.
Comparison with TDCO measurements has identified
no significant differences between measurements from
41
Section 1 Principles and procedures
both techniques in horses and dogs (Young et al., 1996;
Yamashita et al., 2007). Probe size has been a problem,
and the technique requires operator training.
Impedance cardiography
Transthoracic bioimpedance (BICO) involves placement
of electrodes, continuous output of high-frequency, low
magnitude current, measurement of electrical resistance,
and a monitor that calculates CO using an algorithm.
BICO did not produce acceptable values in Beagle dogs
(Yamashita et al., 2007).
Blood loss
Monitoring blood loss should include measuring the
volume of blood aspirated into a suction bottle, estimating
free blood on drapes around the surgical site, and counting
blood-soaked gauze squares. Placing a bucket under the
surgical site to catch free-flowing blood, for example during
rhinotomy in large animals, will assist assessment of blood
loss. Gauze squares of different sizes absorb varying
amounts of blood from 5–8 mL to 12–14 mL. The volume
of blood lost on the gauze squares may be estimated or the
gauzes weighed and, after the weight of the same number
of dry gauzes has been subtracted, applying the formula
that 1 g weight equals 1 mL blood. Measurement of packed
cell volume is not useful during acute blood loss as this
value will not change initially. Once an increased volume
of balanced electrolyte solution with or without colloid
has been infused, the packed cell volume and total protein
concentrations will decrease to a value of use during assess-
ment. When evaluating packed cell volume changes, it is
important to consider that anaesthesia per se will result in
sequestration of red blood cells in the spleen and decrease
the packed cell volume by up to 20%.
In the conscious animal, loss of blood volume is ini-
tially compensated for by increased heart rate and cardiac
contractility, together with peripheral vasoconstriction.
These physiological responses are blunted or abolished
during anaesthesia. Consequently, the significance of the
blood loss may not be appreciated owing to maintenance
of a normal heart rate. Furthermore, it should be remem-
bered that when MAP is decreasing in response to
haemorrhage, cardiac output decreases to a greater extent
(Fig. 2.26) (Weiskopf et al., 1981).
Measurement of arterial pressure is an important step
in the management of blood loss as oxygen delivery to
tissues is impaired when mean arterial pressure decreases
below 60 mmHg. The potential impact of blood loss on
the patient may be evaluated better by assessing the
volume of blood loss against the total blood volume.
The blood volume varies between species and is usually
assessed in mature animals as 86 mL/kg body weight in
dogs, 56 mL/kg in cats, 72 mL/kg in draught horses and
ponies, 100 mL/kg in Thoroughbreds and Arabians,
60 mL/kg in sheep.
42
Haemorrhage % of blood volume
10% 20% 30%
0
-10
Percent decrease
-20
-30
-40 Heart rate
Mean arterial pressure
-50 Cardiac output
Figure 2.26  Cardiovascular responses to graded
haemorrhage in five splenectomized isoflurane-anaesthetized
dogs. Results are presented as percent change from values
measured before blood loss
Adapted from Weiskopf et al., 1981.
Blood volume of paediatric patients may be 50% greater
than the blood volume of the mature animal. The percent-
age of this volume that the animal can lose before circula-
tory shock ensues depends to a large extent on the physical
status of the patient, the preanaesthetic PCV, the depth of
anaesthesia, and the support treatment provided. Signifi-
cant cardiovascular changes occur after loss of 15% of the
blood volume. The maximum blood loss allowed before
giving a blood transfusion is usually 20% of the estimated
blood volume, however, in some animals up to 30% of
the total blood volume may be lost without onset of hypo-
tension or hypoxia if the patient has no major preanaes-
thetic illness, is ventilated with oxygen, the depth of
anaesthesia is lightened, balanced electrolyte and colloid
solutions are infused intravenously, and vasoactive drugs
are administered as needed.
Monitoring the respiratory system
Visual observation of respiratory rate and depth of breath-
ing is a basic estimate of adequacy of breathing. The res-
piratory rate may be counted by observation of chest
movement or movement of the reservoir bag on the anaes-
thesia machine. The excursion of the chest, abdomen, or
bag should be observed to gain an impression of the depth
of breathing. In general, except possibly in horses, a spon-
taneous rate of 6 breaths/min or less is likely indicative of
hypoventilation. Respiratory rates of 10 breaths/min or
greater may provide adequate ventilation or be associated
with hypoventilation when the breaths are shallow. Chest
wall movement with no corresponding movement of the
reservoir bag is indicative of airway obstruction or tension
pneumothorax.
Rate monitors and apnoea alarms
Rate monitors and apnoea alarms may use a thermistor
either connected to the endotracheal tube or placed in
 Patient monitoring and clinical measurement
front of a dog’s nose. The thermistor detects temperature
differences between inspired and exhaled gases to produce
a signal that drives a digital rate meter to make a noise
which varies in intensity or pitch in time with the animal’s
breathing. An alarm sounds if a constant gas temperature
is detected. Like the oesophageal stethoscope that counts
only heart rate, the respiratory rate monitor registers rate
only and not adequacy of ventilation.
Tidal and minute volume monitors
The volume of each breath (tidal volume) and the volume
of gas inhaled or exhaled per minute (minute volume) can
be measured in small animals by attaching a gas meter
such as a Wright’s respirometer within the circle circuit or
to the endotracheal tube. The respirometer has a low
resistance to breathing and is reasonably accurate over
volumes ranging from 4 L/min to 15 L/min but under
reads below 4 L/min.
Blood gas analysis
Measurement of the partial pressure of carbon dioxide in
a sample of arterial blood (PaCO2) using blood gas analy-
sis is the best monitor of ventilation. Arterial blood may
be collected from any peripheral artery used for invasive
blood pressure measurement. Commonly for clinical
patients, a small amount of 1 : 1000 heparin is drawn into
a 3 mL plastic syringe using a 25 gauge needle and the
plunger withdrawn to wash the inside of the syringe with
heparin. Excess heparin is then squirted from the syringe
leaving only syringe dead space filled with heparin and no
bubbles. A larger volume of heparin will increase the
acidity of the sample. A 2 mL sample of blood is collected
from most dogs and 2–3 mL from horses (collecting the
same volume for sequential samples). Individually pack-
aged 1 mL syringes containing a dry lithium heparin pellet
(to decrease dilution) can also be used (for example,
Portex® Line Draw Arterial Blood Sampling Kit, Smiths
Medical ASD, Inc., Keene, NH, USA). After removing the
cap from the nozzle of the syringe, the plunger should be
pushed fully forward before allowing the syringe to fill
with blood. Larger plastic syringes containing lyophilized
heparin are also commercially available.
Blood may be collected by percutaneous puncture or
from a catheter. The contents of the catheter should be
aspirated using a separate syringe before a sample of blood
is collected for analysis. This mixture of saline and blood
may be discarded or, if collected into a syringe containing
some heparinized saline, can be returned into the animal
through a venous catheter. The blood sample should be
collected anaerobically slowly over several respiratory
cycles and without aspirating any air bubbles. Excessive
negative pressure should be avoided as oxygen can be
extracted from the blood sample. After expressing a drop
of blood and any bubbles from the needle, the syringe
should be sealed either with a special cap or by inserting
Chapter 2
the tip of the needle into a rubber stopper. Leaving an air
bubble in the syringe for any length of time allows diffu-
sion of gases between the blood and bubble such that
PCO2 will decrease and PO2 will decrease if the animal is
breathing O2 and increase if the animal is breathing air.
The syringe should be inverted several times over 20
seconds to mix the blood with the heparin. The tempera-
ture of the animal should be measured at the time of
sampling. Firm pressure should be applied to the artery
for 3 minutes after percutaneous needle puncture to avoid
haematoma formation.
Ideally, blood gas analysis should be performed imme-
diately after blood collection into plastic syringes because
there is a significant change in PO2, an increase if PO2 is
12 kPa (90 mmHg) and a decrease when the PO2 is
>33.3 kPa (>250 mmHg), due to diffusion of O2 into or
out of the syringe and metabolism in white blood cells
and platelets that consumes O2 and produces CO2
(Beaulieu et al., 1999). Not all plastic syringes are the
same, even those marketed specifically for blood gas analy-
sis, and the magnitude of PO2 change depends on the
manufacturer and characteristics of the syringe (Wu et al.,
1997). Investigations have discovered that the change in
PO2 over time is greater with a 3 mL syringe than a 5 mL
syringe (Wu et al., 1997) and inaccuracy is greater when
<1.8 mL is collected into a 3 mL syringe compared with
>2 mL (Hedberg et al., 2009). Furthermore, accuracy of
PO2 measurement is related to the method of storage of
the syringe before analysis, in iced water at 0°C or at
ambient temperature of 20–25°C, and the time lapse
between collection and analysis (Pretto & Rochford, 1994;
Deane et al., 2004, Picandet et al., 2007). Iced water
decreases the rate of metabolism in blood and the lower
temperature promotes increased PO2 by facilitating diffu-
sion of O2 from water into the plastic syringe through
increased gas solubility and increased haemoglobin O2
affinity (Wu et al., 1997). A significant change in PO2 has
been measured by 10 minutes after blood collection
(Pretto & Rochford, 1994; Picandet et al., 2007). PCO2
undergoes a clinically insignificant but statistically signifi-
cant change. Picandet et al. (2007) suggested that although
the PCO2 appeared to be stable, the value may have been
a balance between leakage of CO2 out of the blood and
increased CO2 from metabolism. Values other than PO2
may be relied upon from plastic syringes stored at room
temperature up to 60 minutes. It has been suggested that
blood from different species may require different han-
dling but published data reveal differences in results even
within the same species. Despite differences in findings
between investigations, it appears that with an expected
PO2 of about 13.3 kPa (100 mmHg), the increase may be
less if the plastic syringe is kept at room temperature until
analysis (Deane et al., 2004; Picandet et al., 2007) whereas
the decrease may be less in blood with a high PO2 when
the syringe is stored in a slurry of ice and water (Pretto &
Rochford, 1994). Plastic syringes for blood gas analysis
43
Section 1 Principles and procedures

have largely replaced use of glass syringes due to decreased

Table 2.4  Mean normal values for pH, PaCO2, and
cost and increased convenience. Glass syringes are non-
PaO2 in mature conscious unsedated animals
disposable items that must be sterilized before use and not
infrequently the plunger becomes immoveable or the glass
breaks. However, when blood is collected into glass Species pHa PaCO2 PaO2 References
syringes and stored in an ice and water slurry at 0°C, PO2 Dogs 7.40 4.67 13.6 Horwitz et al., 1969
and PCO2 values are minimally changed for 90 minutes (35) (102)
(Pretto & Rochford, 1994; Beaulieu et al., 1999; Deane 7.38 5.3 13.3 Haskins et al., 2005
et al., 2004; Picandet et al., 2007; Noël et al., 2010). (40) (100)
Plastic vacutainer tubes containing lyophilized heparin Cats 7.34 4.5 13.3 Middleton et al., 1981
have been used to collect blood from conscious horses for (34) (100)
blood gas and acid–base analysis. A detailed investigation
Horses 7.38 5.05-6.1 13.3 Steffey et al., 1987;
of this practice revealed that PO2 increases significantly,
(38-46) (100) Wagner et al., 1991;
more than 6.65 kPa (50 mmHg) within 15 minutes, due Wan et al., 1992
to diffusion of O2 through the wall of the tube with a 7.41 4.8 12.2 Clarke et al., 1991;
greater change occurring when tubes are stored at 0°C (36) (91) Tate et al., 1993
than 22°C before analysis (Noël et al., 2010). The change
Cattle 7.40 5.28 11.8 Gallivan et al., 1989
in PCO2 was less dramatic but statistically significant and (39) (89)
was greater when the vacutainer is stored at 22°C than
0°C. The calculated values of bicarbonate (HCO3), total Sheep 7.48 4.4 12.2 Wanner & Reinhart,
(33) (92) 1978
CO2 (TCO2), standard base excess (SBE) were minimally
affected. The authors also noted that the design of the Goats 7.45 5.45 12.6 Forster et al., 1981
vacutainer tube does not allow collection of an anaerobic (41) (95)
blood sample and concluded that plastic vacutainer tubes
Pigs 7.50 5.4 10.5 Hannon, 1983
do not produce accurate results for PO2 and PCO2 but can (41) (79)
be used when HCO3, TCO2 and SBE are the main interest,
in which case the tubes should be stored at 0°C when Values for PaCO2 and PaO2 given as kPa (mmHg)
analysis is delayed.
The blood sample is introduced into equipment incor-
porating electrodes measuring pH, PCO2 and PO2. The
machine uses the measured values to compute HCO3,
TCO2, SBE and oxygen saturation (SaO2). The patient’s Hypercarbia in some anaesthetized dogs and cats during
temperature is entered into the blood gas analyser for anaesthesia may be associated with tachycardia with or
appropriate adjustment of pH and PO2. The patient’s hae- without increased blood pressure. In these animals, inter-
moglobin concentration must be known for an accurate mittent positive pressure ventilation (IPPV) will result
measure of base excess. Fully automated pH and blood gas in decreased heart rate within a few minutes. In other
analysers are highly accurate but expensive. Portable and patients, hypercarbia may be associated with hypotension.
less expensive equipment is available, for example, Hypercarbia in horses during anaesthesia may also cause
STATPAL® (Sendx Medical Inc., Carlsbad, California, USA) stimulation of the sympathetic nervous system, increased
and i-STAT® (Abbott Laboratories, Abbott Park, Illinois, blood pressure and cardiac output (Wagner et al., 1990,
USA), although the cost of individual analyses may be Khanna et al., 1995). Adverse effects of hypercarbia are
higher. observed in some horses as tachycardia of 60–70 beats/
min, or hypotension caused by decreased myocardial con-
Hypercarbia, hypocarbia tractility. These abnormalities are corrected within 5–10
Normal values for PaCO2 in conscious unsedated animals minutes of initiating IPPV. More frequently, the effects of
are given in Table 2.4. Increased PaCO2 (hypercarbia, hypoventilation during inhalation anaesthesia are mani-
hypercapnia) is a direct consequence of hypoventilation fested as an inadequate depth of anaesthesia despite a
and commonly occurs during anaesthesia. An increase of vaporizer setting that should provide a sufficient depth of
10 mmHg above normal is mild hypoventilation, an anaesthesia. In these animals, controlled ventilation
increase of 10–20 mmHg is moderate hypoventilation, expands the lungs, thereby improving uptake of anaes-
and an increase >20 mmHg is severe hypoventilation. thetic agent and resulting in increased depth of anaesthe-
Thus, PaCO2 values exceeding 8 kPa (60 mmHg) are sia (Fig. 2.27).
indicative of severe respiratory depression. A decrease in
PaCO2 (hypocarbia) will occur with increased ventilation. Oxygenation
A PaCO2 less than 2.6 kPa (20 mmHg) causes cerebral PaO2 values are influenced by the inspired oxygen tension
vasoconstriction and cerebral hypoxia. (PIO2), adequacy of ventilation, cardiac output, and blood

44
 Patient monitoring and clinical measurement Chapter 2

TIME 0 15 30 45 60 75 90
O2 L/min 1
Vaporizer 2 2.25 3.5 2.5
Inspired Iso 1.7 1.6 2.1 2
180
End tidal Iso 1.3 1.3 1.6 1.7
End tidal CO2 34 38 46 50 43 37 34
160
SpO2 98 98 98 98 99
140 140

120 120

100 100

80 80

60
Systolic
40
Heart rate
20
C
Resp rate
10
Notes 1 2

Figure 2.27  Part of an anaesthetic record of a 32 kg Golden Retriever anaesthetized for stifle surgery. At Note 1 the dog was
moved into the operating room. The increase in ETCO2 from 34 to 50 mmHg (4.5 to 6.65 kPa) over the next 30 minutes
indicated increasing hypoventilation. An abrupt increase in heart rate from 102 to 180 beats/min was presumed a response to
increased surgical stimulation. Increasing the vaporizer setting to 3.5% was slow to change the circuit isoflurane
concentration. Institution of controlled ventilation quickly increased the depth of anaesthesia (ET isoflurane concentration
increased to 1.6%), decreasing heart rate. Subsequently the vaporizer setting could be decreased.

pressure. A PaO2 of 12–14.6 kPa (90–110 mmHg) is
normal in unsedated animals at sea level and PaO2 values
less than 8 kPa (60 mmHg) constitute hypoxaemia.
The maximum possible PaO2 is governed by the inspired
O2 % and animals breathing oxygen may have PaO2 values
up to five times greater than when breathing air. The
partial pressure of oxygen at the alveolar level (PAO2) can
be calculated from the following formula:
PaO2 = [(barometric pressure − Pwater vapour ) × FIO2 ]
− (PaCO2 /0.8)
where the value for water vapour is 6.25 kPa (47 mmHg),
FIO2 is the fractional concentration of O2 in inspired gas,
and 0.8 is the respiratory exchange ratio. Values for PaO2
greater than 53.2 kPa (400 mmHg) are expected in healthy
dogs and cats breathing oxygen. Horses and ruminants are
subject to lung collapse during recumbency and anaesthe-
sia and, consequently, ventilation and perfusion are
mismatched within the lung, resulting in a lower PaO2 in
some individuals.
Hypoxaemia may develop in dogs and cats during
anaesthesia or recovery as a result of hypoventilation when
breathing air. This situation is most likely to occur in old
animals, animals with hypotension, pneumothorax, pul-
monary disease, CNS depression from metabolic disease,
or after administration of opioids. Hypoxaemia may also
develop during general anaesthesia as a result of severe
lung collapse. Patients at greatest risk are small animals
during thoracotomy or repair of a ruptured diaphragm,
foals with pneumonia and horses with abdominal disten-
sion from pregnancy or colic. Hypoxaemia may be sus-
pected but is not always obvious as the mucous membranes
may be less pink than desired but not cyanotic.
Oxygen content
Oxygen delivery to tissues is dependent on tissue blood
flow and arterial blood oxygen content (CaO2). Oxygen

45
Section 1 Principles and procedures
content comprises O2 carried by haemoglobin (Hb) and
a small amount of dissolved O2. The formula for calculat-
ing CaO2 shows that the Hb concentration of the blood,
the Hb oxygen affinity and the PO2 are important deter-
minants of O2 content:
CaO2 mL/dL = [total Hb − (COHb + metHb)] × SaO2
× 1.39 + PaO2 × 0.003
where SaO2 (oxygen saturation) is a decimal fraction of
1, Hb concentration in g/dL, and 1.39 mL/g is the volume
of O2 in mL that can be bound to 1 g of human Hb. The
number 1.31 or 1.34 is often substituted for 1.39 as being
a practical rather than theoretical value. Correct calcula-
tion of SaO2 should refer to the ratio of oxyhaemoglobin
(O2Hb) to active Hb (O2Hb + deoxyhaemoglobin, HHb).
Inactive Hb has lost the ability to bind O2 and this most
commonly refers to carboxyhaemoglobin (COHb) and
methaemoglobin (metHb) (Toffaletti & Zijlstra, 2007).
Most gas analysers calculate saturation from PO2 by com-
puter and do not actually measure saturation. When the
total Hb value is used in the formula (as with blood
gas analyser results) measured values for SaO2 may be
accurate in most anaesthetized patients because their
quantities of COHb and metHb are small. For accuracy,
the different forms of Hb must be measured by an auto-
mated multiwavelength spectrophotometer commonly
referred to as a cooximeter. Critical care management may
include animals exposed to carbon monoxide poisoning
or animals with methaemoglobinaemia from acetomi-
nophen or benzocaine toxicity, for example. Carbon mon-
oxide displaces O2 from Hb with an affinity approximately
300× that of Hb affinity for O2. Animals with carbon
monoxide poisoning do not have decreased PO2 so that,
unless the different forms of Hb are measured, the decrease
in blood O2 content may not be realized. A value for O2
saturation obtained from a pulse oximeter (SpO2) will not
be decreased in these patients because the wavelengths
used by the monitors are not sensitive to COHb as a con-
sequence of COHb absorbing as much light at 660 nm as
does O2Hb. A patient with increased concentration of
metHb would be reported as having an abnormally low
SpO2. MetHb absorbance is high at both wavelengths used
by pulse oximeters and the resultant effect is to decrease
SpO2 down to 85% regardless of the PaO2 and SaO2 values
(Tremper & Barker, 1990).
Oxygen affinity
The O2 affinity of blood is usually described by the oxygen
dissociation curve (ODC) at standard values of pH = 7.40,
pCO2 = 5.33 kPa (40 mmHg), and temperature of 37°C
(Fig. 2. 28). The relationship between PaO2 and SaO2 is
not linear because Hb changes its affinity for O2 at increas-
ing levels of saturation. Several factors cause the normal
ODC to shift to the right or left along the x-axis, for
example, an increase in PCO2, decrease in pH, increase
46
100 20
Haemoglobin saturation (%)
80 Arterial
O2 content (ml/100ml)
16
sat. 97%
PO2 100
60 Venous 12
sat. 75%
40 PO2 40 8
20 4
0 0
0 20 40 60 80 100
PO2 (mmHg)
Figure 2.28  Graph depicting the relationship between PaO2,
haemoglobin oxygen saturation SaO2, and oxygen content in
humans.
in temperature, and increased concentration of 2,3-
diphosphoglycerate (DPG) in the red cells will produce a
shift to the right, and vice versa. Comparison of O2 dis-
sociation curves is possible by using the P50 value that is
the PO2 required for 50% Hb saturation.
The haemoglobin O2 affinity varies between species.
Human Hb P50 is 3.5 kPa (26.3 mmHg) (Lumb, 2000;
Toffaletti & Zijlstra, 2007). The canine ODC is similar to
human with a range of P50 reported as 3.5–4.2 kPa (26–
31.5 mmHg), however, the small difference may result in
small errors in measurement of canine PO2 produced by
a blood gas analyser using human P50 (Scott et al., 2005).
Bovine, equine, and camelid ODC have lower P50 values
indicating higher O2 affinity. Thus, the llama ODC, P50
3.3 kPa (24.6 mmHg), is to the left of sheep such that the
O2 content of llama blood at a PO2 of 6.7 kPa (50 mmHg)
is similar to that of a PO2 of 8 kPa (60 mmHg) in sheep
(Moraga et al., 1996). Fetal ODC is shifted to the left of
the maternal curve so that the Hb is adapted to operate at
lower PO2 levels present in the fetus. Fetal Hb concentra-
tions are significantly higher than maternal in both llama
and sheep, increasing O2 content, and the camelid pla-
centa is very thin compared with others, facilitating O2
diffusion (Moraga et al., 1996). In animals genetically
adapted to high altitude, the left shift of the ODC improves
oxygenation of arterial blood that outweighs the decrease
in offloading of O2 at the tissues.
The high O2 affinity and increased Hb concentration in
llamas are not different whether the animals are at high
or low altitude, a similarity shared with guinea pigs that
are also considered to be genetically adapted to high alti-
tude (Pairet & Jaenicke, 2010). The high blood-O2 affinity
in camelids (llama, vicuna, alpaca, guanaco) is partly due
to amino acid substitutions in the Hb molecule that
reduce the DPG effect and resists shift of the ODC to the
right (Weber, 2007). Thus, although the intrinsic O2 affin-
ity of llama Hb is lower than camel (lowland species), the
 Patient monitoring and clinical measurement
effect on DPG binding results in greater O2 affinity.
Vicunas have a different amino acid substitution on Hb
that affects Cl binding and increases Hb O2 affinity in
vicuna over llama.
Reduced P50 is critical for maintenance of arterial oxy-
genation in animals at high altitude. Thus, factors that
oppose that state and cause the ODC to shift to the right,
such as hypoventilation and decreased pH, oppose this
effect and are deleterious to tissue oxygen delivery
(Winslow, 2007). Where O2 extraction is high, as in
exercise, hyperventilation, increased cardiac output, and
vasodilation are important for maintaining tissue
oxygenation.
High altitude human residents do not have Hb geneti-
cally adapted to high altitude but a variety of other
physiological adaptations that include increased Hb
concentration, hyperventilation, blunted response of the
chemoreceptors to hypoxia, and higher catecholamine
levels (Hainsworth & Drinkhill, 2007). Hyperventilation
to a PaCO2 3.3 kPa (25 mmHg) is normal at high altitude
and the alkalinization further improves O2 loading in the
lungs. The reduction in O2 release to tissues is partly offset
by a more efficient O2 extraction in the tissues by mecha-
nisms including an increase in tissue capillarization.
Mixed venous, central venous, and venous PO2
Mixed venous PO2 (PmvO2) is obtained from a blood
sample collected from the pulmonary artery after place-
ment of a cardiac catheter. The information obtained is
interpreted based on the fact that PmvO2 is representative
of total body O2 extraction. Factors that influence PmvO2
are: (1) arterial O2 content (CaO2); (2) cardiac output; (3)
distribution of peripheral blood flow; and (4) tissue O2
extraction. Decreases in the first three factors or an increase
in the fourth will cause decreased PmvO2. O2 saturation
of pulmonary artery blood is generally around 70–75%. A
decrease in SmvO2 to less than 65% is significant and indi-
cates an abnormality in the patient, whereas a decrease to
50% is significantly low. Small variations in PmvO2 exert
little influence on PaO2. As the PmvO2 decreases further,
extraction of oxygen from alveolar gas is increased decreas-
ing PaO2, especially in patients with compromised venti-
lation such as hypoventilation or ventilation–perfusion
mismatches. Conditions lowering PmvO2 are low cardiac
output and hypotension or increased oxygen extraction
created by sepsis and postoperative shivering, although the
opposite effect may occur when sepsis results in impaired
tissue oxygen extraction. An abrupt decrease in PmvO2
may occur following a sudden decrease in cardiac output,
decreased venous return, for example, following reposi-
tioning, and increased O2 consumption during muscle
movement. PmvO2 may be higher than normal in animals
in which endotoxaemia has induced a hyperdynamic cir-
culation with increased cardiac output.
Central venous O2 saturation measurement (ScvO2)
may be used as a surrogate for SmvO2. For greatest
Chapter 2
accuracy, ScvO2 should be measured from blood collected
from the tip of a central venous catheter placed close to,
or within, the right atrium (Walley, 2010). The site of
sampling is important because sampling from the tip of a
catheter some distance away from the right atrium pro-
duces inaccurate results when compared to SmvO2.
Peripheral venous blood collected from the cephalic,
femoral, or jugular veins is not comprised of blood from
major organs and cannot be used to evaluate tissue oxygen
extraction but may be used as a screening method for arte-
rial pH and PCO2.
Measurement of pH and blood gases in lingual venous
blood from healthy normotensive, anaesthetized dogs
slightly overestimated arterial pH and overestimated PCO2
and base excess when compared to values measured in
arterial blood (Pang et al., 2009). The differences were
not large and unlikely to significantly alter therapeutic
management. Most of the lingual PO2 values were exces-
sively lower than PaO2 values particularly during admin-
istration of medetomidine. Significant differences were
obtained when comparing mean values for jugular venous
and arterial pH and PCO2. The ranges of values for both
parameters from all three sampling sites were almost
identical.
Pulse oximetry
Pulse oximetry is a non-invasive method of continuously
measuring haemoglobin oxygen saturation (SpO2). The
abbreviation SpO2 is used to identify the method of meas-
urement of SaO2. The pulse oximeter sensor consists of
light-emitting diodes (LEDs) that emit light in the red
(660 nm) and infrared (940 nm) wavelengths and a pho-
todetector that measures the amount of light that has been
transmitted through tissues (Tremper & Barker, 1990). The
principles of measurement are based on the different light
absorption spectra of oxyhaemoglobin and reduced hae-
moglobin, and the detection of a pulsatile signal. Pulse
oximeters are available as single parameter monitors or in
combination, for example, pulse oximetry and NIBP or
pulse oximetry and capnography.
Pulse oximeters display a digital record of saturation
and pulse rate, with an audible beep, and some monitors
display the oxygen saturation waveform (Fig. 2.29). A
limit for acceptable saturation can be entered into the
monitor, allowing an alarm to sound when lower values
are sensed. The pulse rate displayed on the oximeter must
correspond to the rate obtained by palpation or ECG, and
the sensor should be in position for at least 30 seconds
before the measurement can be assumed to be accurate.
The shape of the sensor, thickness of tissue placed within
the sensor, the presence of pigment and hair, and move-
ment of the patient, can be responsible for the oximeter
failing to measure oxygen saturation. Ambient light may
interfere with probe function and covering it with gauze
may produce a reading. It may be impossible to obtain a
47
Section 1 Principles and procedures

Figure 2.29  Multiparameter monitor displays haemoglobin oxygen saturation (SpO2) waveform and value (96%), arterial
blood pressure (systolic 141 mmHg, diastolic 63 mmHg, mean 83 mmHg), and CO2 waveform and values (inspired 4 mmHg
(0.5 kPa), end-tidal 37 mmHg (4.9 kPa), respiratory rate 38 breaths/minute), and temperature of 98.6°F in an anaesthetized
dog (Advisor®, Surgivet™, Smiths Medical PM, Inc., Norwell, MA, USA). Heart rate of 99 beats/minute is obtained from pulse
oximeter and blood pressure. ECG and NIBP are not connected.

reading from a pulse oximeter when peripheral vasocon-

Table 2.5  Relationship between PaO2 and
striction is severe, for example, after administration of
haemoglobin saturation in humans
medetomidine in dogs or patients in circulatory shock.
The pulse oximeter will not accurately reflect blood O2
content in patients with carbon monoxide or methaemo- PaO2 SaO2 Interpretation
globin poisoning (see earlier). Oxygen delivery to tissues kPa mmHg %
may be compromised by low blood O2 content, cardiac
output, or blood flow. Thus a patient with low Hb con- ≥13.3 ≥100 100 Oxygenated
centration may display normal values for SpO2 and yet 10.6 80 94
suffer tissue hypoxia. Anaesthetic management of anaemic
patients should, therefore, include administration of sup- 9.3 70 92
plemental inspired O2 and cardiovascular support. 8.0 60 90 Hypoxaemia

Pulse oximetry saves lives by detecting desaturation 6.7 50 80

before clinically apparent. SpO2 >90% does not 5.3 40 70 Venous
guarantee adequate oxygenation of tissues

A pulse oximeter detects inadequate blood oxygenation,

which should be taken as an indication to supplement
the animal’s inspired oxygen concentration and to search
for the cause. Hypoxaemia is defined as PaO2 of 8 kPa
(60 mmHg) or SaO2 ≤90% (Table 2.5). A pulse oximeter
is a valuable monitor for use on all anaesthetized animals
and specifically for animals anaesthetized with injectable
anaesthetic agents and breathing air, or during inhalation
anaesthesia in patients with pulmonary disease or
traumatic pulmonary contusions or pneumothorax, and
during thoracotomy or major surgery in the cranial
abdomen. It is also important to keep track of oxygenation
in animals during recovery from anaesthesia, in patients
with partial airway obstruction, or when ventilation is
depressed or impaired by systemic opioid administration
or residual pneumothorax after thoracotomy or ruptured
diaphragm repair.

48
 Patient monitoring and clinical measurement
The pulse oximeter is particularly valuable because it
provides an immediate monitor of decreased oxygen satu-
ration, so that corrective treatment can be initiated before
respiratory or cardiovascular failure develops. Use of pulse
oximetry is associated with reduction in odds of anaes-
thetic-related death (Brodbelt, 2009). Evaluation of the
patient should take into account the fact that the pulse
oximeter does not measure CO2 concentration or blood
pressure and may continue to read satisfactorily in the
presence of hypotension. However, it can provide a
warning of a severe decrease in tissue blood flow caused
by hypotension or decreased cardiac output by abruptly
failing to obtain a signal. Loss of signal may also occur
spontaneously with no change in the patient’s condition
due to local blood vessel compression and measurement
is restored by changing the position of the probe. Com-
pression of the base of the tongue between the endotra-
cheal tube and the jaw may decrease blood flow and signal
acquisition from a probe clipped to the tongue.
Although pulse oximetry saves lives by identifying low
SpO2 before desaturation is clinically apparent, it must be
realized that the number observed on the pulse oximeter
is not always accurate and that different results may be
obtained from different probe types, different sites on the
body, different models, and different species of animals.
Most models are reasonably accurate for saturations >90%
but for some models that consistently overestimate SaO2
(Dolphin Voyager in dogs), a higher threshold of 93% has
been suggested (Burns et al., 2006).
Different body sites in dogs have been evaluated for
accuracy of measurement of SaO2. In one investigation, a
multisite clip probe placed on the lip, tongue, toe web,
and the tip of the tail gave accurate and reliable estima-
tions of SaO2 values during conditions of full haemo-
globin saturation and moderate haemoglobin desaturation
(92%) (Huss et al., 1995). In this study, the human finger
probe was accurate only when placed on the dog’s lip and
when haemoglobin saturation was complete. The lip was
found to be the best site in conscious animals. Another
study of conscious dogs in an intensive care unit found
that a circumferential pulse oximeter probe around a digit
or the metatarsus produced excellent correlations between
pulse oximeter and SaO2 values (Fairman, 1993). An eval-
uation of the Ohmeda Biox 3700 with a human ear probe
applied to the tongue provided an accurate evaluation of
SaO2 (Jacobsen et al., 1992). The pulse oximeter underes-
timated SaO2 at higher saturations and overestimated
SaO2 at saturations <70%. However, as the authors pointed
out, detection of hypoxaemia is more important than
measurement of the exact degree of hypoxaemia. One
evaluation of four Nellcor models and the Surgivet V3304
with the probe applied at five sites in anaesthetized dogs
and cats achieved arterial saturations of 98%, 85%, and
72% by varying inspired O2 % (Matthews et al., 2003).
SpO2 measurements were reasonably accurate at SaO2
>90%. The study revealed in dogs that measurements
Chapter 2
obtained from the lip and ear were less accurate and,
although all sites in the cats had low correlation, the hind
paw was the most accurate. Failure to achieve readings was
most frequent with the Surgivet V3304.
Different monitors, types of sensors, and alternative
sites for measurement have been evaluated in horses
(Whitehair et al., 1990; Chaffin et al., 1996; Matthews
et al., 2003). The Ohmeda Biox 3700 pulse oximeter
and the Physio-Control Lifestat 1600 pulse oximeter
were evaluated in mature horses using the human ear
lobe probe (Whitehair et al., 1990). Measurements were
obtained from the tongue and the ear, with the most
accurate measurements obtained from the tongue; the oxi-
meters failed to detect a pulse at the nostril, lip, or vulva.
The results revealed that both oximeters tended to under-
estimate saturation by 3.7%, with 95% of the oxygen
saturation values within 1% above or 8% below SaO2
(Whitehair et al., 1990). The Nellcor N-200 pulse oxime-
ter was evaluated in anaesthetized foals using a fingertip
probe (Durasensor DS-100A) (Chaffin et al., 1996).
Attachment of the probe to the tongue or ear of the foals
slightly underestimated SaO2 within the range of 80–100%
saturation. Evaluation of four Nellcor models and the Sur-
givet V3304 in anaesthetized horses with the probe on the
tongue lip, ear, nostril and prepuce or vulva found that
correlations between SpO2 and SaO2 were fairly high at all
sites except the ear (Matthews et al., 2003). All monitors
except the Nellcor NPB-290 failed to produce readings at
some times, with the V3304 failing 60% of the times.
Reflectance pulse oximeters detect changes in absorp-
tion of light reflected from tissues, rather than transmitted
through tissues as just described (Watney et al., 1993;
Chaffin et al., 1996). Attachment of a reflectance probe
designed for the human forehead to the ventral surface of
the base of the tail in foals had 100% sensitivity for detect-
ing SaO2 <90% but consistently underestimated the actual
value (Chaffin et al., 1996). Therefore, this probe site com-
bination will incorrectly identify some foals as being
hypoxaemic.
Capnography
Capnography indirectly estimates PaCO2 by measuring
the concentration of CO2 in expired gas. Capnography is
also useful for diagnosis of mechanical problems in anaes-
thetic circuits, airway obstruction, and cardiogenic shock.
There are two types of gas sampling. Sidestream sampling
is when gas is aspirated from an adapter inserted between
the endotracheal tube and anaesthetic circuit (Matthews
et al., 1990) and delivered to the capnometer (see Figs.
2.5, 2.29, 2.30). Gases leaving the analyser should be
directed back into the anaesthetic circuit or into the scav-
enging system. Mainstream gas sampling occurs when the
measuring device is placed between the endotracheal tube
and delivery circuit (Fig. 2.31). Measurement of CO2
directly exhaled from the patient provides more accurate
49
Section 1 Principles and procedures

measurement in patients with small tidal volumes or for

Figure 2.30  Gases are aspirated from a T-adapter inserted
between the endotracheal tube and the delivery circuit, and
the capnogram and end-tidal CO2 are displayed on a
monitor distant from the patient. Also attached to this dog is
a pulse oximeter probe on the tongue and blood pressure
cuff and Doppler probe on a forelimb.
non-rebreathing circuits where alveolar gas is diluted by
the fresh gas flow. The CO2 concentration is measured by
infrared absorption and the capnometer provides breath-
by-breath numerical values for CO2 concentration and
usually a CO2 waveform (capnograph). The upward slope
of the waveform represents expiration and the highest
value is the end-tidal CO2 (ETCO2). The downward slope
occurs during inspiration and the inspiratory baseline
should be zero (Fig. 2.32). An increase in baseline to
0.5 kPa (4 mmHg) will occur with rebreathing due to an
increase in apparatus dead space, such as the endotracheal
tube extending beyond the incisors and inclusion of the
sampling adaptor and a humidity and moisture exchanger
(see Fig. 2.29). This degree of rebreathing is not significant
to the patient. A greater increase in baseline to
1.3-1.9 kPa (10-14 mmHg) indicates equipment malfunc-
tion, such as a unidirectional valve on a circle circuit stuck
in the open or closed position, exhaustion of CO2 absorb-
ent, incorrect assembly of a non-rebreathing circuit, or
disconnection of a coaxial circuit (Fig. 2.33A). Respiratory
rate may increase, sometimes panting in dogs, despite eye
signs indicating adequate depth of anaesthesia. Signs of
sympathetic stimulation from hypercarbia such as tachy-
cardia and increased blood pressure may be present.
Falsely low measurements of ETCO2 using side-stream
sampling may occur with the use of non-rebreathing cir-
cuits, because the high gas flow results in dilution of
expired gases, and in animals with very small tidal

Figure 2.31  A CO2 sensor inserted next to the endotracheal tube will more accurately measure end-tidal CO2 in animals with
small tidal volumes (Tidal Wave™, Novametrix, Wallingford, CT, USA). Other monitors on this Bearded Dragon are a pulse
oximeter probe on a foot, Doppler probe on the ventral surface of the tail over the coccygeal artery and a cloacal temperature
probe. After induction of anaesthesia an intraosseous needle was inserted in a femur for fluid therapy and drug
administration. The patient is lying on a heated pad.

50
 Patient monitoring and clinical measurement
D End-tidal CO2
C Table 2.6  Troubleshooting the capnogram
Expiration Inspiration
CO2
A B E Abrupt onset hypotension
Figure 2.32  Schematic diagram of a capnogram. AB = Initial
expiration (dead space), BC = expiration, CD = alveolar gas
plateau, D = end-tidal CO2 value, DE = inspiration.
50
A 0
50
B 0
50
C 0
50
D
Figure 2.33  Interpretation of capnograms. (A). Dog is
panting and inspiratory CO2 is 14 mmHg indicating
significant rebreathing. (B) Normal appearance of an ETCO2
waveform during controlled ventilation. (C) Inspiratory
waveform is sloping indicating a leak during inspiration,
dilution with fresh gas during a long pause between breaths,
or prolonged inspiration. (D) Waveform has a sloping
expiration indicating partial airway obstruction or impaired
lung deflation y-axis = 0-50 mmHg (0-6.65 kPa).
volumes, breathing slowly, or that are panting. Falsely low
CO2 measurements will be obtained in animals that are
ventilating with small tidal volumes, or in small animals
that have significant lung collapse such as diaphragmatic
hernia or thoroscopy, and during spontaneous ventilation
Chapter 2
Unexpectedly low ETCO2
Cardiac arrest
Significant decrease in cardiac output
Air embolism
Pulmonary embolism
Sampling line disconnected or broken
Endotracheal tube cuff deflated
Tidal volume too small
Absent ETCO2
Apnoea
Endotracheal tube disconnect
Airway obstruction
Oesophageal intubation
Failure to read zero on inspiration (rebreathing)
Large apparatus dead space
Expiratory valve in circle stuck open or closed
Exhausted CO2 absorbent
In and out tubes of NRB attached backwards
NRB circuit assembled incorrectly
Breathing rapid and shallow
Prolonged inspiratory or expiratory slope
Gas sampling rate too low
Partial airway obstruction
Leak around endotracheal tube cuff
Bronchoconstriction
Obstruction or crack in the sampling line
NRB = non-rebreathing circuit
in large animals. Bumps and dips in the expiratory plateau
may be caused by spontaneous respiratory efforts, heart-
beats, and movements of the animal by the surgeon
(Fig. 2.34).
Measurement of high ETCO2 confirms respiratory
acidosis. PaCO2 can be high when ETCO2 is normal
or low. CO2 waveform is essential aid for alerting
and troubleshooting abnormalities.
Changes in ETCO2 or waveform are useful indicators of
significant alteration in physiological status or equipment
malfunction (Table 2.6, see Fig. 2.33). A sudden decrease
in ETCO2 to 1.6-2.7 kPa (12-20 mmHg) is cause for
concern and the patient should be checked for hypoten-
sion or cardiac arrest. Absence of CO2 may indicate equip-
ment leaks and disconnection, pulmonary embolism or
air embolism. Detection of CO2 >5 mmHg immediately
after endotracheal intubation may rule out accidental
oesophageal intubation. Exhaled water vapour condenses
51
Section 1 Principles and procedures

Figure 2.34  Cardiac oscillations are seen as regular small dips in the CO2 waveform generated by heartbeats causing small air
movements within the airways. (A) Dog is breathing 13/minute with an end-tidal CO2 concentration of 46 mmHg (6.1 kPa)
indicating mild hypoventilation. (B) Dog is breathing only 5/minute with the same degree of hypoventilation. In both patients,
inspired CO2 of 0–2 mmHg is normal.

in the sampling tubing and water trap but unpredictable
and bizarre values are obtained when water enters the
monitor.
Abrupt decrease ETCO2 to 1.6-2.7 kPa (12-20 mmHg)
occurs with decreased cardiac output or cardiac arrest.
Significant correlation between ETCO2 and PaCO2 has
been recorded in dogs and horses, with the PaCO2 exceed-
ing the ETCO2 by 1.00–4.65 kPa (1–35 mmHg) depend-
ing on the degree of pulmonary shunting and lung
collapse. The difference between PaCO2 and ETCO2 is
usually less in dogs than in horses. In a group of mechani-
cally ventilated dogs in intensive care, the ETCO2 was on
average 0.67 kPa (5 mmHg) less than PaCO2 (Hendricks
& King, 1994). In anaesthetized healthy mature horses, an
average difference of 1.6 kPa (12 mmHg), range 0–4.3 kPa
(0–32 mmHg) was recorded during halothane and 1.9 kPa
(14 mmHg) during isoflurane anaesthesia (Meyer & Short,
1985; Cribb, 1988; Moens, 1989). In one study of 110
horses, the PaCO2−ETCO2 difference was greater in heavier
horses and was increased when horses were in dorsal
recumbency compared with lateral recumbency (Moens,
1989). Institution of controlled ventilation from the start
of anaesthesia in horses may preserve the PaCO2−ETCO2
difference to less than 10 mmHg. A mean PaCO2−ETCO2
difference of 1.8 ± 0.9 kPa (13.4 ± 6.9 mmHg; range
0–37.5 mmHg) was measured in 125 horses anaesthe-
tized with isoflurane in dorsal recumbency for colic
surgery (Trim, 1998). Spontaneously breathing foals
anaesthetized with isoflurane had a mean PaCO2−ETCO2
difference in the first hour of anaesthesia of 0.9 kPa
(7 mmHg) which increased over 90 minutes of anaesthe-
sia to 1.7 kPa (13 mmHg), coincident with an increase in
PaCO2 (Geiser & Rohrbach, 1992). This study emphasized

52
 Patient monitoring and clinical measurement
the limitations of capnometry in spontaneously breathing
anaesthetized foals.
In conditions in which hypoventilation is expected and
the ETCO2 value is normal or low, for example in dogs
with pulmonary disease or during thoracotomy, and
anaesthetized horses at risk for severe lung collapse, such
as colic patients or foals, one direct measurement of
PaCO2 by blood gas analysis is advisable, if available.
ETCO2 values exceeding 6.7 kPa (50 mmHg) represent
increased PaCO2 and significant hypoventilation. The
ETCO2 value at which controlled ventilation is recom-
mended varies between clinicians and is also dependent
on the patient’s disease or procedure.
Transcutaneous CO2 analysis
Carbon dioxide diffuses through tissues and can be
detected by a sensor on the skin. Transcutaneous capnom-
etry is proposed as a non-invasive method of detecting
respiratory depression in patients after anaesthesia and
surgery and in the ICU. The transcutaneous CO2 (TcPCO2)
sensor is warmed electrically and creates a local hyperae-
mia resulting in a measurement that is usually slightly
higher than PaCO2 (Eberhard, 2007). Published investiga-
tions in human patients have cited conflicting results, with
some studies confirming good correlation between TcPCO2
and PaCO2 and others significant bias and limits of agree-
ment with a low degree of correlation. Studies are needed
to determine the value of this monitor in veterinary
medicine.
Acid–base analysis
Maintaining blood pH within a normal range is important
for adequate cellular function. The most dominant buffer
system is the bicarbonate [HCO3−]/carbonic acid, a rela-
tionship that is described by the Henderson–Hasselbalch
equation where the ratio of [HCO3−] to dissolved CO2 is
20 : 1
pH = 6.1 + log[HCO3− ]/(PaCO2 × 0.03)
HCO3− is an important buffer because it is volatile,
being eliminated or retained as CO2 in the lungs, and is
effective at a range of pH values. As a primary acid–base
abnormality develops there is a physiological compensa-
tion in the opposite direction. Thus, when acid is added
to the system, it combines with HCO3 generating CO2 that
can be eliminated through the lungs. In contrast, added
base combines with carbonic acid (H2CO3) generating
HCO3− that can be eliminated via the kidneys. Respiratory
compensation may occur within hours but renal compen-
sation takes days. Other important buffers include pro-
teins and haemoglobin. When interpreting acid–base
status in an anaesthetized animal, it should be remem-
bered that anaesthetic agents depress respiration such that
Chapter 2
the compensatory respiratory response is eliminated. Thus
a patient may have normal acid–base status, respiratory
acidosis or alkalosis, metabolic acidosis or alkalosis, or a
mixture of two or three respiratory and metabolic
components.
Acid–base analysis is underpinned by complex mathe-
matical formulae (Wooten, 2010). The following informa-
tion is a simplified and abbreviated version for clinical
evaluation.
Blood gas and acid-base values
pH: The normal arterial pH of humans is 7.40. A pH <7.35
is referred to as an acidaemia and a pH >7.45 as an alka-
laemia. Blood pH of some other species differs slightly
from pH 7.40 and clinical assessment must take into
account the normal range of values for that species (see
Table. 2.4).
PaCO2: This value is representative of the rate and depth
of breathing and metabolic CO2 production. The normal
average value for PaCO2 is 5.3 kPa (40 mmHg) in most
species, except cats where pCO2 is lower. Venous blood
PCO2 will be approximately 0.8 kPa (6 mmHg) higher
than PaCO2. An increase in PaCO2 (hypercarbia, hyper-
capnia) results in a decrease in pH and is most frequently
due to hypoventilation. A decrease in PaCO2 results in
increased pH and is due to increased ventilation.
HCO3−: This value as reported by an automated blood
gas analyser is calculated from pH and PCO2, thus it is
representative of both respiratory and metabolic status.
For example, a high [HCO3−] may be due to metabolic
alkalosis or to a severe respiratory acidosis.
TCO2: Total CO2 (TCO2) is also representative of both
respiratory and metabolic status as it includes [HCO3−]
and dissolved CO2, although the contribution by dis-
solved CO2 is small (PCO2 mmHg × 0.003 mEq/L). Some-
times chemical determination of TCO2 in serum or plasma
is used as an estimate of blood bicarbonate concentration,
however, results obtained from biochemical autoanalysers
may be significantly different from that obtained by cal-
culation from pH and PCO2. Errors arise from differences
in handling the samples, such as exposure to air, underfill-
ing of blood collection tubes, delay in analysis, and renew-
ing reagents. A combination of these factors may decrease
the TCO2 by as much as 5.3 mEq/L in canine blood and
4.6 mEq/L in feline blood.
Base excess (BE): The BE value describes the buffering
capacity (bicarbonate and haemoglobin) of the blood and
provides a calculated assessment of the metabolic status
of the patient that is almost independent of respiratory
changes. There are a variety of formulae used to calculate
BE and automated blood gas analysers compute BE. The
value of BE describes the amount of acid or base (mEq/L)
that must be added in vitro to return the blood to pH 7.40
under standard conditions of PCO2 5.3 kPa (40 mmHg),
and temperature 37°C. Consequently, BE of zero is neither
53
Section 1 Principles and procedures

acidotic nor alkalotic, positive BE describes a metabolic
alkalosis and negative BE (base deficit) describes a meta-
bolic acidosis. Standard BE (SBE, also called BEecf) is the
BE value when haemoglobin is at 5 g/dL to represent more
clearly the BE of the entire extracellular fluid in vivo.
SBE can indicate the presence of a metabolic acidosis or
alkalosis but may be misleading in cases of mixed acid–
base abnormalities. It also does not provide information
about the cause(s) of the metabolic abnormalities. A cor-
rected formula for SBE (SBEc) can be applied that includes
values for albumin and phosphate (PO4) (Kellum, 2005).
In humans, SBEc = (HCO3 − 24.4) + ([8.3 × Albumin g/dL
−
× 0.15] + [0.29 × Phosphate mg/dL × 0.32]) × (pH − 7.4).
Normal SBE of 0 (range, ± 2.5 mEq/L) is used for
human patients, however, normal values differ between
species (Table 2.7). Since metabolic status is influenced by
diet, in general, species that are carnivores usually have a
mild metabolic acidosis, whereas metabolic alkalosis is
normal in species that are herbivores, as determined by
blood gas analysers using reference values for human
blood. The SBE of venous blood can be used to evaluate
acid–base status because the difference between arterial
and venous PCO2 is small.
Acid–base charts (Siggaard–Andersen) and a PO2 −
PCO2 diagram are available for easy interpretation of
blood gas analyses at sea-level and at high altitude (Paulev
& Zubieta-Calleja, 2005).
Anion gap (AG): The AG is calculated from measured
serum cations and anions as follows:
AG = (Na + + K + ) − (Cl− + HCO3− )
The gap is mainly due to weak acids, primarily albumin
and some PO4, and a minor part due to strong ions, such
as lactate and sulphate (SO4). Plasma proteins other than
albumin can be positive or negative but the final composi-
tion is generally neutral. AG may or may not be helpful
because it can be normal in the face of opposing metabolic
abnormalities. A change in [Na+] without concurrent
change in [Cl−], and vice versa, will alter the AG. Dehydra-
tion can widen the gap by increasing the concentrations
of the measured ions and hypoalbuminaemia decreases
the anion gap. Changes in albumin and PO4 commonly
occur in critically ill patients and must be considered
when interpreting AG (Kellum, 2007; Fidkowski &
Helstrom, 2009). A corrected formula for AG (AGc) is used
for human patients with metabolic acidosis (Kellum,
2005, 2007):

AGc = ([Na + + K + ] − [Cl− + HCO3− ]

Table 2.7  Reference ranges for acid–base and − (2[albumin in g/dL] + 0.5[phosphate in mg/dL])
biochemical parameters − lactate

Parameter Dogs Cats Horses or

HCO3− (mEq/L) 22.2 18 24–30

AGc = ([Na + + K + ] − [Cl− + HCO3− ]
(18.8–25.6) (14.4–21.6)
− (2[albumin in g/dL] + 1.5[phosphate in mmol/L])
SBE (mEq/L) −1.8 −6 ± 4.8 −6 ± 6 − lactate
(−0.2– +3.4) 5±2
−2.1 ± 2.3
Using these formulae, AGc should be approximately
Lactate (mmol/L) <2 <1.46 <2 zero.
Strong ion difference (SID): SID is defined as the differ-
Anion gap (mEq/L) 12–25 15–28 11.6 ± 5.06
17 ± 2.0
ence between the sum of the strong cations (Na+, K+, Ca2+,
and Mg2+) and the sum of the strong anions (Cl− and
Strong ion 34–44 40 ± 8.4 lactate). Ionized concentrations of Mg and Ca are used in
difference* (mEq/L) the formula but are sometimes omitted for simplicity. The
Strong ion gap −8 ± 2 −2 ± 6 apparent SID is defined as:
(mEq/L) 0.36 ± 1.84
SIDa = (Na + + K + + Ca 2 + + Mg 2 + ) − (Cl− + lactate)
ATOT† (mEq/L) 12–15
13.5 ± 0.55
An increase in SID is the result of metabolic alkalosis
* SID = (Na+ + K+) − (Cl− + lactate) and a decrease in SID the result of a metabolic acidosis.
† ATOT = 2.25 × albumin (g/dL) + 1.4 × globulin (g/dL) + 0.59 × Changes in SID not attributable to sodium or chloride fall
Pi (mg/dL) into a category called unidentified ions (UA) that includes
Navarro et al., 2005; Hopper and Haskins, 2008; Valverde et al.,
2008; Viu et al., 2010
substances such as ketoacids. Strong ion difference effec-
tive (SIDe) is calculated from a formula that includes

54
 Patient monitoring and clinical measurement
albumin and PO4 and requires use of a computer program
(Moviat et al., 2008).
SIDe = 2.46 × 10pH − 8 × PCO2 mmHg + (albumin g/dL)
× (0.123 × pH − 0.631) + (phosphate mEq/L)
× (0.309 × pH − 0.469)
Strong ion gap (SIG): SIG is the sum of unmeasured ions
and is equal to SIDe − SIDa. SIG is normally zero, although
a range of values has been reported for healthy human
patients, and does not change with changes in pH or
albumin concentration. Administration of colloids that
include gelatin are known to elevate the SIG. A high SIG
>2 mEq/L indicates accumulation of unmeasured anions as
a cause of acidosis. SIG ≥5 mEq/L has been associated with
increased mortality in human patients (Moviat et al., 2008).
AGc has a strong correlation with SIG, even when the
formula is simplified by omitting PO4 (Gunnerson, 2005).
A simplified calculation of SIG has also been used
(Constable, 2000):
SIG mEq/L = (2.2 [ Total protein g/dL] / 1 + 106.7 − pH ) − AG
Total weak acid concentration (ATOT): The ‘weak’ acids are
mostly proteins, especially albumin, and inorganic phos-
phate, and are not completely dissociated at physiological
pH. They can act as non-volatile buffers, switching between
forms that are associated or dissociated with a proton, i.e.
A− vs HA, in response to pH. These non-volatile buffers are
not in as large a quantity as the volatile buffer, HCO3−, but
still have significant effects on pH. Hypoproteinaemia
results in a non-respiratory alkalosis, whereas hyperprotei-
naemia causes non-respiratory acidosis.
Free water effect: The free water concentration is identi-
fied by sodium concentration, such that a deficit of free
water causes hypernatraemia and alkalosis (concentration
alkalosis) and excess of free water causes hyponatraemia
and acidosis (dilutional acidosis). The free water effect is
calculated by subtracting normal sodium concentration
from measured sodium and multiplying the change in
concentration by 0.25 in dogs and 0.22 in cats (Hopper &
Haskins, 2008).
Interpretation of acid base abnormalities
Step 1: Identification of the critical nature of the patient’s
acid–base status. pH values less than 7.25 and greater
than 7.55 can be associated with significant effects on
physiological function. Extreme values warrant immediate
management.
pH is determined by changes in PCO2, AGc or SID,
and ATOT.
Step 2: Determine whether a respiratory abnormality
exists. An increase in PaCO2 above normal is called a
Chapter 2
respiratory acidosis because increased CO2 causes the car-
bonic acid equilibrium equation to move to the right:
CO2 + H2O  H2CO3  H+ + HCO3−
If the PaCO2 and pH are deviated from normal in oppo-
site directions then a respiratory component is present. If
the PaCO2 and pH are changed in the same direction, then
respiratory and metabolic components are present.
Increased PaCO2 most frequently occurs due to decreased
ventilation caused by CNS depression from anaesthetic
agents or trauma, or to decreased ventilation from partial
airway obstruction, pulmonary disease, lung collapse, or
failure of intercostal or diaphragmatic muscle function. A
decrease in PaCO2 from normal is a respiratory alkalosis
and commonly occurs as a result of hyperventilation when
the patient is anxious or distressed, as a physiological
response to metabolic acidosis or hypoxia in conscious
patients, or due to mechanical overventilation. In human
patients, the change in pH expected from a change in
PaCO2 can be calculated:
• pH decreases by 0.05 unit and [HCO3−] increases
1 mEq/L for every acute 1.33 kPa (10 mmHg)
increase in PCO2
• pH increases 0.10 unit and [HCO3−] decreases
2 mEq/L for every acute 1.33 kPa (10 mmHg)
decrease in PCO2
Hopper & Haskins (2008) reported expected compensa-
tion in dogs as:
• [HCO3−] increases 1.5 mEq/L for every acute 1.33 kPa
(10 mmHg) increase in PCO2
• [HCO3−] decreases 2.5 mEq/L for every acute 1.33 kPa
(10 mmHg) decrease in PCO2
Chronic hypercarbia or hypocarbia generate greater
changes in [HCO3−] so that pH gradually returns to
normal.
Step 3: Determine the metabolic component using
blood gas and laboratory results. Complete assessment of
acid–base balance will require knowledge of electrolyte
and lactate values, patient history and immediate details
(i.e. anaesthesia, ventilatory and circulatory status). It
has been proposed that non-respiratory acid–base abnor-
malities fall into four categories: (1) free water deficit or
excess; (2) increased or decreased [Cl−]; (3) changes in
protein; and (4) presence of unmeasured organic anions
(Fidkowski & Helstrom, 2009).
SBE will determine the direction and magnitude of
metabolic abnormality in most patients. It is less accurate
when abnormal levels of lactate, phosphate, or proteins
are present. Calculation of the AG may or may not reveal
the presence of unmeasured anions as the AG is influenced
by electrolyte abnormalities and hypoproteinaemia.
Diagnosis of hyperchloraemic metabolic acidosis is
determined by measurement of Na and Cl, the absolute
55
Section 1 Principles and procedures
value for Cl, and the ratio of Na to Cl. The ratio of sodium
to chloride is important because the Cl may be within the
accepted normal range but calculation of SBE or SIDa will
reveal a significant change in metabolic status. Calculation
of AGc or SIG more specifically detects changes in unmeas-
ured strong ions, e.g. lactate. Elevated blood lactate may
have several origins but should always be investigated for
unsuspected pathology. Many unmeasured anions have
been identified, including citrate, isocitrate, ketoglutarate,
succinate, and malate.
Simple cases may be managed using pH and blood gas
analysis and routine laboratory tests to provide informa-
tion on pH, PCO2, SBE, and AG or AGc. Accurate determi-
nation of metabolic abnormalities in complex cases can
be made using AGc or SIG when the essential laboratory
test results and computerized formulae are available.
Monitoring body temperature
In the normal animal, body heat is unevenly distributed
with the core temperature being 2–4°C higher than the
peripheral. General anaesthesia inhibits vasoconstriction,
allowing generalized redistribution of body heat. An addi-
tional decrease in body temperature occurs as heat is lost
to the environment by exposure to cold operating room
conditions, skin preparation with cold solutions, and
abdominal surgical exposure. Furthermore, anaesthetics
inhibit thermoregulation, vasoconstriction, and shivering,
thereby decreasing the thresholds for cold responses.
Administration of unwarmed IV fluid contributes substan-
tially to the decrease in body temperature.
One method used in research animals to monitor tem-
perature non-invasively involves subcutaneous injection
of temperature-sensitive microchips. One study in experi-
mental goats compared different sites with core (abdomi-
nal) and rectal temperatures (Torrao et al., 2011). The
results determined that temperature measured from
probes in the shoulder, flank or muscle varied from core
temperature by up to 3.5°C and the differences varied
inconsistently. Microchips implanted in the retroperito-
neum most closely approximated core and rectal body
temperatures with little variability.
Hypothermia
There does not seem to be a generally accepted definition
of hypothermia and the definition should be appropriate
to the species concerned. One study group has defined
mild hypothermia in human patients to be between 34°C
(93.2°F) and 36°C (96.8°F) (Reynolds et al., 2008). A
decrease in temperature of 1–3°C below normal has been
demonstrated to provide substantial protection against
cerebral ischaemia and hypoxaemia in anaesthetized dogs
(Wass et al., 1995). However, perioperative hypothermia
is associated with several significant adverse effects (Table
56
Table 2.8  Adverse effects of perianaesthetic
hypothermia
Impaired cardiovascular function
Hypoventilation
Decreased metabolism and detoxification of anaesthetic drugs
Weakness during recovery from anaesthesia
Decreased resistance to infection
Increased incidence of surgical wound infection
Increased postoperative protein catabolism
2.8) (Carli et al., 1991; Sheffield et al., 1994; Kurz et al.,
1996; Reynolds et al., 2008). Mild hypothermia has been
associated with triple the incidences of adverse myocardial
events in elderly human patients and postoperative surgi-
cal infection; effects that apply to other species. Body tem-
perature <35.6°C (96°F) appears to be associated with
increased ataxia in horses during recovery from inhalation
anaes­thesia. Life-threatening cardiovascular depression
may develop when the temperature decreases below
32.8°C (91°F).
Rectal or oesophageal temperature should be monitored
at regular intervals during inhalation anaesthesia, during
protracted total intravenous anaesthesia, and during
recovery from anaesthesia. Small animals can be insulated
from a cool environment by a variety of methods, includ-
ing plastic covered foam pads and hot water circulating
pads to lie on, and wrapping of extremities with towels
or plastic bubble-wrap or cling-film. Heat loss from
the respiratory tract may be minimized by ensuring
that the inspired air remains warm and humidified. This
can be accomplished by employing rebreathing circuits
and low flow administration, or by attachment of a
humidifier to the endotracheal connection of the anaes-
thetic circuit.
Active skin warming of the limbs may be the most effec-
tive method of preventing heat loss (Cabell et al., 1997).
This can be accomplished by application of hot water or
hot air circulating devices (e.g. Bair Hugger), or warmed
towels, warmed fluid bags identified for this purpose by
injection of food colour, and gel-filled packs. Special care
should be taken to avoid skin sloughing from burns
caused by application of devices that are too hot. Electrical
heating pads and packs heated in a microwave oven are
frequently to blame for tissue damage. It should also be
remembered that warming devices placed over the site of
an intramuscular injection, or an opioid-filled patch
applied to the skin, may alter local blood flow and speed
absorption of the drug. Fluids to be administered IV
should be warm, either in the bag or bottle by storage in
an incubator or at the time of administration by attaching
a warming block or device to the administration line.
 Patient monitoring and clinical measurement Chapter 2

cage and providing sedation, for example, butorphanol,

Table 2.9  Causes of hyperthermia
0.2 mg/kg IM, with or without acepromazine, 0.05–
0.1 mg/kg IM. Circulating iced water through a rigid
Causes Examples plastic pad placed in the cage with the cat is an effective
Fever method of reducing body temperature. Administration of
ketamine or hydromorphone and other opioids to cats has
Increased hypothalamic set Infection, inflammation, also been associated with hyperthermia developing during
point septicaemia, endotoxaemia
recovery from anaesthesia (Posner et al., 2010). Rarely,
Hyperthermia hyperthermia is a manifestation of the malignant hyper-
thermia syndrome (MH) which is a life-threatening
Increased heat generation: Adverse drug reaction including
hypermetabolic condition triggered by stress and certain
increased basal metabolic amphetamines, neuroleptic
rate, increased muscle syndrome, serotonin syndrome anaesthetic agents.
activity, increased thyroid Seizures
hormone, increased Thyrotoxicosis
sympathetic activity Phaeochromocytoma Malignant hyperthermia
Malignant hyperthermia Malignant hyperthermia (MH) occurs most frequently
syndrome
during anaesthesia of human beings and pigs (McGrath,
Decreased heat dissipation Increased ambient temperature 1986; Roewer et al., 1995), but has been reported to occur
Old age in dogs (O’Brien et al., 1990; Nelson, 1991; Roberts et al.,
Decreased cardiac output 2001), cats (Bellah et al., 1989), and horses (Manley et al.,
1983; Klein et al., 1989; Aleman et al., 2009). Clinical
McAllen & Schwartz, 2010
signs of MH in pigs (see Chapter 14) usually include an
increase in temperature, increased respiratory rate and
depth, increased ETCO2 and PaCO2, metabolic acidosis,
tachycardia, hypertension, and arrhythmias. Purple
Prevention of heat loss should be started at the beginning blotches may be observed in the skin of the abdomen and
of anaesthesia. Preparation of the surgical site is often the snout. The soda lime canister on the anaesthesia machine
time of greatest heat loss if active warming is not present may become excessively hot to touch and the absorbent
and alcohol and cold solutions are used in skin prepara- changes colour rapidly, reflecting massive carbon dioxide
tion. An overhead hospital infant radiant heat warmer has production. Rigidity of the jaw and limb muscles may be
proven effective at preventing hypothermia in cats and observed as the condition progresses. The animal dies
small dogs. unless the condition is treated early.
The clinical appearance of dogs developing MH during
anaesthesia may differ from pigs. Tachycardia may not be
Hyperthermia a feature, skeletal muscle rigidity may not occur, and rectal
Increased body temperature is occasionally measured temperature may not increase until the syndrome is well
in anaesthetized animals. Hyperthermia developing in established (Nelson, 1991). The earliest signs may be
dogs and cats is most often caused by either excessive related to increased CO2 production. These signs include
application of heat in an attempt to prevent hypothermia an increased respiratory rate and depth, rapid changing of
or by a pyrogenic reaction to a bacterial infection or CO2 absorbent colour, a hot CO2 absorbent canister, and
inflammation, a contaminant in IV fluids, or drugs. increased ETCO2 in the absence of hypoventilation or mal-
Other causes of intraoperative hyperthermia are loss of functioning one-way valves. Increased respiratory rate
central nervous system temperature regulation, thyrotoxi- would be the only one of these signs present in a dog that
cosis, or phaeochromocytoma (Table 2.9). Symptomatic was merely overheated.
treatment includes wetting the coat or hair with cold The clinical picture of MH in horses is not clear cut.
water, IV administration of cold fluids, and sedation if Abnormal measurements may not be observed for some
applicable. Determination of the cause of hyperthermia time after induction of anaesthesia. Observed signs may
may indicate other specific treatment. Hyperthermia be suggestive that the horse is in a light plane of anaesthe-
(40.5°C; 105°F) quite frequently develops in cats during sia, however, the earliest changes are usually increased
recovery from anaesthesia that included administration PaCO2 and ETCO2. Heart rates may be mildly elevated and
of tiletamine–zolazepam. In these animals, the increase arterial blood pressure is often within the normal range
in temperature is associated with increased muscle for inhalation anaesthesia (Manley et al., 1983; Klein
activity such as paddling, uncoordinated movements, et al., 1989). Changes in anaesthetic management may
or purposeful movements directed at restraints or band- permit the horse to survive anaesthesia but severe rhab-
ages. Treatment that is usually effective includes directing domyolysis developing during recovery from anaesthesia
a flow of air over the cat from a fan placed outside the may necessitate euthanasia.

57
Section 1 Principles and procedures
Monitoring urine volume
The urinary output depends on the renal blood flow that,
in turn, depends on cardiac output and circulating blood
volume, and thus it is a relatively sensitive indicator of the
circulatory state during anaesthesia. Measurement of urine
production is advisable in animals with severe chronic
renal disease, renal failure, or circulatory failure from non-
renal causes. The urinary bladder may be catheterized
using aseptic technique before anaesthesia or after induc-
tion of anaesthesia, and the catheter connected to a plastic
bag for continuous collection of urine. In event of inade-
quate urine flow, the catheter should be checked for block-
age by mucus or blood and that urine is not pooling in
the bladder and cannot drain because of the relationship
between the catheter tip and positioning of the animal.
Alternatively, urine may be collected and measured at the
end of anaesthesia. Urine output of less than 1 mL/kg/
hour is considered to be inadequate. However, urine flow
during anaesthesia is very variable, for example, one group
of healthy dogs anaesthetized for orthopaedic procedures
with oxymorphone, propofol, and isoflurane produced
0–2.2 mL/kg/h (mean 0.46 mL/kg/h) (Boscan et al.,
2010).
Failure of patients to produce an adequate urine volume
over the course of anaesthesia may be unrelated to intra-
operative cardiovascular function. Indeed, fluid retention
is now a recognized complication of surgery in human
patients and has been documented to occur in anaesthe-
tized dogs (Boscan et  al., 2010; Cagini et  al., 2011). Fluid
retention has been measured by a variety of methods
including weighing patients before and after anaesthesia,
calculation of the discrepancy between the volume of fluid
administered and the volume of urine produced, and
bioimpedance analysis. The latter method involves
passing a small undetectable alternating current through
the body, from hand to foot electrodes in humans, and
bioimpedance analysis measures the resistance to flow of
the current. This technique has detected increases in total
body water and extracellular fluid volume after anaesthe-
sia in dogs (Boscan et  al., 2010). The tendency to retain
fluid has been documented in human patients to be
greater on the second postoperative day and apparently
unrelated to age or sex of the patient, early mobilization
after surgery and early oral intake (Cagini et  al., 2011).
Fluid retention occurs even with intraoperative fluid
restriction, although the amount is increased with high
volume fluid therapy. The cause of fluid retention is
thought to be multifactorial. Decreased arterial pressure
or hypovolaemia during anaesthesia causes release of
vasopressin (antidiuretic hormone) and that increases
free water absorption in distal tubules of the kidney
(Hauptman et  al., 2000). Some anaesthetic agents may
influence urine output, for example, decreased urine
production was measured in dogs receiving morphine
for premedication when compared with dogs without
58
morphine (Robertson et  al., 2001). A study of healthy
and traumatized dogs in the ICU receiving LRS 60  mL/
kg/day with a continuous infusion of either morphine,
0.12  mg/kg/h, or fentanyl, 3  µg/kg/h, confirmed that
both opioids decreased urine flow significantly (Anderson
& Day, 2008). Healthy control dogs receiving only LRS
produced urine at a rate of 1.23 ± 0.13  mL/kg/h. Mor-
phine or fentanyl infusion decreased urine production
to approximately 0.7  mL/kg/h and urine specific gravity
increased.
Monitoring blood glucose
Clinical signs of hypoglycaemia may not be obvious
during anaesthesia and the condition may go unrecog-
nized. Consequences of hypoglycaemia are coma, hypo-
tension, or prolonged recovery from anaesthesia with
depression, weakness, or even seizures.
Animals at risk for developing hypoglycaemia during
anaesthesia include paediatric patients, diabetics, and
animals with hepatic disease, portosystemic shunt, insuli-
noma, and septicaemia or endotoxaemia. Occasionally,
healthy adult sheep, goats, and even horses develop
hypoglycaemia which manifests as a prolonged or weak
recovery from anaesthesia. Routine monitoring of patients
at risk for hypoglycaemia should include measurement of
blood glucose at the start and the end of anaesthesia.
Blood glucose can be determined rapidly using reagent
strips and a glucometer. Animals with low blood glucose
concentrations initially or those undergoing major or
prolonged surgery, should have their blood glucose
monitored at approximately 1hour intervals during
anaesthesia.
Patients at risk for hypoglycemia should be given 5%
dextrose in water (D5W) as part of the intraoperative IV
fluid therapy. D5W should be infused at a rate of 3
(2–5) mL/kg/hour to maintain blood glucose between 5.5
and 11.0 mmol/L (100 and 200 mg/dL). Balanced electro-
lyte solution should also be infused at the usual rate of
5–10 mL/kg/hour.
Monitoring neuromuscular blockade
The mechanical response to nerve stimulation (i.e. mus-
cular contraction) may be observed following the applica-
tion of supramaximal single, tetanic or ‘train-of-four’
electrical stimuli to a suitable peripheral motor nerve,
usually a foot twitch in response to stimulation of the
peroneal, tibial, or ulnar nerves. During general anaesthe-
sia the response obtained may be influenced by the anaes-
thetic agents and any neuromuscular blocking drugs
which have been used. Details about neuromuscular
blocking drugs and the monitoring technique are given in
Chapter 8.

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63
 Caso clínico 5
XIII parte

“LUCAS”
Cocker Spaniel
Macho no castrado, 12 kg

Monitorización
Fluidoterapia
ü  Los animales cardiópatas no deben recibir fluídos a una
velocidad superior a 5 ml/kg/h.

ü Lo ideal es usar de fluidoterapia cristaloides hipotónicos, como el

glucosalino isotónico 3,6. Lleva 3,6 gr de glucosa en 100 ml y NaCl
0.3 gr en 100ml. De este cristaloide isotónico se consume
rápidamente la glucosa y queda hipotónico, está indicado en
pacientes renales donde el sodio es peligroso.
ü  Se ha de monitorizar bien la presión arterial (con doppler o
Invasiva) para evitar un exceso de trabajo cardiaco (evitando la
hipotensión, se evita la taquicardia secundaria)

ü  La presión arterial media se ha de mantener ≥ 70 mmHg

(asegura una correcta perfusión renal, coronaria y cerebral)

ü  En caso de hipotensión se pueden usar coloides (isohes 6% 2-5

ml/kg de en 20 min y CRI 20 ml/kg/día)

ü Si no la mejoramos usaremos inyectables inotrópicos positivos

(dobutamina 5 µg/kg/min)
Es preferible a la dopamina que además de inotrópica, es también
vasopresora e incrementa el trabajo cardíaco
Preparación prequirúrgica
•  Analgesia
•  Buprenorfina 20 µg/kg IV
•  Lidocaína 25 µg/kg/min
•  Antibioterapia
•  Cefazolina 25 mg/kg IV q 8h
•  Fluidoterapia
•  Glucosalino 0.3% 5 ml/kg/h
LAPAROTOMÍA

Félix García

Enterotomía para extracción C.E

Hueso de melocotón
Félix García
Félix García

¿Cómo cerrarías esta incisión?

 Caso clínico 5
XI parte

“LUCAS”
Cocker Spaniel
Macho no castrado, 12 kg

Ya sabes cómo ampliar las pruebas

bioquímicas para aclarar más la
hepatopatía de Lucas
El hígado tiene la capacidad de regenerarse y una amplia reserva
funcional, de manera que aunque esté gravemente dañado las pruebas
de laboratorio pueden ser normales o casi normales y los síntomas
clínicos pueden estar ausentes o ser pocos.

Por estas y otras razones es muy importante alcanzar un diagnóstico

preciso cuando las pruebas de laboratorio sobre el hígado son anormales.
Es necesario distinguir en particular entre marcadores de daño hepático
y pruebas funcionales del hígado.

DAÑO HEPÁTICO

Los marcadores principales de daños en el hígado son las enzimas

hepáticas ALT, AST, AP y GGT. Están localizados en diferentes lugares
de las células hepáticas y es posible medirlos en el suero cuando el
hígado está dañado por fugas o necrosis, pero estos daños pueden
deberse a una enfermedad hepática primaria o secundaria. Además, no
todas estas enzimas son específicas del hígado, y por ello pueden estar
elevadas en otras situaciones patológicas o fisiológicas.
 FUNCIONALIDAD HEPÁTICA

Estas pruebas miden la capacidad del órgano para :

o  sintetizar sustancias (albúminas, factores de coagulación,
colesterol, etc.)
o  elaborarlas (bilirrubina)
o  reabsorberlas (ácidos biliares)
o  metabolizarlas (amoniaco, generado por las bacterias entéricas y
absorbido a través de la v. porta)
o  excretarlas (bromosulfoftaleína)
Entre estas pruebas, las de ácidos biliares y bilirrubina se consideran las
más importantes.
 FUNCIONALIDAD HEPÁTICA

Estas pruebas miden la capacidad del órgano para :

o  sintetizar sustancias (albúminas, factores de coagulación,
colesterol, etc.)
o  elaborarlas (bilirrubina)
o  reabsorberlas (ácidos biliares)
o  metabolizarlas (amoniaco, generado por las bacterias entéricas y
absorbido a través de la v. porta)
o  excretarlas (bromosulfoftaleína).
Entre estas pruebas, las de ácidos biliares y bilirrubina se consideran las
más importantes.

Parámetros Resultados V. Referencia

Ac. Biliares pre 23.33 mg/dl 0 -15
Ac. Biliares post 86.37 mg/dl 0 - 30
Bilirrubina total 0.1 g/dL 0 – 0.9
NH4 22 g/dl 0 - 98
Parece que el hígado de lucas no funciona del todo bien.
El siguiente paso para el diagnóstico, sería la biopsia o la citología,
pero los propietarios prefieren no hacer más pruebas.

Además la obstrucción intestinal aunque no sea

completa, es urgente, no es lo mismo una enterotomía
que una enterectomía por culpa de tardar en intervenir, la
primera premisa de la cirugía intestinal es hacerla cuanto
antes si el estado del animal lo permite.
Parece que el hígado de lucas no funciona del todo bien.
El siguiente paso para el diagnóstico (vascular, fibrosis…), sería la
biopsia o la citología, pero los propietarios prefieren no hacer más
pruebas.

¿Qué fármacos no usarías en la anestesia de Lucas teniendo en

cuenta el hígado?

¿Qué fármacos no usarías en la anestesia de Lucas teniendo en

cuenta el soplo?

Indica la fluidoterapia más adecuada, producto y velocidad

81) Duodenogastric Intussusception with Concurrent Gastric
Foreign Body in a Dog: A Case Report and Literature Review
David A. Allman, DVM, DACVS, Michael P. Pastori
(J Am Anim Hosp Assoc 2013; 49:64–69.
http://www.jaaha.org.are.uab.cat/content/49/1/64.full.pdf+html
 
RESUMEN  (INT:  INTUSUSCEPCIONES)  

La  intususcepción  se  define  como  la  introducción  de  un  segmento  intestinal  sobre  
otro.  
El  segmento  que  se  desplaza  se  denomina  intussceptum  y  el  que  lo  recibe  
intususcipiens.  
Las  más  frecuentes  son  las  ileocólicas,  pero  pueden  ocurrir  en  cualquier  tramo  del  
tubo  digestivo.  
 
La  mayoría  de  las  INT.  ocurren  en  sentido  del  peristaltismo  intestinal  
(normógradas),  aunque  también  pueden  ser  en  sentido  inverso  al  peristaltismo  
(retrógradas).  
La  etiología  es  desconocida,  en  animales  menores  de  un  año,  son  en  la  inmensa  
mayoría  de  origen  idiopático.  
Pueden  ocurrir  por  diferencia  de  tamaños  de  diámetros  en  distintos  segmentos  
intestinales,  o  por  obstrucciones  mecánicas  (cuerpos  extraños,  adherencias  
extraluminales,  pólipos  intestinales,  etc).  

Existen  factores  predisponentes:  

-­‐ Parasitosis  intestinales  

-­‐ Cuerpos  extraños  
-­‐ Gastroenteritis  víricas  
-­‐ Intolerancias  alimentarias  
-­‐ Tumores  intestinales  
-­‐ Transplantes  renales  
-­‐ Cirugía  abdominal  
-­‐ anestesias  
-­‐ leptospirosis  
-­‐ intoxicación  por  carbamatos  
La  INT,  se  nombra  citando  primero  el  intusceptum  y  luego  el  intususcepiens.  P  ej:  
INT  ileocólica,  el  ileo  se  invagina  dentro  del  colon.  

Los  perros  con  INT  del  tracto  GI  superior,  presentan  una  sintomatologíaa  aguda  y  
severa,  no  así  los  que  presentan  INT  en  tracto  GI  bajo,  en  la  que  la  sintomatología  
es  más  crónica.  
  
En  ese  artículo  se  presenta  una  INT  duodenogástrica,  en  la  que  el  píloro  y  el  
duodeno  se  invaginan  dentro  del  estómago.  
Son  muy  raras  de  aparecer.    

Su  mortalidad  en  el  estudio  fue  de  un  50%.  

Son  más  frecuentes  en  perros  de  raza  grandes,  pero  también  pueden  aparecer  en  
razas  pequeñas.  
Todos  los  animales  que  las  presentaros  tenían  vómitos  agudos,  fallo  renal,  
intolerancia  alimentaria  y  cuerpos  extraños  gástricos  como  factores  
predisponentes.  
Es  una  urgencia  quirúrgica,  pero  hay  que  estabilizar  al  animal  pues  su  balance  
electrolítico,  su  fallo  renal  y  las  necesidades  cardiovasculares.  
En  algunos  casos  la  ecografía  fue  diagnóstica,  pero  en  otros  se  entró  a  quirófano  
con  la  idea  de  intervenir  un  cuerpo  extraño.  
 
PREGUNTAS  

EN  CUANTO  A  LA  INT.  ,  CUÁLES  SON  MÁS  FRECUENTES?  

Las  ileocólicas.  
CUAL  ES  EL  %  DE  SUPERVIVIENCIA  EN  EL  ESTUDIO?  

50%.  
EN  QUÉ  DIRECCIÓN  SON  MÁS  FRECUENTES?  
En  sentido  del  peristaltismo  intestinal.  
CÓMO  PODEMOS  PREVENIR  LAS  RECIDIVAS?  

Con  gastropexia  y  duodenopexia.    

QUÉ  FACTORES  PREDISPONENTES  HAY?  
Existen  factores  predisponentes:  

-­‐ Parasitosis  intestinales  

-­‐ Cuerpos  extraños  
-­‐ Gastroenteritis  víricas  
-­‐ Intolerancias  alimentarias  
-­‐ Tumores  intestinales  
-­‐ Transplantes  renales  
-­‐ Cirugía  abdominal  
-­‐ anestesias  
-­‐ leptospirosis  
 -­‐ intoxicación  por  carbamatos.  
 

Gastrointestinal  foreign  bodies  in  dogs  and  

cats:  a  retrospective  study  of  208  cases  
 

Journal  of  Small  Animal  Practice  (2009)  50,  (11)  576–583  

 
G.  HAYES*  
 

¿A  qué  porcentaje  de  animales  se  le  realizó  una  laparotomía  exploratoria  sin  tener  
clara  la  presencia  del  cuerpo  extraño?  
 

Un  9%  se  abrió  sin  tener  claro  que  hubiese  cuerpo  extraño  
 
¿Influyó  el  tipo  de  cuerpo  extraño  en  la  supervivencia?  

0·22),  ileum  (P=0·73)  or  colon  

(P=0·63).  

The  presence  of  a  linear  foreign  body  was  associated  with  a  significantly  higher  
mortality  rate  than  the  presence  of  a  discrete  foreign  body  (P<0·01),  and  cases  
undergoing  multiple  gastrointestinal  incisions  

had  a  significantly  higher  mortality  outcome  and  were  rejected  from  the  model.  
This  suggested  

that  the  number  of  incisions  was  a  more  significant  predictor  of  a  poor  outcome  
than  the  presence  of  a  linear  foreign  body  or  an  interaction  between  these  
variables.  
 
 

¿Por  qué  crees  que  llega  a  conseguir  una  supervivencia  del  94%  sin  apenas  
dehiscencias?  
Porque  si  no  lo  ve  claro  lo  eutanasia,  es  un  hospital  de  caridad  donde  no  puede  
proponer  postoperatorios  complicados,  además  reduce  las  enterectomías,  sólo  
hace  dos  de  las  180,  intenta  evitar  hacerlas,  

 
 
Indica  qué  régimen  postoperatorio  instaura  en  los  animales  

 
12-­‐24  líquidos  orales  
18-­‐30  comida  
 

Fluidoterapia  hasta  la  ingestión  de  líquidos  y  Antibiótico  y  analgesia  por  tres  días  
 
¿Cuál  fue  el  principal  factor  que  mejoró  los  resultados  de  los  cuerpos  extraños  
digestivos?  
 
La  supervivencia  fue  mejor  en  los  animales  que  vinieron  antes  al  hospital  porque  
llevaban  menos  días,  también  hubo  mejores  resultados  en  los  cuerpos  extraños  
que  el  propietario  fue  consciente  de  que  su  animal  se  lo  tragaba..  Hubo  peores  
resultados  en  los  animales  que  tenían  los  síntomas  desde  hacía  más  días  y  además  
si  el  propietario  no  sabía  que  se  había  tragado  un  cuerpo  extraño.  
 

¿Qué  porcentaje  de  animales  se  diagnosticó  por  palpación?  

En  el  76%  de  los  perros  se  palpó  el  cuerpo  extraño,  estando  despierto  o  
tranquilizado  

En  el  60%  de  los  gatos  se  palpó  

 
 

Indica  el  %  de  supervivencia  en  perros  y  gatos  tras  la  extracción  de  un  cuerpo  
extraño  digestivo  y  ¿Si  es  lineal?  
 

(94  per  cent  in  dogs  and  100  per  cent  in  cats)  
 as  opposed  to  linear  foreign  bodies  (80  per  cent  in  dogs  and  63  per  cent  in  cats).  
 
Indica  que  patrón  de  sutura  realiza  en  las  enterotomías.  
 

Patron  simple  interrumpido.  

 
¿Cuál  fue  la  localización  más  típica  de  los  cuerpos  extraños  digestivos  en  el  gato?  

En  gatos  el  25%  de  los  cuerpos  extraños  estaban  debajo  de  la  lengua.  
 
 
¿Qué  factores  influyen  en  la  cicatrización  del  intestino?  

1) La  viablidad  de  la  pared  intestinal  

2) El  sobrecrecimiento  bacteriano  en  la  luz  intestinal  
3) La  hipoproteinemia  
4) El  íleo  paralítico  
 

 
 
¿Por  qué  hubo  peores  resultados  en  los  gatos?  
Porque  tardan  más  en  dar  síntomas  y  un  porcentaje  muy  elevado  eran  cuerpos  
extraños  lineales  
 

Feline  gastrointestinal  foreign  bodies  

 

Trevor  N.  Bebchuk,  DVM  

 
Vet  Clin  Small  Anim  32  (2002)  861–880  
 

¿Por  qué  cicatriza  peor  una  herida  en  el  esófago?  

Porque  por  carecer  de  serosa,  no  se  produce  el  sellado  prematuro  de  fibrina  que  
ocurre  en  el  resto  del  tracto  digestivo  
 
 
Enumera  los  tres  lugares  del  esófago  donde  existen  estenosis  anatómicas?  
 

These  include  the  cricopharyngeal  sphincter,  the  base  of  the  heart,  and  the  
esophageal  hiatus  in  the  diaphragm.  

 
 
Additionally,  foreign  bodies  may  lodge  at  the  thoracic  inlet,  where  advancement  

 
 
Indica  el  patrón  de  sutura  que  debes  realizar  en  una  esofagotomía  y  con  qué  
material  de  sutura  lo  realizarías  ¿Cómo  puedes  reforzar  la  sutura?  
 
The  esophagotomy  incision  can  be  closed  in  one  or  two  layers.  The  first  layer  is  an  
appositional  pattern  in  the  mucosa  and  submucosa,  and  the  second  layer  is  an  
appositional  pattern  in  the  muscularis.  
The  holding  layer  is  the  submucosa.  If  the  esophageal  wall  does  not  look  healthy,  a  
resection  and  anastomosis  should  be  performed  on  the  damaged  region.  

Anastomosis  of  the  esophagus  can  be  performed  with  a  one-­‐  or  two  layer    closure.  
Suture  material  for  esophageal  surgery  in  cats  should  be  a  synthetic,  
monofilament,  absorbable  suture,  such  as  polydioxanone,  in  a  4-­‐0  size  and  with  a  
swaged  on  reverse  cutting  needle.  If  there  is  still  concern  relative  to  leakage  of  the  
esophagus  at  the  site  of  the  anastomosis  or  esophagotomy,  an  omental  patch  can  
be  brought  through  the  diaphragm  and  wrapped  over  the  anastomosis,  a  
pericardial  reinforcement  can  be  applied,  or  a  pedicle  intercostal  graft  can  be  used  

 
¿Cuál  es  la  mayor  complicación  y    en  qué  porcentaje  puede  ocurrir  tras  una  
esofagotomía?  
 
La  infección,  y  ocurre  en  un  57%  
 

¿Es    interesante  colocar  un  tubo  de  faringostomía  tras  una  esfagotomía?    Razona  tu  
respuesta.  

 
In  the  postoperative  period,  a  pharyngostomy  

tube  can  be  used  to  provide  caloric  and  fluid  requirements;  however,  
this  is  controversial,  because  the  presence  of  the  intraluminal  tube  may  

impair  esophageal  healing  [5].  

¿Cuando  no  hay  variación  en  el  pH  sanguíneo  de  un  gato  con  cuerpo  extraño  
digestivo?  
Cuando  se  pierden  tanta  secreción  ácida  desde  el  estómago,  como  básica  desde  el  
intestino  delgado,  bilis  y  páncreas.  
 

 
Enumera  los  síntomas  que  puede  presentar  un  gato  con  un  cuerpo  extraño  
digestivo  
 
Clinical  signs  that  may  be  present  include  vomiting,  diarrhea,  regurgitation,  
ptyalism,  inappetence,  anorexia,  depression,  dehydration,  abdominal  pain,  
abdominal  distention,  palpable  firm  segments  of  the  intestines,  palpable  intestinal  
dilation,  and  many  more.    
 

¿Cuál  es  la  modificación  más  típica  del  hemograma  en  un  gato  con  un  cuerpo  
extraño  digestivo?  
 

La  leucocitosis,  con  o  sin  desviación  a  la  izquierda,  dependiendo  de  la  peritonitis  
 
¿Cómo  varían  los  iones  y  el  pH  en  una  obstrucción  pilórica?  

 
Hay  alcalosis  ya  que  sólo  se  pierden  ácidos,  hipokalemia  e  hipocloremia    
 
 

 
 
¿Cómo  puedes  producer  la  emesis  en  un  gato  para  favorecer  la  expulsión  de  un  
cuerpo  extraño  gástrico?  
 
vomiting  can  be  induced  with  xylazine  (Rompun)  at  a  dose  of  1  mg/kg  of  body  
weight  
 
 

Cuál  es  la  mortalidad  tras  la  extracción  quirúrgica  de  un  cuerpo  extraño  digestivo?  
 
Un  7%  si  no  hay  dehiscencia  y  un    80%  si  la  hay  

 
 
¿Cual  es  el  signo  radiológico  patognomónico  en  una  obstrucción  intestinal?  
 

A  small  intestinal  diameter  greater  than  1.6  times  the  depth  of  the  midcentrum  of  
the  

fifth  vertebra  has  been  used  as  a  predictor  of  intestinal  obstruction  in  dogs.  A  
similar  ratio  may  be  useful  in  cats.    
 

 
¿Por  qué  no  se  aconseja  realizar  la  incisión  de  la  enterotomía  proximal  a  la  
obstrucción?  
 

Enterotomy  proximal  to  the  obstruction  is  not  recommended,  because  distention  
with  
gas  and  fluid  and  the  passage  of  the  foreign  body  may  have  caused  some  
degree  of  vascular  compromise  .  

 
 
 

 
Por  qué  un  cuerpo  extraño  lineal  es  más  difícil  de  diagnosticar?  

Porque  no  da  obstrucción  completa  y  cuesta  más  diagnosticar,  no  suelen  haber  
vómitos  frecuentes,  hasta  que  viene  la  perforación  y  el  gato  empeora  de  manera  
suúbita  
  
¿Qué  modificaciones  se  producen  en  el  intestino  para  intentar  superar  el  síndrome  
de  intestino  corto  si  eliminamos  más  del  60´%?  
 

The  pathophysiology  of  this  syndrome  is  a  result  of  decreased  secretin  and  
cholecystokinin  in  the  proximal  duodenum,  thereby  decreasing  pancreatic  and  
biliary  secretions.  The  loss  of  intestinal  brush  border  enzymes  also  contributes  to  
the  syndrome,  with  the  changes  resulting  in  maldigestion.  Decreased  intestinal  
transit  time  and  decreased  mucosal  surface  area  may  also  contribute  to  
malabsorption.  The  decreased  transit  time,  increased  lumenal  osmotic  pressure,  
bacterial  overgrowth,  and  gastric  hypersecretion  ultimately  result  in  diarrhea,  
dehydration,  electrolyte  imbalances,  and  malnutrition.  
 

¿Cual  es  la  complicación  más  frecuente  de  la  extracción  quirúrgica  de  un  cuerpo  
extraño  en  el  intestino?  ¿En  qué  porcentaje  se  presenta  y  cuándo  ocurre,  cuál  es  su  
mortalidad?  
 
El  riesgo  de  dehiscencia  es  de  16%,  ante  una  dehiscencia  el  riesgo  de  mortalidad  es  
del  80%,  sin  dehiscencia  de  un  7%  
 

 
 
¿Cuánto  intestino  de  gato  podemos  retirar  sin  encontrarnos  un  síndrome  de  
intestino  corto?  
No  se  sabe,  pero  extrapolando  informaciones  de  humana,  un  50%  podría  ser  
posible,  aunque  hay  un  estudio  en  perros  donde  se  elimina  el  80%  y  3  de  4  perros  
van  bien..  

 
 
 
¿Cuál  es  la  patofisiología  del  síndrome  de  intestino  corto?  

The  pathophysiology  of  this  syndrome  is  a  result  of  decreased  secretin  and  
cholecystokinin  in  the  proximal  duodenum,  thereby  decreasing  pancreatic  and  
biliary  secretions.  The  loss  of  intestinal  brush  border  enzymes  also  contributes  to  
the  syndrome,  with  the  changes  resulting  in  maldigestion.  Decreased  intestinal  
transit  time  and  decreased  mucosal  surface  area  may  also  contribute  to  
malabsorption.  The  decreased  transit  time,  increased  lumenal  osmotic  pressure,  
bacterial  overgrowth,  and  gastric  hypersecretion  ultimately  result  in  diarrhea,  
dehydration,  electrolyte  imbalances,  and  malnutrition.  
 
¿Por  qué  es  peor  la  morbilidad  de  una  enterotomía  en  el  intestino  grueso?  

 
It  should  be  recognized  that  the  large  intestine  heals  similar  to  the  stomach  and  
small  
intestine  but  that  healing  is  delayed.  Wound  tensile  strength  lags  behind  that  of  the  
small  intestine,  and  suture  line  failure  is  more  likely.  The  blood  supply  is  
segmental,  there  is  a  large  population  of  bacteria,  and  solid  feces  place  more  
tension  on  the  suture  line  than  the  liquid  ingesta  in  the  small  intestine.  
All  these  factors  theoretically  lead  to  greater  morbidity  and  mortality    
 

Explica  una  técnica  original  para  la  extracción  de  los  cuerpos  extraños  lineales  con  
una  sóla  enterotomía  
 

The  procedure  is  performed  by  creating  a  single  enterotomy  in  the  antimesenteric  
border  of  the  proximal  duodenum.  The  linear  foreign  body  is  tied  or  sewn  to  a  red  
rubber  catheter,  which  is  advanced  into  the  duodenum  aborally,  and  the  
enterotomy  is  closed.  The  red  rubber  catheter  is  then  milked  aborally  along  the  
intestine,  relieving  the  placation  as  it  is  advanced,  until  it  is  advanced  the  length  of  
the  colon;  an  assistant  can  
then  retrieve  it  and  the  linear  foreign  body  from  the  anus.  
ç  

BXVII   33   Ellison   G.W.   Complications   of   Gastrointestinal   Surgery   in   Companion  

Animals.  Vet  Clin  North  Am  Small  Anim  Pract    2011,  Sep;41(5):  915–934.  

1. ¿Cómo  se  produce  la  cicatrización  en  el  sistema  gastrointestinal?  

Inmediatamente   después   de   producirse   la   herida/incisión,   las   plaquetas   se  
agregan  al  tejido  lesionado,  el  mecanismo  de  coagulación  se  activa,  y  los  coágulos  
de  fibrina  se  depositan  para  controlar  la  hemorragia.  
Durante   el   primer   día   del   postoperatorio   el   coágulo   de   fibrina   ofrece   una  
resistencia  mínima  en  la  herida,  siendo  las  suturas  las  responsables  del  cierre  de  
esta.  

La   regeneración   del   enterocito   comienza   casi   inmediatamente   después   de  

producirse  la  lesión,  sin  embargo,  el  epitelio  ofrece  poco  apoyo  biomecánico.  Este  
retraso   o   fase   inflamatoria   es   el   período   más   crítico   durante   la   cicatrización   de  
heridas  GI,  y  la  mayoría  de  dehiscencias  tener  lugar  dentro  de  72  a  96  horas.  

Durante   los   3   primeros   días   los   fibroblastos   producen   grandes   cantidades   de  

colágeno   inmaduro,   dando   como   resultado   un   rápido   aumento   en   la   fuerza   de   la  
herida,   pero   este   es   un   proceso   dinámico   en   el   que   la   síntesis   de   colágeno   tiene  
lugar  en  presencia  de  colagenólisis.    

En  el  estómago  y  el  intestino  delgado,  la  actividad  de  la  colagenasa  en  el  borde  de  
la   herida   es   mínima,   por   lo   que   a   los   14   días   la   fuerza   de   tensión   de   la   herida   en   el  
intestino  o  el  estómago  es  del  75%  respecto  a  la  del  tejido  normal.    

Por   el   contrario,   el   colon   se   cura   mucho   más   lentamente   debido   a   la   marcada  

actividad  de  la  colagenasa  en  el  borde  de  la  herida,  y  recupera  sólo  el  50%  de  su  
resistencia  a  la  tensión  normal  a  los  14  días.  Suturas  traumáticas,  la  contaminación  
fecal,   y   la   infección   por   todo   el   aumento   de   la   cantidad   de   colagenasa   locales  
producidos  en  la  herida  pueden  aumentar  el  riesgo  de  infección.  

La   fase   de   maduración   de   la   cicatrización   de   la   herida   se   caracteriza   por   la  

reorganización   y   el   entrecruzamiento   de   las   fibras   de   colágeno.   Esta   fase   se  
extiende  desde  el  día  14  hasta  el  día  180  en  el  tracto  gastrointestinal.  Esta  fase  es  
poco  importante  en  la  cicatrización  de  heridas  GI,  salvo  en  aquellos  casos  en  que  se  
hayan  producido  adherencias,  o  en  casos  de  peritonitis  fibrosante.  

2. ¿Cuáles  son  las  ventajas  e  inconvenientes  de  la  gastropexia  incisional?  

Las  ventajas  de  la  gastropexia  incisional  son:  

- rapidez  
- no  se  produce  una  reducción  del  lumen  del  estómago  
 - la  adhesión  del  estómago  a  la  pared  abdominal  es  fuerte  y  madura.  
El  principal  inconveniente,  si  la  incisión  en  el  peritoneo  se  hace  demasiado  craneal,  
es   el   neumotórax.   Para   evitarlo   hay   que   identificar   el   diafragma   antes   de  
seleccionar  el  sitio  donde  realizar  la  gastropexia.  

3. Tras   realizar   una   entero/enterectomía,   según   los   autores   ¿qué   volumen  

de  suero  salino  debe  introducirse  para  comprobar  la  presencia  de  fugas?  
Si   se   realiza   la   oclusión   con   las   manos,   recomiendan   inyectar   de   11   a   19   mL   de  
suero  salino.  Si  se  realiza  la  oclusión  con  unas  pinzas  Doyen,  la  inyección  debe  ser  
de  10  a    12  mL.  

4. ¿Qué  factores  aumentan  el  riesgo  de  fuga  intestinal?  

1. Eliminación  inadecuada  de  los  tejidos  isquémicos.  
2. Mala  aposición  de  la  herida/incisión  quirúrgica.  
3. Selección  incorrecta  de  la  sutura.  
4. No  colocar  epiplón  en  la  cicatriz  quirúrgica  del  intestino.  
5. Pérdida  crónica  de  peso  (mayor  al  15-­‐20%).  
6. Administración  de  glucocorticoides.  
7. Administración   de   algunos   quimioterápicos   (ciclofosfamida,   metotrexato,  
doxorubicina,  cisplatino…).  
8. Albúmina  sérica  inferior  a  2,5  g/dL.  
 

5. En   el   cierre   de   una   entero/enterectomía   ¿cuáles   son   las   ventajas   de   la  

sutura  de  aposición?  
Una   correcta   aposición   permite   una   reepitelización   rápida   de   la   mucosa   y   la  
formación   del   tapón   de   colágeno   entre   la   submucosa,   muscular   y   serosa   se  
produce   rápidamente   y   estará   bien   vascularizada.   Otras   ventajas   son   que   el  
diámetro  de  la  luz  no  se  ve  comprometida,  la  fuerza  que  se  produce  en  la  incisión  
es   mayor   respecto   a   un   patrón   de   eversión   o   inversión,   y   las   adherencias   son  
mínimas.  
  

6. ¿Por  qué  el  epiplón  es  útil  en  una  entero/enterectomía?  

Epiplón   es   útil   porque   restablece   el   suministro   de   sangre   a   un   área   no  
vascularizada,  facilita  el  drenaje  linfático,  y  minimiza  las  fugas  de  la  mucosa.  

7. En  una  punción  de  líquido  abdominal  ¿qué  otros  parámetros,  a  parte  de  
realizar  una  citología,  son  útiles  para  diagnosticar  una  peritonits  séptica?  
Una   diferencia   mayor   de   20   mg/dL   entre   la   glucosa   sanguínea   y   la   del   líquido  
abdominal   es   muy   útil   para   diagnosticar   una   peritonitis   séptica   (tiene   un   100%   de  
sensibilidad   y   especificidad   en   el   perro;   y   una   sensibilidad   del   86%   y   especificidad  
del  100%  en  el  gato).  

Asimismo   una   diferencia   inferior   a   2,0   mM   entre   lactato   de   la   sangre   y   el   del  

líquido  también  es  efectiva.  Tiene  una  sensibilidad-­‐especificidad  del  100%.    

8. Según   los   autores   ¿cuándo   hay   que   dejar   el   abdomen   abierto   tras   una  
peritonitis  séptica?  
En  general,  el  drenaje  peritoneal  abierto  (abdomen  abierto)  debe  realizarse  en  los  
casos   en   que   la   fuente   de   contaminación   no   ha   sido   identificada,   cuando   la  
contaminación  es  grave  o  de  larga  duración,  o  la  virulencia  de  los  microorganismos  
es  considerada  alta,  como  la  observada  con  la  contaminación  fecal  o  de  infecciones  
anaeróbicas.  En  estos  casos,  el  drenaje  peritoneal  abierto  ofrece  la  posibilidad  de  
una  reexploración  y  de  lavado  posterior.    

Por  otro  lado,  si  la  fuente  de  contaminación  se  ha  eliminado  con  éxito  y  los  lavados  
abdominales   intra-­‐quirúrgicos   son   eficaces   en   la   eliminación   de   los   desechos  
residuales,  el  abdomen  se  puede  cerrar  con  buenos  resultados  en  la  mayoría  de  los  
casos.  

SEWING  NEEDLE  FOREIGN  BODY  INGESTION  IN  DOGS  AND  CATS  :  

65  CASES  (2000-­‐2012)      
Chap  L.  Pratt,  DVM;  Erica  L.  Reineke,  VMD;  Kenneth  J.  Drobatz,  DVM,  MSCE  
JAVMA,  Vol  245,  No.  3,  August  1,  2014  

 
1. ¿Cómo  actuarías  ante  la  sospecha  de  una  aguja  de  coser  en  el  tracto  
digestivo  de  un  animal?  
Los  animales  diagnosticados  de  aguja  como  cuerpo  extraño  en  el  tracto  
digestivo  deben  ser  intervenidos  rápidamente  para  evitar  migraciones  y  
por  lo  tanto  complicaciones.  
 
2. Localizaciones  donde  se  pueden  hallar  objetos  punzantes.  
-­‐ Región  orofaríngea  
-­‐ Región  superior  del  tracto  gastrointestinal  
-­‐ Región  inferior  del  tracto  gastrointestinal  
 

3. ¿Que  tipos  de  pruebas  hematológicas  realizarías  y  que  cambios  observarías  

y  cuando?  
Basándose  en  la  localización  de  las  agujas  no  se  aprecia  diferencia  entre  los  
valores  obtenidos.  Se  encuentra  citología  y  cultura  microbial  en  animales  
con  perforación  e  infección.  
 

4. Indica  cuales  son  las  técnicas  diagnósticas  apropiadas  y  en  que  casos.  
-­‐ Radiografía  sirve  para  la  localización  orofaríngea  y  del  tracto  
gastrointestinal  superior.  
-­‐ Ultrasonografía  para  verificar  las  sospechas  de  perforación  que  se  tenía  
en  sospecha.  
-­‐ Fluoroscopia  para  agujas  que  había  perforado  la  porción  cranial  del  
esófago  y  en  intestino  delgado  que  no  había  sido  detectadas  mediante  
palpación.  
 
5. ¿Cuáles  son  los  tratamientos  definitivos?  
Todas  las  agujas  localizadas  en  la  región  orofaríngea  fueron  retiradas  sin  
complicaciones.  Las    localizadas  en  el  estómago  pueden  ser  extraídas  
fácilmente  por  endoscopia.,  salvo  que  exista  una  perforación  del  estómago  
que  requerirá  laparotomía  o  gastrostomía.    Las  agujas  que  se  encuentran  en  
el  intestino  requieren  enterotomía  y  también  son  extraídas  sin  
complicaciones.      
 
6. ¿Cuáles  son  las  causas  de  retraso  de  cicatrización  en  el  esófago  por  
perforación?  
La  curación  del  esófago  se  limita  por  la  capa  serosa  y  su  movilidad  
constante  que  provoca  un  aumento  de  estrés  de  incisión  y  retrasa  la  
curación.    
 
 
 
  
7. ¿Consideras  imprescindible  intervenir  quirúrgicamente  una  aguja  que  ya  ha  
superado  el  píloro?  
No,  pero  vigilaremos  todos  los  días  con  radiografía  el  avance  del  cuerpo  
extraño  estableciendo  3  días  como  período  máximo  que  puede  permanecer  
la  aguja  en  esa  disposición  y  la  presencia  de  signos  clínicos.  
 
8. ¿Sabes  que  mecanismos  dispone  el  intestino  para  permitir  el  avance  del  
cuerpo  extraño  atreves  de  él?  ¿Cómo  responde  el  intestino  al  cuerpo  
extraño  para  evitar  ser  perforado?  
-­‐ Retracción  de  la  mucosa  intestinal  local  
-­‐ Incremento  de  producción  mucosa  
-­‐ Dilatación  intestinal  por  estimulación  mecánica  
 
13) Linear versus non-linear gastrointestinal foreign bodies in 499 dogs: clinical
presentation, management and short-term outcome
http://onlinelibrary.wiley.com.are.uab.cat/doi/10.1111/jsap.12271/epdf  

 
Introducción  
Los  cuerpos  extraños  (CE)  gastrointestinales  se  diagnostican  con  mucha  frecuencia  
en  medicina  veterinaria  de  urgencias.  Tras  su  ingestión  los  signos  clínicos  pueden  
variar  desde  horas  hasta  semanas.  Los  signos  clínicos  más  comunes  son:  anorexia,  
vómitos,  diarrea,  dolor  abdominal  y  letargia,  aunque  ninguno  de  estos  signos  son  
específicos  y  pueden  variar  en  su  presentación.  La  radiografía  se  usa  
habitualmente  para  evaluar  la  sospecha  de  cuerpos  extraños  gastrointestinales,  
pero  en  algunos  casos  se  requiere  de  la  ecografía  para  poder  llegar  al    diagnóstico  
definitivo.  

Estudios  previos  sugieren  que  los  perros  con  cuerpos  extraños  lineales  (CEL)  
tienen  mayor  frecuencia  de  complicaciones  postoperatorias  así  como  un  peor  
pronóstico  que  los  perros  con  cuerpos  extraños  no  lineales  (CENL).  
Materiales  y  métodos  

Se  realizó  un  estudio  retrospectivo  de  pacientes  con  un  diagnóstico  confirmado  de  
CEL  y  CENL  gastrointestinal  comparando  la  presentación  clínica,  el  manejo  y  el  
seguimiento  a  corto  plazo  de  ambos  grupos.  
Resultados  
De  los  499  casos,  el  35,3%  eran  CEL,  mientras  que  el  64,7  eran  CENL.  Las  razas  
más  representadas  fueron;  Labrador  retriever,    Golden  retriever,  y  Pit  bull  
americano.  Los  signos  clínicos  que  presentaron  los  pacientes  de  ambos  grupos  
fueron:  vómitos,  anorexia,  letargia,  dolor  abdominal  y  diarrea.  Los  pacientes  con  
CEL  presentaron  con  mayor  frecuencia  todos  estos  signos  clínicos,  a  excepción  de  
la  diarrea.  Los  perros  con  CEL  presentaban  mayor  dolor  a  la  palpación  que  los  del  
otro  grupo.  El  grupo  de  CEL  presentaron  niveles  más  bajos  de  sodio,  potasio  y  
cloro  y  mayores  valores  de  bicarbonato,  hematocrito  y  urea  comparados  con  los  de  
CENL.  La  radiografía  fue  diagnóstica  en  un  62,5%  de  los  CEL  y  del  71,8%  de  los  
CENL.  A  pesar  de  ello  no  hubo  diferencias  significativas  en  cuanto  a  la  capacidad  de  
la  radiografía  para  diagnosticar  un  CEL  o  un  CENL.  Radiografías  de  contraste  con  
bario  se  utilizó  en  30  perros  y  fue  diagnóstica  en  el  86%  de  los  pacientes  con  CEL  y  
en  el  88%  de  los  pacientes  con  CENL.  La  ecografía  abdominal  se  utilizó  en  123  
casos  y  fue  diagnóstica  en  todos  los  casos  en  los  que  se  utilizó.    

Los  perros  con  CEL  presentaban  de  forma  mayoritaria  el  cuerpo  extraño  anclado  
en  el  estómago  en  un  85,2%  mientras  que  en  los  CENL  el  cuerpo  extraño  se  alojaba  
mayoritariamente  en  el  yeyuno  en  un  65,3%.    
Se  realizó  endoscopia  a  57  perros  (5  con  CEL  y  52  con  CENL)  de  los  cuales  se  
consiguió  extraer  el  CE  en  un  20%  de  los  CEL  y  en  un  63,5%  de  los  CENL.  Se  realizó  
laparotomía  exploratoria  en  el  92%  de  los  casos;  en  el  99%  de  los  casos  de  CEL  y  
en  el  88,5%  de  los  casos  de  CENL.  En  el  grupo  de  CEL  se  presentó  con  mayor  
frecuencia  una  gastrotomía  y  al  menos  una  enterotomía,  y  enterectomia  y  
anastomosis,  así  como  perforación  intestinal,  peritonitis  y  necrosis  intestinal.    
La  anestesia  resultó  ser  más  larga  en  el  grupo  CEL  que  en  el  otro  grupo.  El  96%  de  
los  pacientes  sobrevivieron  al  alta.  La  media  del  tiempo  de  hospitalización  fue  de  3  
días  en  el  grupo  CEL,  y  de  2  días  en  el  CENL.  El  coste  del  tratamiento  fue  mayor  en  
el  grupo  de  CEL  que  en  el  grupo  CENL.  

Discusión  
Estudios  previos  sugieren  que  los  CEL  producen  una  obstrucción  parcial,  por  lo  
que  los  signos  clínicos  pueden  no  ser  tan  intensos  como  en  una  obstrucción  
completa.  Sin  embargo  en  este  estudio  los  pacientes  con  CEL  mostraron  mayor  
frecuencia  en  anorexia,  vómitos,  letargia  y  dolor  abdominal  que  en  el  grupo  de  
CENL.  La  diarrea  y  la  capacidad  de  palpar  el  CE  en  la  exploración  fueron  poco  
comunes  en  ambos  grupos.  La  mayor  prevalencia  en  la  presencia  de  dolor  
abdominal  en  perros  con  CEL  puede  relacionarse  con  la  mayor  presencia  de  
necrosis,  perforación  y  peritonitis.  

La  radiografía  fue  diagnóstica  en  un  62,5%  de  CEL  y  en  70,1%  CENL.  Por  otro  lado,  
una  radiografía  de  revisión  o  radiografías  con  contraste  de  bario  o  el  uso  de  
ecografía  fue  necesario  en  23%  de  los  casos.  
Al  igual  que  estudios  previos,  perros  con  CEL  presentaron  con  mayor  frecuencia  
hiponatremia,  hipocalemia,  hipocloremia,  hemoconcentración,  mayor  
concentración  de  urea  y  de  pH  que  los  perros  con  CENL.  A  pesar  de  ello,  estos  
datos  no  son  útiles  para  diferenciar  el  tipo  de  CE.  
Los  perros  con  CEL  necesitaron  mayor  número  de  gastrotomías,  enterotomías,  
enterectomias  y  anastomosis  que  los  perros  con  CENL.  La  endoscopia  resultó  más  
efectiva  en  los  CENL  que  en  los  CEL.  Los  tiempos  quirúrgicos  fueron  mayores  en  
CEL.    
A  pesar  de  que  el  grupo  de  CEL  presentó  mayor  frecuencia  de  necrosis  intestinal,  
perforación  intestinal,  peritonitis,  mayor  tiempo  quirúrgico,  mayor  tiempo  de  
hospitalización  y  mayor  coste,  no  hubo  diferencias  en  cuanto  al  índice  de  
supervivencia,  siendo  excelente  en  ambos  grupos.  
  
 

Preguntas  
1-­‐ ¿Qué  crees  que  aporta  de  nuevo  este  artículo  con  respecto  a  artículos  
anteriores?  
Estudios  previos  sugieren  que  los  perros  con  cuerpos  extraños  lineales  (CEL)  
tienen  mayor  frecuencia  de  complicaciones  postoperatorias  así  como  un  peor  
pronóstico  que  los  perros  con  cuerpos  extraños  no  lineales  (CENL).  Sin  embargo,  a  
pesar  de  que  el  grupo  de  CEL  presentó  mayor  frecuencia  de  necrosis  intestinal,  
perforación  intestinal,  peritonitis,  mayor  tiempo  quirúrgico,  mayor  tiempo  de  
hospitalización  y  mayor  coste,  no  hubo  diferencias  en  cuanto  al  índice  de  
supervivencia,  siendo  excelente  en  ambos  grupos.  
 
2-­‐ ¿Cuáles  signos  clínicos  se  observaron  en  los  pacientes  con  CE?  
Los  signos  clínicos  que  presentaron  los  pacientes  de  ambos  grupos  fueron:  
vómitos,  anorexia,  letargia,  dolor  abdominal  y  diarrea.  
 
 
3-­‐ Indica  los  lugares  más  frecuentes  donde  puedes  encontrar  un  CE:  
Los  perros  con  CEL  presentaban  de  forma  mayoritaria  el  cuerpo  extraño  
anclado  en  el  estómago  en  un  85,2%  mientras  que  en  los  CENL  el  cuerpo  
extraño  se  alojaba  mayoritariamente  en  el  yeyuno  en  un  65,3%.  
 
4-­‐ ¿Cuál  es  el  porcentaje  de  supervivencia  de  los  pacientes  de  este  estudio?  
El  96%  de  los  pacientes  sobrevivieron  al  alta.  
 
5-­‐ Indica  los  porcentajes  de  éxito  de  la  endoscopia  para  extraer  CE  en  este  
estudio  
Se  realizó  endoscopia  a  57  perros  (5  con  CEL  y  52  con  CENL)  de  los  cuales  se  
consiguió  extraer  el  CE  en  un  20%  de  los  CEL  y  en  un  63,5%  de  los  CENL.  
 
6-­‐ ¿Por  qué  se  planteaba  en  otros  estudios  que  un  CEL  podía  producir  menos  
signos  clínicos  que  un  CENL?  
Estudios  previos  sugieren  que  los  CEL  producen  una  obstrucción  parcial,  por  lo  
que  los  signos  clínicos  pueden  no  ser  tan  intensos  como  en  una  obstrucción  
completa.  
 
BXVII 33 Ellison G.W. Complications of Gastrointestinal Surgery in Companion
Animals. Vet Clin North Am Small Anim Pract 2011, Sep;41(5): 915–934.

Ahora ya puedes ir a uab.cat allí clica debajo a la derecha en Bibliotecas después clica
en acceso desde fuera de la UAB, te pedirá que te identifiques, hazlo y ves al Trobador
de la UAB y clica REVISTAS ELECTRONICAS pon Vet Clin North Am Small Anim
Pract CLICA en CONTIENE pon los datos 2011 41 5 915 y tendrás el artículo

1. ¿Cómo se produce la cicatrización en el sistema gastrointestinal?

2. ¿Cuáles son las ventajas e inconvenientes de la gastropexia incisional?

3. Tras realizar una entero/enterectomía, según los autores ¿qué volumen de

suero salino debe introducirse para comprobar la presencia de fugas?

4. ¿Qué factores aumentan el riesgo de fuga intestinal?

5. En el cierre de una entero/enterectomía ¿cuáles son las ventajas de la sutura de

aposición?
6. ¿Por qué el epiplón es útil en una entero/enterectomía?
7. En una punción de líquido abdominal ¿qué otros parámetros, a parte de
realizar una citología, son útiles para diagnosticar una peritonits séptica?
8. Según los autores ¿cuándo hay que dejar el abdomen abierto tras una
peritonitis séptica?
SEWING  NEEDLE  FOREIGN  BODY  INGESTION  IN  DOGS  AND  CATS  :  
65  CASES  (2000-­‐2012)      
Chap  L.  Pratt,  DVM;  Erica  L.  Reineke,  VMD;  Kenneth  J.  Drobatz,  DVM,  MSCE  
JAVMA,  Vol  245,  No.  3,  August  1,  2014  
 
http://avmajournals.avma.org/doi/pdfplus/10.24
60/javma.245.3.302  
 
1. ¿Cómo  actuarías  ante  la  sospecha  de  una  aguja  de  coser  en  el  tracto  
digestivo  de  un  animal?  
 
2. Localizaciones  donde  se  pueden  hallar  objetos  punzantes.  
 
3. ¿Que  tipos  de  pruebas  hematológicas  realizarías  y  que  cambios  observarías  
y  cuando?  
 
4. Indica  cuales  son  las  técnicas  diagnósticas  apropiadas  y  en  que  casos.  
 
5. ¿Cuáles  son  los  tratamientos  definitivos?  
 
6. ¿Cuáles  son  las  causas  de  retraso  de  cicatrización  en  el  esófago  por  
perforación?  
 
7. ¿Consideras  imprescindible  intervenir  quirúrgicamente  una  aguja  que  ya  ha  
superado  el  píloro?  
 
 
8. ¿Sabes  que  mecanismos  dispone  el  intestino  para  permitir  el  avance  del  
cuerpo  extraño  atreves  de  él?  ¿Cómo  responde  el  intestino  al  cuerpo  
extraño  para  evitar  ser  perforado?  
 
Complications of
Gastrointestinal Surgery in
Companion Animals
Gary W. Ellison, DVM, MS

KEYWORDS
• Gastric dilatation • Volvulus • Gastropexy
• Laparoscopic gastropexy • Intestinal anastomosis
• Intestinal dehiscence • Short bowel syndrome
• Subtotal colectomy

The small animal surgeon routinely creates wounds in the gastrointestinal (GI) tract for
biopsy, for foreign body or neoplasm removal for correction of gastric dilatation
volvulus, or to relieve intestinal and colonic obstruction. Unlike dehiscence of a skin
wound, which is often easily remedied with appropriate local wound treatment,
dehiscence of a wound of the GI tract often leads to generalized bacterial peritonitis
and potentially death. Consequently, technical failures and factors that negatively
affect GI healing are of great clinical significance to the surgeon. Surgery of the GI
tract must be considered clean-contaminated at best, and as one progresses aborally
down the GI tract, the bacterial population increases. Therefore, intraoperative
spillage, wound dehiscence, or perforations that occur in the lower small intestine or
colon tend to be associated with a higher mortality rate than those of the stomach or
upper small intestine.

WOUND HEALING OF THE GI TRACT

Basic understanding of GI tract healing is essential to the surgeon since it dictates

proper clinical approach in those cases in which GI complications develop. Immedi-
ately after wounding, platelets aggregate, the coagulation mechanism is activated,
and fibrin clots are deposited to control hemorrhage.1 The fibrin clot offers minimal
wound strength on the first postoperative day, but the main wound support during the
lag phase of healing comes from the sutures.2 Fibrin also has adhesive properties and
may increase the risk of secondary obstruction since these fibrinous adhesions may
ultimately be converted to fibrous adhesions. Enterocyte regeneration begins almost
immediately after wounding; however, the epithelium offers little biomechanical

The author has nothing to disclose.

Department of Small Animal Clinical Sciences, College of Veterinary Medicine, PO Box 100126,
Health Science Center, University of Florida, Gainesville, FL 32610-0126, USA
E-mail address: ellisong@ufl.edu

Vet Clin Small Anim 41 (2011) 915–934

doi:10.1016/j.cvsm.2011.05.006 vetsmall.theclinics.com
0195-5616/11/$ – see front matter © 2011 Elsevier Inc. All rights reserved.
916 Ellison

support.2 This lag or inflammatory phase is the most critical period during GI wound
healing, and most dehiscences take place within 72 to 96 hours.2
The proliferative or logarithmic phase of GI wound healing lasts from days 3 through
14.1 Fibroplasia occurs logarithmically during this period. The fibroblasts produce
large amounts of immature collagen, resulting in rapid gains in wound strength, but
this is a dynamic process in which collagen synthesis takes place in the presence of
collagenolysis. In the stomach and small intestine, collagenase activity at the wound
edge is minimal and rapid gains in tensile and bursting strength occur. At the end of
14 days, gastric and small intestinal wound bursting strength is approximately 75%
that of normal tissue.1 Conversely, the colon heals much more slowly due to marked
collagenase activity at the wound edge and regains only about 50% of its normal
tensile strength 14 days post wounding.1 Factors such as traumatic suturing, fecal
contamination, and infection all increase the amount of local collagenase produced at
the wound and hence can increase the risk of infection.1
The maturation phase of wound healing is characterized by reorganization and
cross-linking of collagen fibers. This phase extends from day 14 through day 180 in
the gastrointestinal tract of the dog.1 Similar to skin wounds, the size and thickness
of the scar decrease during this time without weakening the wound. The maturation
phase is relatively unimportant clinically in GI wound healing, except in those cases
where significant adhesions are present or in cases of sclerosing encapsulating or
fibrosing peritonitis.3,4

COMPLICATIONS ASSOCIATED WITH GASTRIC DILATATION VOLVULUS

Predictors of Mortality and Gastric Necrosis
Mortality continues to occur in all published reports of gastric dilatation volvulus
(GDV). However, over the past four decades, survival rates have improved due to early
recognition, rapid gastric decompression, earlier cardiovascular resuscitation, and
availability of better medical and surgical care. In older studies from the 1970s and
early 1980s, GDV-related mortality rates ranged from 43% to 60%.5,6 However, in a
large epidemiologic study of over 1900 dogs with GVD, the mortality rate had reduced
to 33% in cases evaluated during the late 1980s and early 1990s7 and was even
reported to be as low as 15% in the mid 1990s.8 In a recent study the postoperative
mortality rate of 306 dogs with GDV was 10%. Those dogs receiving gastropexy alone
had mortality of only 3%, while dogs receiving partial gastrectomy with gastropexy
had a rate of 9% and those receiving partial gastrectomy, splenectomy, and
gastropexy had a rate of 20%.9 That study also showed a reduction of mortality in
dogs if the clinical signs occurred less than 6 hours prior to presentation. While one
study suggested that reduced duration of clinical signs and shorter time from
presentation to the surgery table also decreased mortality rate in 166 dogs with
GDV,10 a second study contradicted these findings.11 Severity of clinical presentation
has also been related to outcome, with recumbency at presentation increasing risk of
death by 4.4 times and dogs with varying degrees of obtundation having mortality that
ranged between 3% and 36%.7–9,12
The presence of preoperative cardiac ventricular dysrhythmias has been evaluated
as a predictive indicator for survival in dogs with GDV since they may act as a sentinel
for gastric or splenic ischemia. In one study, dogs having intermittent ventricular
arrhythmia on admission had a significantly higher mortality rate than did dogs with
ventricular tachycardia. Additionally, 48% of those dogs presenting with preoperative
cardiac arrhythmias underwent splenectomy or partial gastrectomy, whereas just
27% of the dogs without arrhythmias required those procedures.9 However, in
 Complications of Gastrointestinal Surgery 917

another study of 295 dogs with GDV, 40% of the animals developed arrhythmias
perioperatively and survival rate was unaffected by their presence.8
Approximately 40% of dogs with GDV also develop concurrent disseiminated
intravascular coagulopathy (DIC). Reported abnormal hemostatic profiles with GDV
include prolonged prothrombin time (PT), prolonged activated partial thromboplastin
time (aPTT), reduced fibrinogen concentration, increased fibrin degradation product
(FDP) concentration, reduced platelet counts, and reduced antithrombin III (ATIII)
activity, and these may be useful in estimating gastric ischemia/necrosis and DIC. In
a study of 20 dogs with GDV, thrombocytopenia occurred in 9 of 20 dogs, followed
by decreased ATIII (8 of 20), elevated FDP (6 of 20), prolonged PT (6 of 20),
hypofibrinogenemia (6 of 20), hyperfibrinogenemia (5 of 20), prolonged aPTT (5 of 20),
and shortened aPTT (4 of 20). Approximately 70% of dogs with more than one
abnormal hemostatic test result had gastric necrosis, whereas dogs with one or no
abnormality rarely had gastric necrosis.13
Considerable attention has turned to serum lactate as predictor of gastric necrosis
and increased mortality. In an original retrospective study of 102 dogs with GDV, dogs
with serum lactate values less than 6 mM had a survival rate of 99%, whereas dogs
with initial lactate concentrations of greater than 6 mM were associated with only a
58% survival rate.13 A more recent study showed a positive predictive correlation
between lactate values before and after intravenous fluid resuscitation. In that study,
even animals with an elevated initial serum lactate less than 9 mM were likely to
survive, as long as the post resuscitation value dropped to 5.6 mM or less.14 Other
factors reported to increase postoperative mortality include hypotension, concurrent
peritonitis, DIC, and blood plasma transfusions.10
Although the timing of surgery varies between studies, what is clear is that shock
therapy and gastric decompression need to be followed by definitive surgical
management of GDV. Definitive management of GDV involves (1) repositioning of the
stomach with resection or involution of any devitalized gastric wall and (2) a
prophylactic gastropexy technique to prevent recurrence. In studies using shock
therapy and gastric decompression without gastropexy, the recurrence rate of GDV
was 56% to 76%, with many recurrences within 3 months after initial presenta-
tion.15,16 Because of this we now advocate laparotomy as soon as the patient is a
reasonable anesthetic risk. This allows for early assessment of gastric wall viability
and gastric derotation, which increases gastric circulation and helps with cardiovas-
cular resuscitation.
DIAGNOSIS AND MANAGEMENT OF GASTRIC NECROSIS

Intraoperative clinical criteria for determining gastric wall viability include assessment
of color, peristalsis, and tissue thickness. Viable gastric wall may be discolored and
blue or dark red in appearance but is normal thickness upon palpation and will often
contract when pinched. Ischemic or necrotic gastric wall, on the other hand, is black,
gray, or green and is thin on palpation and lacks peristalsis.17 Fluorescein dye is not
an accurate indicator of ischemia since the gastric wall is too thick to be affected by
vital dyes. However, surface laser Doppler flowmetry of the gastric serosal surface
has been shown to be a relatively good predictor of viability.18
Standard methods for gastrectomy involve ligation of branches of the left gastro-
epiploic arteries and veins, allowing areas along the greater curvature of the stomach
to be resected. The stomach is resected back to areas of healthy bleeding. Spillage
is prevented through the use of Babcock forceps or stay sutures. The mucosa and
submucosa are closed with a continuous inverted Cushing pattern. The serosa and
muscularis are then closed with a similar pattern. We have also used utostapling
918 Ellison

Fig. 1. (A) Intraoperative image of the stomach of a 3-year-old Chinese sharpei presenting for
GDV. A 3 ⫻ 3 cm area of full-thickness necrosis exists along the ventral gastric fundus. (B) The
area of gastric necrosis has been invaginated using a continuous Lembert suture pattern.

equipment for rapid gastrectomy procedures with minimum risk of spillage. The TA 90
autostapler is used with the green (4.8 mm) or blue (3.5 mm) cartridge. Often the
surgeon needs to overlap the staple lines by a few mm to prevent leakage between
the staples. The author has seen one clinical case in which perforation and leakage
occurred between the overlapping staple lines several months after the original
resection. Partial invagination of the stomach has been a useful technique for those
animals with small areas of gastric necrosis (Fig. 1A). With this technique, ligation of
some of the short gastric vessels may be necessary to allow transection of the
gastrosplenic ligament.19 The area of gastric necrosis is then invaginated using a
continuous Lembert suture pattern (see Fig. 1B). Since the invaginated tissue will
ultimately slough, an H2 antagonist such as cimetidine or mucosal protectant such as
sucralfate should be given for 5 to 7 days postoperatively. While the development of
a bleeding ulcer in a single dog 21 days after gastric resection prompted a
recommendation for prolonged administration of gastric protectants after this proce-
dure,20 the author has used the invagination technique successfully on many dogs
that failed to develop overt signs of gastric ulceration after surgery.
RATIONAL FOR PROPHYLACTIC GASTROPEXY

There are reports documenting the occurrence of GDV following splenectomy for
large splenic tumors or splenic torsion in dogs.21,22 Because of this, many veterinary
 Complications of Gastrointestinal Surgery 919

surgeons in North America advocate the practice of performing a prophylactic

gastropexy after a splenic mass is removed in large or giant breeds of dogs. A recent
report from the United Kingdom controverts these earlier studies, suggesting that
there was no increased risk of dogs with splenectomy developing GDV compared to
the risk incidence for the general population of dogs.23 The contradictory conclusions
of these studies may be related to differences in breed distribution, leaving the issue
of prophylactic gastropexy after splenectomy somewhat controversial.
While gastropexy is clearly indicated as a therapeutic procedure in cases of
naturally occurring GDV,11 there is now growing evidence that it may be indicated as
a prophylactic procedure in dogs at risk for developing the syndrome. In 136 dogs
with GDV, there was only a 4.3% recurrence rate in dogs and a 547-day median
survival time in dogs receiving a gastropexy procedure. Conversely, there was a
recurrence rate of 54.5% with a median survival time of 188 days in those dogs not
receiving a GDV. The mortality associated with GDV recurrence was reported to be
83% in those dogs not receiving gastropexy.11
Breed incidence of GDV has been closely evaluated, with giant and large breeds
having a lifetime probability of 22% to 24% in 1914 dogs as determined by studies using
the Veterinary Medical Data Base.7 Also, great Danes with moderate and high abdominal
height-to-width ratios were approximately 5½ to 8 times as likely to develop GDV as were
those with low abdominal height-to-width ratios. Breeds such as the great Dane and
bloodhound had reported lifetime incidences of 53% and 39%, respectively.24 A
decision-tree analysis for prophylactic gastropexy using lifetime probability of death from
GDV and expected cost savings for veterinary services as outcome measures was
undertaken to determine the preferred course of action in several dog breeds.25
Prophylactic gastropexy was the preferred choice of action for all breeds examined, with
the reduction in mortality (vs no gastropexy) ranging from 2.2-fold (Rottweiler) to 29.6-fold
(great Dane). Assuming a prophylactic gastropexy costs US$400, the procedure was cost
effective when the lifetime risk of GDV was 34% or greater.25

Complications associated with gastropexy

Most North American surgeons use an antral gastropexy procedure to affix the
stomach to the right abdominal wall and prevent GDV. Common antral gastropexy
techniques used in North America include the tube gastrostomy,26 the incisional
gastropexy,27 the circumcostal gastropexy,28 the belt-loop gastropexy,29 and the
ventral midline gastropexy.16 Recurrence rates are typically reported 5% to 29% for
the tube gastrostomy and between 3% and 8% with the other techniques.30 In most
reports, recurrence is typically defined to include the occurrence of gastric dilatation
without volvulus and does not necessarily indicate failure of the gastropexy site.
Prophylactic gastropexy techniques may also be performed using minimally invasive
techniques such as laparoscopy or endoscopy.31
Potential advantages of the tube gastropexy are that the tube not only creates a
permanent adhesion of the gastric antrum to the abdominal wall but also allows for
continued gastric decompression in the early postoperative period. In addition, slurried
food or medications can be offered through the tube. The main disadvantages of the
technique are the nursing care and long hospital period required for tube management
and the potential for fatal peritonitis secondary to leakage around the tube or early
removal by the dog (Fig. 2). In a study by Fox and others, complication rate of tube
gastropexy was approximately 18%, with local cellulitis around the tube site being the
most common complication and 2 of 24 dogs developing fatal peritonitis.32
Incisional gatropexy is performed by making a 3- to 4-cm longitudinal incision in the
seromuscular layer of the antrum, suturing this to a similar length incision in the
920 Ellison

Fig. 2. Necropsy specimen of a dog receiving a tube gastrostomy for GDV that had prema-
turely removed its Foley catheter. Gastric spillage occurred from the open gastrostomy site,
resulting in fatal septic peritonitis.

transversus muscle and peritoneum of the right ventral abdominal wall. Advantages of
the incisional gastropexy are that the procedure is rapidly performed, the stomach
lumen is not entered, and fibrous connective tissue enters the abdominal rectus
muscle and stomach wall to form a strong mature adhesion. Pneumothorax is a
potential complication if the incision in the peritoneum is made too far cranially, so the
surgeon must take care to identify the caudal extent of the diaphragm before
selecting the site of gastropexy. Incisional gastropexy is popular among many North
American surgeons, but unfortunately few retrospective studies are available to
determine the rate of failure or recurrence rate with this technique.
The circumcostal gastropexy technique uses a viable muscle flap to create a
mechanically strong adhesion by wrapping the flap around one of the caudal ribs. In
a clinical study by Lieb and others, circumcostal gastropexies were associated with
a lower recurrent rate (2.6% at 13.7 months) than tube gastrostomy.32,33 Use of this
technique allows the surgeon to achieve proper anatomic placement of the stomach,
although the complicated nature of the technique prolongs surgical time compared to
other methods of gastropexy. Complications of circumcostal gastropexy include rib
fracture during dissection for passage of the flap and pneumothorax because of the
close proximity to the diaphragm.32,33
The belt-loop gastropexy offers similar advantages to the circumcostal and
incisional gastropexies in that the gastric lumen is not entered and the risk of
peritonitis if properly performed is minimal. A seromuscular flap is threaded through
a tunnel in the transversus and peritoneum of the right ventral abdominal wall, before
being sutured back down to the donor bed. In a series of 20 dogs receiving this
technique there were no reported recurrences of GDV within 3 to 13 months after the
procedure was performed. The technique can be performed by an unassisted
surgeon but is technically more difficult than the incisional gastropexy and, as a result,
is not as popular in the United States. Although the gastric flap has the potential to
undergo necrosis if a narrow flap is created, this complication has not been
recognized in clinical studies of the technique.29 The ventral midline gastropexy is
possibly the easiest gastropexy to perform. The gastric antrum is incorporated into
the celiotomy closure with this technique. After the serosa is abraded with a dry
surgical sponge, the seromuscular layer of the stomach is incorporated in the linea
alba closure using 0 polypropylene sutures. The main disadvantage of this technique
 Complications of Gastrointestinal Surgery 921

is that if a future laparotomy is performed, there is risk that an inadvertent gastrotomy

might occur with secondary gastric spillage.16
Laparoscopy-assisted or extracorporeal gastropexy procedures have been used
as elective procedures in breeds at risk for developing GDV. These elective proce-
dures are commonly done on an outpatient basis and consistently are reported as
creating less pain for the patient and good efficacy for creation of a permanent
adhesion. Potential complications include perforation of the gastric lumen or any
laparoscopy-related complication such as splenic laceration during insufflation. In a
series of 25 client-owned dogs, 23 received laparoscopy-assisted gastropexy as an
elective procedure and 2 as a treatment for GDV. None of the dogs developed GDV
the year after surgery and 20 evaluated with ultrasonography were found to have
intact gastropexy attachments.31
In summary, with the exception of the tube gastrostomy a variety of open and
minimally invasivegastropexy techniques are associated with a low failure rate and
minimal complications if properly performed. There are inherent advantages and disad-
vantages with each technique, making the choice of the procedure a matter of surgeon’s
preference.
COMPLICATIONS FOLLOWING PARTIAL GASTRECTOMY

Gastric resection for GDV related necrosis usually has few long-term side effects
since the gastrectomy site is typically fundic in origin. Unfortunately, since most
malignant neoplasms involve the pyloric antral area, resection of the pylorus is
required. Pyloric resection may necessitate an end-to-side anastomosis of the
duodenum to the stomach also known as a Billroth I gastroduodenostomy procedure.
Alternatively, creation of a blind duodenal loop with end-to-side-to-side anastomosis
of the stomach to the jejunum is known as a Billroth II gastrojejunostomy. Of these 2
procedures, there is less postoperative vomiting and morbidity associated with the
gastoduodenostomy procedure.34 The tumor mass may also invade the proximal
duodenum and common bile duct, forcing the surgeon to anastomose the gallbladder
to the duodenum (cholecystoduodenostomy) to reestablish bile flow back into the
intestine. Ascending cholecystitis has been reported as a common sequelae to a
cholecystoenterostomy. The pathogenesis is thought to be due to a reflux of
duodenal contents into the gallbladder. Clinical signs include fever, abdominal pain,
vomiting, neutrophilia, and elevation of liver enzymes. Patients usually respond to oral
antibiotic therapy, but recurrent episodes are common. Creation of a stoma at least
2.5 cm in length may decrease gallbladder retention of ingesta and minimize the
occurrence of postoperative cholecystitis (see Complications of Biliary Surgery).
Other reported complications of cholecstoenterostmy in dogs include hepatic ab-
scess, acquired portosytemic shunts, pancreatitis, and vomiting.35
Gastric bypass procedures are technically difficult to perform and have numerous
complications associated with them, such as the dumping syndrome, marginal ulcers
at the anastomosis site, and cholecystitis.34 After gastric resection and especially
gastojejunostomy procedures, rapid gastric emptying (dumping) occurs, which may
lead to abdominal bloating, pain, vomiting, and diarrhea as well as vasomotor
symptoms, which also cause tachycardia.36 Since the pyloric antrum contains the
mucus-secreting cells of the stomach and is often removed during the resection,
marginal ulceration of the anastomosis site may also occur.34 Damage to the
pancreatic duct may cause resultant pancreatitis after any of the aforementioned
gastrectomy techniques.35 Sporadic vomiting is usually seen during the first 24 to 72
hours after pyloric surgery and is possibly due to bilious duodenal reflux into the
causing secondary gastritis. We therefore recommend treating the animal with gastric
922 Ellison

protectants such as sucralfate or using H2 blockers such as ranitidine or famotidine

for 5 to 7 days postoperatively.
COMPLICATIONS ASSOCIATED WITH INTESTINAL SURGERY
Intestinal Wound Dehiscence
Wound dehiscence of intestinal biopsy, enterotomy, or intestinal resection and
anastomosis sites often leads to generalized bacterial peritonitis and subsequent
death. Risk of intestinal anastomotic leakage can be affected by the cause of the
obstruction, failure to adequately identify ischemic tissue, improper suturing or
stapling technique, and a variety of factors that negatively affect wound healing such
as sepsis, malnutrition, and antineoplastic therapy. In a retrospective study of 115
cases of intestinal anastomosis in dogs and cats, leakage occurred in 13 of 90 dogs
but in none of 25 cats.37 The incidence of leakage and postoperative complications
was directly related to the cause of the problem, and mortality was higher in dogs that
needed intestinal surgery because of foreign body obstruction compared to those
with intestinal neoplasia.37 In this study, discriminate analysis indicated that dogs with
preoperative peritonitis, intestinal foreign body, and serum albumin concentration of
2.5 g/dL or less were also most likely to have leakage from the intestinal wound.37 A
simple method of checking the anastomotic wound site for leakage is to inject the
sutures site with saline to check for an adequate seal. In a recent study, 38 jejunal
biopsies in dogs were performed and closed using 3 or 4 full-thickness simple
interrupted sutures. Saline volumes needed to achieve intraluminal pressures of 20
and 34 cm H2O in a 10-cm canine jejunal segment containing a closed biopsy site
using 2 methods of luminal occlusion were recorded. The 95% confidence intervals
for the volume of saline needed to achieve 20 and 34 cm H2O intraluminal pressure
with digital occlusion were 10.9 to 13.6 mL and 16.3 to 19.0 mL, respectively, and with
Doyen occlusion, 8.5 to 11.1 mL and 12.1 to 14.8 mL, respectively. Therefore,
intestinal surgical sites can be checked intraoperatively for leakage by intraluminal
injection of 10 to 12 mL of saline if the loop of intestine is sealed with Doyen forceps
placed 10 cm apart.38
FACTORS INCREASING THE RISK OF INTESTINAL LEAKAGE
Inadequate removal of ischemic tissue
Ischemic intestine is often black or gray and easily discernible from normal bowel.
Determining viability in cyanotic appearing bowel is sometimes difficult. The intestine
first should be decompressed with a needle and suction apparatus to relieve
venous congestion. Intraoperative criteria for establishing intestinal viability are
color, arterial pulsations, and the presence of peristalsis. Questionable areas of
bowel should be pinched to determine whether smooth muscle contraction and
peristalsis are present. If clinical criteria are inadequate to determine viability,
intravenous fluorescein dye or surface oximetry can be used. A 10% fluorescein
solution is given at a dosage of 1 mL/5 kg intravenously through any peripheral vein.39
After 2 minutes, the tissues are subjected to long-wave ultraviolet light (Wood’s
lamp). Areas of bowel are considered viable if they have a bright green glow. Areas
of bowel are not viable if they have a patchy density with areas of nonfluorescence
exceeding 3 mm, have only perivascular fluorescence, or are completely nonfluo-
rescent.39 Oxygen saturation may also be a reliable method of determining
intestinal wall viability. A sterile probe is placed on the surface of the bowel and
an oxygen saturation level reading will occur. According to published reports in
rabbits, saturation levels above 81% typically indicate that the bowel is viable,
whereas values below 76% were consistent with mucosal necrosis and those
below 64% indicated transmural intestinal necrosis.40
 Complications of Gastrointestinal Surgery 923

Poor wound apposition

Direct approximation of the wound edge allows for optimum rapid healing character-
ized by primary intestinal wound healing. Accurate apposition allows for rapid
mucosal reepithelialization, and early formation occurs of young well-vascularized
collagen between the submucosa, muscularis, and serosa. Other advantages of
approximating patterns for intestinal anastomosis are that (1) the lumen diameter is
not compromised, (2) the wound strength meets or exceeds everting or inverting
wound strengths after 24 hours, and (3) the adhesions are minimal.2 Sutures should
not be tied too tight since crushing of tissue has been shown to cause more tissue
ischemia directly at the suture line and is discouraged. Mucosal eversion or tissue
overlap retards healing and should be avoided. Mucosal eversion results in delayed
fibrin seal formation, delayed mucosal reepithelialization, increased mucocele forma-
tion, prolonged inflammatory response, and marked adhesion formation. Eversion
may initially widen the intestinal lumen diameter, but the prolonged inflammatory
response eventually narrows the lumen, contributing to the risk of stenosis. Everting
anastomoses also have an increased tendency for leakage, especially in the face of
septic peritonitis, and should never be used in the colon. Inversion of the wound edge
creates an internal cuff of tissue that reduces lumen diameter. Hemodynamic
compromise of the inverted submucosa occurs, resulting in mucosal edema and
necrosis. After 5 days the internal cuff usually sloughs. Inverting anastomoses are
characterized by a rapid serosa-to-serosa seal and minimal adhesion formation. Yet
because of their safety against leakage, inverting patterns may be the preferred
technique for the colon.
As an alternative to hand suturing, autostapling may be used for intestinal
anastomosis. The GIA and TA auto staplers lay an overlapping double row of staples
for security and, when used in combination, create a functional “end-to-end anasto-
mosis.” The GIA portion of the anastomosis is inverted, whereas the TA portion of the
anastomosis is everted. Recent studies in human have shown that leakage rates are
similar to hand-sewn techniques but autostapler use significantly reduces surgical
time.41 In veterinary surgery, direct comparisons between hand-sewn and stapled
anastomosis are poorly documented, but in a recent study, nonspecialists were able
to achieve very good results with stapling devices in 25 of 30 dogs, with anastomotic
problems occurring in only 2 dogs.42 An alternative to sutured anastomosis is the use
of an AutoSuture Premium 35 skin stapler with stainless skin staples (Covidien,
Norwalk, CT, USA). After triangulating the intestine with 3 stay sutures, the skin
stapler is used to place staples every 2 to 3 mm around the perimeter of the wound.
These closures are more rapidly done than hand-sewn anastomosis and have similar
bursting strengths. However, mucosal eversion may occur between staples.43

Improper selection of suture material

For hand-sewn anastomoses, either continuous or interrupted patterns can be used
with equal efficacy. Although both absorbable and nonabsorbable suture materials
have been used successfully for anastomosis, the braided nonabsorbable suture
materials such as silk may harbor bacteria and create granulomatous inflammatory
reaction or draining suture sinus. Monofilament nonabsorbable sutures such as Nylon
and polypropylene are safe in contaminated environments. However, polypropylene
has been associated with foreign body adherence in one case series.44 Absorbable
suture materials reported in the veterinary literature for intestinal suturing include chromic
gut, polyglycolic acid (Dexon), polygalactin 910 (Vicryl), polydioxanone (PDS), polyg-
lyconate (Maxon), and poliglecaprone (Monocryl). Of these, surgical gut is not
recommended for anastomosis because it is rapidly broken down by collagenase.
924 Ellison

Polygalactin 910 and polyglycolic acid are braided and retain good tensile strength for
up to 28 days. Vicryl is commonly used for intestinal anastomosis in humans with
good published success and is popular in Europe for veterinary use. In North America,
monofilament sutures such as polydioxanone (PDS) and polyglyconate (Maxon) are
more commonly used. These polyester monofilament suture materials are absorbed
by hydrolysis and therefore are unaffected by contaminated environment. They
maintain up to 40% of their original tensile strength after 3 weeks. Many surgeons are
also starting to use shorter acting monofilament suture such as Monocryl or Biosyn
for intestinal anastomosis. They have similar handling properties to PDS but are
degraded more quickly. The newer “Plus” sutures are impregnated with the antibac-
terial agent Triclosan. Their efficacy in reducing infection in contaminated dermal
wounds may foster an increased use in intestinal anastomosis.

Omentalization
All anastomoses should be covered with a vascularized omental flap that is tacked in
place. Omentum is useful in (1) restoring blood supply to a devascularized area, (2)
facilitating lymphatic drainage, and (3) minimizing mucosal leakage and secondary
peritonitis. The role of omentum is significant when one considers that in one study
90% mortality rates were seen with intestinal anastomoses after omental resection
was performed in dogs.45 Free omental flaps are not as effective as pedicle omental
flaps and may in fact lead to anastomosis failure.45

OTHER FACTORS AFFECTING DEHISCENCE

Healing of visceral wounds is negatively affected by a number of other factors.

Chronic weight loss of 15% to 20% due to cancer cachexia or other reasons has a
negative effect on visceral wound healing. Correction of cachexia as well as early
postoperative enteral feeding appears to increase collagen deposition and bursting
wound strength.46 Glucocorticoids have a negative effect on wound healing when
given in large doses prior to the third day after wounding.1 NSAIDs appear to affect
the early inflammatory phase of wound healing but do not appear to interfere with the
proliferative phase of wound healing or have a significant negative effect on visceral
healing strength.47 Radiation therapies interfere with fibroblast mobilization, replica-
tion, and collagen synthesis as well as causing sclerosis of microvasculature, thereby
reducing oxygenation at the wound site. Whenever possible, radiation therapy should
be initiated after visceral wound healing is complete. The negative effects of cancer
on wound healing appear to be secondary to nutritional deficiencies rather than direct
tumor impairment on wound healing. Visceral wound healing may actually be mildly
augmented, owing to release growth factors by the neoplasm. Effects of chemother-
apeutic agents on visceral wound healing are variable. Drugs such as vincristine,
vinblastine, and azathioprine seem to be safe when used in therapeutic doses. Drugs
such as cyclophosphamide, methotrexate, 5-FU, and doxorubicin have been shown
to delay wound healing in both experimental and clinical studies.46,48 Cisplatin
appears to significantly impair intestinal wound healing in rats and should be used
with caution after intestinal surgery.49

EFFECT OF EARLY POSTOPERATIVE ENTERAL FEEDING ON VISCERAL HEALING

Malnutrition induces intestinal mucosal atrophy, reduced motility, increased inci-

dence of ileus, and the potential for bacterial translocation through the bowel wall,
with resultant sepsis.50 Impaired wound healing due to nutritional causes may be
reversed by feeding an enteral or a parenteral diet that supplies energy needs in the
 Complications of Gastrointestinal Surgery 925

form of fatty acids and sugars and provides essential amino acids. Feedings of high
protein meals after injury can optimize conditions for normal visceral wound healing.
Amino acids provided through enteral nutrition are utilized for the synthesis of
structural proteins such as actin, myosin, collagen, and elastin. Early, if not immedi-
ate, postoperative enteral feeding has been shown to have a positive influence on the
healing rate of intestinal anastomosis in dogs.51 Bursting pressures and collagen
levels of ileal and colorectal anastomosis were compared in beagles fed elemental
diets versus those fed only electrolytes and water for 4 days.51 The dogs fed orally
had nearly twice the bursting strengths of the control group and nearly double the
amount of both immature and mature collagen at the wound site.51 Total parenteral
nutrition (TPN) does not appear to ameliorate the mucosal atrophy or increase
collagen deposition as did enteral nutrition.50 In human studies, the incidence of
septic complications is significantly lower in people fed between 8 and 24 hours after
surgery versus those maintained on TPN. Additionally, early-fed patients had a
reduced incidence of postoperative ileus and reduced hospital stay.50
EFFECTS OF MASSIVE SMALL INTESTINAL RESECTION

The propensity for short-bowel syndrome after massive intestinal resection depends
on the amount of tissue excised, the location of the resection, and the time allowed
for adaptation. Resection of up to 80% of the small intestine in puppies may allow for
normal weight gain, whereas resection of 90% produces morbidity and mortality in
dogs.52 After resection of large portions of small intestine, maldigestion, malabsorp-
tion, diarrhea induced by fatty acids or bile salts, bacterial overgrowth, and gastric
hypersecretion may occur. Location of the resection is important in people. High
resection of the duodenum and upper jejunum may decrease pancreatic enzyme
secretion because pancreatic-stimulating hormones such as secretin and cholecysto-
kinin are produced in the mucosa of these sections. These reductions in release of
pancreatic enzymes contribute to maldigestion. Maldigestion of protein, carbohy-
drate, and fat leads to catabolism, negative nitrogen balance, and steatorrhea.
Unabsorbed sugars also may cause osmotic diarrhea. If the ileocecal valve is
resected, bacteria may ascend, overgrow in the small bowel, and contribute to
diarrhea. After massive resection, the remaining small intestine adapts by increasing
lumen diameter, enlarging microvilli, and increasing mucosal cell number. These
compensatory changes may take several weeks; during this period, parenteral fluids,
electrolytes, and hyperalimentation may be necessary for the survival of the animal.
With proper supportive care, the animal will be able to maintain weight even with
diarrhea. Medical treatments for unresponsive diarrhea after massive resection in
dogs include frequent small meals, low-fat diets such as intestinal diet (I/D Hills,
Topeka, KS), elemental diet supplements, medium-chain triglyceride oils, pancreatic
enzyme supplements, B vitamins, kaolin antidiarrheals, and poorly absorbed oral
antibiotics such as neomycin.
A recent retrospective study determined outcome in 13 dogs and 7 cats that
underwent extensive (ie, ⬎50%) resection of the small intestine.53 In this study, in all
7 cats and 8 of the 13 dogs, extensive intestinal resection was performed because of
a foreign body. Mean ⫾ SD estimated percentage of intestine that was removed was
68 ⫾ 14% (range, 50%–90%). Two dogs were euthanized 3 days after surgery
because of dehiscence of the surgical site and development of septic peritonitis; 1
dog died of acute respiratory distress syndrome 5 days after surgery. The remaining
10 dogs and 7 cats were discharged from the hospital, and follow-up information
was available for 15 of the 17. Median survival time was 828 days, and 12 of the
15 animals for which long-term follow-up information was available had good
926 Ellison

outcomes. However, none of the factors examined, including percentage of

intestine resected, were significantly associated with outcome. In summary, most
dogs and cats that underwent extensive resection of the small intestine had a
good outcome after a variable period of intestinal adaptation. The amount of
intestine resected was not always associated with outcome.

SURGICAL MANAGEMENT OF INTESTINAL LEAKAGE

Revision of the primary surgical site, copious abdominal lavage, and broad-spectrum
intravenous antibiotic therapy are the mainstays of addressing intestinal anastomotic
leakage and are addressed separately in this chapter (Diagnosis and Drainage
Options for Septic Abdomen). After revision of the primary anastomotic site, mechan-
ical reinforcement if the anastomosis is typically performed. Use of an omental pedicle
graft (described earliere) is sufficient in most animals; however, when the omentum is
devitalized or when more substantial mechanical reinforcement is desired, intestinal
serosal patching is recommended. The serosal patch technique uses the antimesen-
teric surface of the small bowel to cover or buttress an adjacent area of questionable
tissue viability or an area that cannot be reliably sutured. Jejunum is commonly used
because its freely movable mesentery allows it to be mobile. The serosal patch
provides mechanical stability and will help to induce and localize a fibrin seal over the
questionable area. A section of jejunum free of mesenteric tension is transposed over
the perforation or area to be buttressed. It is important not to stretch, kink, or twist its
mesenteric root or the vascular supply may be disrupted. The bowel chosen for the
patch is then gently looped to prevent luminal bowel obstruction. Multiple perfora-
tions sometimes require patching using a back-and-forth looping of the entire
segment of bowel. The lateral aspects of the bowel wall or antimesenteric border are
used for the patch (Fig. 3A). The patch is not sutured directly to the edges of the
defect but rather 3 to 4 mm beyond its margins. Simple interrupted sutures of 4-0
nylon or polypropylene are placed 3 to 4 mm from the wound edges and 3 to 4 mm
apart (see Fig. 3B). The sutures grasp the submucosa of the patch and bowel wall but
do not penetrate the lumen.
Externalized intestinal anastomosis has been used in humans in the management of
leaking colonic anastomosis, and this novel approach was successfully used to
manage a leaking ileocolic anastomosis in a dog.54 A 6-year-old, spayed female
Labrador retriever was presented 48 hours after an intestinal resection and anasto-
mosis for management of a small intestinal foreign body. Abdominal ultrasound
confirmed the presence of peritoneal effusion. Cytology of fluid collected by abdom-
inocentesis revealed a large number of degenerate neutrophils with intracellular cocci.
A diagnosis of septic peritonitis was made, presumably because of dehiscence of the
anastomosis. Upon repeat exploratory celiotomy, the intestinal anastomosis was
found to be leaking intestinal contents into the abdomen. An end-to-end, ileocolic
anastomosis was performed and subsequently exteriorized into the subcutaneous
space via a paramedian incision through the abdominal wall. The anastomosis was
inspected daily for 4 days before it was returned to the abdomen and the subcuta-
neous defect was closed. Serial cytology of the peritoneal fluid, which was performed
during this 4-day postoperative period, confirmed progressive resolution of the
peritonitis and the dog was discharged from the hospital with a successful recovery.

DIAGNOSIS AND DRAINAGE OPTIONS FOR SEPTIC ABDOMEN

With generalized septic peritonitis, massive fluid and protein movement to the
peritoneal cavity result in a shift of fluid away from the intravascular space, causing
 Complications of Gastrointestinal Surgery 927

Fig. 3. (A) Intraoperative image of a leaking enterotomy that had been closed with chromic
gut. (B) A loop of jejunum has been sutured in place over the previous enterotomy site to
create a serosal patch.

hemoconcentration and eventual hypovolemic shock. The presence of large numbers

of free bacteria or endotoxins causes massive shifts of neutrophils to the abdomen,
vasodilation of the visceral vasculature, high hepatic energy demand (hypoglycemia),
metabolic acidosis, and often fatal septic shock. Mortality rates with septic peritonitis
secondary to leaking intestinal anastomosis may be as high as 70%. In cases
where cytologic evaluation of peritoneal fluid is not diagnostic, clinicians are now
using comparisons of serum versus intraperitoneal glucose and lactate values as
a means of determining the diagnosis of septic peritonitis. In a study evaluating 18
dogs and 12 cats with septic effusion dogs with septic effusion, all animals had
peritoneal fluid glucose concentration lower than the blood glucose concentration.55
A blood-to-fluid glucose (BFG) difference greater than 20 mg/dL was 100% sensitive
and 100% specific for the diagnosis of septic peritoneal effusion in dogs. Also, in the
7 dogs in which it was evaluated, a blood-to-fluid lactate (BFL) difference less than
⫺2.0 mM was also 100% sensitive and specific for a diagnosis of septic peritoneal
effusion. In cats, the BFG difference was 86% sensitive and 100% specific for a
diagnosis of septic peritonitis. In dogs and cats, the BFG difference was more
accurate for a diagnosis of septic peritonitis than was peritoneal fluid glucose
concentration alone.55
Once diagnosed, treatment of septic peritonitis is directed toward the correction of
electrolyte and colloid abnormalities, appropriate antimicrobial therapy, and explor-
atory celiotomy to determine and surgically correct the underlying cause of the
peritonitis. After aerobic and anaerobic culture and correction of the offending
928 Ellison

problem, aggressive peritoneal lavage is performed; either the abdomen is closed

primarily or closed peritoneal drainage techniques are used. Thorough peritoneal
lavage of the abdominal cavity is performed with body-temperature 0.9% NaCl or
lactated Ringer’s solution. Lavaging a cat with 500 to 750 mL and a large dog with 3
to 5 L of fluid will help remove the bacteria and foreign debris, which are the initiators
of the peritoneal inflammation. Although lavage of the peritoneum may have the
theoretical disadvantage of spreading bacterial contamination, peritoneal lavage is
well established as a means of reducing morbidity and mortality due to septic
peritonitis. All lavage fluid should be aspirated because when bacteria are suspended
in residual lavage fluid, phagocytosis is impaired. Three cycles of lavage and
aspiration are recommended.
Peritoneal drains, when used, vary in their effectiveness with single-lumen passive
drains such as Penrose tubes, recovering much less fluid than that collected by
double-lumen active drains in most studies.56 Gravity drains have several other
disadvantages, including early occlusion of the drain by the omentum, fibrin, or
exudate and mechanical irritation of the peritoneum. Last, passive drains may
facilitate migration of bacteria into the peritoneal cavity. Active suction drains, such as
the Jackson-Pratt drain, improve efficacy of fluid removal and maintain a closed
system that minimizes bacterial contamination of the peritoneum, making them the
clear choice if closed abdominal drainage is elected for following surgery. As an
added benefit to the use of closed suction drains, the clinician is able to monitor
changes in gross and cytologic features of peritoneal fluid on a daily basis until drain
removal is performed. Intra-abdominal drains may also be used to perform a
technique called intermittent peritoneal lavage. Isothermic, sterile fluids are adminis-
tered via a peritoneal catheter or fenestrated tube. The fluids are then removed by
gravity flow back through a separate outflow tube. Our clinical impressions are that
this technique has been helpful in reducing mortality associated with diffuse perito-
nitis. However, experimental results suggest that good lavage of the entire abdomen
is not provided.57 The development of hypoproteinemia and hypokalemia is common,
although these complications are less severe than those noted during open peritoneal
drainage.
Open peritoneal drainage is a process by which the linea alba and skin are left
partially or completely open and covered with sterile dressings, which are changed at
frequent intervals. The main advantages of open peritoneal drainage are that it allows
unimpeded drainage of fluid and exudate from the peritoneal cavity and at the same
time alters the anaerobic environment of the peritoneum. Many surgeons advocate
open peritoneal drainage as the optimal treatment for generalized septic peritoni-
tis.58 – 60 The mortality rate associated with open peritoneal drainage for management
of septic peritonitis in dogs and cats ranges between 11% and 48%.56 –58 Most
studies document that mortality is increased if sepsis is secondary to GI leakage
compared to leakage from the reproductive tract.58,59 The author facilitates open
peritoneal lavage by placing continuous or interrupted Nylon or polypropylene sutures
loosely in the linea alba, allowing it to gap 1 to 2 cm. The skin and subcutaneous
tissues are not closed and are covered with antibiotic ointment and nonadherent
gauze dressing before applying a large cotton padded bandage (Fig. 4). The animal
is continuously observed and the bandage aseptically changed at 12- to 24-hour
intervals under general anesthesia and strict aseptic technique. The abdominal
wound is closed primarily in 1 to 5 days depending on when the peritoneal
inflammation has resided. Common complications associated with open peritoneal
drainage are patient dehydration and hypoproteinemia secondary to massive fluid
and protein loss into the bandage.
 Complications of Gastrointestinal Surgery 929

Fig. 4. (A) Image from a cat with multiple intestinal perforations secondary to an arrow
traversing the abdomen. After repair of all intestinal wounds, the abdomen was thoroughly
lavaged and open abdominal drainage was performed. The abdominal wall has been partially
closed with a loosely placed polypropylene sutures. (B) The abdomen is covered with a sterile
dressing that is changed under general anesthesia or deep sedation on a daily basis. The
abdominal is typically closed within 1 to 5 days depending on the degree of inflammation.

It is unclear whether open or closed peritoneal drainage is superior in the treatment

of septic peritonitis in dogs and cats. Open peritoneal drainage is a more effective
technique for achieving peritoneal drainage than is tube drainage56 and is generally
recommended if contamination is diffuse and not readily removed during the initial
exploratory celiotomy. With open drainage, large volumes of abdominal fluid and
exudate can be removed from the abdomen and the bacterial environment can be
favorably altered, therefore decreasing the number of anaerobic microorganisms. In
humans it has been reported that open abdominal drainage can improve a patient’s
metabolic condition, reduce abdominal adhesion formation, and leave access for
repeated exploration and inspection of the abdomen.61 Yet that same study actually
indicated a higher mortality rate associated with patients managed with open peritoneal
drainage compared to patients managed with closed abdomens, largely due to the
acquisition of nosocomial infections. Other reported complications included massive fluid
and protein loss, increased nursing care, increased cost, additional anesthetic, enteric
fistula formation, incisional herniation, evisceration, small bowel obstruction secondary
to adhesion formation, and nosocomial infection.61 Information provided by a limited
number of retrospective studies in veterinary medicine offer guidelines as to when
open peritoneal drainage may be indicated.58 – 60,62,63 In general, open peritoneal
drainage is considered in cases where the source of contamination cannot be
930 Ellison

identified, the contamination is severe or longstanding, or the virulence of organisms

is considered high, such as that seen with fecal contamination or anaerobic
infections. In these situations, open peritoneal drainage offers the possibility of
reexploration and subsequent lavage. On the other hand, if the source of contami-
nation is successfully eliminated and lavaging the abdomen is effective at removing
residual debris, the abdomen may be closed with good results in a majority of the
cases.62
Vacuum-assisted closure (VAC) (V.A.C., Kinetic Concepts, Inc, San Antonio, TX,
USA) is a relatively new concept in veterinary medicine that can be adopted for use
in cases of septic peritonitis. Vacuum-assisted therapy consists of placing a dressing
sponge made of open-cell polyurethane ether foam over the partially closed abdom-
inal incision. Embedded in this sponge is a noncollapsible, side-ported evacuation
tube that is connected to an adjustable pump. The vacuum applied may be used
intermittently or continuously. All the cells in the open cell foam communicate so the
vacuum is evenly applied to all wound surfaces in contact with the sponge. A plastic
adhesive drape (Ioban) is placed around the abdomen to create an air-tight seal. The
excellent drainage characteristics provided by vacuum therapy appear to be a
therapeutic option for the treatment of septic peritonitis. One human study compared
different bandaging techniques for the management of patients with open abdomens
and found a 40% reduction in mortality in patients treated with VAC therapy.64 There
are limited studies in the human literature supporting the use of VAC therapy in
patients with septic peritonitis, but the positive results from these studies are
encouraging.64,65

COMPLICATIONS AFTER SUBTOTAL COLECTOMY

Subtotal colectomy is a salvage technique for treatment of recurrent megacolon. In

North America, dogs have traditionally been treated medically because of their
propensity for postoperative diarrhea after removal of large segments of the colon.
However, in a recent UK study, 8 dogs with acquired megacolon underwent subtotal
colectomy with preservation of the ileocolic junction.66 The diagnosis was confirmed
in all animals by abdominal palpation, plain radiography, and postoperative histo-
pathologic findings. There were no intraoperative complications, although 1 dog died
postoperatively as a result of septic peritonitis. Long-term follow-up was obtained by
clinical records and telephone interviews with the owners of the 7 surviving dogs.
Resolution of obstipation and improved stool consistency of the remaining dogs were
improved at discharge and all surviving animals eventually returned to normal
defecation in 5 to 10 weeks and were alive 11 to 48 months (mean 40.5 months) after
surgery. These results emphasized the long-term effectiveness of subtotal colectomy
with preservation of the ileocolic junction in dogs with idiopathic megacolon.
In cats, subtotal colectomy has been a successful salvage procedure for idiopathic
megacolon for more than 25 years.67–70 Some controversy exists as to whether the
cecum should be preserved and a colon-to-colon anastomosis (colocolostomy) done
or whether it can be sacrificed and an ileum-to-colon anastomosis (ileocolostomy)
performed. Ileocolostomy has the inherent luminal disparity to deal with but ligation of
the ileocolic artery and removal of the cecum allow easy transposition of the mobile
ileum down to the colonic stump. With colocolostomy, luminal disparity is kept to
minimum, but the technique may be technically demanding because the relatively
immobile mesocolon places considerable tension on the suture line. Studies indicate
that removal of the cecum does not lead to ascending bacterial enteritis, and cats
with ileocolostomies do as well clinically as those with the cecum preserved.69,70
 Complications of Gastrointestinal Surgery 931

Colocolostomy can also be performed using an end-to-end anastomosis autostapler,

but it must be done via a typhlotomy incision (EEA; Covidien Inc).
Cats are often somewhat depressed and anorectic for 48 hours following subtotal
colectomy. They will sometimes have a moderate fever of 103° to 103.5°F in the
absence of leukocytosis.68 Dark tarry liquid feces are usually noted for about 3 to 4
days. The presence of abdominal tenderness, vomiting, detection of intracellular
bacteria on peritoneal fluid cytology, or significant glucose differential between
peritoneal fluid and serum warrants early reexploration of the abdomen. Normally,
feces remain liquid and poorly formed for 2 to 6 weeks after surgery, at which time
they usually become soft and poorly formed for the remainder of the cat’s life.
Long-term follow-up studies indicate that most cats seem to maintain their normal
body weight or even gain weight after the procedure.67,68 After surgery, cats generally
use the litter box 2 or 3 times a day, but the total amount of water loss in the feces
equals that of normal cats.63 The ileum increases it absorptive capacity by increasing
villous height. Bacterial overgrowth, folic acid deficiency, and anemia are not
uncommon, despite initial concerns.70 The major complaint of cat owners is chronic
perineal soiling caused by the loose feces. If this becomes a problem, it can often be
managed by clipping hair in the perineal area. Occasionally cats become reconsti-
pated and must be treated medically with lactulose and cisapride for a period of time.
In recurrent cases, reexploration and removal of additional residual colon are
sometimes necessary.
SUMMARY

A large number of naturally occurring disease conditions are treated by GI surgery in

small animals. The GI tract is rich in blood supply and has the potential to heal in rapid
fashion but GI effluent is contaminated and surgery is fraught with many pitfalls, the
most notable of which is leakage of the surgical site due to technical error, patient
cachexia, chemotherapy, metabolic disorders, or preexisting septic peritonitis. Once
present, septic peritonitis requires reoperation, patching techniques for the leakage
sites, aggressive fluid resuscitation, and appropriate antibiotic therapy based on
culture and sensitivity. Innovative surgical techniques such as the VAC drainage or
extra abdominal anastomosis placement may increase the survival rates in these
critical patients but need further investigation.
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tool for septic peritonitis in dogs and cats. Vet Surg 2003;32(2):161– 6.
56. Donner GS, Ellison GW. The use and misuse of abdominal drains in small animal
surgery. Cont Educ Pract Vet 1986;8:705–15.
57. Hosgood G, Salisbury SK, Cantwell HD, et al. Intraperitoneal circulation and drainage
in the dog. Vet Surg 1989;18:261– 8.
58. Greenfield CL, Walshaw R. Open peritoneal drainage for treatment of contaminated
peritoneal cavity and septic peritonitis in dogs and cats: 24 cases. J Am Vet Med
Assoc 1987;191:100 –5.
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peritonitis in 25 dogs and cats. Vet Surg 1986;15:27–32.
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Surg 1984;13:222– 6.
61. Bosscha K, Hulstaert PF, Visser MR, et al. Open management of the abdomen and
planned reoperations in severe bacterial peritonitis. Eur J Surg 2000;166:44 –9.
62. Lanz OI, Ellison GW, Bellah JR, et al. Surgical treatment of septic peritonitis without
abdominal drainage in 28 dogs. J Am Anim Hosp Assoc 2001;37:87.
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the treatment of septic peritonitis in dogs and cats: 42 cases (1993-1999). Vet Surg
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diffuse peritonitis. Zentralbl Chir 2006;131(Suppl 1):S108 –10.
66. Nemeth T, Solymosi N, Balka G. Long-term results of subtotal colectomy for acquired
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 Sewing needle foreign body ingestion
SMALL ANIMALS

in dogs and cats: 65 cases (2000–2012)

Chap L. Pratt, DVM; Erica L. Reineke, VMD; Kenneth J. Drobatz, DVM, MSCE

Objective—To characterize clinical signs, diagnostic test results, foreign body location,
treatment, and outcome for dogs and cats with sewing needle foreign bodies.
Design—Retrospective case series.
Animals—65 dogs and cats with sewing needle foreign bodies.
Procedures—Medical records of 27 dogs and 38 cats examined because of sewing needle for-
eign bodies from January 2000 to February 2012 were reviewed for signalment, medical history,
physical examination findings, diagnostic test results, interval from witnessed exposure and
radiographic imaging to definitive treatment, definitive treatment, sewing needle location,
complications, and outcome.
Results—7 (10.8%) animals had sewing needles in extragastrointestinal locations that
were not causing clinical signs. The remaining 58 (89.2%) animals had known sewing nee-
dle exposure or acute clinical signs associated with ingestion. The esophageal and gastric
regions were the most common location for a sewing needle (10/21 [47.6%] dogs; 19/37
[51.4%] cats), followed by the oropharynx (7/21 [33.3%] dogs; 11/37 [29.7%] cats) and
small and large intestines (4/21 [19.0%] dogs; 7/37 [18.9%] cats). Gastrointestinal perfora-
tion was detected in 10 of 58 (17.2%) animals (5/21 [23.8%] dogs; 5/37 [13.5%] cats). Sew-
ing needles in the esophagus and stomach were successfully removed endoscopically in 8
of 9 dogs and 18 of 19 cats. Survival rate was 98.1% (51/52) for animals receiving definitive
treatment.
Conclusions and Clinical Relevance—Endoscopic removal of ingested sewing needles was
highly successful and should be recommended to prevent gastrointestinal tract perforation
and associated morbidity. Prognosis for dogs and cats receiving definitive treatment for sew-
ing needle foreign body ingestion was excellent. (J Am Vet Med Assoc 2014;245:302–308)

F oreign body ingestion is a common reason for emer-

gency visits in small animal practice. Depending
on the nature of the foreign body and risk of gastroin-
testinal tract obstruction or perforation, various treat-
ments may be recommended. Treatment options may
include intensive monitoring, induction of emesis, and
endoscopic or surgical removal. Treatment recommen-
dations often are dependent on clinician experience
and rarely supported by evidence in the peer-reviewed
literature.
Retrospective studies of humans have found that
65% of ingested sharp-pointed objects pass without in-
cidence,1 with perforation occurring in 15% to 35% of
cases.2 On the basis of this information, the American
Society for Gastrointestinal Endoscopy Practice Guide-
lines recommend endoscopic removal of all amendable
ingested sharp objects in people.3 If retrieval is not pos-
sible by minimally invasive routes (eg, foreign body has
passed into the jejunum) and the patient has no clini-
cal signs associated with the foreign body, monitoring
via examination of serial radiographs is recommended
until passage of the foreign body.3 Surgical intervention
is recommended in patients who develop clinical signs
From the Department of Clinical Studies-Philadelphia, School of Veter-
inary Medicine, University of Pennsylvania, Philadelphia, PA 19104.
Presented in abstract form at the International Veterinary Emergency
and Critical Care Conference, San Antonio, Tex, September 2012.
Address correspondence to Dr. Pratt (chappratt06@gmail.com).
or patients in which the foreign body fails to advance
after 3 days.3
The authors are not aware of similar veterinary
consensus statements for nonobstructive foreign bod-
ies, such as sewing needles. Case reports4–7 of sewing
needle migration and a few retrospective studies8–10
that include descriptions of sewing needle foreign bod-
ies have been published in the veterinary literature. To
the authors’ knowledge, these reports do not include
descriptions of the ability for sewing needles to pass
through the gastrointestinal tract, incidence of perfora-
tion, or diagnostic and interventional options that will
aid in clinical decision making. It is common to rec-
ommend endoscopic or surgical retrieval of a sewing
needle foreign body from an animal, despite the lack
of evidence in the veterinary literature to support such
a recommendation. The purpose of the study reported
here was to characterize the clinical signs, diagnostic
evaluation, location of a sewing needle, frequency of
perforation, definitive treatment, and outcome in dogs
and cats with sewing needle foreign body ingestion.
Materials and Methods
Case selection—The medical record database at
the Matthew J. Ryan Veterinary Hospital of the Uni-
versity of Pennsylvania for the period between January
2000 and February 2012 was searched by use of the
terms sewing needle and needle to identify cases. Cases

302 Scientific Reports JAVMA, Vol 245, No. 3, August 1, 2014

were included if physical examination or radiography
confirmed the presence of a sewing needle foreign
body. Cases were excluded if a sewing needle foreign
body could not be confirmed or the medical record was
incomplete.
Animals were allocated into 2 groups: those with a
suspected or witnessed sewing needle ingestion or clin-
ical signs associated with ingestion of a sewing needle
and those with a sewing needle identified in an extra-
gastrointestinal location as an incidental finding with-
out associated clinical signs or pathological lesions. An-
imals with clinical signs associated with a foreign body
were grouped on the basis of sewing needle location
(oropharyngeal region [oral cavity and pharynx], up-
per gastrointestinal tract [esophagus and stomach], and
lower gastrointestinal tract [small and large intestines])
identified during physical examination or radiography.
Medical records review—Medical records were re-
viewed for signalment, medical history (witnessed in-
gestion, clinical signs, and evidence of dietary indiscre-
tion), and physical examination findings. Hematologic
analyses at the time of admission included venous blood
gas results, PCV, and total solids, electrolytes, glucose,
BUN, and blood creatinine concentrations. Diagnostic
imaging information included modality (radiography,
fluoroscopy, or ultrasonography) and interval from ob-
taining the last diagnostic image until anesthetic induc-
tion. Definitive care and outcome measures collected
included interval from witnessed exposure to definitive
care, definitive treatment (including procedural suc-
cess or failure), secondary procedures performed, sew-
ing needle location, presence or absence of perforation,
and outcome.
Statistical analysis—Continuous variables were
assessed for normality by means of the Shapiro-Wilk
test. None of the variables were normally distributed;
thus, they were reported as median and range. The
Wilcoxon rank sum test was used to compare continu-
ous variables among groups. Categorical variables were
reported as proportions and percentages. The Kruskal-
Wallis test was used to compare categorical variables
when > 2 groups were assessed, which was followed
by the Wilcoxon rank sum test for paired comparisons
when the Kruskal-Wallis test was significant (P ≤ 0.05).
The Wilcoxon rank sum test was used to compare cat-
egorical variables between 2 groups. Values of P ≤ 0.05
were considered significant for all comparisons. A sta-
tistical software programa was used for all analyses.
Results
Sewing needle foreign bodies were diagnosed in 65
animals (27 dogs and 38 cats), of which 58 (89.2%)
had clinical signs associated with sewing needle inges-
tion and 7 (10.8%) had a sewing needle identified at an
extragastrointestinal location as an incidental finding.
Of the 58 animals with clinical signs associated with
a sewing needle foreign body, there were significant-
ly (P = 0.017) more cats (37 [63.8%]) than dogs (21
[36.2%]). The animals with clinical signs associated
with the foreign body were grouped by region of the
body (oropharyngeal, upper gastrointestinal tract, or
JAVMA, Vol 245, No. 3, August 1, 2014
lower gastrointestinal tract) in which the sewing needle
SMALL ANIMALS
was found during physical examination or examination
of radiographs (Table 1). In approximately half of the
animals (10/21 [47.6%] dogs and 19/37 [51.4%] cats),
a sewing needle was identified in the upper gastrointes-
tinal tract, whereas 2 (5.4%) cats and 1 (4.8%) dog had
a sewing needle in the esophagus, and the remaining
animals (10 [47.6%] dogs and 16 [43.2%] cats) had a
sewing needle in the stomach. For 2 animals in which
a sewing needle was identified in the stomach during
initial examinations, the needle had migrated into the
small intestines (jejunum in 1 dog and ileum in 1 cat)
at the time of surgical intervention. Approximately one-
third of sewing needles (7/21 [33.3%] dogs and 11/37
[29.7%] cats) were found in the oropharyngeal region.
At the time of diagnostic imaging, sewing needle
foreign bodies were least commonly identified in the
lower gastrointestinal tract (4/21 [19.0%] dogs and
7/37 [18.9%] cats). A sewing needle was detected
radiographically in the jejunum of 2 animals (1 dog and
1 cat), the ileum of 1 animal (1 dog), and the rectum of
another animal (1 cat). One dog was monitored until
passage of the sewing needle, and definitive surgical in-
tervention was declined for the remaining 6 animals (1
dog and 5 cats), which limited information on the exact
location within the lower gastrointestinal tract.
Clinical signs for a sewing needle foreign body—
Of the 21 dogs with clinical signs, 16 (76.2%) were males
(6 sexually intact and 10 neutered) and 5 (23.8%) were
females (3 sexually intact and 2 spayed). Most dogs were
young, with a median age of 1 year (range, 3 months to
11 years). Breeds represented included 4 (19.0%) mixed-
breed dogs, 3 (14.3%) Labrador Retrievers, and 2 (9.5%)
Boston Terriers. The remaining 12 (57.1%) dogs were
purebreds (1 each of 12 other breeds).
For the 37 cats with clinical signs, 17 (45.9%)
were males (1 sexually intact and 16 neutered) and 20
(54.1%) were females (6 sexually intact and 14 spayed).
Similar to the ages of the dogs in the study, most cats
were young, with a median age of 1.5 years (range, 0.2
to 19 years). Almost all were domestic shorthair cats
(36/37 [97.3%]); the other cat was a purebred Siamese.
Recent medical history—Sewing needle ingestion
was witnessed or suspected for 13 of 21 (61.9%) dogs
Table 1—Number (percentage) of animals with sewing needle
foreign bodies examined because of suspected or witnessed in-
gestion or because of clinical signs associated with sewing nee-
dle ingestion, described by anatomic location identified during
physical examination or radiography in 58 animals from January
2000 to February 2012.
Dogs Cats
Anatomic location (n = 21) (n = 37) P value
Oropharyngeal region 7 (33.3) 11 (29.7) 0.776
Upper gastrointestinal tract 10 (47.6) 19 (51.4) 0.785
Lower gastrointestinal tract 4 (19.0) 7 (18.9) 0.990
Sewing needles were detected in an extragastrointestinal loca-
tion as an incidental finding in 7 other animals. The oropharyngeal
region was defined as the oral cavity and pharynx, the upper gas-
trointestinal tract was defined as the esophagus and stomach, and
the lower gastrointestinal tract was defined as the small and large
intestines.
Scientific Reports 303
 with clinical signs. Only 5 of these 13 dogs had other
historical findings noted by the owner at home. Retch-
SMALL ANIMALS
ing (4/7 dogs) was significantly (P = 0.006) associated
with sewing needle foreign bodies found in the oropha-
ryngeal region, compared with sewing needles found in
the other locations. A prior history of dietary indiscre-
tion was reported in 4 of the 21 (19.0%) dogs.
Sewing needle ingestion was witnessed or suspect-
ed for 29 of 37 (78.4%) cats with clinical signs. Only 11
of these 37 (29.7%) cats with suspected sewing needle
ingestion had other abnormalities noted by the owner
at home. When evaluated on the basis of location of
a sewing needle, significantly more cats with a sewing
needle in the oropharyngeal region had anorexia (5/11;
P = 0.035), retching (4/11; P = 0.051), and cervical
swelling (3/11; P = 0.021), compared with the number
of cats with a sewing needle in the upper or lower gas-
trointestinal tract.
Cats with a sewing needle foreign body in the up-
per gastrointestinal tract were significantly more com-
monly lethargic (2/18; P = 0.024) and anorectic (1/18;
P = 0.017) than were cats with a sewing needle in the
oropharyngeal region or lower gastrointestinal tract.
Cats with a sewing needle in the lower gastrointestinal
tract did not have distinguishing historical abnormali-
ties. Only 1 of 37 (2.7%) cats with clinical signs had a
prior history of dietary indiscretion.
Oropharyngeal location of a foreign body—The
median body weight of the 7 dogs with a sewing nee-
dle foreign body in the oropharyngeal region was 7.2
kg (15.84 lb; range, 3.5 to 49.2 kg [7.70 to 108.24 lb]).
Physical examination findings for 6 of these 7 dogs were
suggestive of an oropharyngeal location for the foreign
body; these findings included resistance to examination
of the oral cavity (2 dogs), excessive swallowing (1 dog),
sensitivity to ventral cervical flexion (1 dog), or ventral
mandibular swelling (1 dog). The sewing needle was vis-
ible during examination in 1 dog. Additional physical ex-
amination findings included a median rectal temperature
of 39.33°C (102.8°F; range, 38.11° to 39.83°C [100.6°
to 103.7°F]) and a median heart rate of 126 beats/min
(range, 120 to 168 beats/min).
For the 11 cats with a sewing needle foreign body
in the oropharyngeal region, median body weight was
5.2 kg (11.44 lb; range, 1.4 to 7.6 kg [3.08 to 16.72
lb]), median rectal temperature was 38.83°C (101.9°F;
range, 37.5° to 40.61°C [99.5° to 105.1°F]), median
heart rate was 190 beats/min (range, 160 to 240 beats/
min), and median respiratory rate was 49 breaths/min
(range, 30 to 140 breaths/min). Physical examination
findings consistent with a foreign body in the oropha-
ryngeal region included a visible needle (8 cats) and
ventral cervical swelling (3 cats). Of these 11 cats, there
was 1 with a ruptured abscess, 1 with ptyalism, and 1
with signs of ventral cervical discomfort. One cat did
not have physical examination findings suggestive of
oropharyngeal involvement; however, only a brief ex-
amination was performed because of the cat’s aggressive
behavior.
The proportion of cats with a sewing needle foreign
body in the oropharyngeal region was not significantly
(P = 0.776) different, compared with the proportion of
dogs with a sewing needle foreign body in the oropha-
304 Scientific Reports
ryngeal region (Table 1). However, a needle was visible
during physical examination in significantly (P = 0.05)
more cats than dogs.
Upper gastrointestinal tract (esophagus and
stomach) location of a foreign body—The 10 dogs
with a sewing needle foreign body in the stomach had a
median body weight of 17.9 kg (39.38 lb; range, 5.6 to
29.7 kg [12.32 to 65.34 lb]). Median rectal temperature
was 39.22°C (102.6°F; range, 38.44° to 39.78°C [101.2°
to 103.6°F]), and median heart rate was 132 beats/min
(range, 95 to 176 beats/min). Hydration status was as-
sessed as normal. Respiratory rate was reported for only
5 dogs, with a median of 48 breaths/min (range, 28 to
80 breaths/min). Four dogs had physical examination
findings suggestive of a foreign body in the stomach;
these findings included tensing of the abdominal mus-
cles or signs of pain during palpation of the abdominal
region. Thread presumably attached to a sewing needle
was not detected in the sublingual region in any of the
dogs.
For the 19 cats with a sewing needle foreign body
in the upper gastrointestinal tract, median body weight
was 4.2 kg (9.24 lb; range, 2.5 to 6.6 kg [5.50 to 14.52
lb]), median rectal temperature was 39.22°C (102.6°F;
range, 37.72° to 40.28°C [99.9° to 104.5°F]), median
heart rate was 200 beats/min (range, 150 to 240 beats/
min), and median respiratory rate was 40 breaths/min
(range, 24 to 72 breaths/min). Hydration status was as-
sessed as normal for 18 of these 19 cats. Physical ex-
amination findings suggestive of a foreign body in the
upper gastrointestinal tract were found in 6 cats; these
findings included tensing of the abdominal muscles or
signs of pain in 5 cats and coughing in 1. Thread pre-
sumably attached to a sewing needle was not detected
in the sublingual region in any of the cats.
Lower gastrointestinal tract (small and large in-
testines) location of a foreign body—For the 4 dogs
with a sewing needle foreign body in the lower gastro-
intestinal tract, median body weight was 7.4 kg (16.28
lb; range, 4.4 to 21.6 kg [9.68 to 47.52 lb]), median
rectal temperature was 39.11°C (102.4°F; range, 38.39°
to 39.44°C [101.1° to 103.0°F]), and median heart rate
was 115 beats/min (range, 72 to 180 beats/min). Re-
spiratory rate was reported for only 2 dogs (28 and 30
breaths/min). Hydration status was abnormal in 2 of
the 4 dogs. Tensing of abdominal muscles or signs of
pain were detected during palpation of the abdominal
region in 3 dogs; in 1 of those dogs, thread presumably
attached to a sewing needle was visible protruding from
the rectum.
For the 7 cats with a sewing needle foreign body
in the lower gastrointestinal tract, median body weight
was 5.1 kg (11.22 lb; range, 3.1 to 5.6 kg [6.82 to 12.32
lb]), median rectal temperature was 38.56°C (101.4°F;
range, 37.33° to 39.5°C [99.2° to 103.1°F]), median
heart rate was 200 beats/min (range, 120 to 240 beats/
min), and median respiratory rate was 35.5 breaths/
min (range, 30 to 80 breaths/min). Hydration status
was assessed as abnormal for 3 cats. Physical examina-
tion findings were suggestive of a sewing needle foreign
body in the lower gastrointestinal tract in 2 cats (tens-
ing of abdominal muscles or signs of pain in one cat
JAVMA, Vol 245, No. 3, August 1, 2014
and thread [presumably attached to a sewing needle]
protruding from the rectum of the other cat). A thread
was also visible in the sublingual region of 1 cat with a
sewing needle in the lower gastrointestinal tract.
Hematologic and laboratory findings—Determina-
tion of electrolyte (sodium, chloride, and potassium) sta-
tus, PCV, and total solids, BUN, blood creatinine, blood
glucose, and venous blood gas concentrations was per-
formed on an emergency basis for 40 of 58 (69.0%) ani-
mals (11/21 dogs and 29/37 cats). The median values for
all variables were within reference ranges, and there were
no significant differences in the median values based on
the location of the sewing needle for both dogs (range
of P values, 0.204 to 0.907) and cats (range of P values,
0.086 to 0.887).
Cytologic examination findings, microbial culture re-
sults, or gross description of local discharge was available
for 7 of 10 animals (2/5 dogs and 5/5 cats) with perfora-
tion and suspected infection. In all animals, the discharge
was described as septic or suppurative inflammation. Aer-
obic bacterial culturing was performed on samples from
2 animals. An α-hemolytic Streptococcus sp was cultured
from a cat with perforation of the thoracic portion of the
esophagus, and Escherichia coli and an Enterococcus sp
were isolated from a dog with septic peritonitis secondary
to perforation in the ileocolic region.
Diagnostic imaging—Radiography was performed
on 50 (86.2%) animals (19/21 [90.5%] dogs and 31/37
[83.8%] cats), but correlation of radiographic findings
with clinical findings at the time of sewing needle re-
moval could be compared in only 34 animals. Radio-
graphic findings correlated well with the surgical loca-
tion of a sewing needle for the oropharyngeal region
(7/7) and upper gastrointestinal tract (21/23) but poor-
ly for the lower gastrointestinal tract (1/4). Advanced
imaging techniques were required for 4 of 58 (6.9%)
animals; this included ultrasonography in 2 animals to
confirm radiographic suspicion of perforation and fluo-
roscopy in 2 other animals to identify a sewing needle
that perforated the cervical portion of the esophagus of
1 dog and to identify the location of a sewing needle in
the small intestines that was not detected via palpation
during initial assessment of 1 cat.
Definitive treatment—Definitive treatment was
provided to 52 (89.7%) animals (20/21 [95.2%] dogs
and 32/37 [86.5%] cats). For 6 animals, treatment was
declined, and animals (1 dog and 5 cats) were dis-
charged from the hospital and lost to follow-up moni-
toring. Sewing needle foreign bodies were radiographi-
cally identified in the lower gastrointestinal tract of
each of these 6 animals.
Overall, the median interval from witnessed ex-
posure to definitive treatment increased as the sewing
needle in the gastrointestinal tract became less acces-
sible in both dogs (oropharyngeal region, 240 minutes;
upper gastrointestinal tract, 375 minutes; and lower
gastrointestinal tract, 365 minutes) and cats (oropha-
ryngeal region, 87 minutes; upper gastrointestinal tract,
250 minutes; and lower gastrointestinal tract, 722 min-
utes); however, there were too few animals with a for-
eign body in the lower gastrointestinal tract to make
meaningful statistical comparisons.
JAVMA, Vol 245, No. 3, August 1, 2014
All sewing needle foreign bodies in the oropha-
ryngeal region were removed in animals (7 dogs and
SMALL ANIMALS
11 cats) that had been sedated or anesthetized. There
were no immediate complications recorded. Endoscopy
was initially performed in all animals with a suspected
sewing needle foreign body in the stomach. Endoscopic
removal of the foreign body was successful in 8 of 9
dogs and 18 of 19 cats; the 2 failures resulted because
the sewing needle had moved into the small intestines.
A sewing needle foreign body was successfully removed
via enterotomy, with no postoperative complications, in
3 of 3 dogs (2 jejunum and 1 ileum) and 2 of 2 cats
(1 jejunum and 1 ileum); these 5 animals included the
2 animals in which attempts to endoscopically remove
a sewing needle from the stomach were unsuccessful.
One dog was monitored in the hospital and passed the
sewing needle from the lower gastrointestinal tract in
< 24 hours with no complications. One dog was trans-
ferred to another hospital, where a laparotomy and
gastrotomy were used successfully to remove a sewing
needle that had perforated the stomach; there were no
postoperative complications in that dog.
Perforation was confirmed at the time of surgery
in 10 of 58 (17.2%) animals (5/21 [23.8%] dogs and
5/37 [13.5%] cats); there was no significant (P = 0.471)
difference between dogs and cats with regard to perfo-
ration. The most common location for perforation was
the oropharyngeal region in 5 of 10 animals (2/5 dogs
and 3/5 cats). Perforation of the upper gastrointestinal
tract was the second most commonly identified site (2/5
dogs and 2/5 cats), with specific locations including the
cervical portion of the esophagus (1 cat and 1 dog),
thoracic portion of the esophagus (1 cat), and stomach
(1 dog). Only 1 dog had a perforation in the lower gas-
trointestinal tract, which was at the ileocolic junction.
Perforation was significantly (P < 0.001) more common
in animals for which an owner was unaware of sewing
needle ingestion (8/16), compared with the proportion
of animals for which an owner witnessed or suspected
sewing needle ingestion (2/42 [4.8%]).
Thread was attached to the sewing needle in 13 of
18 (72.2%) dogs and 24 of 33 (72.7%) cats. None of the
animals underwent surgery because of signs of intes-
tinal obstruction caused by the thread, and intestinal
plication was not evident at the time of surgery. The
length of the attached thread was rarely and inconsis-
tently recorded.
Fifty-one of 52 (98.1%) animals that received de-
finitive treatment made a complete recovery. The 1
nonsurvivor was a cat in which a sewing needle had
perforated the distal aspect of the thoracic portion of
the esophagus, which resulted in septic mediastinitis.
The cat was euthanized at the owner’s request because
of a poor prognosis and the estimated cost of care.
Incidental finding of a sewing needle foreign
body—Sewing needle foreign bodies were identified in-
cidentally in 7 of 65 (10.8%) animals (6 dogs and 1 cat).
Dogs were significantly (P = 0.017) more likely than
cats to have a sewing needle identified as an incidental
finding. Location of the sewing needle included 4 in
the abdominal region (2 in the liver, 1 in the omentum,
and 1 unspecified), 1 in the thoracic region, and 2 in
the oropharyngeal or cervical region. The incidentally
Scientific Reports 305
 identified sewing needle was surgically removed from 4
SMALL ANIMALS
of 7 animals; thread was attached to only 1 of these 4
sewing needles. All 4 animals recovered without com-
plications. The remaining 3 animals with incidentally
identified sewing needle foreign bodies did not receive
further treatment. Variable amounts of follow-up infor-
mation were available on these animals for 7 days to 6
weeks. During the follow-up period, no complications
or signs of further migration of the sewing needle were
detected for these 3 untreated animals.
Discussion
To our knowledge, the study reported here is the
first in which there is a description of sewing needle
foreign bodies in a large number of dogs and cats. It is
standard care at our veterinary medical teaching hospi-
tal that animals with known sewing needle ingestion or
clinical signs attributable to a sewing needle receive de-
finitive treatment for the sewing needle because of con-
cerns about extragastrointestinal migration4–7 that may
result in life-threatening complications. This treatment
approach to sewing needle ingestion was highly suc-
cessful and resulted in survival to discharge of 98.1%
of treated patients. In the present study, the perforation
rate for the gastrointestinal tract was 17.2% (10/58).
The authors are not aware of any comparable rates in
the veterinary literature, but similar rates for perfora-
tion of sharp foreign bodies (15% to 35%) have been
reported in humans.2
Sewing needles were found in an oropharyngeal
location in approximately one-third of animals with
clinical signs associated with the foreign body. Pets
with a sewing needle foreign body in the oropharyn-
geal region typically had a shorter interval from time of
ingestion or suspected exposure until time of evalua-
tion at the emergency service. In contrast to findings in
animals with a sewing needle foreign body in the upper
or lower gastrointestinal tract, 6 of 7 dogs and 10 of 11
cats with a sewing needle in the oropharyngeal region
had abnormalities that were detected during physical
examination. It could be hypothesized that the clini-
cal abnormality increased the owners’ concerns, which
led them to bring their animal in for evaluation. The
clinical signs most commonly found during physical
examination included retching in dogs and anorexia,
retching, or cervical swelling in cats.
Both anatomic and physiologic barriers likely
contribute to resistance of passage of sewing needles
through the oropharynx. To pass successfully through
the gastrointestinal tract, a sewing needle must traverse
over the base of the tongue without penetrating the hard
or soft palate, then pass through the oropharynx, which
is located dorsal to the cervical portion of the esopha-
gus. Additionally, the physiologic barrier of the gag reflex
must be overcome before a sewing needle can pass into
the esophagus because the horizontal fibers of the crico-
pharynx typically are under involuntary control. These
barriers all inhibit progression of a sewing needle foreign
body into the upper gastrointestinal tract. In the present
study, a sewing needle foreign body was successfully re-
moved without complication for all animals with a sew-
ing needle located in the oropharyngeal region.
306 Scientific Reports
Three animals with a sewing needle foreign body
in the upper gastrointestinal tract that had clinical signs
associated with the foreign body also had esophageal
perforation. Foreign bodies in the esophagus typically
are found at 4 naturally narrow locations: immediately
caudal to the pharynx (cricopharyngeus muscle or su-
perior esophageal sphincter), thoracic inlet, heart base,
or distal portion of the esophagus.11 In the present study,
2 of 3 sewing needles were suspected to have penetrated
the esophagus at a point immediately caudal to the phar-
ynx, and the third was suspected to have penetrated the
esophagus at a point immediately caudal to the heart.
Surgical versus medical management of esophageal
lacerations remains a debated subject. Healing potential
of the esophagus is limited by its lack of a serosal sur-
face and constant mobility, which increases incisional
stress and delays healing.11 However, healing of experi-
mentally induced esophageal perforations up to 12 mm
in diameter without surgical intervention has been de-
scribed in dogs.12 In that study,12 an effective seal was
formed as a result of substantial local contraction of
the esophagus after removal of the perforating object,
and no additional surgical debridement or repair was
needed. However, delayed intervention (ie, removal of
the penetrating foreign body) increases tissue exposure
to bacteria-laden saliva, which increases the risk of de-
layed healing and may complicate recovery secondary
to extension of bacteria into the mediastinum.11,13–15
Prognosis for an animal with esophageal perfora-
tion differs depending on the location, extent of esoph-
ageal trauma, and time to intervention.16 In humans,
mortality rates of 6% for perforation of the cervical por-
tion of the esophagus and 44% for perforation of the
thoracic portion of the esophagus have been reported.17
To our knowledge, mortality rates have not been report-
ed for perforation of the cervical portion of the esopha-
gus in domestic animals, but in the present study, none
of the animals developed fatal complications. However,
the mortality rate for animals with perforation of the
thoracic portion of the esophagus reportedly is 42% in
those managed medically16 and as high as 75% in those
requiring surgical intervention.13,14 Esophageal perfo-
ration secondary to ingestion of other foreign bodies,
most commonly reported secondary to ingestion of
bones or rawhides, has been described in dogs.13,14,16,18
Esophageal perforation secondary to a bone foreign
body with successful recovery after esophageal resec-
tion and anastomosis was described in a cat in 2011.19
In the present study, the only death was a cat that was
euthanized; that cat had ingested a sewing needle 77
hours prior to hospitalization, which perforated the
caudal aspect of the esophagus and caused local septic
mediastinitis. The location of the lesion and delay until
examination and potential treatment were suspected to
have increased the risk for development of septic me-
diastinitis. It is unknown whether this cat would have
survived had the owners opted for treatment.
In the present study, 8 of 10 perforations in animals
with clinical signs associated with the foreign body
were orad to the stomach. Although the exact etiology
has not yet been determined, the narrow anatomic loca-
tions throughout the upper gastrointestinal tract are, at
least in part, responsible for the increased risk of perfo-
JAVMA, Vol 245, No. 3, August 1, 2014
ration. There were only 2 perforations in the stomach
and lower gastrointestinal tract, despite the fact they
have similar narrow locations. Possible explanations for
the decreased incidence of perforations of the stomach
and lower gastrointestinal tract include retraction of the
local intestinal mucosal, increased mucous production,
and local intestinal dilation attributable to mechanical
stimulation by the needle. Interestingly, investigators in
previous studies20,21 found that mechanical stimulation
of the intestines by a sharp needle results in mucosal
retraction, marked localized pallor, increased mucous
production, and local dilation. This local physiologic
response may in part explain the decreased incidence
of perforations.
Given the high incidence of perforation (10/58
[17.2%]) in the present study and the known risk of
problematic migration of sewing needle foreign bod-
ies, which may result in septic peritonitis (which was
reported in 1 dog of the present study), traumatic peri-
carditis,4 caval syndrome,6 and urolithiasis,7 we urge
adoption of the American Society for Gastrointestinal
Endoscopy Practice Guidelines.3 These guidelines rec-
ommend endoscopic removal of all amendable ingested
sharp objects.3 In the present study, there was a high
success rate for endoscopic retrieval of a sewing needle
foreign body from the stomach, with the only failures
occurring secondary to advancement of the sewing
needle aboral to the stomach. Increased gastric ingesta,
debris, or fluid can complicate endoscopic retrieval,22
although we did not find evidence of this in the present
study. A previous veterinary study13 conducted to eval-
uate the success of endoscopy for foreign body retrieval
revealed success rates of 26% to 86%. This is similar to
the results for the present study, in which endoscopy
was successful in 26 of 28 (92.9%) animals. To the au-
thors’ knowledge, the present study is the first in which
endoscopic success rates for retrieval of sewing needle
foreign bodies in the stomach of cats (18/19) has been
reported.
Further investigation is needed for sewing needle
foreign bodies that migrate into the intestines beyond
the reach of an endoscope. Successful surgical retrieval
of the sewing needle was performed in 6 animals in
the present report. Even though there were no com-
plications in the present study, there is still a risk of
anesthetic and postoperative complications, such as
dehiscence of the enterotomy incision, which has been
reported in 7% to 17% of animals.24 This treatment
protocol is in contrast to traditional veterinary expert
opinion and reports3,23 for humans, which have sug-
gested that if a sewing needle reaches the stomach, it
typically will pass through the intestinal tract without
complications. Evidence for intensive monitoring ver-
sus surgical removal is lacking in veterinary medicine.
In humans, the American Society for Gastrointestinal
Endoscopy Practice Guidelines recommend intensive
monitoring for signs of perforation and daily radiogra-
phy. Surgical intervention is indicated when the patient
has an acute onset of clinical signs or the sharp object
fails to advance for 3 consecutive days.3 In the present
study, only 1 dog was managed medically; that dog suc-
cessfully passed the sewing needle. Because only 1 dog
was managed medically and, to the authors’ knowledge,
JAVMA, Vol 245, No. 3, August 1, 2014
there have been no other reports of medically managed
SMALL ANIMALS
animals, future prospective studies are needed to evalu-
ate the safety of this conservative treatment approach.
In the present study, 7 (10.8%) sewing needles were
found incidentally; 4 of these were found in the ab-
dominal cavity. The authors are aware of 1 other report5
of a dog with a sewing needle that migrated without
causing clinical signs. In that report,5 the sewing needle
migrated into the caudal mediastinum and heart of a
3-year-old dog, which remained free of clinical signs
for 6 months before being lost to follow-up monitoring.
Clinical signs following perforation are dependent on
the duration of penetration, microenvironment at the
site of perforation, and migration path. As indicated by
the 7 animals in the present report, perforation does not
always result in acute onset of clinical signs, and there
is a possibility that migration of a sewing needle foreign
body may be a subclinical condition.
However, extraintestinal migration of an ingested
sewing needle can lead to serious morbidity and poten-
tially to death. The authors of 1 case report4 described
transdiaphragmatic migration in a dog that resulted
in life-threatening pericardial effusion and hemotho-
rax secondary to a myocardial laceration. In addition,
various other aberrant migrations with serious clinical
consequences have been reported, although most had
positive outcomes.6,7
Further evaluation is needed to determine the most
appropriate monitoring and intervention for subclini-
cal extragastrointestinal migration of a sewing needle.
A report25 of humans with asymptomatic extragastro-
intestinal migration of sewing needle foreign bodies
reveals that foreign bodies can remain stable for 22
years. Analysis of results of the present study suggested
that the clinical approach to a patient with an extragas-
trointestinal sewing needle foreign body may include
intensive monitoring to detect clinical signs resulting
from the migration of the sewing needle. Although ini-
tial interventions may be avoided with this approach,
removal may still be necessary, depending on the risks
associated with the procedures and continued migra-
tion of the sewing needle.
The present study had inherent limitations, includ-
ing lack of long-term follow-up monitoring, missing
data, treatment bias, and referral bias. Although our
veterinary teaching hospital is a tertiary referral cen-
ter, none of the animals were referred because of con-
cerns about perforation, and many of the patients were
evaluated by personnel in the emergency service, which
possibly made the population more representative of a
non–tertiary referral hospital.
Another potential limitation was the reported rate
of perforation, excluding the 7 animals with a sewing
needle identified as an incidental finding, which may
have underestimated the true incidence. Animals with
incidentally detected sewing needle foreign bodies
represented a unique population, and despite surgical
removal in many animals, definitive perforation of the
gastrointestinal tract was not proven. In humans, abuse
and mental disorders have led to percutaneous inser-
tion of sewing needles, which has resulted in aberrant
migration.25 Although abuse was not suspected in any
of the animals in the study reported here, it could not
Scientific Reports 307
 be ruled out. Gastrointestinal tract perforation without
clinical signs has been reported in humans.3,25,26 In the
SMALL ANIMALS
present study, only 8 of 21 (38.1%) dog owners and 8 of
37 (21.6%) cat owners reported that clinical signs were
detected at home; therefore, there is a possibility that
more animals may have had unwitnessed sewing needle
ingestion and needle migration without clinical signs.
The actual rate of perforation could not be determined.
Analysis of results of the present study suggested
that an animal that ingests a sewing needle foreign
body and receives definitive treatment has an excellent
prognosis. Perforation was detected in 10 of 58 (17.2%)
animals and may result in severe, potentially life-threat-
ening complications. Future studies are required to de-
termine whether an ingested sewing needle that passes
atraumatically into the stomach can pass through the
remainder of the intestines with minimal risk and
whether such animals can be managed medically.
a. Stata, version 12 for Mac, Stata Corp, College Station, Tex.
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JAVMA, Vol 245, No. 3, August 1, 2014
ttp://www.bsava.com PAPER

Linear versus non-linear gastrointestinal

foreign bodies in 499 dogs: clinical
presentation, management
and short-term outcome
M. M. Hobday, G. E. Pachtinger, K. J. Drobatz and R. S. Syring

Department of Clinical, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104-6010, USA

OBJECTIVES: To compare clinical signs, clinicopathological abnormalities, imaging findings and outcome
of dogs with linear and non-linear foreign bodies in the gastrointestinal tract.
METHODS: Retrospective review of case records of dogs with a confirmed diagnosis of gastrointestinal
foreign body. Signalment, history, clinical signs, clinicopathological data, diagnostic imaging stud-
ies, surgical and endoscopic procedures, hospital stay, costs and outcome were compared between
groups.
RESULTS: A total of 176 dogs had linear and 323 had non-linear foreign bodies. Dogs with a linear
foreign body were more likely to have a history of vomiting, anorexia, lethargy and pain on abdominal
palpation. They were also more likely to have the foreign body anchored in the stomach and continuing
into the small intestine, experience intestinal necrosis, perforation and peritonitis, and require intesti-
nal resection and anastamosis. The duration of hospitalisation was longer for dogs with linear foreign
body (3 versus 2 days), and the cost of treatment was 10% higher. However, in both groups, 96% of
dogs survived to hospital discharge.
CLINICAL SIGNIFICANCE: Dogs with a linear foreign body had more severe clinical signs and gastrointesti-
nal pathology, and an increased duration of hospitalisation and cost of care. However, overall survival
rates were not different in dogs with linear and non-linear foreign bodies.

Journal of Small Animal Practice (2014) 55, 560–565

DOI: 10.1111/jsap.12271
Accepted: 29 July 2014

INTRODUCTION gastrointestinal foreign bodies, plain abdominal radiographs may

Gastrointestinal foreign bodies are a common diagnosis amongst
dogs presenting for emergency veterinary care and yet they often
represent a diagnostic challenge (Clark 1968, Guilford 1996,
Aronson et al. 2000, Tyrrell & Beck 2006, Hayes 2009, Sharma
et al. 2011). After ingestion, the onset of clinical signs can vary
from hours to weeks (Capak et al. 2001, Gianella et al. 2009,
Hayes 2009). Clinical signs commonly associated with gastroin-
testinal disease such as anorexia, vomiting, diarrhoea, abdominal
discomfort and lethargy are non-specific and are variably pres-
ent in dogs with gastrointestinal foreign bodies (Mishra et al.
1974, Capak et al. 2001, Hayes 2009). Moreover, while radi-
ography is commonly used to evaluate patients with suspected
be unremarkable in many cases and abdominal ultrasonography
may be required to confirm the diagnosis (Root & Lord 1971,
Tidwell & Pennick 1992, Graham et al. 1998, Tyrrell & Beck
2006, Sharma et al. 2011).
Previous studies suggest that dogs with linear foreign bodies
(LFB) have a higher frequency of postoperative complications
and a worse prognosis compared with non-linear foreign bodies
(NLFB) (Evans et al. 1994, Hayes 2009). The purpose of the
current study was to compare the clinical signs, clinicopatho-
logical abnormalities, diagnostic imaging findings, treatment
and outcome between a group of dogs with LFB and a group
with NLFB to determine if the groups would have a similar
prognosis.

560 Journal of Small Animal Practice • Vol 55 • November 2014 • © 2014 British Small Animal Veterinary Association

MATERIALS AND METHODS
Using a retrospective case-ascertainment design, the computer-
ised medical record database of the Mathew J. Ryan Veterinary
Hospital at the University of Pennsylvania was searched to iden-
tify dogs that were presented to the emergency service between
1997 and 2008 and diagnosed with a gastrointestinal foreign
body. The records were then grouped into those with LFB and
NLFB. To maximise case identification, the computerised medi-
cal record database was cross-referenced with both the complete
surgical case log and abdominal fluid analysis submissions.
Dogs were included in the study if a foreign body was the cause
of any of the presenting clinical signs of vomiting, anorexia, leth-
argy or diarrhoea. Dogs with objects in the oral cavity or colon
were included only if those objects extended to or from another
portion of the gastrointestinal tract. Finally, the foreign mate-
rial had to be confirmed by surgical or endoscopic removal, or
necropsy. Dogs were excluded from the study if the clinical signs
were caused by aetiologies other than a foreign body. Incomplete
medical records were not grounds for exclusion from the study.
Clinical variables extracted from the medical record included:
history, signalment, body weight, age at presentation, clinical
signs (anorexia, lethargy, vomiting, diarrhoea), physical exami-
nation findings (abdominal pain, ability to palpate a foreign
body), clinicopathological data (venous blood gas, complete
blood count, biochemistry, lactate concentration), diagnostic
procedures (radiography, ultrasonography, contrast radiography),
surgical procedures (gastrotomy, enterotomy, intestinal resection
and anastamosis), endoscopic evaluation, surgical time, anaes-
thesia time, intraoperative findings (perforation, peritonitis,
bowel necrosis), location of the foreign body, outcome (survival,
euthanasia, death), necropsy results, cost for hospitalisation and
treatment and length of hospitalisation. Dogs were categorised
as having peritonitis based solely on the surgical report, and a
distinction between septic and aseptic peritonitis was not made.
Abdominal radiograph reports, which were completed by
board certified radiologists, were reviewed. Additional diagnostic
imaging tools, such as repeated radiographs, contrast radiography
or ultrasonography were also recorded.
Flexible gastrointestinal endoscopy was used for foreign body
retrieval, and was performed by internal medicine specialists and
house officers directly supervised by internists. The endoscopy
reports and patient discharge summaries were reviewed for for-
eign body location and gross pathological changes resulting from
the foreign body ingestion.
In dogs that underwent an exploratory coeliotomy, a ventral
midline incision was made, and a routine examination of the gas-
trointestinal tract was carried out. Foreign body location, surgi-
cal method and anatomical pathology as a result of the foreign
body were recorded from the surgical report. Surgical specialists
or house officers under the guidance of the surgical specialists
performed all surgeries.
Dogs were categorised as having either LFB or NLFB on the
basis of the attending veterinarian’s description of the gastrointes-
tinal abnormalities from the surgical or endoscopic procedures,
Journal of Small Animal Practice • Vol 55 • November 2014
Linear and non-linear foreign bodies
or necropsy. Linear foreign bodies were classified as compliant
objects anchored at one anatomic site, inducing plication through
one or more aboral sites in the gastrointestinal tract. Non-linear
foreign bodies were defined as ingested, discrete objects causing
clinical signs of vomiting, anorexia, lethargy, abdominal pain
and/or diarrhoea.
Statistical analysis
T-test for independent groups was used to examine the differences
in the mean values of continuous dependent variable measures
(days hospitalised, hospital costs, age, surgery time and related
factors) and the independent categorical measures (linear foreign
bodies, non-linear foreign bodies). Chi-squared test (χ2) was used
to compare differences in categorical factors (e.g. linear foreign
bodies/non-linear foreign bodies with intervention categories,
presenting signs and the remaining signalment parameters). All
reported P-values are two-sided with P-values lower than 0·05
indicating statistical significance. Descriptive statistics utilised
proportions by group and or variable. The calculations were
completed using Epi Info (2013) and SPSS (2011).
RESULTS
Between January 1997 and January 2008, there were 499 dogs
that met the criteria for inclusion into the study. The LFB group
included 176 dogs (35·3%) and the NLFB included 323 dogs
(64·7%). There were 87 different breed classifications. The
majority of the dogs were pedigree, with the most common
breeds being the Labrador retriever (67/499 13·4%; 23/176 LFB
13·1%, 44/323 NLFB 13·6%; P=0·86), golden retriever (28/499
5·6%; 12/176 LFB 6·8%, 17/323 NLFB 5·3%; P=0·39) and
the American pit bull terrier (21/499 4·2%; 9/176 LFB 5·1%,
12/323 NLFB 3·7%; P=0·46). Additionally, there were 69
mixed breed dogs (69/499 13·8%; 34/176 LFB 19·3%, 35/324
NLFB 10·8%). Of the 499 dogs, 337 were male (67·5%; 116
LFB 23·2%, 221 NLFB 44·3%; P=0·31) and 162 were female
(32.5%; 60 LFB 12·0%, 102 NLFB 20·4%; P=0·63). Overall,
354 of patients were neutered (70·9%; 42 spayed female LFB
8·4%, 78 castrated male LFB 15·6% and 75 spayed female NLFB
15·0%, 159 castrated male NLFB 31·8%). The mean ±sd age of
LFB dogs at the time of admission was 4·06 ±3·32 years (range
0·21-14·0 years). The mean ±sd age of NLFB dogs at the time of
admission was 4·27 ±3·51 years (range 0·085-14·5 years), which
was not statistically significantly different (P=0·51).
Several clinical signs and examination findings were evaluated
in the dogs with LFB and NLFB (Table 1). As per the inclusion
criteria, all dogs had at least one clinical sign associated with the
gastrointestinal foreign body, and with the exception of diarrhoea,
each of these clinical signs was more frequently present in dogs with
LFBs. Dogs in the LFB group were also more likely to have pain
on abdominal palpation. The ability to palpate the foreign object
on initial physical examination was uncommon and similar in both
groups (LFB 27/176, 15·3%, NFLB 43/323, 13·3%; P=0·53).
The results of the most common laboratory studies are
summarised in Table 2. Dogs with LFB had significantly lower
• © 2014 British Small Animal Veterinary Association 561
 M. M. Hobday et al.

Table 1. Frequency of presenting clinical signs and body in 26 of 30 dogs (LFB 12/14; 86%, NLFB 14/16; 88%).
examination findings at admission for dogs with LFB For the four dogs where contrast radiography was considered
(n=176) compared to NLFB (n=323) insufficient for definitive diagnosis, ultrasound was ultimately
Variable LFB LFB NLFB NLFB P-value used. Abdominal ultrasonography was performed on 123 dogs
(n=176) % (n=323) % in this study and confirmed the diagnosis of foreign body in all
Vomiting 173 98·3 286 88·6 0·0001 cases, based on ultrasound reports. This was true if ultrasound
Anorexia 164 93·1 261 80·8 0·0002 was the sole imaging study, or if it was performed when survey or
Lethargy 162 92·0 254 78·6 0·0001
contrast radiography failed to yield a diagnosis.
Abdominal pain 96 54·5 122 37·8 0·0003
Diarrhoea 35 16·5 77 23·8 0·2798 Of the 499 dogs evaluated in the study, 494 underwent gen-
Ability to palpate 27 15·3 43 13·3 0·53 eral anaesthesia for a surgical or endoscopic procedure. Five dogs
foreign body were euthanased before any treatment with a diagnosis of foreign
LFB Linear foreign bodies, NLFB Non-linear foreign bodies, n Number of dogs body later confirmed at necropsy (one LFB, four NLFB). The
324 dogs with NLFB had a total of 374 foreign bodies removed,
sodium, potassium and chloride, and higher bicarbonate, haema- while 176 were removed from the 176 dogs with LFB. The loca-
tocrit and blood urea nitrogen as compared to those with NLFB. tions of the LFB and NLFB retrieved from the gastrointestinal
Percentages of blood work parameters below and above reference tract are reported in Fig 1. Dogs with LFB most commonly had
ranges were calculated for each group. foreign material anchored in their stomach (150 dogs, 85·2%),
Survey abdominal radiography was performed in 483 of 499 whereas the foreign material was most commonly found in the
dogs. In the 16 patients for which radiographs were not per- jejunum in dogs with NLFB (211 dogs, 65·3%)
formed, 10 dogs had ultrasound as the sole diagnostic imaging Endoscopic foreign body retrieval was attempted in 57 dogs
study, 2 dogs had a string foreign body under the tongue and (5 LFB, 52 NLFB), and was successful in 34 dogs (LFB 1/5,
were taken directly to surgery, 2 dogs were euthanased prior to 20·0%; NLFB 33/52, 63·5%). The remaining dogs required
diagnostics, with the foreign body confirmed on necropsy, and 2 exploratory coeliotomy following the unsuccessful endoscopic
case records lacked documentation of imaging studies. The initial procedure. A gastrotomy was performed in 248 dogs (157 LFB,
set of radiographs was considered sufficient to provide a diagno- 91 NLFB) for the removal of foreign material. Six more
sis of foreign body in 337 dogs (LFB 110/166; 62·5%, NLFB gastrotomies were performed (1 LFB, 5 NLFB) to assess the
227/318; 71·8%). There was no statistically significant difference gastric lumen for further foreign material or to inspect the
in the ability to diagnose LFB or NLFB based on the initial radio- pylorus, but foreign material was not found.
graphic evaluation (P=0·271). Radiographs were repeated in 10 Exploratory coeliotomy was performed in 460 dogs (460/499,
dogs (five LFB, five NLFB), where the initial set had not yielded 92%; LFB 174/176, 99%; NLFB 286/323, 88·5%). Dogs in
a diagnosis. This confirmed the presence of a foreign body in the LFB group were more likely to have a gastrotomy, at least
seven dogs (two LFB, five NLFB). Barium contrast radiography one enterotomy, and intestinal resection and anastamosis, as
was utilised in 30 dogs and it confirmed a diagnosis of foreign well as intestinal perforation, peritonitis and intestinal necrosis.

Table 2. The mean values for the most common laboratory tests ordered on admission and between-group comparisons
for dogs with LFB (n=176) and NLFB (n=323)
Variable Reference LFB NLFB P-value
intervals
Mean (sd) %* Mean (sd) %*
+ – + –
Significant
pH 7·35-7·45 7·44 (0·06) 44·1 8·2 7·42 (0·05) 27·4 8·3 0·02
Na (mmol/L) 139-154 143·70 (6·00) 1·1 16·0 145·53 (6·07) 3·4 9·9 0·001
K (mmol/L) 3·6-5·5 3·76 (0·49) 0·0 33·1 3·92 (0·49) 0·6 24·7 0·001
Cl (mmol/L) 102-120 104·55 (9·59) 0·6 33·5 108·30 (8·52) 2·2 12·9 <0·001
HCO3 (mmol/L) 21-24 28·70 (5·36) 82·4 2·4 26·57 (6·97) 64·6 11·5 0·001
HCT (L/L) 0·36-0·60 0·49 (0·093) 11·0 13·3 0·47 (0·08) 6·9 3·7 0·006
BUN (mmol/L) 2·14-11·1 7·90 (7·26) 0·19 0·6 6·12 (6·57) 6·1 1·3 0·009
Non significant
Lactate (mmol/L) 0·5-2·5 2·56 (1·55) 41·1 1·2 2·38 (1·46) 36·5 1·6 0·21
Glucose (mmol/L) 3·85-7·59 6·26 (1·98) 14·9 1·1 5·97 (1·02) 5·9 0·9 0·07
ALT (U/L) 12-118 69·83 (69·03) 11·8 1·3 68·76 (114·47) 8·3 0·4 0·92
AST (U/L) 15-66 69·20 (67·27) 33·6 0·0 63·64 (70·55) 24·2 0·0 0·43
Albumin (g/L) 24-42 31·9 (8·87) 9·0 17·4 32·1 (7·12) 4·5 8·2 0·88
WBC (×109/L) 4·1-15·5 16·24 (6·35) 47·5 0·6 15·60 (7·54) 45·9 1·8 0·37
Creatinine (µmol/L) 44·2-141·4 86·63 (44·2) 6·7 3·0 91·94 (76·91) 5·3 1·4 0·37
n Number of dogs, LFB Linear foreign bodies, NLFB Non-linear foreign bodies, sd Standard deviation, Cl Chloride, K Potassium, Na Sodium, BUN Blood urea nitrogen, WBC White blood cells,
HCO3 Bicarbonate, HCT Haematocrit
*
Percentage of dogs above (+) and below (–) reference range

562 Journal of Small Animal Practice • Vol 55 • November 2014 • © 2014 British Small Animal Veterinary Association
 Linear and non-linear foreign bodies

FIG 1. Location of 550 foreign bodies (176 linear, 374 non-linear) in 499 dogs

Table 3. Summary of surgical techniques, intraoperative findings, and procedure times between the LFB and NLFB groups
Dogs having surgery LFB n=174 LFB 174/176 (99%) NLFB n=286 NLFB 286/324 (88%) P-value
Gastrotomy 159 90·3 96 29·7 <0·001
Enterotomy (one or more) 130 73·9 167 52 <0·001
Resection and anastamosis 57 32·4 51 15·8 <0·001
Intestinal perforation 34 19·3 16 4·9 <0·001
Peritonitis 31 17·6 22 6·8 <0·001
Intestinal necrosis 48 27·3 46 14·2 <0·001
Mean surgical time (minutes) ±sd 122·7 ±sd 50·84 – 94·2 ±sd 37·26 – <0·0001
Mean anaesthesia time (minutes) ±sd 176·5 ±sd 53·27 – 144·8 ±sd 51·97 – <0·0001
Total number of dogs having surgery 460/500 (92%). LFB Linear foreign bodies, NLFB Non-linear foreign bodies, sd Standard deviation

Table 4. Summary of mortality for the dogs with LFB and Both groups had a 96% survival rate to time of discharge from
NLFB hospital. The reasons for death or euthanasia are summarised in
LFB NLFB Table 4.
7/176 (4%) 13/323 (4%)
Dogs eutha- 1 – financial reasons 2 – financial reasons Duration of hospitalisation and cost of care
nased preop- 2 – undocumented The median length of hospitalisation for LFB dogs was 3 days
eratively reasons
(range 1-18 days) compared with 2 days (range 1-22 days)
Dogs eutha- 0 2 – significant intestinal
nased intra- necrosis, perforation for dogs in the NLFB group, which was significantly differ-
operatively and sepsis ent (P<0·0001). Similarly, the LFB group median total costs
Dogs euthana- 1 – recurrent septic 1 – intestinal infarct were $2479·25 (range $486-$18,307), which was significantly
sed postop- abdomen 2 – ARDS
eratively 1 – ARDS 1 – financial reasons greater than costs for dogs with NLFB, median $2263·50 (range
1 – financial reasons 1 – sepsis $215-$7490). The difference in mean costs was significant with
3 – undocumented reasons 1 – undocumented reason the LFB group having increased costs (P<0·001).
Dogs that died 0 1
LFB Linear foreign bodies, NLFB Non-linear foreign bodies, ARDS, Acute respiratory distress
syndrome
DISCUSSION

This is the largest retrospective study to date evaluating the

Surgery and anaesthesia time were significantly longer in dogs
with LFB. These results are summarised in Table 3.
Mortality risk
Four hundred and seventy-nine dogs (96%) survived to dis-
charge, while 19 dogs were euthanased (5 preoperatively,
2 intraoperatively, 12 postoperatively) and 1 died postoperatively.
clinical course of LFB and NLFB in dogs. It reports excellent
rates of survival, following diagnosis of a gastrointestinal foreign
body (96%) with no difference in outcome when comparing
dogs with LFB to those with NLFB, despite a higher frequency
of intestinal necrosis, intestinal perforation, peritonitis, longer
surgical times, longer hospital stay and increased costs in dogs
with LFB.

Journal of Small Animal Practice • Vol 55 • November 2014 • © 2014 British Small Animal Veterinary Association 563
 M. M. Hobday et al.
Previous reports suggest that LFBs cause partial obstruction,
and animals may not present with clinical signs as severe as those
with a discrete, complete obstruction (Aronson et al. 2000,
Brown 2012). In the current study, however, this was not the
case, as dogs with LFBs had more frequent reports of anorexia,
vomiting, lethargy and pain on abdominal palpation compared
to dogs presenting with NLFBs. These results are comparable
to another study where 94% of dogs had vomiting, 66% had
anorexia and 63% had signs of lethargy, with LFB obstructions
(Evans et al. 1994). Diarrhoea and clinician ability to palpate the
foreign body was an uncommon finding in dogs in either group.
The increased prevalence of abdominal pain in dogs with LFB
may have been related to the increased occurrence of intestinal
necrosis, perforation and peritonitis in that study population.
In this study, survey radiographs were adequate to confirm
a diagnosis of gastrointestinal foreign body in the majority of
cases (LFB 62·5%, NLFB 70·1%). While radiographs may fail
to demonstrate radiolucent foreign bodies, they can reveal seg-
mental dilation of intestines with fluid and or gas or disparate
bowel populations; however, this is not pathognomonic for for-
eign body obstruction (Clark 1968, Root & Lord 1971, Gibbs
& Pearson 1973, Graham et al. 1998, McNeel & Riedesel 1998,
Tyrell & Beck 2006, Sharma et al. 2011, Ciasca et al. 2013). It is
important to note that this study was not designed to assess the
accuracy of radiography for detection of gastrointestinal foreign
bodies, as all dogs included in this study had confirmed foreign
bodies. When survey radiographs alone were not diagnostic,
either repeated radiographs or other diagnostic modalities, such
as barium contrast studies or abdominal ultrasonography were
used to confirm the diagnosis. Of the 483 dogs that had survey
radiographs, repeat survey radiographs, or barium contrast stud-
ies, an abdominal ultrasound examination was still required to
confirm the diagnosis of foreign body in 23% of the cases.
Hypochloraemia, metabolic alkalosis, hypokalaemia and
hyponatraemia have been reported in dogs with various gastro-
intestinal foreign bodies, with LFB being more likely associated
with hyponatraemia (Boag et al. 2005). Similarly, the present
study demonstrated that dogs with LFB were more likely to have
lower sodium, potassium and chloride concentrations, but also
demonstrated haemoconcentration, an increase in blood urea
nitrogen concentrations, and higher pH than dogs with NLFB.
While these findings were statistically different between dogs
with LFB and NLFB, these clinicopathological parameters are
unlikely to be useful in distinguishing LFB from NLFB in indi-
vidual cases, as many values remained within their respective ref-
erence intervals. There were no statistical differences between the
two groups of dogs when comparing admission values for white
blood cell count, serum lactate, glucose, albumin or creatinine
concentrations and alanine aminotransferase activity.
Dogs with LFB required significantly more gastrotomies,
enterotomies, and intestinal resection and anastamosis, than
dogs with NLFB. This finding is consistent with the linear
nature of the foreign body and the difficulty in their remov-
ing through one gastrointestinal incision. A high frequency of
gastrotomy in dogs with LFB is expected as the majority of cases
had linear material anchored in the stomach, which is similar
564 Journal of Small Animal Practice
to other studies (Evans et al. 1994, Hayes 2009). In contrast,
33 of 52 (63·5%) of dogs with NLFBs were able to have the
material removed by endoscopy, while only 1 dog had a LFB
removed by endoscopy. This is likely because the linear material
was anchored further along the gastrointestinal tract. This study
had one successful case of endoscopic removal of a LFB (a needle
and thread from the stomach into the duodenum); however, this
is unique and the current authors do not advocate endoscopy as
a means to remove LFBs. Surgical times were nearly 30 minutes
longer in the LFB group, likely related to the greater complexity
of the surgical procedures. Similar findings were reported in a
study comparing large and small bowel surgery, where increased
gastrointestinal surgical time did not adversely affect mortality
(Wylie & Hosgood 1994).
Reported survival rates of dogs undergoing surgery of the gas-
trointestinal tract vary from 80 to 99% (Evans et al. 1994, Boag
et al. 2005, Shales et al. 2005, Hayes 2009), with the present
study results being 96% for both groups. However, it should be
noted that the current study was unable to provide follow-up past
the time of discharge for all patients, and it is therefore difficult
to directly compare survival rates with other studies. Overall, it
appears that surgical management is more complex, costly and
time consuming in dogs with LFBs, and variable rates of dehis-
cence and septic peritonitis are reported (Allen et al. 1992, Wylie
& Hosgood 1994, Ralphs et al. 2003, Shales et al. 2005). Despite
these findings, treatment for a linear foreign body was not associ-
ated with a worse outcome in the present study, as it was in pre-
vious studies that investigated LFBs or one that compared both
groups (Evans et al. 1994, Hayes 2009). Reasons for improved
outcome in the dogs with LFB in this study may be the result of
the improved resources at a specialty centre.
This study occurred in a large specialty care facility, where
there are many practitioners of varying experience. This may
cause variations in surgical technique, efficiency in surgery and
postoperative care. For this reason it was hard to objectively com-
pare cases. The retrospective nature of the study made it difficult
to standardise results to fit a specific category, as the informa-
tion retrieved was based on the documentation of the supervising
clinician. Additionally, even though several steps were taken to
ensure all dogs meeting the inclusion criteria were enrolled in the
study, it is not possible to determine if any records were omitted.
This is particularly true of septic peritonitis, which has been asso-
ciated with an unfavourable prognosis. The current search criteria
may have failed to identify dogs presenting with septic peritoni-
tis, whereby inclusion of such cases may have resulted in fewer
surviving to discharge. Finally, any complication occurring past
time of discharge may not be known if the clients elected follow-
up care through their first opinion practice. This is particularly
important when considering the high success rate in the current
study, as some dogs could have had intestinal dehiscence and sep-
tic peritonitis, without the authors’ knowledge, if follow-up was
performed elsewhere.
Despite a higher frequency of clinical signs, intestinal
necrosis, perforation, peritonitis, surgical procedures, longer
hospitalisation and a greater cost in dogs with LFB, the overall
short-term outcome was excellent for both groups.
• Vol 55 • November 2014 • © 2014 British Small Animal Veterinary Association
 Linear and non-linear foreign bodies
Acknowledgements
The authors thank Dr. Peter Chapman for his and guidance in
manuscript preparation, Kathleen Carr for graphics and Dr. Gary
Leonardson for statistical assistance.
Conflict of interest
The authors have no conflicts to declare.
References
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dehiscence and associated clinical factors: a retrospective study of 121 dogs.
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Boag, A. K., Coe, R. J., Martinez, T. A., et al. (2005) Acid-Base and electrolyte
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Brown, D. C. (2012) Small intestine. In: Veterinary Surgery: Small Animal. Eds K.
Tobias and S. Johnson. Saunders, Philadelphia, PA, USA. pp 1533-1536
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occlusive ileus in dogs. Veterinarski Arhiv 71, 345-359
Ciasca, T. C., David, F. H. & Lamb, C. R. (2013) Does measurement of small
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207-211
Clark, W. T. (1968) Foreign bodies in the small intestine of the dog. Veterinary
Record 83, 115-119
Evans, K. L., Smeak, D. D. & Biller, D. S. (1994) Gastrointestinal linear foreign
bodies in 32 dogs: a retrospective evaluation and feline comparison. Journal of
the American Animal Hospital Association 30, 445-450
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Gianella, P., Pfammatter, N. S. & Burgener I. A. (2009) Oesophageal and gastric
endoscopic foreign body removal: complications and follow-up of 102 dogs.
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Gibbs, C. & Pearson, H. (1973) The radiographical diagnosis of gastrointestinal
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tinal dilation as a predictor of obstruction in the dog. Journal of Small Animal
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Hayes, G. (2009) Gastrointestinal foreign bodies in dogs and cats: a retrospective
study of 208 cases. Journal of Small Animal Practice 50, 576-583.
McNeel, S. V. & Riedesel, E. A. (1998) Small bowel. In: Textbook of Veterinary Diagnostic
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Mishra, N. K., Appert, H. E. & Howard, J. M. (1974) The effects of distention and
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Ralphs, S. C., Jessen, C. R. & Lipowitz, A. J. (2003) Risk factors for leakage follow-
ing intestinal anastomosis in dogs and cats: 115 cases (1991-2000). Journal
of the American Veterinary Medical Association 223, 73-77
Root, C. R. & Lord, P. F. (1971) Linear radiolucent gastrointestinal foreign bodies in
cats and dogs: Their radiographic appearance. Journal of American Veterinary
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Shales, C. J., Warren, J., Anderson, D. M., et al. (2005) Complications following
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Linear versus non-linear gastrointestinal foreign bodies in 499 dogs: clinical presentation,
management and short-term outcome

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Preguntas  

1-­‐ ¿Qué  crees  que  aporta  de  nuevo  este  artículo  con  respecto  a  artículos  anteriores?  
 
2-­‐ ¿Cuáles  signos  clínicos  se  observaron  en  los  pacientes  con  CE?  
 
3-­‐ ¿Qué  alteraciones  en  el  ionogramapresentan  los  pacientes  con  Los  pacientes  con  CE  
pueden  presentar:  
 
4-­‐ Indica  los  lugares  más  frecuentes  donde  puedes  encontrar  un  CE:  
 
5-­‐ ¿Cuál  es  el  porcentaje  de  supervivencia  de  los  pacientes  de  este  estudio?  
 
6-­‐ Indica  los  porcentajes  de  éxito  de  la  endoscopia  para  extraer  CE  en  este  estudio  
 
7-­‐ ¿Por  qué  se  planteaba  en  otros  estudios  que  un  CEL  podía  producir  menos  signos  
clínicos  que  un  CENL?  
 
Feline gastrointestinal foreign bodies
Trevor N. Bebchuk, DVM

Vet Clin Small Anim 32 (2002) 861–880 BUSCA

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Indica el patrón de sutura que debes realizar en una esofagotomía y con qué material de
sutura lo realizarías ¿Cómo puedes reforzar la sutura?

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esofagotomía?

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¿Cuando no hay variación en el pH sanguíneo de un gato con cuerpo extraño digestivo?

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 Vet Clin Small Anim 32 (2002) 861–880

Feline gastrointestinal foreign bodies

Trevor N. Bebchuk, DVM
Department of Small Animal Clinical Sciences, Western College of Veterinary Medicine,
University of Saskatchewan, 52 Campus Drive, Saskatoon, Saskatchewan, S7N 5B4 Canada

Gastrointestinal foreign bodies are responsible for a wide range of clinical

presentations in veterinary practice. Cats may demonstrate vague mild signs
of a chronic nature, they may have acute or severe vomiting and diarrhea, or
they may be in hypovolemic or septic shock. The clinical signs vary depend-
ing on the location of the obstruction, the degree of obstruction, the foreign
body causing the obstruction, and the chronicity of obstruction. The
required treatment depends on numerous clinical and laboratory variables,
which must be evaluated before developing a treatment plan. The goal of
treatment is always relief of the obstruction with minimum morbidity. This
article focuses on some of the different types of obstructions reported in cats,
how they affect the animal at different levels of the gastrointestinal tract,
diagnostic techniques, and the recommended treatments.
The vast range of clinical presentations possible with gastrointestinal for-
eign bodies precludes any specific generalizations regarding the appearance
of a cat with this problem. Clinical signs that may be present include vomiting,
diarrhea, regurgitation, ptyalism, inappetence, anorexia, depression, dehy-
dration, abdominal pain, abdominal distention, palpable firm segments of the
intestines, palpable intestinal dilation, and many more. It is imperative that a
complete physical examination, including an oral examination, be performed.
It is recommended that laboratory assessment, including routine hematology
tests, a serum biochemical profile, and urinalysis, be performed. Radiographs
are essential for the diagnosis of most gastrointestinal foreign bodies, and a
contrast study is necessary in some cases. Obtaining both left and right lateral
recumbent radiographs of the abdomen may prove beneficial in some animals.
Fluid and gas contents are extremely mobile and tend to move to the depen-
dent portion of the stomach during postural changes. The redistribution of
gas can act as a negative contrast medium to highlight foreign objects or dis-
orders only visible on one lateral projection [1]. The same principle applies to

E-mail address: trevor.bebchuk@usask.ca (T.N. Bebchuk).

0195-5616/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved.
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862 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880

the intestinal tract. Ultrasonography is useful for the diagnosis of certain for-
eign body obstructions. Ultimately, either endoscopy or surgery is required
for definitive diagnosis and treatment of foreign body obstruction.
The most common hematologic abnormalities in cats with foreign body
obstruction range from a leukocytosis with or without a mild left shift to
a degenerative left shift in cases with peritonitis from intestinal perforation.
Dehydration and electrolyte imbalance are expected in animals that are
vomiting. These animals may have a normal pH or primary metabolic
acidosis. A normal pH results from equal loss of gastric acid secretions and
base secretions from the proximal duodenal, bile, and pancreatic juices. Pri-
mary metabolic acidosis is caused by a relatively greater loss of base secre-
tions from the upper intestinal tract, and lactic acidosis results from
dehydration and inadequate perfusion of splanchnic viscera, skin, and
muscle [2]. Cats with pyloric obstruction may demonstrate a hypokalemic,
hypochloremic, metabolic alkalosis. The dehydration and laboratory abnor-
malities should be corrected by appropriate intravenous fluid therapy, which
should be initiated before surgical intervention. Definitive correction
requires removal of the inciting cause of the vomiting and inflammation.

Foreign body location

Esophagus
The esophagus is responsible for the transport of food, water, and saliva
from the pharynx to the stomach. It is frequently under tension during the act
of swallowing and bolus formation. Unlike the intestines, the esophagus does
not have a serosal surface, and this may delay early fibrin sealing of entero-
tomy sites compared with the rest of the intestines. Vascular supply to the
esophagus is segmental, with the cervical portion supplied by branches of the
thyroid and subclavian arteries and the thoracic portion supplied by the bron-
choesophageal arteries and segmental branches of the aorta [3].
Esophageal obstruction is less common than other gastrointestinal
obstructions. When it occurs, it can be complete or partial, each of which
demonstrates different clinical signs and sequelae. The most common clini-
cal signs are dysphagia and regurgitation depending on the level of obstruc-
tion. When the obstruction is incomplete, signs of chronic wasting, such as
emaciation, may be observed. If aspiration has occurred as a result of the ob-
struction, abnormal pulmonary sounds, such as crackles, may be auscultable,
and clinical signs, including coughing, mucopurulent nasal discharge, and
fever, may be observed. If a foreign body has perforated the esophagus, a
secondary mediastinitis or pyothorax may develop [4]. Esophagobronchial
fistula formation secondary to a perforating foreign body can occur, leading
to secondary pulmonary pathologic findings [5].
There are three narrowed anatomic regions in the esophagus where a for-
eign body is likely to become lodged. These include the cricopharyngeal
 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880 863

sphincter, the base of the heart, and the esophageal hiatus in the diaphragm.
Additionally, foreign bodies may lodge at the thoracic inlet, where advance-
ment may be impeded by surrounding soft tissues [4].
Diagnosis of esophageal foreign body obstruction is based on clinical
signs, a normal pharyngeal examination, and radiographs. In most cats, the
esophagus is not normally visible on radiographs. When distended with air
or fluid, it becomes a visible structure. Esophageal dilatation can be evi-
dence of an esophageal foreign body if the cat has no previous history of
megaesophagus. The presence of a radiopaque object (Fig. 1) in the region
of the esophageal lumen provides a definitive diagnosis of foreign body
obstruction, but not all foreign objects are radiographically visible. An
esophagram can be performed to visualize radiolucent objects (Fig. 2).
When an esophagram is performed, there is a risk of aspiration, and fluid
barium rather than barium paste can be used to reduce the risk [3]. A fluo-
roscopic examination, in conjunction with a contrast esophagram, should be
used when possible because it allows assessment of swallowing, esophageal
motility, and gastroesophageal sphincter function. If there is evidence of
periesophageal gas or fluid accumulation, mediastinal effusion, or pleural
effusion, there may be an esophageal rupture, and barium should not be
used. In these cases, aqueous iodine or iohexol should be used [6].
Removal of esophageal foreign bodies should be considered an emer-
gency procedure, because the longer an object remains in the esophagus, the
greater is the risk of aspiration and esophageal wall injury by pressure
necrosis. Most esophageal foreign bodies can be definitively diagnosed and
removed endoscopically [4,7]. This includes fishhooks, some of which may
be large or embedded in the esophageal wall [8]. The equipment needed to
be successful at endoscopic removal of esophageal foreign bodies includes
but is not limited to a rigid proctoscope or flexible fiberoptic endoscope, a
light source, long blunt-ended grasping forceps, flexible alligator forceps,
and Foley catheters. In the event a foreign body is located in the caudal
thoracic esophagus and cannot be removed endoscopically, an attempt
should be made to gently push it into the stomach. This should only be per-
formed if it is possible without causing further injury to the esophagus.
When successful, this technique allows for a laparotomy and gastrotomy
to remove the foreign body rather than the higher morbidity thoracotomy
and esophagotomy. When perforations are present or when removal of a
foreign body endoscopically carries a high risk of perforation, surgical
removal via esophagotomy is recommended. With some foreign bodies, such
as embedded fishhooks, a combined surgical and endoscopic approach may
be used. A surgical approach is made, and without an esophagotomy, the
portion of the hook protruding through the esophageal wall is cut and
removed. The endoscope is then used to retrieve the rest of the hook that
remains within the lumen [8].
The surgical approach to the cervical esophagus is via a ventral midline in-
cision, and the thoracic esophagus is approached via a left lateral intercostal
864 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880

Fig. 1. Right lateral (A) and ventrodorsal (B) projections of the neck and thorax of a 1-year-old
female domestic shorthair cat. A 5-cm needle was ingested, punctured the pharynx, and is now
lying ventral to the larynx and trachea extending to the level of the fifth cervical vertebral body.

thoracotomy at the appropriate intercostal space for the level of the obstruc-
tion. At the level of the heart base, where the aorta pushes it to the right, the
esophagus can be approached via a right lateral intercostal thoracotomy
at the fourth or fifth intercostal space. The esophagus is then packed off from
the rest of the neck or thorax using moistened laparotomy sponges. Ideally,
 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880 865

Fig. 2. Right lateral (A) and ventrodorsal (B) projections of an esophagram in a 3-year-old
castrated male domestic longhair cat. There is a large filling defect in the thoracic esophagus
extending from the fourth thoracic vertebral body to the diaphragm. This is best viewed on the
lateral projection. This foreign body was not visible on survey radiographs. It was determined
to be clumps of hair and vegetation and was removed endoscopically.
866 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880

the cranial esophagus can be suctioned of contents before the esophagotomy

incision, but if this is not possible, an assistant can hold the esophagus
closed cranial and caudal to the proposed esophagotomy site to prevent con-
tamination from leakage. If the esophageal wall over the foreign body looks
healthy, the incision can be made over the object and should be made large
enough to remove the foreign body with no additional damage to the esoph-
ageal wall. If the esophagus seems compromised, the incision should be
made aboral to the foreign body, beginning at the foreign body but large
enough to remove the object with minimal manipulation. Once the foreign
object has been removed, the esophageal mucosa is examined for any evi-
dence of perforation. The esophagotomy incision can be closed in one or
two layers. The first layer is an appositional pattern in the mucosa and sub-
mucosa, and the second layer is an appositional pattern in the muscularis.
The holding layer is the submucosa. If the esophageal wall does not look
healthy, a resection and anastomosis should be performed on the damaged
region. Anastomosis of the esophagus can be performed with a one- or two-
layer closure. Suture material for esophageal surgery in cats should be a syn-
thetic, monofilament, absorbable suture, such as polydioxanone, in a 4-0
size and with a swaged on reverse cutting needle. If there is still concern rel-
ative to leakage of the esophagus at the site of the anastomosis or esopha-
gotomy, an omental patch can be brought through the diaphragm and
wrapped over the anastomosis, a pericardial reinforcement can be applied,
or a pedicle intercostal graft can be used [9,10]. Anastomosis of the esoph-
agus should not be under tension, because the esophagus is constantly in
motion as a result of swallowing and respiration. The anastomosis may
dehisce if the tension is excessive. The major complication of surgery for
esophageal perforation is infection, and this occurred in 57% of cases in one
study with and without dehiscence [5]. In the postoperative period, a phar-
yngostomy tube can be used to provide caloric and fluid requirements; how-
ever, this is controversial, because the presence of the intraluminal tube may
impair esophageal healing [5].

Stomach
Foreign bodies of the stomach are common and may be an incidental
finding in some cases (Fig. 3). Clinical signs of gastric foreign bodies range
from asymptomatic to intermittent or persistent vomiting as a result of out-
flow obstruction, gastric distention, and mucosal irritation. Vomiting is
more common with foreign bodies in the pyloric antrum, because distention
or noxious stimulation of the duodenum and/or pyloric antrum stimulates
vomiting, whereas similar distention of the fundus does not [3]. Cats com-
monly ingest string, yarn, and other string-like material when they play.
This can result in a linear foreign body, which is frequently anchored under-
neath the tongue or at the pylorus, causing intestinal plication. A gastric for-
eign body is generally not an emergency unless it is a linear foreign body or
 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880 867

Fig. 3. Right lateral (A) and ventrodorsal (B) projections of a gastric foreign body (vintage
Canadian nickel) discovered as an incidental finding when obtaining radiographs of a 10-year-
old cat after trauma.
868 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880

the foreign object is lodged in the pylorus and causing obstruction and
severe vomiting.
Young animals are presented with gastric foreign bodies more frequently
than older animals, and this should be a differential diagnosis for any kitten
that has clinical signs of vomiting. The cats are presented with a history of
intermittent or persistent vomiting or a more chronic history of inappetence/
anorexia and depression. Physical examination of these cats may be unre-
markable; however, many have some level of dehydration or abdominal
pain, and a gastric foreign body is palpable in some cats. The stomach is cra-
nially located in the abdomen and is shielded by the caudal costal arches,
making routine palpation of gastric foreign bodies difficult. If a linear for-
eign body is present, plicated intestines may be palpable.
Laboratory abnormalities most commonly include evidence of dehydra-
tion. For example, an elevated hematocrit as well as elevated blood urea
nitrogen, creatinine, and total protein levels can be expected. In cases of
severe vomiting as a result of pyloric obstruction, a hypochloremic and
hypokalemic metabolic alkalosis may be present. In cases of vomiting with-
out pyloric obstruction, a metabolic acidosis would be expected as a result
of losses of base-rich duodenal and pancreatic secretions as would dehydra-
tion and lactic acidosis.
Radiopaque foreign bodies may be diagnosed radiographically; however,
this is not always the case. Radiolucent foreign bodies may require a con-
trast gastrogram for diagnosis. This can be performed using barium; how-
ever, if an esophageal, gastric, or intestinal rupture is suspected, aqueous
iodine or iohexol should be used [6]. As in the case of the esophagus, many
gastric foreign bodies can be diagnosed and removed endoscopically. Con-
trast radiographs and endoscopy allow the clinician to discern between for-
eign bodies and other causes of vomiting, such as gastric neoplasia and
gastric ulceration. An additional tool for the diagnosis of a gastrointestinal
foreign body is ultrasonography. Using ultrasound, foreign bodies of the
stomach and intestines may be identified, and many foreign bodies have a
characteristic ultrasonographic appearance depending on the tendency to
transmit or attenuate the ultrasound beam [11]. If the foreign body is
smooth and rounded, vomiting can be induced with xylazine (Rompun) at
a dose of 1 mg/kg of body weight [12]. This should only be attempted with
objects that can be expulsed with no harm to the esophagus and no risk of
lodging in the esophagus.
Foreign bodies that have sharp edges or are large should not be removed
by endoscopy because of the risks of esophageal laceration and lodging the
foreign body in the esophagus. These foreign bodies are best removed by
gastrotomy [12]. Radiographs should be taken just before surgery to ensure
that the object has not moved from the stomach. The surgical approach to
the stomach for gastrotomy is via a cranial ventral midline laparotomy.
Because the intestines and stomach can contain foreign bodies concurrently,
a thorough exploratory laparotomy should be performed. The stomach is
 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880 869

packed off from the rest of the abdomen with moistened laparotomy

sponges, and stay sutures are placed between the greater and lesser curva-
tures, near the cardia, and in the pyloric antrum. The gastrotomy incision
is created between these stay sutures in the hypovascular region between the
greater and lesser curvatures on the ventral surface of the stomach. The inci-
sion should not be made too close to the pylorus to prevent excessive nar-
rowing of the gastric lumen. Closure of the gastrotomy can be performed
in one or two layers. If a two-layer closure is used, the first layer is an appo-
sitional pattern that must incorporate the submucosa, and the second layer
is an inverting pattern in the serosa and muscularis [12]. Suture material
should be synthetic, monofilament, absorbable, and size 3-0 or 4-0.
In the postoperative period, hydration status and electrolyte levels should
be monitored. Intravenous fluid therapy should be continued and adjusted to
address any abnormalities. If the animal has been anorexic and vomiting for a
sustained period, hypokalemia is expected. This can be treated with intrave-
nous fluids containing 20 to 40 mEq/L of potassium chloride. The animal
should not receive more than 0.5 mEq/kg/h of potassium chloride. If vomiting
continues, treatment with an antiemetic may be necessary. If vomiting has
ceased, the cat should be started on a bland diet 12 to 24 hours after surgery.
The prognosis for removal of gastric foreign bodies via gastrotomy is
good. Recovery can be complicated by local or generalized peritonitis if
there is gastric perforation present or if spillage of gastric contents occurs
during gastrotomy. The latter is uncommon if moist laparotomy sponges are
used effectively to isolate the stomach from the rest of the abdomen before
making the gastrotomy incision.

Small intestine
Small intestinal obstruction by a foreign body is a common condition in
cats. This obstruction can be complete or partial. The clinical signs vary in
severity as a result of the level and degree of obstruction. The location of the
obstruction also contributes to variability in the presenting clinical signs.
Common clinical abnormalities include vomiting, anorexia, depression, and
abdominal tenderness. Many intestinal foreign bodies can be detected with
careful abdominal palpation. Results of abdominal palpation include intes-
tinal distention, a palpable object, and abdominal pain.
The diagnosis of foreign body obstruction is usually made radiographi-
cally. The classic radiographic sign of mechanical obstruction is the presence
of multiple loops of gas-filled small intestine of various diameters. A small
intestinal diameter greater than 1.6 times the depth of the midcentrum of the
fifth vertebra has been used as a predictor of intestinal obstruction in dogs
[13]. A similar ratio may be useful in cats. The dilation may not be present to
the same degree in cases of partial intestinal obstruction. If the object is
radiopaque, it can be identified on plain radiographs (Fig. 4); however,
many foreign objects are radiolucent and require contrast radiography for
870 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880

identification (Fig. 5) [14]. Some foreign objects, such as various fruit seeds
and corn cobs, although nonopaque, can be identified on survey radio-
graphs because of their characteristic shape and contained gas lucencies
[14]. Liquid barium or barium paste in food can be used if there is no sus-
picion of gastrointestinal perforation. If perforation is suspected, aqueous
iodine or iohexol should be used [6]. Most proximal small intestinal obstruc-
tions are visible within 6 hours, whereas a 24-hour study may be required for
more distal obstructions [15,16]. The presence of a nonopaque foreign body
is seen as a filling defect in the intestinal lumen or as a complete obstruction
to the flow of barium in some cases. Another imaging modality that can be
used to diagnose and characterize intestinal foreign bodies is ultrasono-
graphy [11,17]. Using ultrasonography, gastrointestinal motility can be
assessed; when increased, it often signals the location of a mechanical
obstruction. The presence of fluid/gas distention also indicates the location
of the foreign object, and some objects may have characteristic acoustic sig-
nals. Ultrasonography may not accurately predict the presence of intestinal
perforation even when wall thickness is measured [11].
The treatment of intestinal foreign body obstruction is surgical. The sur-
gical approach is via a ventral midline laparotomy extending from the
xiphoid to the pubis. The entire intestinal tract should be explored to deter-
mine if there are multiple foreign bodies and to assess if the object caused
any intestinal trauma in transit. If the bowel segment containing the foreign
body is healthy, the foreign object can be removed through an antimesen-
teric enterotomy incision just aboral to the obstruction. This placement
ensures that the intestine excised is healthy. There is potential for the intes-
tine immediately overlying the foreign body to be compromised as a result
of pressure necrosis of the intestinal wall contacting the object. Enterotomy
proximal to the obstruction is not recommended, because distention with
gas and fluid and the passage of the foreign body may have caused some
degree of vascular compromise [2,18]. The enterotomy incision is made large
enough to manipulate the foreign material out of the intestinal lumen with-
out causing further intestinal trauma. This usually requires an incision the
length of the diameter of the obstructing object [18]. The enterotomy inci-
sion is then closed with size 4-0, synthetic, monofilament, absorbable suture
material, such as polydioxanone, in a simple continuous or simple interrup-
ted appositional pattern [19,20]. If the bowel segment demonstrates evidence
of necrosis, such as a thin intestinal wall and dark discoloration, a resection
and anastomosis should be performed. End-to-end anastomosis can be
accomplished using a simple interrupted appositional pattern or a modified
simple continuous appositional pattern with the same type of suture material
used for enterotomy closure [20,21]. The modified simple continuous pattern
is performed by first placing two separate sutures at the mesenteric and anti-
mesenteric borders. They are tied, leaving a 3- to 4-cm end for a stay suture,
to which mosquito forceps are attached. The needle end of the suture is then
used to complete the anastomosis. One strand advances the perimeter of the
 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880 871

Fig. 4. Right lateral (A) and ventrodorsal (B) radiographic projections of the abdomen of a 2-
year-old male domestic shorthair cat after ingestion of fishing tackle. Three radiopaque foreign
bodies are visible, including two hooks (one with leader attached) and a lead fishing weight.
872 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880

Fig. 5. Right lateral (A) and ventrodorsal (B) survey radiograph projections of a 3-year-old cat
with a 4-day history of vomiting and depression. The stomach is distended with gas, and there is
a large and primarily fluid-filled bowel loop in the caudal right abdomen. (C,D) A barium
contrast gastrointestinal study in the same cat. This contrast study confirms the presence of
foreign body obstruction of the proximal jejunum, and the distended bowel seen on the survey
radiographs is proximal to the obstruction. Complete obstruction is confirmed by the fact that
the barium does not flow past the lesion. There is mild gastroesophageal reflux.
 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880 873

Fig. 5 (continued).

intestine with bites 2 to 3 mm apart from mesenteric to antimesenteric knots

and a square knot tied to the tagged end of the knot at the antimesenteric
border. The other strand is advanced on the other side in the opposite di-
rection and tied in the same fashion [20]. After the anastomosis has been
874 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880

completed, an omental or serosal patch can be used to aid in sealing the

anastomosis [10,19,22].
A unique form of intestinal obstruction that is seen commonly in cats is
linear foreign body obstruction. This is caused by foreign bodies, such as
string, thread, a nylon stocking, or carpet fibers. One of the most common
causes is sewing thread alone or in combination with sewing needles [23].
The linear object becomes fixed around the base of the tongue or in the pylo-
rus. The intestinal peristaltic waves attempt to move the object aborally, and
the intestine gradually gathers up in a pleated fashion like an accordion on
the foreign object. The linear object becomes imbedded in the mesenteric
border of the small intestine and can erode through the intestinal wall, lead-
ing to leakage of intestinal contents and a local or generalized peritonitis
[24]. Clinical signs with these foreign bodies are generally not severe, because
the obstruction is not complete. Vomiting tends to be less frequent and
severe than with other foreign bodies. If peritonitis develops, a rapid deteri-
oration in the cat’s status may be observed. The linear object is generally not
palpable even with careful abdominal palpation; however, plication and
clumping of the intestine often are observed.
The radiographic signs of a linear foreign body include small intestinal
accordion-like pleating, shortening or gathering of the intestine, increased
luminal gas bubbles, and peritonitis secondary to bowel lacerations [23].
When clumping and plication of the intestine are visible on survey radio-
graphs, this is strong circumstantial evidence for the presence of a linear for-
eign body (Fig. 6). Another common radiographic sign of a linear foreign
body is a pattern of small, eccentrically located, luminal gas bubbles that are
tapered at one or both ends [23]. In a review of 64 cats with linear foreign
bodies, if three or more of these bubbles were seen, a definitive diagnosis
of a linear foreign body could be made [23]. Both ventrodorsal and lateral
projections should be obtained. The lateral view is preferred to determine
whether intestinal clumping is present, because the intestines are often on
the right side in a ventrodorsal view of a normal cat. The purpose of the ven-
trodorsal projection is to confirm that suspicious gas bubbles are located in
the small bowel. If a barium contrast study is used to confirm the diagnosis,
the abnormal plication of the intestines should be more evident, and the for-
eign object may appear as a linear filling defect. Once the contrast material
has passed through to the colon, a small amount may remain in the foreign
body, making it look like a linear opaque structure in the intestinal lumen.
On ultrasonographic examination, the bowel may have a ‘‘ribbon candy’’
appearance. Ultrasonography of linear foreign bodies reveals plication or
corrugation of the intestinal tract that can be similar to the ultrasonographic
appearance of intussusception. The two disorders can be differentiated by
the presence of a hyperechoic structure within the lumen and lack of the wall
layers to form a complete concentric ring [11].
Linear foreign bodies may cause only mild chronic intermittent signs
because of the partial nature of the intestinal obstruction [25]. Continued
 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880 875

Fig. 6. Right lateral (A) and ventrodorsal (B) survey radiographic projections of a 2-year-old
spayed female domestic shorthair cat with a linear foreign body (sewing thread). There is
clumping of the intestines on the lateral projection, and several eccentric tapered gas bubbles
can be seen in the small intestine. There is generalized decreased detail suggesting some free
peritoneal fluid.
876 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880

peristaltic activity may lead to erosion of the mesenteric border intestinal

wall with subsequent local or generalized peritonitis and vascular compro-
mise of the intestinal wall. For this reason, linear foreign body ingestion
should be treated as an emergency condition. Surgical management is the
traditional approach to this disorder. It has been reported that cats with
mild clinical signs, no pyrexia or severe abdominal pain, a linear foreign
body located around the base of the tongue, and evidence of only a mild left
shift on a complete blood cell count can be managed conservatively by cut-
ting free the sublingual attachment of the foreign body and maintaining the
cat in the hospital for observation and intravenous fluid therapy. Contrain-
dications to this conservative management approach include obvious pyloric
anchoring of the linear foreign body, the presence of severe abdominal pain
and pyrexia, radiographic evidence of peritonitis, and a degenerative left
shift on routine hematology testing [24].
Unlike most other intestinal foreign bodies, linear foreign bodies are not
easily removed from a single enterotomy incision. Pulling the object out
through a single proximal enterotomy can cause friction of the object against
the intestinal mesenteric border, and occult perforations may develop. It is
preferable to remove the object in short segments via multiple enterotomies
on the antimesenteric border. To begin, the anchor point, which is usually sub-
lingual or pyloric, must be released. Incising the string under the tongue or
performing a gastrotomy to release a pyloric anchor point accomplishes this.
The linear object can then be removed by one or more intestinal enterotomies.
A technique has been described for removal of linear foreign bodies from a
single enterotomy incision. The procedure is performed by creating a single
enterotomy in the antimesenteric border of the proximal duodenum. The lin-
ear foreign body is tied or sewn to a red rubber catheter, which is advanced
into the duodenum aborally, and the enterotomy is closed. The red rubber
catheter is then milked aborally along the intestine, relieving the plication
as it is advanced, until it is advanced the length of the colon; an assistant can
then retrieve it and the linear foreign body from the anus [26]. This technique
may not be effective for certain linear objects that have caused more severe pli-
cation or are knotted or matted and cannot be advanced aborally [27]. It is dif-
ficult to detect perforations on the mesenteric border should they occur,
because they are shielded by the attachment of the mesentery and mesenteric
vasculature. Where laceration has occurred, inflammation and infection at the
site are occasionally walled off, making removal of the string difficult. In these
cases, the intestine may not resume normal functioning after surgery [12].
At our teaching hospital, we see a combination of local clients and refer-
ral cases. Over the past 10 years, we have treated 113 cats for gastrointesti-
nal foreign bodies, with 2 of these cats presented on two different occasions.
Linear foreign bodies caused almost 50% of these cases. Over half of these
cases were caused by needles and thread or thread alone. Other foreign
objects identified were coins, earplugs, small toys, trichobezoars, an almond,
fishing tackle, and a cork. Cats are susceptible to intestinal obstruction by
 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880 877

many different types of foreign bodies, but linear foreign body obstruction is
clearly the most common type.
Although most feline intestinal foreign bodies can be removed with a
good prognosis, intestinal surgery is not without morbidity. Intestinal dehis-
cence is the most significant complication and has been associated with an
80% mortality rate in cats and dogs after intestinal surgery. This compares
with a mortality rate of only 7.2% in animals without dehiscence [28]. In a
series of 121 dogs undergoing small intestinal anastomosis or enterotomy,
dehiscence was identified in 15.7% of the animals, with a mortality rate of
73.7% [29]. It has also been shown that the survival rate is negatively corre-
lated with multiple intestinal procedures [28]. For these reasons, it is impor-
tant to ensure that only a single enterotomy or resection and anastomosis is
performed whenever possible, only healthy intestine is sutured, and intesti-
nal closure is meticulous.
When extensive intestinal injury results from the passage of a foreign
body or the presence of a linear foreign body, there may be a large or multi-
ple areas of intestinal necrosis. This would require the resection of a large or
multiple segments of the small intestine. This can result in various clinical
signs known as short bowel syndrome. The pathophysiology of this syn-
drome is a result of decreased secretin and cholecystokinin in the proximal
duodenum, thereby decreasing pancreatic and biliary secretions. The loss of
intestinal brush border enzymes also contributes to the syndrome, with the
changes resulting in maldigestion. Decreased intestinal transit time and
decreased mucosal surface area may also contribute to malabsorption. The
decreased transit time, increased lumenal osmotic pressure, bacterial over-
growth, and gastric hypersecretion ultimately result in diarrhea, dehydra-
tion, electrolyte imbalances, and malnutrition. The precise percentage of
small intestinal length that can be removed in cats without causing short
bowel syndrome is not known. In people, 40% to 50% can be removed
safely, but when greater then 75% is removed, nutritional status cannot be
maintained on enteral nutrition alone [30]. In four of five experimental dogs,
resection of 85% of the small intestine did not affect their ability to live for
11 to 24 months with no special therapy [31]. If massive resection of the
small intestine is required, it must be anticipated that the cat is going to need
nutritional support until adaptive changes in the intestine can occur. These
adaptive changes include increased bowel diameter, crypt and villus mucosal
cell hyperplasia, an increase in villus height and crypt depth, and an increase
in the number of epithelial cells per unit length of the villus. In the interim,
antidiarrheal therapy may be necessary as well as antibacterial therapy to
limit bacterial overgrowth [30].

Large intestinal foreign bodies

Large intestinal foreign body obstruction is exceedingly rare in cats.
Once passed into the colon, most objects are passed in the feces without
878 T.N. Bebchuk / Vet Clin Small Anim 32 (2002) 861–880

complication. In the rare case where colonic obstruction is identified, it can

be treated in a similar fashion as small intestinal obstruction. It should be
recognized that the large intestine heals similar to the stomach and small
intestine but that healing is delayed. Wound tensile strength lags behind that
of the small intestine, and suture line failure is more likely. The blood supply
is segmental, there is a large population of bacteria, and solid feces place
more tension on the suture line than the liquid ingesta in the small intestine.
All these factors theoretically lead to greater morbidity and mortality with
colonic surgery [19]. One study, however, did not detect a difference in dehis-
cence between animals undergoing large or small intestinal surgery [28].

Conclusion
Cats can be affected by foreign body obstruction at all levels of their gas-
trointestinal tract. Foreign bodies can be diagnosed and identified by a com-
bination of physical examination and palpation techniques, medical
imaging, and endoscopy. Medical imaging can consist of survey radio-
graphs, contrast radiographs, or any combination of the three. Endoscopy
is useful for the identification and removal of both esophageal and gastric
foreign bodies. If possible, esophageal surgery should be avoided. Small
intestinal foreign bodies are most commonly linear foreign bodies in cats,
and these constitute an emergency presentation. Traditionally, these have
been addressed as a surgical emergency, but in selected cases, conservative
management is appropriate. When surgery is performed for intestinal for-
eign bodies, the object should be removed using the fewest number of enter-
otomies necessary for removal with minimal intestinal trauma. If there is
evidence of intestinal necrosis, a resection and anastomosis is performed.
To prevent leakage and to aid in intestinal healing, an omental or serosal
patch can be placed over the enterotomy and anastomotic sites after suture
closure. If large intestinal segments must be removed, the cat may need to be
managed for short bowel syndrome with nutritional and pharmacologic
support.
The successful management of cats with gastrointestinal obstruction is
based on a knowledge of the relevant anatomy, proper use of diagnostic and
therapeutic techniques, an understanding of the physiologic effects of
obstruction, and an appreciation for intestinal tract healing at the affected
location. If all these factors are considered, most cats with gastrointestinal
foreign bodies can be managed with a good prognosis.

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beagle, including laboratory data in severe undernutrition. Surgery 1970;68:698–705.
Gastrointestinal  foreign  bodies  in  dogs  and  cats:  
a  retrospective  study  of  208  cases  
Journal of Small Animal Practice (2009) 50, (11) 576–583

G. HAYES*

¿A qué porcentaje de animales se le realizó una laparotomía exploratoria sin tener clara la
presencia del cuerpo extraño?

¿Influyó el tipo de cuerpo extraño en la supervivencia?

¿Por qué crees que llega a conseguir una supervivencia del 94% sin apenas dehiscencias?

Indica qué régimen postoperatorio instaura en los animales

¿Cuál fue el principal factor que mejoró los resultados de los cuerpos extraños digestivos?

¿Qué porcentaje de animales se diagnosticó por palpación?

Indica el % de supervivencia en perros y gatos tras la extracción de un cuerpo extraño

digestivo y ¿Si es lineal?

Indica que patrón de sutura realiza en las enterotomías.

¿Cuál fue la localización más típica de los cuerpos extraños digestivos en el gato?

¿Qué factores influyen en la cicatrización del intestino?

¿Por qué hubo peores resultados en los gatos?

PAPER

Gastrointestinal foreign bodies in dogs

and cats: a retrospective study of 208
cases
OBJECTIVES: To establish predilection sites of obstruction and to impaired oral intake of fluid and nutrients
(Boag and others 2005). Gastrointestinal
investigate clinical factors associated with a poor outcome. foreign bodies may cause complete or par-
METHODS: A retrospective study of 208 consecutive cases over a tial obstruction. In general, complete ob-
struction is associated with more dramatic
48-month period from first-opinion practice. clinical signs and a rapid deterioration
RESULTS: Overall, 91 per cent of cases recovered with higher whereas partial obstruction may be associ-
ated with more chronic signs of maldiges-
survival rates from discrete foreign bodies (94 per cent in dogs and tion and malabsorption (Papazoglou and
100 per cent in cats) as opposed to linear foreign bodies (80 per others 2003).
The majority of obstructive non-linear
cent in dogs and 63 per cent in cats). English bull terriers, springer gastrointestinal foreign bodies compro-
spaniels, Staffordshire bull terriers, Border collies and Jack Russell mise the blood supply to the intestinal
segment by luminal distention leading
terriers were over-represented. In dogs, 63 per cent of obstructions to intestinal wall oedema and progressive
occurred in the jejunum but foreign objects were encountered at all necrosis. These factors contribute to ileus
and to an increase in the number of patho-
points along the gastrointestinal tract. A longer duration of clinical genic intraluminal bacteria leading to the
signs, the presence of a linear foreign body and multiple intestinal breakdown of the mucosal barrier and sys-
temic endotoxaemia (Ellison 1993a).
procedures were associated with significantly increased mortality. Alongside the challenges of diagnosis
Neither the degree of obstruction (partial or complete) nor the and anaesthesia, surgical treatment and
wound healing are compromised by intes-
location of the foreign body was shown to have a significant tinal wall viability, intraluminal bacterial
influence on survival. overgrowth, ileus and hypoproteinaemia
(Allen and others 1992, Ellison 1993b,
CLINICAL SIGNIFICANCE: Prompt presentation, diagnosis and surgical Ralphs and others 2003). Enteric wound
intervention improve the outcome of gastrointestinal obstruction breakdown and leakage are the most se-
rious and catastrophic complications of
by foreign bodies. At surgery, the minimal number of intestinal surgery on the gastrointestinal tract (Allen
procedures should be performed to restore the integrity of the and others 1992, Evans and others 1994,
Shales and others 2005).
alimentary tract. Retrospective studies concerning lin-
ear foreign bodies exist (Felts and others
1984, Evans and others 1994) and two
case series in dogs have been published
G. HAYES* INTRODUCTION (Capak and others 2001, Boag and oth-
Journal of Small Animal Practice (2009) ers 2005). These studies all originate from
50, 576–583 Gastrointestinal foreign bodies are com- veterinary teaching hospitals, report a re-
DOI: 10.1111/j.1748-5827.2009.783.x monly encountered in first-opinion com- ferral caseload and focus on different as-
Accepted: 27 April 2009; Published online: panion animal practice and may present pects of presentation and treatment. To
8 October 2009 with a variety of clinical signs depending the author’s knowledge, there are no stud-
on the location, the degree and the dura- ies from first-opinion practice despite the
tion of the obstruction (Aronson and oth- fact that the vast majority of gastrointesti-
ers 2000, Papazoglou and others 2003). nal foreign bodies are probably managed
Gastrointestinal obstruction results in in first-opinion practice.
disturbances of fluid balance, acid-base The aims of the present study are: to
RSPCA Greater Manchester Animal Hospital, 411
Eccles New Road, Salford, Manchester M5 5NN status and serum electrolyte concentra- report a large series of cases of gastrointes-
tions due to hypersecretion and seques- tinal obstruction from first-opinion (char-
*Current Address: The Queen’s Veterinary School
Hospital, University of Cambridge, tration within the gastrointestinal tract ity) practice; to report predilection sites of
Madingley Road, Cambridge CB3 0ES which is exacerbated by vomiting and obstruction and types of objects recovered

576 Journal of Small Animal Practice • Vol 50 • November 2009 • © 2009 British Small Animal Veterinary Association

and to investigate clinical factors associ-
ated with a poor outcome.
MATERIALS AND METHODS
The case records of all cats and dogs ad-
mitted to the RSPCA Greater Manches-
ter Animal Hospital with a diagnosis of
gastrointestinal obstruction due to a for-
eign body during the period June 2003
to May 2007 (48 months) were reviewed.
Gastrointestinal foreign bodies were de-
fined as all clinically significant ingested
foreign bodies (whose main bulk was) lo-
cated distal to the cardia. Case details re-
trieved included age, breed, bodyweight,
presenting clinical signs, duration of
clinical signs, surgical findings and treat-
ment, postoperative complications and
outcome. The duration of clinical signs
was either the time since known inges-
tion or from the start of clinical signs if
ingestion was not observed. The surgi-
cal findings and treatment recorded were
the site of obstruction, type of foreign
body (that is linear or discrete), the de-
gree of obstruction (that is partial or
complete) and the treatment (that is gas-
trotomy, enterotomy or enterectomy and
the number of incisions made into the
alimentary tract). Patients which passed
the foreign body before diagnosis were
excluded.
Dog breeds which were over-represent-
ed had a relative risk calculated (relative to
crossbreed dogs) taking into account the
prevalence of these breeds in the hospital
population. Selected ratio measurements
were summarised as mean (±sd) and sta-
tistical comparisons (independent t-tests,
with the type indicated by Levene’s test for
equality of variances) were made between
surviving patients and those with a fatal
outcome. Nominal data were statistically
compared between surviving patients and
those with a fatal outcome (Fisher’s exact
test). All variables were examined with the
null hypothesis of homogeneity between
the groups with significance taken at p
less than 0⋅05 (two-tailed tests). Logistic
regression was performed on selected vari-
ables using forward stepwise regression
and verified with forced entry regression.
All statistics were performed using SPSS
for Windows 16⋅0 (SPSS Inc).
Journal of Small Animal Practice • Vol 50
Gastrointestinal foreign bodies
Diagnosis
Cases were investigated and treated by nine
veterinary surgeons with variable clinical
experience working within the limited re-
sources of a charity hospital in the context
of a persistently high caseload. Diagnostic
workup was limited to that necessary to
make a tentative diagnosis or to indicate the
need to surgically explore the abdomen. In
most cases, the decision to perform a co-
eliotomy was based on history and careful
clinical examination, with particular em-
phasis on abdominal palpation. If further
investigations were necessary, abdominal
palpation under sedation (or anaesthesia),
abdominocentesis, radiography and endos-
copy could be performed. In certain cases
blood tests and radiographs had been per-
formed at private veterinary practices be-
fore a charitable referral with or without a
diagnosis.
Presurgical treatment and
surgical technique
All cases with a history of vomiting received
fluid therapy before anaesthesia and coeli-
otomy. All cases received intramuscular or
subcutaneous 15 mg/kg amoxicillin (Be-
tamox; Norbrook) preoperatively and pa-
tients undergoing enterotomy or enterecto-
my also received iv 10 mg/kg metronidazole
(Flagyl; Aventis) intra-operatively. A ventral
midline coeliotomy was performed and the
entire gastrointestinal tract was examined
before replacement within the abdomen.
The obstructed segment was exteriorised
and packed off with swabs. Enterotomy
incisions were made on the antimesenteric
border and all enterotomy, enterectomy
and gastrotomy sites were closed using two
metric polydioxanone (PDS II; Ethicon) in
a simple interrupted appositional pattern.
A two-layer closure was performed follow-
ing gastrotomy. The exteriorised segment
was lavaged before omentalisation (simple
wrapping with or without tacking sutures)
and routine abdominal closure.
Cases with multiple ruptures, gener-
alised peritonitis or extensive non-viable
bowel were generally euthanased intra-op-
eratively at the discretion of the individual
surgeon (with informed owner consent).
Postoperative treatment
All patients were offered oral fluids 12 to
24 hours postoperatively (unless vomiting)
• November 2009 • © 2009 British Small Animal Veterinary Association
and food 18 to 30 hours postoperatively, at
the discretion of the surgeon. Intravenous
fluids were continued until oral intake was
sufficient. Antibiotics and analgesics were
normally continued for at least three days
postoperatively. No cases underwent re-
operation.
RESULTS
Eligibility, clinical signs and pre-
sentation
One hundred and seventy-four dogs com-
prising 24 different breeds were included
in the study (summarised in Tables 1 and
2). Ten individuals were presented on two
separate occasions with gastrointestinal
foreign bodies, hence 184 distinct inci-
dents (cases) were recorded.
Twenty-one cats were included in the
study (summarised in Tables 1 and 2).
Three individuals were presented on two
separate occasions with gastrointestinal
foreign bodies, hence 24 distinct incidents
(cases) were recorded.
Presenting clinical signs included vom-
iting (87 per cent), anorexia (72 per cent),
greater than 10 per cent bodyweight loss
(8 per cent), diarrhoea (5 per cent) and
haemorrhagic diarrhoea (2 per cent). In
14 cases animals were presented before
clinical signs developing as the owner had
witnessed ingestion of an object. In a total
of 54 cases (26 per cent) the owner was
aware of foreign body ingestion (Fig 1).
Dogs
Diagnosis In six of 184 cases (3 per cent)
a linear foreign body was evident in the oral
cavity or at the anus during clinical examina-
tion. In 139 of 184 cases (76 per cent) the
foreign object (or an intestinal abnormality)
was palpable in the conscious patient (111
cases) or anaesthetised/sedated patient. Ab-
dominal radiography was performed in 42
cases, which was essential to the diagnosis
in 21 of 184 cases (11 per cent), and two of
184 cases (1 per cent) underwent endoscopy
to confirm the diagnosis. An exploratory co-
eliotomy was performed in 16 of 184 cases
(9 per cent) without a definitive diagnosis
for the investigation of chronic vomiting, the
owner’s insistence of foreign body ingestion,
previous history of foreign body ingestion or
the presence of fragments of foreign material
577
 G. Hayes

Table 1. Breeds represented dogs the linear foreign body originated

Breed Number Relative risk* 95 per cent
at the pylorus in 20 cases (67 per cent) as
confidence interval summarised in Fig 3.
Dogs (n=174)†
Staffordshire bull terrier 52 3⋅3 2⋅2-5⋅1
Complications and outcome Of 184
English bull terrier 13 10⋅9 6⋅0-20⋅0 cases admitted into the hospital, 169 were
Jack Russell terrier 13 2⋅2 1⋅2-4⋅2 discharged (92 per cent) and made a full
Border collie 9 3⋅0 1⋅4-6⋅1 recovery with follow-up for at least 10
Springer spaniel 9 8⋅3 4⋅1-16⋅8 days (summarised in Table 5).
Yorkshire terrier 7 1⋅0 0⋅5-2⋅3 Of the five cases euthanased, one case
German shepherd dog 6 1⋅1 0⋅5-2⋅6 was euthanased preoperatively (on hu-
Labrador 5 2⋅2 0⋅9-5⋅6 mane grounds), two cases were euthana-
Bull mastiff 4
sed intra-operatively (both linear foreign
Cocker spaniel 3
bodies of five days duration, with multiple
Golden retriever 3
Shih-tzu 2
ruptures and generalised peritonitis) and
West Highland white terrier 2
two cases were euthanased postoperatively
Dobermann, Dalmatian, Rough collie, 1 of each (mean 4⋅5 days later; range 4 to 5 days)
great Dane, boxer, Rottweiler, Samo- with signs of peritonitis suggestive of en-
yed, Toy poodle, Lurcher, Border terrier teric dehiscence. Four of the five cases eu-
Crossbreed 36 1⋅0
thanased were linear foreign bodies.
Cats (n=21)†
Of the 10 cases which died, one died
Domestic shorthair 20
Siamese 1
preoperatively (six hours after admission)
and nine cases died postoperatively (mean
*Based on incidence proportion per breed relative to crossbreeds in the hospital population, calculated for breeds with at
least five individuals represented. 3⋅1 days later; range 0⋅13 to 10 days). Of
†Ten dogs and three cats presented on two separate occasions (174 individual dogs and 21 individual cats with
208 distinct incidents of foreign body obstruction).
these nine cases, one was an anaesthetic
recovery death, one developed pancreatitis
and jaundice and seven developed signs
Table 2. Patient details at presentation of peritonitis suggestive of enteric dehis-
Dogs (n=174)* Cats (n=21)* cence. Three of these seven cases (and the
Age (years)
one case which died preoperatively) had
Mean (sd) 2⋅5 (3⋅0) 1⋅8 (1⋅8)
been treated with anti-emetics for periods
Range 0⋅10-14⋅0 0⋅2-5⋅3 of between 3 and 14 days by the refer-
Bodyweight (kg) ring practices which were thought to have
Mean (sd) 13⋅8 (9⋅8) 2⋅8 (0⋅8) masked the progression of their clinical
Range 1⋅1-39⋅4 1⋅4-4⋅9 signs. It was not possible to statistically de-
Duration of clinical signs termine the contribution of preoperative
(days)
anti-emetic usage to the outcome.
Mean (sd) 4⋅8 (6⋅8) 6⋅2 (7⋅7)
Minor complications were recorded in
Range 0⋅04-60 0⋅08-30
seven of 184 cases (4 per cent) and includ-
*Ten dogs and three cats presented on two separate occasions (174 individual dogs and 21 individual cats with 208
distinct incidents of foreign body obstruction). ed postoperative pyrexia, anorexia or vom-
iting treated medically (five cases), wound
infection or seroma (one case of each).
in vomit or faeces. These 16 cases had no pal- 152 cases as summarised in Fig 2. Fifteen The average period of hospitalisation
pable gastrointestinal abnormality and no ab- cases ingested two or more different objects; postoperatively was 2⋅8 days (range 1 to
normalities on abdominal radiography. One in six of these, concurrent obstructions 10 days).
case died between diagnosis and surgery. were present at different levels of the gas-
trointestinal tract. In 126 of 180 cases (70 Cats
Surgical findings Overall, 199 foreign per cent) the foreign object was subjective- Diagnosis In six of 24 cases (25 per cent)
objects were recovered from 183 cases ly judged to be causing complete luminal a linear foreign body was evident under the
(Table 3). Two cases passed the foreign obstruction and partial obstruction in the tongue or protruding from the anus dur-
object in vomit or faeces after diagno- remaining 54 of 180 cases (30 per cent). ing clinical examination. In 14 of 24 cases
sis but before surgery. One hundred and One foreign object was removed from the (58 per cent) the foreign body (or an intes-
eighty cases underwent a coeliotomy omentum, having penetrated through the tinal abnormality) was evident during gen-
(summarised in Table 4). duodenum (Hunt and others 2004). tle abdominal palpation of the conscious
Discrete foreign objects were found at Linear foreign bodies were found in 30 patient (13 cases) or anaesthetised patient.
all points along the gastrointestinal tract in cases (16 per cent of all canine cases). In Abdominal radiographs were taken in six

578 Journal of Small Animal Practice • Vol 50 • November 2009 • © 2009 British Small Animal Veterinary Association
 Gastrointestinal foreign bodies

80 obstruction in the remaining 14 of 24 cas-

es (58 per cent). In one case a trichobezoar
70 was removed from the duodenum (Barrs
Owner aware of foreign body and others 1999).
ingestion (n=54) The majority of discrete foreign objects
60
were found in the proximal parts of the
Owner not aware of foreign gastrointestinal tract as summarised in
Number of patients

50 body ingestion (n=154) Fig 2. One patient had foreign objects at

two locations.
40 Linear foreign bodies were found in
eight cases (33 per cent) originating from
30 the base of the tongue in five cases (63 per
cent) as summarised in Fig 3.
20
Complications and outcome Of the 24
cat cases admitted into the hospital, 21
10 were discharged (88 per cent) and made
a recovery with follow-up for at least 10
0 days (summarised in Table 5).
<1d 1-3d 4-6d 7-9d 10-12d 13-15d >15d Three cases were euthanased intra-
Duration of clinical signs or time since operatively (linear foreign bodies of over
ingestion (days [d])
14 days duration with multiple ruptures
FIG 1. Graph to show the duration of clinical signs or the time since known ingestion before and generalised peritonitis). No cats died
presentation for definitive treatment postoperatively and only one minor com-
plication was recorded (an upper respira-
tory tract infection). The average period
Table 3. Foreign objects recovered from the gastrointestinal tract of hospitalisation postoperatively was 2⋅2
Type of foreign body Dogs* Cats† days (range 1⋅5 to 4 days).
Latex teat 58 5
Plastic/rubber object 32 6 Statistics
String/rope/fishing line 22 8 The relative risk for eight dog breeds with
Stone 19 at least five individuals represented was
Balls 15 calculated based on the incidence propor-
Underwear/nappy 9 tion per breed relative to crossbreeds in
Corn-cob 9 the entire hospital population. Five breeds
Leather 5
were at significantly higher risk of requir-
Metallic object/coins 5‡
ing treatment for a gastrointestinal foreign
Bone 3
body than the “bench-mark” crossbreed
Cassette tape 2
Needle and thread 1 3
dogs (summarised in Table 1).
Fish hook and line 1 Owners aware of foreign body inges-
Plastic bag, blanket, 2 ft electric cable, peach 1 of each tion presented animals for treatment
stone, wooden skewer, potato, pine cone, bead, significantly earlier (mean 2⋅8 ± 3⋅6 days
lolly stick
of clinical signs) than those not aware of
Dustbin contents (multiple small objects) 9
foreign body ingestion (mean 5⋅7 ± 7⋅6
Sellotape, almond, trichobezoar 1 of each
days of clinical signs; P<0⋅01).
*One hundred and ninety-nine foreign objects from 183 dogs (12 dogs had two types of objects and two dogs had
three different types of objects). One dog died preoperatively and the foreign object was not identified. There was no statistical difference be-
†Twenty-five foreign objects from 24 cats. tween surviving cases and those with a fa-
‡One case had 20 coins in the stomach.
tal outcome with regard to age (P=0⋅98)
or bodyweight (P=0⋅65), but surviving
cases which were essential to make a diag- Surgical findings Overall, 25 foreign cases had a significantly shorter duration
nosis in three of 24 cases (13 per cent). In objects were recovered from 24 cases of clinical signs (mean 4⋅6 ±6⋅8 days) than
one of 24 cases (4 per cent) an exploratory (Table 3). All 24 cases underwent a coeli- those with a fatal outcome (mean 8⋅7 ±
coeliotomy was performed without a diag- otomy (summarised in Table 4). In 10 of 7⋅7 days; P=0⋅02).
nosis to investigate chronic vomiting and 24 cases (42 per cent) the foreign object There was a trend for foreign bodies
anorexia following unremarkable blood was subjectively judged to be causing judged to be causing a complete obstruc-
results and radiographs. complete luminal obstruction and partial tion to present earlier (mean 4⋅1 ±3⋅5

Journal of Small Animal Practice • Vol 50 • November 2009 • © 2009 British Small Animal Veterinary Association 579
 G. Hayes

Table 4. The results of coeliotomy in dogs and cats days) than those causing partial obstruc-
Treatment Dogs (n=180) Cats (n=24)
tion (mean 6⋅7 ±10⋅8 days; P=0⋅06), but
there was no statistical difference in the
Gastrotomy only 28 3
outcome between foreign bodies causing
One or more enterotomies only 115 14
complete or partial obstruction of the
Gastrotomy and one or more enterotomies 24 3
Enterectomy 2
gastrointestinal tract (P=0⋅59). Too few
One gastrointestinal incision 137 14 enterectomies were performed to judge
Two gastrointestinal incisions 14 2 whether this treatment was associated
Three gastrointestinal incisions 8 1 with a poor outcome. There was no signif-
Four gastrointestinal incisions 1 1 icant difference in the outcome in relation
Five gastrointestinal incisions 5 2 to the location of discrete foreign bodies:
above five gastrointestinal incisions 2 stomach (P=0⋅36), duodenum (P=0⋅28),
Foreign body removed per rectum 8 1 jejunum (P=0⋅22), ileum (P=0⋅73) or co-
Foreign body removed from omentum 1 lon (P=0⋅63).
Euthanased intra-operatively 2 3
The presence of a linear foreign body
was associated with a significantly higher
mortality rate than the presence of a dis-
crete foreign body (P<0⋅01), and cases
undergoing multiple gastrointestinal inci-
sions had a significantly higher mortality
than those treated with a single gastroto-
my or enterotomy (P=0⋅01). However, the
presence of a linear foreign body closely
correlated with multiple gastrointesti-
Oesophagus† nal incisions (P<0⋅01) making it diffi-
cult to evaluate which variable was more
significant.
Stomach 16% 2.9 ±3.5 days 24% Independent variables entered into the
logistic regression model included the
duration of clinical signs, type of foreign
Duodenum 14% 4.1 ±2.3 days 24% body (linear or discrete), number of in-
cisions, degree of obstruction (partial or
Omentum 1%
complete) and the interaction type of for-
Prox-jejunum 23% 4.3 ±4.6 days 29% eign body times number of incisions. The
Jejunum* 7%

dependent variable investigated was out-

Mid-jejunum 26% 5.5 ±9.1 days 18%
come (dead or alive). The only indepen-
dent variable included in the final model
Distal-jejunum 6% 11.2 ±18.5 days was the number of incisions (OR 1⋅807;
95 per cent CI 1⋅255 to 2⋅601). All other
Ileum 3% 2.6 ±0.6 days 6% variables were insignificantly associated
with predicting the outcome and were
rejected from the model. This suggested
that the number of incisions was a more
Colon 4% 3.0 ±1.4 days significant predictor of a poor outcome
than the presence of a linear foreign body
or an interaction between these variables.

DISCUSSION
FIG 2. Diagram to illustrate the locations of 160 discrete foreign bodies in 152 dogs‡ (left side)
and 17 discrete foreign bodies in 16 cats (right side). For the dogs the mean duration of clinical Presentation
signs (±sd) is also displayed for each location
* Sub-division of jejunum not specified.
Staffordshire bull terriers, English bull
†Oesophageal foreign bodies were excluded from this study due to the differing pathophysiology terriers, Jack Russell terriers, Border col-
and treatment. However, to increase the usefulness of this diagram the author would like to report lies and springer spaniels were found to be
that one feline and 10 canine oesophageal foreign bodies were presented during the course of this
study.
at higher risk than crossbreeds to require
‡ One dog died and one patient vomited the foreign body preoperatively after diagnosis. treatment for a gastrointestinal foreign

580 Journal of Small Animal Practice • Vol 50 • November 2009 • © 2009 British Small Animal Veterinary Association
 Gastrointestinal foreign bodies

intestinal tract, with the jejunum being

Tongue / Mouth
the most common location. Most patients
presented within one day of ingestion had a
gastric foreign body, although foreign bod-
ies were found which had moved to the
mid-jejunum within one day. With increas-
ing duration of clinical signs objects were
Oesophagus more likely to be found in the proximal and
10%

3%

3%

38%

25%
mid-jejunum. This suggests that (initially
at least) the majority of foreign bodies will
slowly move distally along the small intes-
Stomach
tine despite causing clinical signs of obstruc-
tion. Some may pass all the way through
but most are eventually immobilised by the
47%

13%

Duodenum
distended small intestine or a physical bar-
rier such as the ileocolic junction.
The location of the canine discrete for-
eign bodies in this study is comparable to

13%
that recorded by Capak and others (2001)
25%
Jejunum
13%

7%

where the mean duration of clinical signs

at presentation was six days. The series
reported by Boag and others (2005) re-
Ileum corded 50 per cent of foreign bodies in
3%

the stomach in comparison with 16 per

cent in the present study. The median du-
ration of vomiting in the Boag study was
Colon two days (mean not reported, 124 dogs),
whereas the median duration of clinical
signs in this study was three days (mean
5⋅0 ±7⋅0 days, 184 cases). These factors
imply that the referral population of dogs
in the Boag study was different from the
Anus first-opinion (charity hospital) population
of dogs in the present study. It is possible
FIG 3. Diagram to illustrate the location of linear foreign bodies in 30 dogs (left side) and eight
cats (right side). The circle at the beginning of each arrow indicates the proximal “anchorage
that many of the cases in the present study
point” and the arrowhead indicates the most distal extent of the linear foreign body had a gastric foreign body for a period of
time and were presented for treatment
only when the foreign body entered the
proximal small intestine and their condi-
Table 5. Summary of major complications and outcome
tion deteriorated.
Species Foreign Total inci- Total surviv- Euthanased Died Total surviving
body dents ing (per cent) (per cent)
The survival rate for the treatment of
discrete foreign bodies in dogs in the pres-
Dogs Discrete 154 145 (94) 1 8

Cats
Linear
Discrete
Linear
30
16
8
24 (80)
16 (100)
5 (63)
4
0
3
2
0
0
169 (92)

Totals 208
body. Breed predispositions have not been
previously reported.
Owners aware of foreign body ingestion
tended to present their animals for treat-
ment significantly earlier than those not
aware of ingestion. This is important be-
cause this study also found that the success
21 (88)
} 190 (91)
190 8 10
rate declined with increasing duration of
clinical signs of obstruction. These intuitive
findings have not previously been reported.
Discrete foreign bodies
This study reports foreign bodies causing
obstruction at all points along the gastro-
ent study was 94 per cent. This compares
favourably with the 83 per cent survival
rate reported by Capak and others (2001),
but is less than the 99 per cent survival
rate in the study by Boag and others
(2005). These are “crude statistics” and
do not take into account any confound-
ing factors between the study populations
and institutions. Capak and others (2001)
reported a higher survival in dogs less than
two years of age but this was not found in
the present study.
For cats neither the locations of discrete
gastrointestinal foreign bodies nor the

Journal of Small Animal Practice • Vol 50 • November 2009 • © 2009 British Small Animal Veterinary Association 581

surgical survival rate has previously been
described. There appears a more uniform
distribution of locations than in dogs, al-
though far fewer cases were recorded. All
cats with discrete foreign bodies in this
study survived.
Linear foreign bodies
In dogs, linear foreign bodies accounted
for 16 per cent of the foreign bodies in
the present study, and the most common
anchorage point was the pylorus (67 per
cent) with the foreign material extending
into the proximal jejunum. Canine linear
foreign bodies are usually fabrics, plastic
and textile materials.
In cats, linear foreign bodies accounted
for 33 per cent of the foreign bodies in the
study, and the pylorus was an unusual lo-
cation, with the majority being anchored
around the tongue (63 per cent) and
mostly comprising single strands of thread
or string.
Gastrointestinal foreign bodies have
been previously reported to be linear in
50 to 61 per cent of feline cases (Felts and
others 1984, Basher and Fowler 1987,
Bebchuk 2002) and 36 per cent of canine
cases (Boag and others 2005). These pro-
portions are higher than in the present
study which may indicate differences in
first-opinion and referral populations or
in the definition of a linear foreign body.
The survival rate for linear foreign bod-
ies in the present study was 80 per cent for
dogs which is very similar to the 78 per
cent survival rate reported by Evans and
others (1994) but less than the 98 per cent
survival eluded to in the study by Boag
and others (2005).
For cats the survival rate for linear for-
eign bodies was 63 per cent which is lower
than the 84 per cent survival rate reported
by Felts and others (1984) and the 92
per cent survival reported by Basher and
Fowler (1987). The duration of clinical
signs was not recorded in the Felts study,
and for the Basher and Fowler study the
median duration of clinical signs was only
two days (range 0⋅5 hours to 10 days). In
the present study, the median duration of
clinical signs for cats presented with linear
foreign bodies was four days (mean 10 ±
9⋅9 days, range 2 to 30 days). Of the cats
not surviving in the present study, all had
clinical signs of over 14 days duration.
582
G. Hayes
This study reports a significantly higher
mortality rate in animals presented with a
linear foreign body (rather than a discrete
foreign body) and in animals treated with
more than one gastrointestinal incision.
There are likely to be many reasons for the
lower survival rates for linear foreign bod-
ies. First, linear foreign bodies may cause
a chronic partial obstruction. Secondly, a
greater proportion of the bowel is likely
to be affected and compromised. Thirdly,
multiple ruptures and peritonitis were a
common finding during exploratory co-
eliotomy in this study. Multiple incisions
were required for most linear foreign bod-
ies (and in some cases with multiple foreign
bodies in the gastrointestinal tract) which
increases surgical time, contamination
and suture material usage. It is intuitive
to minimise the number of gastrointesti-
nal incisions, and in certain cases foreign
objects can be manipulated along the ali-
mentary tract to the rectum or stomach.
A technique of single enterotomy removal
of linear foreign bodies has been reported
and used with good success by others (An-
derson and others 1992), although many
chronic foreign objects cannot be safely
manipulated due to severe compromise
of the local gastrointestinal segment. The
number of intestinal procedures performed
was found to have a detrimental effect on
survival in a study reported by Wylie and
Hosgood (1994) but this association was
not found by Evans and others (1994).
Over half of the animals euthanased
in this study were euthanased intra-op-
eratively due to multiple ruptures and
generalised peritonitis as a consequence
of chronic linear foreign bodies. This was
performed at the discretion of the surgeon
(with informed owner consent) due to the
perceived poor prognosis (Evans and oth-
ers 1994, Ralphs and others 2003) and the
inability to provide intensive care postop-
eratively. Some of these cases may have
survived with extensive bowel resections
and intensive management of peritonitis
(King 1994, Mueller and others 2001,
Staatz and others 2002, Costello and oth-
ers 2004, Boag and others 2005).
In this study, of 189 cases that under-
went intestinal surgery, two were euthana-
sed postoperatively and nine died. Nine
of these cases showed signs of peritonitis
suggestive of enteric wound breakdown,
Journal of Small Animal Practice • Vol 50
although further investigations (such as
abdominocentesis and cytology) were not
performed to confirm this diagnosis. How-
ever, these figures do allow an estimate to
be made of the dehiscence rate of five per
cent. This dehiscence rate may have been
higher if treatment had been attempted
on the five cases euthanased intra-opera-
tively. The comparison of dehiscence rates
from different studies is complicated by
the large numbers of variables between
and within studies. The presence of a gas-
trointestinal foreign body, preoperative
peritonitis and greater than 15 per cent
preoperative weight loss all increase the
risk of dehiscence (Allen and others 1992,
Ellison 1993b, Evans and others 1994,
Ralphs and others 2003). Reported dehis-
cence rates following foreign body surgery
are 27⋅7 per cent (n=36), 13⋅9 per cent
(n=122) and 2⋅9 per cent (n=138) (Allen
and others 1992, Capak and others 2001,
Boag and others 2005).
This study reports a low incidence of
cases treated by enterectomy (two of 189)
in comparison with other studies [13 of 32
dogs with linear foreign bodies (Evans and
others 1994), 12 of 123 dogs (Capak and
others 2001) and 38 of 138 dogs (Boag
and others 2005)]. The five cases eutha-
nased intra-operatively may have been
treated with this procedure, had treatment
been attempted. This low rate of resection
and anastomosis may reflect differences in
the way surgeons judge intestinal viabil-
ity, may reflect a reluctance to perform a
more complex procedure in a first-opin-
ion practice or may be another reflection
of the different patient populations seen
in first-opinion and referral practices.
In this study neither the location of the
foreign body nor the degree of obstruc-
tion were shown to affect the outcome.
This finding does not seem to support
the widely held belief that patients with
complete or proximal obstructions tend to
deteriorate more quickly than those with
partial or more distal obstructions. An-
other interpretation could be that animals
with more proximal or complete obstruc-
tions recover better or were treated more
quickly.
Limitations of this study
There are many limitations inherent in a
retrospective study performed in a busy,
• November 2009 • © 2009 British Small Animal Veterinary Association

first-opinion urban charity hospital. The
treatment performed and surgical success
rate achieved depended on many factors
including the owner’s wishes and expecta-
tions and the experience and clinical skills
of the veterinary surgeon managing the
case. There was no financial motivation
to treat cases or perform extensive workup
and in some cases the perception of owner
neglect or indifference to the outcome
may have influenced the decision to rec-
ommend euthanasia. It was impossible to
correct for such confounding factors.
Diagnostic techniques were limited to
those necessary to make a diagnosis of
gastrointestinal obstruction or to indicate
the need for surgical exploration of the ab-
domen. The goal of treatment was to re-
move the gastrointestinal obstruction and
promptly restore enteric nutrition. The
limited facilities did not allow the routine
measurement of biochemical, acid-base or
electrolyte abnormalities which common-
ly occur with gastrointestinal obstruction
(Papazoglou and others 2003, Boag and
others 2005). However, attempts were
made to correct fluid deficits preopera-
tively, followed by the prompt restoration
of oral alimentation to rectify electrolyte
abnormalities. Routine biochemical, acid-
base and electrolyte stabilisation may
have improved patient recovery times and
reduced the incidence of adverse postop-
erative complications.
Better imaging investigations and tech-
nological skill may have reduced patient
morbidity; foreign bodies past the ileoco-
lic junction may not have undergone co-
eliotomy and some gastric foreign bodies
may have been recovered endoscopically.
Antibiotic protocols were not opti-
mal; intravenous, broad spectrum cepha-
losporins or potentiated amoxicillins at
induction are recommended (Papazoglou
and others 2003), used according to the
cascade, for a duration determined by
the classification of the surgery. Inten-
sive postoperative management, prompt
re-operation and open-abdominal drain-
age techniques may have reduced patient
mortality.
Journal of Small Animal Practice • Vol 50
Gastrointestinal foreign bodies
A limitation of one aspect of this study
is the low number of cats presented, with
insignificant numbers for statistical analy-
sis. Only 12 per cent of the cases reported
were in felines despite cats accounting for
35 per cent of the surgical caseload of the
hospital. It would seem that cats are genu-
inely less likely to ingest significant gastro-
intestinal foreign objects than dogs, but
it is nevertheless interesting to compare
these cats with the dogs.
Despite these justifiable criticisms this
study does present new information on
the predilection sites for obstruction and
on clinical factors associated with a poor
outcome.
CONCLUSIONS
This study has demonstrated that certain
dog breeds are predisposed to gastrointes-
tinal obstruction by foreign body and that
obstruction mostly occurs in the jejunum.
A longer duration of clinical signs, the
presence of a linear foreign body and mul-
tiple intestinal procedures were shown to
be significantly associated with increased
mortality. Neither the degree of obstruc-
tion (partial or complete) nor the location
of the foreign body was shown to have a
significant influence on survival.
Acknowledgements
The author would like to thank Dick
White (for assistance with the manu-
script), T. J. McKinley (for statistical
advice) and the staff at the RSPCA Great-
er Manchester Animal Hospital.
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BOAG, A. K., COE, R. J., MARTINEZ, T. A. & HUGHES, D.
(2005) Acid-base and electrolyte abnormalities in
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(2001) Treatment of the foreign body induced oc-
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FELTS, J. F., FOX , P. R. & BURK, R. L. (1984) Thread and
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583
81) Duodenogastric Intussusception with Concurrent Gastric
Foreign Body in a Dog: A Case Report and Literature Review
David A. Allman, DVM, DACVS, Michael P. Pastori
(J Am Anim Hosp Assoc 2013; 49:64–69.
http://www.jaaha.org.are.uab.cat/content/49/1/64.full.pdf+html

 
PREGUNTAS
 

 

1.  EN  CUANTO  A  LA  INT.  ,  CUÁLES  SON  MÁS  FRECUENTES?  

2.  CUAL  ES  EL  %  DE  SUPERVIVIENCIA  EN  EL  ESTUDIO?  
3.  EN  QUÉ  DIRECCIÓN  SON  MÁS  FRECUENTES?  

4.  CÓMO  PODEMOS  PREVENIR  LAS  RECIDIVAS?  

5.  QUÉ  FACTORES  PREDISPONENTES  HAY?  
 
CASE REPORTS

Duodenogastric Intussusception with Concurrent

Gastric Foreign Body in a Dog: A Case Report and
Literature Review
David A. Allman, DVM, DACVS, Michael P. Pastori

ABSTRACT
A 3 yr old spayed female boxer weighing 22.8 kg was presented for severe, acute vomiting and tenesmus. Tachycardia, tachy-
pnea, dehydration, and abdominal pain were present on physical examination. Abdominal radiographs showed a foreign
object (golf ball) in the fundus of the stomach, and a larger, round, soft-tissue opacity mass in the region of the pylorus.
Endoscopic removal of the foreign object was unsuccessful. A large soft-tissue mass (duodenogastric intussusception) was
visualized with endoscopy, but was not correctly diagnosed until surgery. A midline exploratory celiotomy was performed and
the duodenogastric intussusception was diagnosed and manually reduced. Severe pyloric wall edema and minimal bruising
were present. A routine fundic gastrotomy was performed and the foreign object was removed. A right-sided incisional
gastropexy and duodenopexy were performed in attempt to prevent recurrence of the intussusception. The dog was dis-
charged from the hospital 38 hrs after surgery, and was normal on follow-up 1 yr after surgery. The dog in this report is the
sixth documented case of duodenogastric/pylorogastric intussusception in the veterinary literature. This is the first reported
case with a concurrent gastric foreign body and endoscopic visualization of the intussusception. (J Am Anim Hosp Assoc 2013;
49:64–69. DOI 10.5326/JAAHA-MS-5827)

Introduction On presentation, the dog’s temperature was 39.38C, heart

The purpose of this article is to report the first known case of
a duodenogastric intussusception with a concurrent foreign body
and to review the literature surrounding this topic.
Case Report
A 3 yr old spayed female boxer weighing 22.8 kg presented to the
Michigan State University Veterinary Teaching Hospital for severe,
acute vomiting and tenesmus. The vomiting began the morning of
presentation and . 10 episodes, some including hematemesis,
occurred prior to presentation. There was no known dietary in-
discretion associated with the episodes of severe vomiting. It was
reported that for the last 1 yr the dog had a history of vomiting
when in situations of high anxiety. Those situations occurred 2–3
times/mo and usually only involved one episode of vomiting.
From the Department of Small Animal Clinical Sciences, College of
Veterinary Medicine, Michigan State University, East Lansing, MI.
Correspondence: dr.allman@mvsaustin.com (D.A.)
rate was 150 beats/min, respiratory rate was 60 breaths/min,
and mucous membranes were tacky. The dog appeared un-
comfortable, and the abdomen was painful upon palpation.
Packed cell volume, total solids, venous blood gas, complete
blood cell count, and serum biochemical panel were obtained
prior to initiating fluid therapy. A 500 mL bolus of Normosol-
R a was administered IV followed by a constant rate infusion at
120 mL/kg/day. Hydromorphoneb (0.1 mg/kg) was adminis-
tered IV.
Three-view abdominal radiographs showed a rounded, well-
defined foreign object in the stomach, the rim of which had
a mineral opacity. Cranial to that object (also in the body of the
stomach), a larger, round, soft-tissue opacity was present (Figures
1A–C). On the left lateral projection, a distinct, gas-filled pylorus
was not seen (Figure 1B). The small intestine was empty of both
ingesta and air. Based on the history, physical examination, and
radiographic findings, a diagnosis of gastric outflow obstruction
secondary to a gastric foreign body and an undefined, round, soft-
tissue opacity mass near the pyloric region was made. Differential

64 JAAHA | 49:1 Jan/Feb 2013 ª 2013 by American Animal Hospital Association

 Intussusception and a Foreign Body in a Dog

FIGURE 1 Right lateral (A), left lateral (B), and ventrodorsal (C) abdominal radiographs prior to surgery. Within the body of the stomach
there is a well-defined, soft-tissue opacity mass. The rim of the mass has a mineral opacity (solid arrow). Cranial to this is a larger, round, soft-
tissue opacity mass (hollow arrow). The pylorus is not air-filled on the left lateral view, and the small intestines are empty in all views. L, left;
R, right.

diagnoses for the round, soft-tissue opacity were a second foreign stomach as well as a golf ball measuring 4 cm in diameter (Figure
body, neoplasia, polyp, and granuloma. 2). Attempts to remove the golf ball failed due to its smooth, firm
Clinicopathologic abnormalities included a packed cell vol- surface and size. Endoscopy showed that the round, soft-tissue
ume and total solid of 68% and 8.1 g/dL, respectively (references opacity mass seen on radiographs was about 7 cm in diameter,
ranges, 41–55 and 6.0–7.4, respectively). Venous blood gas showed firm, and deep purple in color. The pyloric sphincter could not be
hyperglycemia (148 mg/dL; reference range, 66–115 mg/dL) and identified. Based on the need to correct the gastric outflow
hyperlactatemia (6.2 mmol/L; reference range, 0.3–3.4 mmol/L).
The complete blood cell count revealed a leukocytosis (18.12 3
103/mL; reference range, 5.90–11.60 3 103/mL) with a mature
neutrophilia (16.49 3 103/mL; reference range, 4.00–8.20 3 103/
mL). The serum biochemical panel revealed an increased creati-
nine (2.3 mg/dL; reference range, 0.7–2 mg/dL), hypochloremia
(100 mmol/L; reference range, 107–116 mmol/L), hypercalcemia
(11.4 mg/dL; reference range, 9.4–10.9 mg/dL), hyperphosphatemia
(7.3 mg/dL; reference range, 2.1–4.6 mg/dL), hypermagnesemia
(3.5 mg/dL; reference range, 1.5–2.4 mg/dL), hyperproteinemia (8.4
g/dL; reference range, 5.6–7.5 g/dL), and hyperalbuminemia (4.6
g/dL; reference range, 2.8–4 g/dL).
After adequate cardiovascular stabilization, the dog was
anesthetized for endoscopic examination of the upper gastroin-
testinal tract, biopsy of the round, soft-tissue opacity mass, and
possible foreign body removal using a 9.5 mm diameter flexible FIGURE 2 Photograph of the foreign body (a golf ball) after
endoscopec. A small amount of green ingesta was present in the removal from the stomach.

JAAHA.ORG 65
obstruction, remove the golf ball, and address the large, soft-tissue
mass, the patient was taken to surgery.
A routine ventral midline celiotomy was made from the
xyphoid process to the pubis. Exploration of the abdomen revealed
a duodenogastric intussusception involving the pylorus, proximal
duodenum, and right limb of the pancreas (Figure 3A). The
duodenogastric intussusception was the cause of the gastric out-
flow obstruction and was the round, soft-tissue mass seen on the
radiographs and via endoscopy. Gentle yet firm traction was
placed on the descending duodenum and the stomach was
simultaneously squeezed to force the intussuscepted duodenum
and pyloric sphincter aboral. With forceful steady traction and
digital pressure (Figure 3A), the intussusception was reduced with
minimal serosal tearing. After reduction of the intussusception,
the pyloric and proximal duodenal walls were markedly edema-
tous (w 2 cm thick), had mild serosal bruising, and almost no
palpable lumen in the region of the pyloric antrum. The portion
of the right limb of the pancreas that was involved in the intus-
susception was mildly edematous. A gastrotomy was performed in
the body of the stomach, and the golf ball was removed. A two
d
layer gastrotomy closure was performed with 3-0 polydioxanone .
The mucosal layer was closed with a simple continuous pattern,
and the seromuscular layer was closed with a continuous Lembert
pattern. A routine, right-sided incisional gastropexy was per-
formed in a minimally bruised region of the pylorus using 3-0
FIGURE 3 Intraoperative photographs of the intussusception
before (A) and after (B) reduction, gastropexy, and duodenopexy. A:
The intussusception was reduced with digital pressure before the
gastrotomy. The hollow and solid stars indicate the location of the
duodenum and body of the stomach, respectively. B: A continuous
pattern was used for the gastropexy (solid arrow) and five inter-
rupted sutures were used for the duodenopexy (hollow arrow). Cd,
caudal; Cr, cranial; L, left; R, right.
66 JAAHA | 49:1 Jan/Feb 2013
polydioxanone.1 Following the gastropexy, the duodenum was
placed in its correct anatomic position along the right dorsolateral
body wall caudal to the last rib. Starting 10 cm aboral to the
pyloric sphincter, a duodenopexy was performed by placing
simple interrupted 3-0 polydioxanone sutures 1 cm apart in an
aboral direction as shown in Figure 3B. An effort was made to
leave enough distance between the pyloric sphincter and the start
of the duodenopexy for peristalsis and the passage of large boluses
of ingesta. The surgical sites were lavaged with warm, sterile sa-
line, and the abdomen was closed routinely.
Postoperatively, buprenorphinee (0.01 mg/kg) was adminis-
tered IV q 6 hr. Famotidinef (0.5 mg/kg) was administered IV q 12
hr. Acepromazineg (0.001 mg/kg) was administered IV pro re nata
for sedation. Normosol-R was administered IV at a rate of 120
mL/kg/day until the dog ate a small amount of a bland canned
dog food 14 hr after surgery. Fourteen hr after surgery, the IV
fluid rate was decreased to 60 mL/kg/day, and treatment with
buprenorphine and famotidine was continued until the dog was
discharged from the hospital. Normal urination and defecation of
soft stools were noted during the hospital recovery. The dog’s
appetite continued to improve, and neither vomiting nor regur-
gitation occurred during recovery. The patient was discharged 38
hr after surgery and was prescribed tramadolh (4.3 mg/kg per os q
8–12 hr pro re nata) for pain.
Two wk after surgery, the owner contacted the hospital by
phone to report the dog had one episode of vomiting associated
with eating the contents of a soiled baby diaper. The dog was
otherwise bright, alert, and responsive. Instructions were given to
monitor the dog closely and to return to the veterinarian if another
episode of vomiting occurred. One month after surgery, the dog
was re-examined at the Michigan State University Veterinary
Teaching Hospital. No further episodes of vomiting were reported,
and the physical exam was within normal limits. The owner was
contacted by phone 1 yr postsurgically and reported that the dog
was completely normal. The owner had no knowledge of any
episodes of vomiting since the previously reported episode 2 wk
after surgery.
Discussion
Intussusception is defined as the taking up or receiving of one part
within another, especially the enfolding of one segment of intestine
within another.2 The segment of intestine that is displaced into the
lumen of another is referred to as the intussusceptum. The receiv-
ing segment of the intestine is referred to as the intussuscipiens.
Intussusceptions most commonly occur in the direction of nor-
mal peristalsis (normograde) but can occur in a reverse peristalsis
direction (retrograde).1

The exact etiology of intussusceptions is unknown, and an
intussusception has not been reproduced experimentally. The
pathophysiology of intussusceptions may involve either an inho-
mogeneity in a bowel segment or a mechanical linkage of non-
adjacent bowel segments, leading to either a kink or fold in the
bowel wall that is propagated circumferentially and longitudinally
3,4
into an intussusception. Examples of inhomogeneity include
a flaccid or indurated segment of bowel or a region of the gas-
trointestinal tract that undergoes a sudden change in diameter.
Examples of mechanical linkage include pedunculated polyps,
5
linear foreign bodies, or extraluminal adhesions. Most intussus-
ceptions occur in dogs , 1 yr of age and are considered idio-
pathic.5–7 Other reported causes of intussusception include
parasitism, viral enteritis, acute gastroenteritis, dietary indiscre-
tion, foreign bodies, intestinal masses, renal transplants, anes-
thesia, and abdominal surgery.5–9 More recently, case series have
reported leptospirosis and methiocarb toxicity as causes of
intussusceptions in dogs.10,11
Intussusceptions are named by citing the intussusceptum
followed by the intussuscipiens. For example, an ileocolic intus-
susception is a normograde intussusception in which the ileum has
invaginated into the colon. Ileocolic intussusceptions are most
common; however, intussusceptions can occur anywhere along the
gastrointestinal tract. Dogs with intussusceptions in the lower
gastrointestinal tract may present with a chronic history of clinical
signs. In contrast, dogs with intussusceptions high in the gastro-
intestinal tract usually present with severe, acute clinical signs, and
death can occur from hypovolemia, electrolyte disturbances, and
5,8
acid-base imbalances.
The dog described in this report had a duodenogastric in-
tussusception in which the pylorus and duodenum were invagi-
nated into the stomach. Duodenogastric intussusceptions, being
both high within the gastrointestinal tract and retrograde, are rare.
The authors are aware of only five previously reported cases of
pylorogastric/duodenogastric intussusceptions.12–16 The mean age
of the five previously described patients was 4 yr. The reported
breeds consisted of an Old English sheepdog (case 1), a basset
hound (case 2), a rottweiler (case 3), a Saint Bernard (case 4), and
12–16
a Maltese (case 5). Three out of the six cases of pylorogastric/
duodenogastric intussusception (including the present case) had
had a known history of dietary indiscretion associated with the
12,13,15
onset of clinical signs. All dogs presented for an acute onset
of severe vomiting. Tachycardia, abdominal discomfort, dehy-
dration, and electrolyte abnormalities were consistent findings.
The diagnosis of pylorogastric/duodenogastric intussusception
was made during surgery in all dogs except case 5. Case 1 acutely
died postoperatively of suspected toxemia, and case 2 was
Intussusception and a Foreign Body in a Dog
euthanized due to extensive gastric necrosis.12,13 Case 3 presented
in acute renal failure, underwent surgical correction of the pylo-
rogastric intussusception, and renal biopsies were taken. Mild
glomerulonephritis with occasional hyaline cast was diagnosed
based on the renal biopsies, and the dog survived . 20 mo. Case
4 also presented in acute renal failure, underwent a Y-U pylo-
roplasty during surgery to relieve the outflow obstruction caused
by profound pyloric edema, and survived . 1 yr.15,17 Likewise,
case 5 presented in acute renal failure. In that case, the pylo-
rogastric intussusception was diagnosed with ultrasound, the in-
tussusception reduced spontaneously, but the dog was euthanized
due to renal failure.16
The five previously reported cases and the case described in
this report are similar in both history and clinical findings. Clinical
signs and diagnostic test results were consistent with a pyloric
outflow obstruction in all dogs. In each case, the differential di-
agnoses included foreign body, gastric neoplasia, and soft-tissue
proliferation. The correct diagnosis of an intussusception was
made intrasurgically. Abdominal ultrasonography of case 3 showed
a large, echogenic mass that extended into the lumen of the gastric
fundus, but the individual wall layers of the intussusception could
not be seen.14 The case described in this report did not have an
abdominal ultrasound performed due to the known indication for
surgery (i.e., foreign body). Endoscopy was performed based on
the potential for foreign body retrieval, mass identification, and
obtaining biopsies. Due to edema and venous congestion, it was
not possible to identify the mass as an intussusception with en-
doscopy in the dog described herein. The foreign body had no
surface for grasping; thus, it was not removable via endoscopy.
Despite the use of endoscopy in this case, the authors recommend
abdominal ultrasonography as the diagnostic test of choice due to
its reliability for diagnosing intussusceptions.16,18
This is the first reported case of a pylorogastric/duodenogastric
intussusception in conjunction with a foreign body. In most of the
previously reported cases of pylorogastric/duodenogastric intus-
susception, a foreign body was suspected on preoperative abdominal
radiographs, but no foreign object was found during surgery. The
dog reported herein had a 1 yr history of vomiting (several times/
mo), which resolved after surgery. Multiple possibilities exist to
explain this resolution, including a chronic, spontaneously reducing,
mild duodenogastric intussusception similar to case 5.16 Chronic
foreign bodies have been described in the veterinary literature, and
it is reasonable to theorize that the golf ball was the cause of this
dog’s chronic vomiting.6,19 Another possible explanation for the
resolution of vomiting after surgery is fixation of the stomach in
a new position by gastropexy, similar to the manner in which the
left-sided gastropexy functions in the repair of hiatal hernias.20
JAAHA.ORG 67
 Significant pyloric wall edema has been described in all cases
of pylorogastric/duodenogastric intussusception. The actual py-
13
loric wall thickness was measured to be up to 2 cm in one case. In
a previously reported case, a Y-U pyloroplasty was performed
during surgery in attempt to increase the diameter of the pyloric
outflow tract.15 In the case described herein, the pyloric wall
edema was palpated and estimated to be about 2 cm thick after
reduction of the intussusception. The surgeon chose not to in-
tervene with a Y-U pyloroplasty based on its potential morbidity
and the gastrointestinal tract’s ability to repair itself after removal
of the insult. The patient described in this report ate well without
vomiting 14 hr after surgery. Although severe pyloric wall edema
is commonly encountered in cases of pylorogastric intussuscep-
tion, the decision to perform a Y-U pyloroplasty should be made
on a case-by-case basis until further information is available.
To reduce the possibility of intussusception recurrence,
a gastropexy and duodenopexy were performed in this case. Given
that most cases of high intussusceptions occur in large breed dogs,
a right-sided gastropexy can also serve as a prophylactic procedure
for the prevention of gastric dilatation-volvulus. The duodenopexy
in this case was performed without either incision or abrasion of
the seromuscular layer. This decision was based on multiple fac-
tors, including easy reversal if complications resulted, and stronger
adhesions were not thought to be needed as the probable cause
(i.e., the foreign body) was removed. The entire length of the in-
testinal tract was not plicated in this case (or in any other case of a
high intussusception). Recurrence of a pylorogastric/duodenogastric
intussusception has not been described; however, recurrence
rates of up to 17% have been reported for other types of intus-
susceptions.8 Early publications promoted the use of routine
enteroplication with surgical correction of intussusceptions.5,21
Since that time, publications have shown no recurrence without
enteroplication, and no significant difference in the need for
a second surgical procedure between plicated and nonplicated
groups was noted.7–9 Complications of enteroplication, such as
small intestinal obstruction from plant material or strangulation,
have been described in up to 19% of cases.7 Randomized, mul-
ticenter, prospective clinical studies are needed to evaluate the role
of enteroplication with both high and low intussusceptions. Until
then, the authors advocate the use of gastropexy and duodeno-
pexy for high intussusceptions, knowing that each individual
surgeon must balance the potential benefits with the risk of
complications.
Conclusion
Pylorogastric/duodenogastric intussusception is a rare problem in
veterinary medicine. It appears to be more common in large breed
68 JAAHA | 49:1 Jan/Feb 2013
dogs, but can occur in small breeds. All cases reported to date have
presented with severe, acute vomiting. Dietary indiscretion, renal
failure, and gastric foreign body are possible predisposing factors.
The survival rate of the six reported cases of pylorogastric/
duodenogastric intussusception is 50%. High intussusceptions
are a surgical emergency, but preoperative stabilization of the
patient’s cardiovascular needs, electrolyte imbalances, and un-
derlying disease (such as renal failure) is important. Reduction of
the intussusception may be difficult and require a gastrotomy. The
use of a right-sided incisional gastropexy and duodenopexy has
been proposed to help prevent recurrence.15 Increasing knowl-
edge, improved diagnostics (e.g., ultrasonography), and early
treatment seem to be improving the survival rates associated with
high intussusceptions; however, more information is needed
about this rare condition to guide further recommendations.
The authors would like to acknowledge Laurent Guiot, DMV,
DACVS, and Christine Venema, DVM, DACVIM, for their contri-
butions to this manuscript.
FOOTNOTES
a
Normosol-R; Hospira Inc., Lake Forest, IL
b
Hydromorphone; Hospira Inc., Lake Forest, IL
c
Olympus GIF-100; Olympus Corp., Center Valley, PA
d
Polydioxanone; Ethicon Inc., Somerville, NJ
e
Buprenorphine; Bedford Laboratories, Bedford, OH
f
Famotidine; Baxter Healthcare Corp., Deerfield, IL
g
Acepromazine; Boehringer Ingelheim Vetmedica Inc.,
St. Joseph, MO
h
Tramadol; Amneal Pharmaceuticals, Glasgow, KY
REFERENCES
1. Hedlund CS, Fossum TW. Surgery of the digestive system. In:
Fossum TW, ed. Small animal surgery. 3rd ed. St. Louis (MO):
Mosby; 2007:409–24, 470–4.
2. Pugh M. Stedman’s medical dictionary. 27th ed. Baltimore (MD):
Lippincott, Williams & Wilkins; 2000.
3. Reymond RD. A mechanism of the kink formation which precedes
intussusception. Invest Radiol 1971;6(1):61–4.
4. Reymond RD. The mechanism of intussusception: a theoretical
analysis of the phenomenon. Br J Radiol 1972;45(529):1–7.
5. Lewis DD, Ellison GW. Intussusception in dogs and cats. Compend
Contin Educ Pract Vet 1987;9:523–34.
6. Wilson GP, Burt JK. Intussusception in the dog and cat: a review of
45 cases. J Am Vet Med Assoc 1974;164(5):515–8.
7. Applewhite AA, Hawthorne JC, Cornell KK. Complications of
enteroplication for the prevention of intussusception recurrence in
dogs: A retrospective study (1989–1999). J Am Vet Med Assoc 2001;
219(10):1415–8.
8. Applewhite AA, Cornell KK, Selcer BA. Diagnosis and treatment of
intussusceptions in dogs. Compend Contin Educ Pract Vet 2002;24:
110–27.

9. Rallis TS, Papazoglou LG, Adamama-Moraitou KK, et al. Acute
enteritis or gastroenteritis in young dogs as a predisposing factor
for intestinal intussusception: A retrospective study (1995–1999).
J Vet Med 2000;47:507–11.
10. Schweighauser A, Burgener IA, Gaschen F, et al. Small intestinal
intussusception in five dogs with acute renal failure and
suspected leptospirosis (L. australis). J Vet Emerg Crit Care
2009;19:363–8.
11. Corfield GS, Connor LM, Swindells KL, et al. Intussusception fol-
lowing methiocarb toxicity in three dogs. J Vet Emerg Crit Care
2007;18:68–74.
12. Marks DL. Canine pylorogastric intussusception. Vet Med 1983;78:
677–80.
13. Bowersox TS, Caywood DD, Hayden DW. Idiopathic, duodeno-
gastric intussusception in an adult dog. J Am Vet Med Assoc 1991;199
(11):1608–9.
14. Huml RA, Konde LJ, Sellon RK, et al. Gastrogastric intussusception
in a dog. Vet Radiol Ultrasound 1992;3(3):150–3.
Intussusception and a Foreign Body in a Dog
15. Applewhite AA, Cornell KK, Selcer BA. Pylorogastric intussuscep-
tion in the dog: a case report and literature review. J Am Anim Hosp
Assoc 2001;37(3):238–43.
16. Lee H, Yeon S, Lee H, et al. Ultrasonographic diagnosis—pylo-
rogastric intussusception in a dog. Vet Radiol Ultrasound 2005;46(4):
317–8.
17. Bright RM, Richardson DC, Stanton ME. Y-U antral flap
advancement pyloroplasty in dogs. Compend Contin Educ Pract
Vet 1988;10:139–44.
18. Lamb CR, Mantis P. Ultrasonographic features of intestinal intus-
susception in 10 dogs. J Small Anim Pract 1998;39(9):437–41.
19. Matz ME. Chronic vomiting & diarrhea in a dog. NAVC Clinician’s
Brief 2008;6(5):29–33, 80.
20. Guiot LP, Lansdowne JL, Rouppert P, et al. Hiatal hernia in the dog:
a clinical report of four Chinese shar peis. J Am Anim Hosp Assoc
2008;44(6):335–41.
21. Oakes MG, Lewis DD, Hosgood G, et al. Enteroplication for the
prevention of intussusception recurrence in dogs: 31 cases
(1978–1992). J Am Vet Med Assoc 1994;205(1):72–5.
JAAHA.ORG 69
 Caso clínico 5
V parte de X

“LUCAS”
Cocker Spaniel
Macho no castrado, 12 kg

¿Por qué están aumentados los eritrocitos

y el hematocrito?
El aumento de glóbulos rojos o el aumento del hematocrito se
conoce también como eritrocitosis. La eritrocitosis puede ser de 2
tipos:
1. eritrocitosis vera. Causas:
. Policitemia vera: trastorno de la médula ósea que ocasiona
demasiada producción de glóbulos blancos, glóbulos rojos y plaquetas
. Hipoxia: intoxicación CO, altura, shunts izda-dcha
. Tumores: feocromocitoma
. Enfermedad renal
2. Eritrocitosis relativa o espuria: hemoconcentración secundaria a
deshidratación.

¿Cómo diferenciarías de manera sencilla una eritrocitosis

vera de una relativa?
El aumento de glóbulos rojos o el aumento del hematocrito se
conoce también como eritrocitosis. La eritrocitosis puede ser de 2
tipos:
1. eritrocitosis vera. Causas:
. Policitemia vera: trastorno de la médula ósea que ocasiona
demasiada producción de glóbulos blancos, glóbulos rojos y plaquetas
. Hipoxia: intoxicación CO, altura, shunts izda-dcha
. Tumores: feocromocitoma
. Enfermedad renal
2. Eritrocitosis relativa o espuria: hemoconcentración secundaria a
deshidratación.

¿Cómo diferenciarías de manera sencilla una eritrocitosis

vera de una relativa?

MIDIENDO LAS PROTEÍNAS TOTALES.

Veamos la bioquímica de Lucas
BIOQUÍMICA e IONES

Parámetros Resultados V. Referencia

Potasio 4.1 mmol/L 4.37 – 5.35
Sodio 147 mmol/L 141 - 152
Cloro 115 mmol/L 109 - 220

Parámetros Resultados V. Referencia

Creatinina 0.5 mg/dl 0.5 - 1.5
Glucosa 98 mg/dl 65 - 120
Albúmina 3.5 g/dL 2.3 - 4
Proteínas totales 8.9 g/dl 5.4 - 7.5
ALT 40 U/L 10-100
Urea 30 mg/dl 21.4 - 59.9
Fosfatasa alcalina 69 UI/L 20 - 156
BIOQUÍMICA

Parámetros Resultados V. Referencia

Creatinina 0.5 mg/dl 0.5 - 1.5
Glucosa 98 mg/dl 65 - 120
Albúmina 3.5 g/dL 2.3 - 4
Proteínas totales 8.9 g/dl 5.4 - 7.5
ALT 40 U/L 10-100
Urea 30 mg/dl 21.4 - 59.9
Fosfatasa alcalina 69 UI/L 20 - 156

Las proteínas totales están elevadas, lo que confima la

deshidratación de Lucas. ¿Y ahora?

IMPORTARTE REHIDRATAR ANTES DE LA CIRUGÍA

 BIOQUÍMICA

Parámetros Resultados V. Referencia

Creatinina 0.5 mg/dl 0.5 - 1.5
Glucosa 98 mg/dl 65 - 120
Albúmina 3.1 g/dL 2.3 - 4
Proteínas totales 8.9 g/dl 5.4 - 7.5
ALT 40 U/L 10-100
Urea 30 mg/dl 21.4 - 59.9
Fosfatasa alcalina 69 UI/L 20 - 156

Los parámetros hepáticos son normales, pero ¿qué pruebas

nos ayudan a valorar la función hepática?
 Evaluación hepática
Entra en https://login.are.uab.cat identifícate y y consulta
este libro: Handbook of Small Animal Practice 5th ed.
Rhea V. Morgan, Section 5ª Digestive System
CHAPTER 37 - Diseases of the Hepatobiliary System
Pages 416-432/, de Kenneth Harkin verás todas las
posibilidades de enfermedades hepáticas, clica abajo ó
pega la dirección en la barra de tu navegador

<http://www.sciencedirect.com/science/
article/pii/B9781416039495500418>

HAZ UN RESUMEN DEL CAPÍTULO

 CHAPTER 37

Diseases of the Hepatobiliary

System
| Kenneth Harkin

Diagnosis
CONGENITAL/DEVELOPMENTAL
DISEASES I. Screening laboratory tests
A. Complete blood count (CBC)
Congenital Por tosystemic Shunt s 1. Mild anemia: hypochromic, microcytic
2. Poikilocytosis in cats
Definition and Causes B. Serum biochemistry profile
I. Congenital portosystemic shunt (PSS) is a vascular anomaly 1. Hypoalbuminemia, hypocholesterolemia, hypogly-
resulting in direct communication between the portal and cemia
systemic circulation. 2. Low blood urea nitrogen (BUN)
II. Extrahepatic shunts are the most common type in small 3. Normal or mildly elevated serum alanine trans-
breeds of dogs and cats. aminase (ALT) and alkaline phosphatase (ALP)
III. Intrahepatic shunts are the most common shunt in large 4. Often normal in cats
breed dogs with a patent ductus venosus being the most C. Urinalysis
frequent anomaly. 1. Ammonium biurate crystalluria
IV. Prevalence is unknown, but it is relatively common in the 2. Hyposthenuria or isosthenuria
dog (0.5%) (Tobias and Rohrbach, 2002). 3. Active sediment with urate cystic calculi
V. Commonly affected breeds include the Havanese, Yorkshire D. Postprandial serum bile acids: significantly elevated
terrier, Maltese, Dandie Dinmont terrier, pug, miniature II. Imaging techniques
schnauzer, Irish wolfhound, and Cairn terrier. A. Abdominal radiographs usually document micro-
VI. PSS is uncommon in cats. hepatica.
B. Abdominal ultrasonography may reveal microhepatica
Pathophysiology with homogenous echogenicity.
I. Diversion of portal blood from the liver to the systemic 1. Visualization of the shunting vessel is often possible
circulation deprives the liver of trophic factors, resulting in (d’Anjou et al., 2004).
hepatic atrophy. 2. Renomegaly and urolithiasis may be identified.
II. Shunting of portal blood prevents normal clearance of C. Rectal portal scintigraphy
toxins and bacteria by the liver. 1. 99mTechnetium-pertechnetate placed in the rectum
III. Bacteremia is rarely significant, but toxins result in hepatic eventually enters the portal circulation.
encephalopathy (see Hepatic Encephalopathy). 2. Radioactivity occurs in the liver before the heart in
normal animals.
Clinical Signs 3. Radioactivity is seen in the heart and lungs before
I. Hepatic encephalopathy the liver with PSS.
A. Most commonly occurs after a meal D. Intraoperative portography
B. Depression, stupor, or coma 1. Catheterization of mesenteric vein at laparotomy
C. Circling, head pressing, amaurosis (blindness) 2. Radiographs or fluoroscopic images obtained during
D. Pica, personality changes, ptyalism (cats) injection of contrast
E. Seizures (more common in cats) 3. Often unnecessary, as the shunting vessel usually
II. Intermittent vomiting visible during laparotomy
III. Polyuria, polydipsia: may resolve with antibiotics
IV. Pollakiuria, stranguria, or hematuria associated with urate Differential Diagnosis
urolithiasis I. Hypoglycemia in puppies (toy breeds)
V. Growth retardation II. Cobalamin deficiency in the border collie

416

III. Cirrhosis
IV. Intrahepatic arteriovenous fistula, acquired PSS
V. Hydrocephalus, idiopathic epilepsy, other causes of
encephalopathy
Treatment
I. Medical management: see treatment of Hepatic Encephalo-
pathy
II. Surgical correction of PSS
A. The preferred treatment method
B. Surgical options
1. Silk ligation: partial or complete
2. Ameroid constrictor
a. Most popular technique
b. Shorter surgery time than silk ligation (Hurn and
Edwards, 2003)
3. Cellophane banding
4. Transvenous coil embolization
C. Liver biopsy for histopathology
III. Surgical complications
A. Portal hypertension occurs with a rapid onset of con-
gestive enteropathy and ascites.
1. Most common with complete silk ligation
2. May require emergency surgery to remove the
ligature
3. Possible acquired shunts in some dogs
B. Generalized motor seizures may develop 12 to 72 hours
after ligation and are accompanied by a high mortality
rate.
C. Persistent clinical signs may be explained by the
following:
1. Concurrent presence of portal vein hypoplasia
2. Development of acquired shunts from portal hyper-
tension
3. Incomplete ligation or failure to ligate additional
PSSs
D. Persistent signs may need long-term medical manage-
ment or repeated ligation.
Monitoring of Animal
I. Monitoring after surgical ligation
A. With partial ligation, rectal portal scintigraphy is re-
peated in 3 months to evaluate the need for additional
ligation.
B. With complete ligation or ameroid constrictor place-
ment, follow-up is dependent on the presence of clinical
signs.
1. Asymptomatic animals are rechecked at 3 to 6
months, with evaluation of serum biochemistry
profile and serum bile acids.
2. In symptomatic animals, rectal portal scintigraphy,
abdominal ultrasonography, biochemistries, and
bile acids are repeated.
II. Monitoring during chronic medical therapy
A. Serial serum bile acids are not very helpful, as the
degree of dysfunction cannot be predicted by comparing
levels from various times.
CHAPTER 37 | Diseases of the Hepatobiliary System 417
B. Asymptomatic animals are reevaluated every 6 to
12 months.
C. Animals that remain symptomatic require frequent
evaluation to optimize therapy and monitor nutritional
status.
Por tal Vein Hypoplasia
Definition and Cause
I. It is abnormal microscopic circulation of the hepatic portal
system that is poorly understood.
II. It is also termed hepatic microvascular dysplasia, although
the term portal vein hypoplasia is preferred.
III. Despite the general acceptance of this condition as a disease,
the histological changes identified can be seen in healthy
dogs with normal serum bile acids.
IV. Although some liver disease is likely to be present in these
dogs, portal vein hypoplasia has not been definitively proven.
Pathophysiology
I. Decreased portal vein circulation results in hepatic arterial
overcirculation that maintains sinusoidal perfusion.
II. Sinusoidal pressure increases, resulting in dilation of portal
lymphatics and hepatic venules.
III. Embryological sinusoidal vessels reopen from the hyper-
tension, shunting blood away from sinusoids.
IV. These shunting vessels have a variable effect on the
development of clinical signs.
Clinical Signs
I. No apparent clinical signs: most common
II. Signs of hepatic encephalopathy
Diagnosis
I. Screening laboratory tests
A. CBC: usually normal in most cases; rarely, changes
similar to PSS
B. Serum biochemistry profile: usually normal; mild eleva-
tions in liver enzymes; changes similar to PSS (rare)
C. Urinalysis: ammonium biurate crystals possible
D. Serum bile acids: postprandial levels not as high as with
PSS (median = 41 mmol/L) (Allen et al., 1999)
II. Imaging tests
A. Liver size is usually normal on radiography.
B. Ultrasonography and transcolonic scintigraphy are
usually normal.
C. Intraoperative contrast portography is usually normal.
III. Histopathologic findings
A. Hepatic arteriolar tortuosity (duplication), portal venule
hypoplasia
B. Iron granuloma formation
C. Also identified in dogs with PSS
Differential Diagnosis
I. Portosystemic shunt
II. Lysosomal storage diseases
III. Urea cycle enzyme deficiency
418 SECTION 5 | Digestive System

Treatment III. Secondary to immunosuppressive conditions: diabetes

I. Most dogs require no therapy. mellitus, hyperadrenocorticism, exogenous corticosteroids
II. Symptomatic dogs are treated with medical therapy as for IV. Ascending biliary tract infection, pancreatitis
PSS. V. Hepatic neoplasia or infarcts

Urea Cycle Enzyme Defect s Pathophysiology

See Table 37-1. I. Inflammation from necrosis or infection results in fever
and pain.
INFECTIOUS DISEASES II. Release of toxins from bacteria cause systemic signs of
sepsis.
Hepatic Abscess III. Abscess rupture may result in peritonitis.

Definition Clinical Signs

I. Abscesses are variably sized, focal or multifocal, localized I. Lethargy, fever
collections of purulent material that form from necrosis II. Vomiting, diarrhea
of hepatic tissue. III. Weight loss
II. They may be infected (primary or secondary) or sterile.
Diagnosis
Causes I. CBC
I. Unknown in most cases A. Leukocytosis, often with a left shift
II. Hematogenous spread from infections of the skin, heart, B. Thrombocytopenia, possible evidence of disseminated
gastrointestinal (GI) tract, etc. intravascular coagulation (DIC)

TA BL E 37-1

Miscellaneous Hepatobiliary Diseases

DISORDER CAUSE(S) CLINICAL FINDINGS DIAGNOSIS TREATMENT/PROGNOSIS

Urea cycle enzyme Congenital defect Hyperammonemia, HE Biopsy and measurement Supportive therapy for HE
deficiency of enzyme levels Poor prognosis
Vacuolar hepatopathy Cortisol excess Asymptomatic, polyuria/ Biopsy, tests for Treat underlying disease
Idiopathic polydipsia, elevated ALP hyperadrenocorticism Good prognosis
Hyperlipidemia
Idiopathic hepatic Unknown Ascites, weight loss, Biopsy Colchicine, diuretics,
fibrosis polyuria/polydipsia, HE others as for chronic
hepatitis
Poor prognosis
Intrahepatic Congenital defect Ascites, HE, GI signs, Ultrasonography, Surgical resection of
arteriovenous hypoalbuminemia laparotomy, affected liver lobe
fistula arteriography Guarded prognosis
Granulomatous Bacterial and fungal Anorexia, fever, Biopsy with special stains Underlying etiology
hepatitis infection hepatomegaly for fungi, culture, determines therapy and
Immune disorders antinuclear antibody prognosis
Neoplasia assay
Idiopathic forms
Cholecystitis/ Mucocele Abdominal pain, fever, Ultrasonography, bacterial Antibiotics, supportive
cholangitis Cholelithiasis vomiting, icterus, culture of bile care, ± cholecystectomy
Pancreatitis leukocytosis Good prognosis
Immune suppression
Scottish terrier Idiopathic Asymptomatic, elevated Biopsy No treatment needed
hepatopathy ALP Prognosis excellent
Biliary flukes (cat) Platynosomum spp. GI signs, icterus Fecal flotation Praziquantel 20-40 mg/kg
Amphimerus spp. SC, PO SID for 3 days
Variable prognosis
HE, Hepatic encephalopathy; ALP, alkaline phosphatase; GI, gastrointestinal.
 CHAPTER 37 | Diseases of the Hepatobiliary System 419

C. Mild anemia Feline Acute Cholangiohepatitis

II. Serum biochemistry profile
A. Elevated ALP and ALT Definition and Causes
B. Hypoalbuminemia I. It is an acute bacterial infection of the liver and biliary
C. Hyperbilirubinemia (less common) tract.
D. Hyperglobulinemia with chronicity II. It may result from an ascending infection with enteric
III. Coagulation profile: abnormal prothrombin time and bacteria.
partial thromboplastin time consistent with DIC III. The most common organisms isolated include Escherichia
IV. Abdominal radiography coli, Enterobacter spp., Streptococcus spp., Klebsiella spp.,
A. ± Hepatomegaly Clostridia spp., and Bacteroides spp.
B. ± Focal gas accumulation
C. ± Poor abdominal detail Pathophysiology
V. Ultrasonography I. The predominant finding on histopathology is a neutro-
A. Hyperechoic, mixed-echoic, or anechoic masses philic infiltration.
B. ± Localized peritoneal effusion II. Although some degree of biliary stasis may be necessary for
VI. Definitive diagnosis this to occur, diseases that cause biliary stasis (cholelithiasis,
A. Laparotomy or laparoscopy with biopsy, aerobic and pancreatitis) are not often identified.
anaerobic bacterial culture
B. Ultrasound-guided aspiration with cytology and Clinical Signs
culture I. It typically affects young to middle-aged cats; males may be
predisposed.
Differential Diagnosis II. Duration of clinical signs is usually short (<5 days).
I. Hepatic neoplasia: primary, metastatic III. Jaundice, vomiting, diarrhea, and fever are common.
II. Nodular regeneration of the liver
III. Extramedullary hematopoiesis Diagnosis
I. Laboratory findings
Treatment A. Increased ALT: fivefold to tenfold increase
I. Antibiotic treatment is optimally guided by culture and B. Increased ALP: twofold to fourfold increase
sensitivity. C. Elevated bilirubin (mean total bilirubin 5.0, range
A. Good first choices in dogs pending culture results 0.1 to 20)
include the following: D. Leukocytosis with a left shift in 30% to 50% of cases
1. Ampicillin 22 mg/kg IV, PO TID and enrofloxacin II. Imaging tests
5 mg/kg IV, PO BID A. Liver may be enlarged or normal in size on radio-
2. Cefoxitin 30 mg/kg IV TID to QID graphs.
3. Metronidazole 20 to 30 mg/kg IV, PO SID, cefazolin B. Liver may appear hypoechoic, and the biliary tree may
22 mg/kg IV TID or cephalexin 22 mg/kg PO TID, appear thickened and dilated on ultrasonography.
and enrofloxacin or marbofloxacin 5 mg/kg PO C. Evidence of cholelithiasis may occasionally be found.
BID III. Definitive diagnosis by hepatic biopsy
B. Long-term antibiotic therapy (4 to 6 months) is A. Periductal and periportal suppurative inflammation
recommended. and edema
II. Surgery is indicated for large abscesses, when the abscess B. Accumulation of suppurative exudate in intrahepatic
has ruptured and septic peritonitis has occurred, and for bile ducts
abscesses localized to a single lobe. C. Piecemeal necrosis with local extension of inflammation
III. Ultrasound-guided drainage and alcoholization is effective D. Dilation of intrahepatic bile ducts
for confined lesions.
Differential Diagnosis
Monitoring of Animal I. Acute pancreatitis
I. Underlying or predisposing conditions are identified and II. Feline infectious peritonitis (FIP)
managed to prevent recurrence. III. Toxoplasmosis
II. For animals that are managed medically, perform an ultra- IV. Tularemia
sound examination monthly until resolution or reduction V. Cytauxzoonosis
in size is noted, and then every 3 months for 6 to 12 months VI. Salmonellosis
after completing antibiotics.
Treatment
I. Intravenous fluid therapy is usually required, with fluid
Other Infectious Causes of Hepatitis deficits corrected over 8 to 12 hours and potassium supple-
See Section 15. mented as needed.
420 SECTION 5 | Digestive System
II. Antibiotic therapy is started pending the results of culture.
A. Ampicillin 22 mg/kg IV, PO TID and enrofloxacin
5 mg/kg IV, PO SID
B. Cefazolin 22 mg/kg IV TID and enrofloxacin
C. Ticarcillin/clavulanic at acid 33 to 50 mg/kg of ticarcillin
IV QID
D. Amoxicillin/clavulanic acid 13.75 mg/kg PO BID
E. Cefoxitin 30 mg/kg IV TID
III. Long-term, antibiotic therapy (3 to 6 months) is recom-
mended.
IV. Cats rarely require surgery to relieve an extrahepatic bile
duct obstruction or obstruction from inspissated bile.
Monitoring of Animal
I. Reevaluate liver enzymes every 1 to 2 weeks until antibiotic
therapy is discontinued.
II. If liver enzymes are not normal after completing therapy,
further evaluation (repeat biopsy) may be indicated.
INFLAMMATORY DISEASES
Canine Chronic Hepatitis and Cirrhosis
Definition
I. Chronic hepatitis is an inflammatory disease of the liver
that is characterized by bridging fibrosis, hepatocellular
necrosis, piecemeal necrosis, and predominantly non-
suppurative inflammation.
II. Most dogs are identified only when the disease is
advanced.
III. Cirrhosis is the end result, with bridging fibrosis, nodular
regeneration, and permanent distortion of the hepatic
architecture.
IV. The term chronic active hepatitis has often been used
previously for this disease.
Causes
I. In some cases the etiology may be identified; however, in
most dogs the underlying cause is never defined.
II. Possible etiologies include canine adenovirus 1 (CAV-1),
leptospirosis, and long-term administration of medications
(e.g., phenobarbital, primidone, phenytoin, carprofen).
III. See also Copper Storage Hepatopathies.
Pathophysiology
I. The predominant inflammatory cells are lymphocytes and
plasma cells.
II. Nonspecific, immunological response leads to chronic
hepatic injury.
III. Antibodies are directed against liver-specific antigens and
perpetuate hepatic injury.
Clinical Signs
I. Commonly affected breeds include the Doberman pinscher,
American and English cocker spaniels, Labrador retriever,
and German shepherd dog.
II. Typical age is 4 to 7 years.
III. Lethargy, anorexia, vomiting, and weight loss are common.
IV. Small bowel diarrhea, polyuria, and polydipsia are seen
occasionally.
V. Ascites, icterus, and hepatic encephalopathy occur in severe
cases.
VI. In some dogs the disease is subclinical and identified on
routine laboratory testing.
Diagnosis
I. Serum biochemistry results
A. Increased ALT and ALP occur in most affected dogs.
B. Hypoalbuminemia is seen in many affected dogs.
C. BUN is usually subnormal.
D. Hyperbilirubinemia occurs early in the course of dis-
ease when the primary lesion is periportal.
1. Clinical jaundice is not seen until bilirubin
>2.0 mg/dL.
2. Jaundice may not be apparent until bilirubin
>4.0 mg/dL.
E. Hyperglobulinemia is uncommon and occurs from
chronic inflammation.
F. Serum cholesterol may be increased, normal, or de-
creased.
G. Hypoglycemia is rarely seen except in end-stage
cirrhosis.
II. Coagulation profile results
A. Variable, depending on the stage of chronic hepatitis
B. Uncommonly associated with vitamin K deficiency
III. Bile acids concentrations: postprandial levels almost always
abnormal
IV. Radiographic findings
A. Survey radiography: small or normal sized liver
B. Ultrasonography: normal or diffuse hyperechogenicity,
microhepatica, irregular margins, cirrhotic nodules
V. Histopathologic examination of liver biopsy
A. It provides the definitive diagnosis.
B. Also submit samples for culture and mineral analysis.
C. Samples obtained at laparotomy and laparoscopy are
preferred.
1. Tru-cut biopsies may not always provide the
diagnosis.
2. Fine-needle aspirate cytology often is not accurate
enough to make the diagnosis.
VI. Recommendations for biopsy
A. Persistently elevated liver enzymes without an obvious
cause
B. Not precluded by absence of clinical signs
Differential Diagnosis
I. Hepatic neoplasia
II. Protein-losing enteropathy
III. Systemic lupus erythematosus
IV. Right-sided congestive heart failure
V. Hypoadrenocorticism
Treatment
I. The goals of therapy are to control inflammation, arrest
fibrosis, resolve infection, improve bile flow and decrease
toxic bile acids, provide antioxidants, decrease absorption

of hepatic encephalopathic toxins, support hepatic re-
generation, and manage or prevent GI complications.
II. Various drugs are used to control inflammation.
A. Give prednisone at 1 mg/kg PO SID for 2 to 3 weeks,
then taper.
1. Do not give if cultures are positive.
2. Dexamethasone (0.2 to 0.4 mg/kg PO SID) is an
alternative in dogs with ascites, as it has less
mineralocorticoid activity.
B. Use azathioprine in combination with corticosteroids
to reduce their dosage.
1. Dose is 2 mg/kg PO SID for 10 to 14 days, then
QOD for 3 to 6 months, then 1 mg/kg PO QOD
indefinitely.
2. Side effects include GI upset, myelosuppression,
and pancreatitis.
C. D-penicillamine is principally used as a copper
chelator.
1. Dose is 10 to 15 mg/kg PO BID.
2. It may cause persistent vomiting.
D. Metronidazole is given at 15 mg/kg PO SID or divided
BID for its possible immunomodulatory and anti-
oxidant effects.
III. Colchicine may be given to combat fibrosis.
A. Recommended dose is 0.03 mg/kg PO SID (do not use
the probenecid/colchicine combination).
B. Side effects include hemorrhagic gastroenteritis, myelo-
suppression, nephrotoxicity, and neuromyopathies.
IV. Resolve or control infections.
A. Antibiotics are recommended in the following
situations:
1. Positive culture results
2. Significant suppurative component on biopsy
3. To reduce any bacterial contribution to hepatic
encephalopathy
4. Prophylaxis after liver biopsy or episodes of gastro-
enteritis
B. Antibiotic choices include the following:
1. Ampicillin 22 mg/kg IV TID, amoxicillin 22 mg/kg
PO TID, or amoxicillin-clavulanic acid 13.75 mg/
kg PO BID
2. Cephalexin 22 mg/kg PO TID or cefadroxil 22 mg/
kg PO BID
3. Enrofloxacin 5 mg/kg PO BID
4. Metronidazole 15 mg/kg PO SID for anaerobic
infections
V. Ursodeoxycholate 10 to 15 mg/kg PO SID is used to im-
prove bile flow and reduce toxic bile acids.
VI. Antioxidant therapy helps protect against ischemic,
hypoxic, oxidative, or free radical damage.
A. Zinc acetate or gluconate
1. Prescribed for copper hepatopathy
2. May also have antifibrotic activity
B. d-Alpha-tocopheryl-1000-polyethylene glycol succi-
nate (Liqui-E; TwinLab, New York, N.Y.)
1. It is a water-soluble form of vitamin E that accu-
mulates in hepatocytes to a greater degree than
does the acetate form.
CHAPTER 37 | Diseases of the Hepatobiliary System 421
2. Dose is 25 IU/kg PO BID.
3. The sweet taste may be objectionable to some dogs.
C. S-adenosyl-L-methionine (SAMe)
1. It is normally produced in the liver from dietary
methionine, but in cirrhosis, SAMe synthetase is
reduced.
2. Administer SAMe on an empty stomach at a dose
of 20 mg/kg PO SID.
VII. Decrease absorption of hepatic encephalopathic toxins.
A. Give antibiotics to reduce production of toxins by
enteric bacteria.
B. Give lactulose at 0.5 mL/kg PO TID.
VIII. Institute dietary changes that support hepatic regeneration.
A. Protein requirements are at least as high as those of
healthy individuals.
B. Protein is necessary to maintain a positive nitrogen
balance and stimulate hepatic regeneration.
C. In the animal without encephalopathy, give a diet
that contains between 25% and 32% protein in a
highly digestible source.
D. Protein-restricted diets are given only to treat hepatic
encephalopathy, which most commonly occurs in
dogs with PSS and severe hepatic dysfunction.
IX. Prevent or treat GI complications.
A. GI ulcers and subsequent hemorrhage can complicate
hepatic encephalopathy, precipitate an encephalo-
pathic crisis, and cause anorexia.
B. Famotidine is given at 0.5 to 1.0 mg/kg PO SID to
BID to decrease gastric acid production.
C. Consider sucralfate as a GI protectant at 250 to
1000 mg PO TID.
X. Recommendations for managing ascites include the
following:
A. Furosemide is given at 1.0 mg/kg PO BID.
B. Spironolactone may be tried at 1 to 2 mg/kg PO BID,
alone or in combination with furosemide.
C. Restricted exercise and decreased salt intake are rarely
effective.
D. Abdominocentesis is performed in dogs with signifi-
cant ascites or compromised cardiac or respiratory
functions or anorexia, and it is followed with diuretics.
Monitoring of Animal
I. Evaluate body weight, liver enzymes, serum albumin and
bilirubin monthly until they are stable, then every 3 to
6 months.
II. Monitor serum bile acids every 6 to 12 months.
A. Changes in degree of elevation do not correlate well
with changes in hepatic function.
B. Return to normal signals normalization of hepatic
function (rare).
III. Any dog that suddenly decompensates with ascites,
hepatic encephalopathy, or vomiting requires immediate
reevaluation.
IV. Ascites is a poor prognostic sign.
V. For dogs that are receiving azathioprine, check a CBC at
2 and 4 weeks initially, then monthly while on 2 mg/kg
QOD, and every 3 months when on the lowest dose.
422 SECTION 5 | Digestive System
Feline Chronic Cholangiohepatitis
Definition and Causes
I. It is also referred to as nonsuppurative cholangitis, lympho-
plasmacytic cholangitis, or cholangiohepatitis.
II. It is presumed to be immune-mediated.
III. It often occurs as a component of other inflammatory
diseases of the intestine or pancreas.
Pathophysiology
I. Predominant infiltrating cells are lymphocytes and plasma
cells.
II. Nonspecific, immune-mediated destruction of the liver may
arise from an unknown insult and be self perpetuating.
III. It may be a component of lymphoplasmacytic inflammatory
diseases of the cat.
A. In one study, 15 of 18 cats with chronic cholangio-
hepatitis had inflammatory bowel disease (IBD), 9 of
18 had pancreatitis, and 7 of 18 had both pancreatitis
and IBD (Weiss et al., 1996).
B. Other disorders associated with chronic cholangio-
hepatitis include toxoplasmosis, feline immuno-
deficiency virus (FIV) infection, and idiosyncratic
reactions to chronic medications.
Clinical Signs
I. It is less severe than acute cholangiohepatitis, but cats are
usually ill for longer periods.
II. Most are middle-aged cats.
III. Duration of illness is typically ≥3 weeks.
IV. No sex or breed predilection has been found.
V. Vomiting, diarrhea, and jaundice are common.
VI. Most cats have good appetites.
Diagnosis
I. ALT and bilirubin are mildly to moderately increased.
II. Abdominal radiography is usually unremarkable, but
ultrasonography may reveal a diffuse to patchy hyperecho-
genicity of the hepatic parenchyma.
III. Definitive diagnosis is by biopsy.
A. Mixed lymphoplasmacytic periportal inflammation
B. Piecemeal necrosis and extension of lymphoplasma-
cytic inflammation into surrounding parenchyma
C. Focal invasion of bile duct epithelium with lymphocytes
D. Reduction in number of bile ducts
E. Bridging portal fibrosis in later stages
Differential Diagnosis
I. Idiopathic hepatic lipidosis
II. Hepatobiliary neoplasia
III. Chronic pancreatitis
IV. Acute cholangiohepatitis
V. Toxoplasmosis
VI. Lymphocytic portal hepatitis
A. It is a waxing and waning disease similar to chronic
cholangiohepatitis.
B. Affected cats are older (≥11 years) and have intermittent
vomiting and jaundice for months to years.
C. Hepatomegaly, marked leukocytosis, mild elevations in
ALT and ALP, and hyperglobulinemia are common.
D. A biopsy is required for diagnosis and demonstrates
periportal lymphocytic infiltrates.
E. Treatment is similar to chronic cholangiohepatitis,
although some cats require no therapy if the disease is
waning.
Treatment
I. Give prednisolone (which may be superior to prednisone
in cats, as it needs no conversion to an active form) at 2 to
4 mg/kg PO SID for 4 to 8 weeks, and taper gradually to a
dose that controls clinical signs.
II. Ursodeoxycholate acid may be tried at 10 to 15 mg/kg PO
SID, but its efficacy is unproven.
III. Start antibiotics if there is evidence of infection based on
culture of bile or hepatic tissue.
IV. Antioxidant therapy may be helpful.
A. Give d-alpha-tocopheryl-1000-polyethylene glycol suc-
cinate (Liqui-E) at 25 IU/kg PO BID.
B. Give SAMe at 20 mg/kg PO SID on an empty stomach.
V. Use cyclosporine at 5 mg/kg PO SID to BID in cats that
have a poor response to prednisone or develop diabetes
mellitus from chronic prednisone administration.
Monitoring of Animal
I. Monitor body weight and serum liver enzymes, bilirubin,
and albumin every 2 to 4 weeks for several months.
II. If response to therapy is poor, perform a complete re-
evaluation, including liver biopsy.
III. Prognosis is variable, although most affected cats have good
long-term survival.
Copper Storage Hepatopathies
Definition
I. It is a chronic progressive hepatitis of dogs associated with
the accumulation of copper in hepatocytes.
II. It is well characterized in the Bedlington terrier and West
Highland white terrier.
III. It also occurs in the Dalmatian, Labrador retriever, Doberman
pinscher, keeshond, and Skye terrier.
Causes
I. It is often a hereditary disease.
II. Cholestasis can also result in copper accumulation in
hepatocytes.
Pathophysiology
I. In the Bedlington terrier, an autosomal trait leads to
expression of an abnormal hepatic metallothionein, with
resultant reduced biliary copper excretion.
II. As hepatic copper concentration increases progressively
over time, hepatic injury increases.
III. Above a critical concentration, acute hepatic necrosis
develops.

Clinical Signs
I. Many dogs are asymptomatic.
II. Acute episodes of anorexia, vomiting, weakness, lethargy,
and dehydration may occur.
III. In chronic cases, anorexia or inappetence, poor body
condition, and intermittent vomiting and diarrhea may
occur weeks to months before onset of liver failure, and
these dogs eventually develop jaundice, ascites, cachexia,
and hepatic encephalopathy.
IV. Peracute episodes of hemolytic anemia and jaundice may
occur.
Diagnosis
I. ALT is consistently elevated; ALP values are variable.
II. Bile acid assays indicate presence of liver disease.
III. Radiographic and ultrasonographic findings are variable.
IV. The measurement of serum or plasma copper or cerulo-
plasmin is not diagnostic.
V. Definitive diagnosis requires hepatic biopsy with quantita-
tive measurement of hepatic copper.
A. Dry matter copper >400 ppm is abnormal.
B. Clinical disease usually occurs with copper levels
>2000 ppm (dry matter).
VI. Affected Bedlington terriers accumulate copper as they
age, so biopsies of the liver are performed at 6 months, and
at 14 to 15 months of age.
A. Normal dogs have normal liver copper content on both
biopsies.
B. Affected homozygotes have increased hepatic copper
on both biopsies.
C. Heterozygotes have elevated copper at 6 months but
normal values at 14 to 15 months.
VII. In the West Highland white terrier, copper accumulation
is not progressive with age.
A. After 2 years, they do not appear to accumulate more
copper.
B. Maximum documented hepatic copper is much lower
than in Bedlingtons.
Treatment
I. Zinc acetate or gluconate stimulates the production of
intestinal metallothionein, which preferentially binds intes-
tinal copper.
A. Dose is 5 to 10 mg/kg PO SID of elemental zinc, or
alternatively, give 50 to 100 mg SID to medium- and
large-breed dogs.
B. Some dietary constituents inhibit absorption, so zinc
must be administered 1 hour before or 2 hours after a
meal; however, it can be mixed with meat (tuna fish,
ground beef) to prevent GI upset.
C. The goal is to double baseline plasma zinc levels.
II. d-Penicillamine is a copper chelator that results in urinary
excretion of copper.
A. Dose is 10 to 15 mg/kg PO BID.
B. Side effects include GI upset, renal disease, proteinuria,
and cutaneous eruptions.
III. Trientine (2,2,2 tetramine, Syprine) is a copper chelator
with no serious side effects.
CHAPTER 37 | Diseases of the Hepatobiliary System 423
A. It is given at 10 to 15 mg/kg PO BID.
B. It has substantially greater copper chelation ability than
d-penicillamine.
C. 2,3,2 Tetramine has greater than fourfold to ninefold
potency compared to trientine, but is not commercially
available.
Monitoring of Animal
I. Hepatic biopsy may be obtained every 1 to 6 months to
monitor success of copper chelation.
II. Monitor serum liver enzymes, bilirubin, albumin, and
cholesterol every 3 to 6 months.
III. The prognosis is good if the disease is identified before the
onset of liver failure.
PARASITIC DISORDERS
See Table 37-1.
IDIOPATHIC DISEASES
Feline Idiopathic Hepatic Lipidosis
Definition
I. It is characterized by the accumulation of fat (triglycerides)
in vacuoles within hepatocytes.
II. It is a syndrome of cyclic anorexia or inappetence that
exacerbates the lipidosis, which in turn worsens the
anorexia.
Causes
I. The exact etiology remains a mystery.
II. It usually occurs secondary to some stressful illness or
event (e.g., upper respiratory infection, boarding, addition
of new cats to the household, recent diet change), although
an initiating event may not be identified.
III. It can occur secondary to other diseases.
A. Examples include diabetes mellitus, other hepatic
diseases, renal failure, hyperthyroidism, pancreatitis,
neoplasia, small intestinal diseases, and starvation.
B. Resolution of the primary disease may result in re-
solution of the lipidosis once the cat starts eating.
C. Chronic pancreatitis is associated with a worse prognosis
in cats with hepatic lipidosis.
Pathophysiology
I. Mechanisms for hepatic lipidosis include the following:
A. Excess delivery of triglycerides to the liver during
anorexia and insulin-deficient or insulin-resistant
states
B. Impaired formation and release of very low density
lipoprotein
C. Impaired oxidation of fatty acids
II. Acute hepatic failure is a consequence when treatment is
delayed.
A. Lipid vacuoles cause peripheral displacement of hepato-
cyte organelles and disruption of normal hepatocyte
function.
424 SECTION 5 | Digestive System

B. The prognosis for recovery worsens with progressive III. Gastrointestinal diseases: IBD, lymphoma
hepatic failure, because hepatic encephalopathy may IV. Pancreatitis
develop.
C. Coagulopathy may occur from decreased synthesis of Treatment
clotting factors in the liver and decreased absorption
I. Enteral feedings are the most critical component of
of vitamin K.
therapy.
Clinical Signs A. Force feeding or appetite stimulants usually do not
result in adequate food intake.
I. No breed, age, or sex predilection
B. Insert a feeding tube in all affected cats.
II. Indoor cats more often affected
1. Nasoesophageal tube
III. Many cats initially obese
a. A 5-French infant feeding tube is placed through
IV. Anorexia or decreased appetite for several days to weeks
the nose and into the esophagus.
V. Early signs: weight loss, dehydration, ptyalism, vomiting
b. It allows for temporary nutritional support (2 to
VI. Late signs: severe wasting, icterus, hepatic encephalopathy
4 days) and is a good option for initial stabiliza-
(e.g., depression, head pressing, circling)
tion of the cat in the hospital.
Diagnosis 2. Esophagostomy tube: preferred if there is no esopha-
geal disease
I. CBC
3. Gastrostomy tube options
A. Mild, nonregenerative anemia
a. Percutaneous endoscopic gastrostomy (PEG)
B. Stress leukogram
tube
II. Serum biochemistry profile
b. Many blind percutaneous gastrostomy tube tech-
A. ALP: often the most significantly elevated liver enzyme
niques
B. ALT also elevated
c. Major problems: splenic entrapment, pressure
C. Hyperbilirubinemia
necrosis of the skin
D. Evidence of liver failure: hypoalbuminemia, hypogly-
C. Provide a diet that has adequate calories and good
cemia, low BUN, hypocholesterolemia (bad prognostic
quantities of protein, carbohydrates, and fat.
indicator)
1. Canned cat food can be blended and strained.
E. Elevated creatine kinase: associated with anorexia, not
2. On the first day, give 1/3 the daily requirement,
muscle damage
followed by 2/3 on the second day, and then the full
III. Bilirubinuria: always abnormal in cats
requirement thereafter.
IV. Serum bile acids: usually abnormal in both fasting and
3. Divide food into 6 to 8 meals for the first 1 to 2
postprandial samples
weeks, then gradually reduce the number of feedings
V. Other tests to consider: feline leukemia virus (FeLV), FIV,
to TID to QID.
toxoplasmosis, serum thyroxine
4. Some cats require nutritional support for ≥60 to
VI. Abdominal radiography
90 days, although most start eating on their own
A. It may reveal no significant findings.
within 2 to 4 weeks.
B. Many previously obese cats still have abundant falci-
5. Let the cats eat on their own for 4 to 7 days (without
form fat.
nutritional supplementation) to evaluate whether
C. The liver may be normal in size or slightly enlarged,
they are eating enough before the tube is pulled.
with rounded edges.
II. Antiemetics may help reduce any associated vomiting,
VII. Abdominal ultrasonography: diffuse hyperechogenicity
especially when tube feeding is started.
of liver parenchyma
A. Metoclopramide 0.2 to 0.4 mg/kg PO TID
VIII. Cytological and histopathologic examinations
B. Cisapride 0.5 mg/kg PO BID
A. They are usually diagnostic.
C. Ondansetron 0.1 to 0.3 mg/kg IV BID to TID or
B. Fine-needle aspirate (FNA) reveals multiple hepato-
dolasetron 0.5 mg/kg IV SID for refractory, severe
cytes packed with small and large vacuoles.
vomiting
C. Liver biopsy is superior to FNA, but may not be
III. Give antacid therapy for GI hemorrhage (hematemesis,
necessary.
melena).
1. Obtaining a biopsy allows identification of other
A. Not routinely required
diseases (e.g., cholangiohepatitis).
B. Famotidine 0.5 mg/kg IV, PO SID to BID
2. It may be obtained via ultrasound guidance, lapar-
C. Sucralfate 250 mg PO BID to TID
oscopy, or laparotomy.
3. A coagulation profile is usually performed before
biopsy. Monitoring of Animal
I. Evaluate hepatic biochemistries and body weight every 1 to
Differential Diagnosis 2 weeks during therapy and recovery.
I. Acute or chronic cholangiohepatitis II. Do not discontinue tube feeding or remove tube too
II. Hepatic neoplasia: lymphoma early.
 CHAPTER 37 | Diseases of the Hepatobiliary System 425

Gallbladder Mucocele 1. Antibiotics: amoxicillin-clavulanic acid, cephalo-

sporins, fluoroquinolones, metronidazole
Definition and Causes 2. Ursodeoxycholate 10 to 15 mg/kg PO SID
I. It is a pathologic collection of mucus in the gallbladder. B. Surgical therapy is often required.
II. It is one of the most common causes of extrahepatic biliary II. Symptomatic animal
disease in the dog. A. Surgical treatment is required.
III. There is no known etiology. B. Cholecystectomy is the treatment of choice.
IV. An infectious cause has been suggested, but cultures from C. Obtain bile and gallbladder wall samples for aerobic
bile or gallbladder wall are usually sterile. and anaerobic bacterial culture.
D. Adhesions to liver, omentum, stomach, and diaphragm
Pathophysiology may complicate removal.
I. Mucus accumulation admixed with bile can extend into E. Gallbladder rupture requires copious lavage to remove
the biliary tree, resulting in bile duct obstruction. contents from the abdomen.
II. Progressive distension of the gallbladder may result in F. Assess patency of the common bile duct.
necrosis of the gallbladder wall. G. Intraoperative hemorrhage from the hepatic fossa
may occur after cholecystectomy, but is often readily
Clinical Signs controlled.
I. Most dogs are older (≈10 years), although dogs as young H. Necrosis of the common bile duct may necessitate
as 3 years may be affected. euthanasia.
II. Dogs may be asymptomatic.
III. Acute to subacute onset of vomiting, anorexia, lethargy, Monitoring of Animal
and icterus may occur. I. Prognosis is dependent on the severity of signs, but is good
IV. Polyuria/polydipsia and abdominal discomfort may be for most dogs.
noted. II. Ultrasonography and hepatic biochemistries are repeated
every 2 to 4 weeks while on medical therapy.
Diagnosis III. Immediate postoperative therapy includes IV fluid therapy,
I. CBC IV antibiotics (e.g., ampicillin, cefazolin, cefoxitin), and
A. Leukocytosis is common, often with a mature neutro- pain control (e.g., buprenorphine, fentanyl, morphine).
philia. IV. Complications after surgery include pancreatitis, bile perito-
B. Mild anemia may be present but is uncommon. nitis from bile duct leakage, pulmonary thromboembolism,
II. Serum biochemistry profile and aspiration pneumonia.
A. ALP is significantly elevated (as high as 11,100 U/L)
(Pike et al., 2004). Vacuolar Hepatopathies
B. Moderate to significant elevations occur in ALT (as See Table 37-1.
high as 4827 U/L).
C. Hyperbilirubinemia (as high as 17.5 mg/dL) is common. Idiopathic Hepatic Fibrosis in Young Dogs
III. Abdominal radiography: normal, hepatomegaly See Table 37-1.
IV. Ultrasonography
A. It is the definitive diagnostic test. Hepatocutaneous Syndrome
B. Echogenic material in the gallbladder can appear
striated, stellate, or amorphous. Definition and Causes
C. Dilated common bile ducts may be identified. I. It is also known as superficial necrolytic dermatitis and
D. Gallbladder wall rupture may appear as a loss of necrolytic migratory erythema.
continuity in the wall. II. Although a hepatopathy is recognized in most cases, the
E. Echogenic peritoneal effusion is often seen but not etiology is unknown except for those with a glucagonoma
diagnostic for rupture. (rare).
III. A classic triad of findings occurs.
Differential Diagnosis A. Ulcerative and crusting lesions of foot pads, muco-
I. Acute pancreatitis cutaneous junctions, ears, pressure points
II. Leptospirosis B. Vacuolar hepatopathy
III. Gallbladder neoplasia C. Late onset glucose intolerance: diabetes mellitus
IV. Acute hepatitis
V. Cholelithiasis Pathophysiology
I. There are two theories for the development of the cutaneous
Treatment lesions.
I. Asymptomatic animal A. Increased portal glucagon with increased hepatic gluco-
A. Medical therapy may be attempted, but is not often neogenesis, decreased plasma amino acids, and protein
successful. depletion of the epidermis
426 SECTION 5 | Digestive System
B. Hyperglucagonemia with increased arachidonic acid
synthesis in keratinocytes, inflammation, and necrosis
II. Dermatohistopathology reveals the following:
A. Epidermal parakeratotic hyperkeratosis
B. Severe intercellular and intracellular edema
C. Clefts and subcorneal vesicles
D. Foci of epidermal necrosis
E. Hyperplasia of the basal layers of the epidermis
III. Liver histopathology is characterized by the following:
A. Large, nodular areas of normal hepatic parenchyma are
isolated by areas of parenchymal collapse.
B. Collapsed areas contain severely vacuolated hepato-
cytes (lipid), numerous small bile ductules, and a net-
work of reticulin and fine collagen fibrils.
C. There is no evidence of cirrhosis.
Clinical Signs
I.Typically older dogs (6.5 to 16 years)
II.GI signs: diarrhea, vomiting, inappetence
III.Hyperkeratosis of footpads with severe crusting
IV. Reluctance to walk
V. Mucocutaneous ulcerations, ear crusting, pressure point
ulcers, deformed nails
VI. Polyuria and polydipsia with diabetes mellitus
Diagnosis
I. Laboratory test results
A. ALP is elevated (often >1000 U/L) in all dogs.
B. ALT is mildly elevated in many dogs.
C. Low BUN and cholesterol are common.
D. Variable hyperglycemia is present.
E. Mild, normocytic, normochromic, nonregenerative
anemia may be detected.
II. Abdominal ultrasonography
A. Liver can be small, normal (most common), or large in
size.
B. Surface of liver is often slightly irregular.
C. A distinctive “honeycomb” pattern is present in the
parenchyma, with variably sized hypoechoic regions
surrounded by highly echogenic areas.
III. Specialized testing
A. Hypoaminoacidemia, especially low glutamine and
proline (<10% of normal)
B. Serum glucagon levels
1. Normal in all dogs with vacuolar hepatopathy
2. Elevated with glucagonoma
IV. Histopathology of skin and liver: definitive
Differential Diagnosis
I. Diseases with similar gross cutaneous lesions
A. Pemphigus foliaceous
B. Lupus erythematosus
C. Zinc-responsive dermatosis
D. Generic dog-food dermatosis
II. Differentiated by skin biopsy
Treatment
I. Goals of treatment
A. Resolution of the cutaneous lesions
B. Prevention of deterioration of hepatic dysfunction
C. Effective management of diabetes mellitus
II. Short-term amino acid infusions for dogs with severe
cutaneous lesions
III. Long-term treatment nutritional therapy
A. Do not feed a protein-restricted diet.
B. Attempt to correct hypoaminoacidemia.
C. Feed a high-quality, easily digestible protein.
1. Minimum of 28% to 35% protein (dry matter basis)
2. High-protein, low-fat diets (approximately 50%
protein) preferred
D. Supplement diet to provide additional amino acids.
1. Egg yolks and cottage cheese
2. Amino acids (variety of products high in branched
chain amino acids are available over the counter) at
1 to 2 g/5 to 10 kg body weight PO TID
3. Whey protein supplement at 1 to 2 g/kg/day PO
(unflavored or vanilla preferred)
4. Powders mixed with yogurt or broth
IV. Zinc therapy is given as for copper hepatopathy.
V. Water-soluble vitamin E is given as for chronic hepatitis.
VI. Essential fatty acid therapy is also helpful
A. Dose: 30 to 90 mg/kg PO SID
B. Side effects: lethargy, vomiting, diarrhea
VII. Ursodeoxycholate is not a critical component of therapy,
but is used as for chronic hepatitis.
Monitoring of Animal
I. Skin lesions
A. They improve within 4 to 6 weeks with successful
therapy.
B. Monitor for secondary bacterial and fungal podo-
dermatitis.
II. Hepatic lesions
A. Monitor liver enzymes, bilirubin, albumin, glucose,
and cholesterol every 1 to 3 months.
B. Values improve within 2 to 4 months with successful
therapy, but ALP may never normalize.
III. Diabetes mellitus
A. Develops in most dogs
B. Requires insulin therapy (see Chapter 44)
METABOLIC AND TOXIC DISEASES
Hepatic Encephalopathy
Definition and Causes
I. Hepatic encephalopathy (HE) is a complex neurological
syndrome associated with acquired and congenital liver
disease.
II. Causes include the following:
A. Portal vascular anomalies
B. Idiopathic feline hepatic lipidosis
C. Fulminant hepatic failure
D. End-stage chronic hepatitis/cirrhosis
E. Urea cycle enzyme deficiencies
III. Contributing factors include the following:
A. Anesthesia, surgery
 CHAPTER 37 | Diseases of the Hepatobiliary System 427

B. High protein meal H. Polyuria, polydipsia

C. GI bleeding: ulceration, intestinal parasites I. Vomiting, diarrhea
D. Hypokalemia: enhances renal ammonia production
E. Bacterial infections or septicemia Diagnosis
F. Alkalosis: enhances transfer of ammonia into central I. High index of suspicion in certain breeds
nervous system (CNS) A. Yorkshire terriers and other breeds known to have a
G. Constipation, dehydration high prevalence of PSS
H. Transfusions of stored blood B. Doberman pinschers or other breeds with a high prev-
I. Diuretics alence of chronic hepatitis
C. Bedlington terrier or other breeds with a high prev-
Pathophysiology alence of copper toxicosis
I. HE involves the accumulation of neurotoxins. II. Compatible physical examination findings
II. Ammonia is converted to glutamine in the brain, and this A. The presence of icterus
pathway can be rapidly overwhelmed. 1. Unexpected in dogs with PSS
A. Serum glutamine levels are increased in dogs with HE. 2. Common in dogs with acute hepatic failure
B. Blood ammonia is typically high in advanced liver B. Copper-colored irises in cats with PSS
failure. C. Hypersalivation in cats
1. The level correlates poorly with severity of HE. D. Microhepatica
2. Blood levels are not very useful in the diagnosis of III. Supportive laboratory results
HE. A. Hypoalbuminemia, hyperbilirubinemia, hypocholes-
C. In the CNS, chronic hyperammonemia impairs the terolemia, hypoglycemia, and elevated liver enzymes
glutamate-nitric oxide-cGMP pathway (neurostimula- B. Abnormal serum bile acids
tory pathway), which contributes to the neurological C. Elevated blood ammonia levels
impairment. 1. Only accurate if assayed immediately and against
III. False neurotransmitters are formed from excessive delivery a control sample
of aromatic amino acids to the CNS. 2. Not elevated in every animal with HE
A. Tryptophan and phenylalanine are converted to false D. Presence of PSS on ultrasonography
neurotransmitters, such as octopamine and phenyl-
ethanolamine. Differential Diagnosis
B. The false neurotransmitters are depressive in their I. Hypoglycemia: see Chapter 46
action. II. Diabetic ketoacidosis
IV. Activation of central gamma-amino butyric acid (GABA)- III. Azotemia
benzodiazepine receptors also produces a depressive effect IV. Cerebral infarction
on the CNS. V. Meningitis or encephalitis: see Chapter 23
V. Manganese intoxication produces clinical signs similar to VI. Epilepsy
HE (Schenker and Bay, 1997). VII. Distemper encephalitis
VI. Serum levels of tumor necrosis factor-a are increased in VIII. Propane inhalation, carbon monoxide intoxication
acute and chronic liver disease, and increase peripheral- IX. Inherited cobalamin deficiency: giant schnauzer, border
type benzodiazepine receptors in the cerebral cortex. collie
VII. Other factors that may play a minor role include short-
chain fatty acids, mercaptans, phenols, brain lactate, and Treatment
zinc deficiency. I. Emergency therapy
A. Lactulose can be given as an enema for grade 3 to
Clinical Signs 4 disease.
I. Grading scheme for HE 1. Dose is 100 mL in 200 mL water, given at 5 to
A. Grade 0: normal 15 mL/kg QID.
B. Grade 1: irritability, restlessness, altered sleep, agitation 2. The stool pH will be <6 if therapy is effective.
C. Grade 2: lethargy, sluggishness, decreased inhibitions B. Povidone iodine enema
D. Grade 3: somnolent, but can be roused 1. A 1:10 dilution of povidone iodine with water is
E. Grade 4: comatose given at 20 mL/kg QID.
II. Common signs 2. It acidifies the colon and decreases bacterial
A. Depression, lethargy, stupor, coma numbers.
B. Ataxia, circling, compulsive pacing C. IV fluid therapy is started with crystalloid solutions
C. Head pressing, disorientation, amaurosis that do not contain lactate.
D. Hysteria, aggression D. Give supplemental dextrose to animals with acute or
E. Excessive panting fulminant hepatic failure.
F. Ptyalism in cats II. Long-term management
G. Seizures (more common in cats) A. Surgically correct any PSS, if possible.
428 SECTION 5 | Digestive System
B. Institute therapy specific for any underlying, acquired
liver disease.
C. Restrict dietary protein.
1. Establish the protein tolerance of the animal and
feed the highest amount tolerated.
2. Supplementation of vegetable protein-based diets
may allow a higher protein content to be fed.
3. When restricting protein in cats, make sure the diet
is high in arginine to prevent deficiency.
D. Lactulose is a nonabsorbable disaccharide that is
metabolized in the colon by certain bacteria.
1. Lactulose is converted to lactic acid, acetic acid,
formic acid, and carbon dioxide, which decrease
the breakdown of amino acids, protein, and blood,
and minimize the formation of short-chain fatty
acids.
2. Acidification of the colon draws ammonia out of
the blood into the gut, where it is trapped for ex-
cretion.
3. Low pH decreases the survival of urease-producing
bacteria and promotes growth of non–urease-
producing bacteria.
4. Cathartic action decreases the retention of nitro-
genous waste.
5. Give lactulose at 0.5 to 1.0 mL/kg PO TID and titrate
to produce a soft stool.
E. Antibiotics kill the bacteria that produce ammonia
and may have a synergistic effect with lactulose.
1. Neomycin 20 mg/kg PO BID to TID for 10 to 14 days
2. Metronidazole 15 mg/kg PO SID
3. Ampicillin 20 mg/kg PO TID
F. Zinc may be given, as for Copper Hepatopathy.
Monitoring of Animal
I. See specific monitoring advice for the primary disease
conditions.
II. Monitoring blood ammonia levels is not indicated because
they correlate poorly with therapeutic success.
III. Regular evaluation of serum albumin is indicated for
animals on low-protein diets.
IV. Avoidance of ulcerogenic medications (e.g., nonsteroidal
antiinflammatory drugs) is warranted.
Hepatic Necrosis and Failure
Definition
I. Fulminant hepatic failure is characterized by hypoalbumi-
nemia, hypoglycemia, hypocholesterolemia, decreased
coagulation factors, and cholestasis of short (<2 weeks)
duration, with the potential for complete recovery.
II. Not all forms of necrosis and failure are toxic in origin.
Causes
I. Blunt abdominal trauma with liver lobe rupture
II. Liver lobe torsion
A. With or without diaphragmatic hernia
B. Can lead to ischemic necrosis, endotoxic shock, and
death
III. Postcaval syndromes: right-sided congestive heart failure
(CHF), pericardial disease, Budd-Chiari-like syndrome
from occlusion of the caudal vena cava between the heart
and liver
IV. DIC with thromboembolic disease and infarction
V. Acute pancreatitis: shock, DIC, bacteremia, extrahepatic
bile duct obstruction
VI. Gastric dilatation-volvulus: disrupted portal and vena
caval blood flow
VII. Immune-mediated hemolytic anemia: hypoxia, damage
from unconjugated bilirubin and hemoglobin, thrombo-
embolism from autoagglutination
VIII. Vasculitis: infectious, noninfectious causes
IX. IBD: absorption of inflammatory mediators, endotoxin,
and enteric bacteria
X. Hyperthermia: direct thermal injury, shock, DIC
XI. Neoplasia: tumor invasion (especially lymphoma), im-
paired perfusion, release of vasoactive substances
XII. Infections
A. Viral: infectious canine hepatitis, canine herpesvirus
B. Bacterial
1. Bacteremia: Staphylococcus spp. or Streptococcus
spp.
2. Anaerobic bacteria of enteric origin
3. Bacillus piliformis (Tyzzer’s disease), salmonellosis
4. Bacterial cholangiohepatitis
5. Leptospirosis
6. Tularemia
C. Rickettsial
1. Ehrlichia canis: liver disease uncommon, vasculitis-
induced necrosis
2. Rocky Mountain spotted fever: necrosis from
vasculitis
D. Protozoal
1. Toxoplasmosis: hepatic necrosis from host response
to tachyzoites
2. Neosporosis: hepatic infiltration, necrosis
E. Fungal: histoplasmosis, blastomycosis, coccidioido-
mycosis, aspergillosis
F. Toxins
1. Uncommon in dogs and cats
2. Amanita mushroom poisoning: rare
3. Drugs
a. Thiacetarsamide, metofane, halothane, keto-
conazole
b. Cats: oral diazepam, griseofulvin
c. Dogs: carprofen, trimethoprim-sulfa, amioda-
rone, methotrexate
4. Blue-green algae
Pathophysiology
I. Distribution of necrosis
A. Widespread: CAV-1, trimethoprim-sulfa, oral diazepam
B. Focal: any insult, hypotension and local hypoxia
during anesthesia, often seen in surgical biopsies
C. Centrilobular: hypoxemia, hypoperfusion, chronic
passive congestion, certain toxins (thiacetarsamide,
aflatoxins, amanita mushrooms)

D. Midzonal: rare and usually associated with centrilobu-
lar necrosis
E. Periportal: uncommon; associated with some hepato-
toxins, endotoxins, IBD, chronic pancreatitis
F. Paracentral: involves an entire hepatic acinus, occurs
secondary to ischemia from thromboembolism
II. Consequences of fulminant hepatic failure
A. Hepatic encephalopathy
B. Cerebral edema
1. Major cause of death
2. Occurs from vasogenic edema, cytotoxic edema,
cerebral ischemia
C. Coagulopathies
D. Hypotension: from endotoxemia, retention of vasogenic
amines, etc.
E. Cardiac dysfunction and arrhythmias
F. Pulmonary edema
G. Acid-base and electrolyte disturbances: hyponatremia,
hypokalemia, metabolic acidosis
H. Pancreatitis, renal failure
I. Hypoglycemia: develops rapidly
J. Secondary infections
K. Portal hypertension: grave prognostic sign
L. Cholestasis
Clinical Signs
I. Signs may be absent or vague.
II. Nonspecific signs occur in animals with focal, mild, or
moderate hepatic necrosis.
III. Signs may relate to another organ system that is affected
(e.g., CHF, pyometra, severe shock).
IV. With severe or massive acute hepatic necrosis, signs are
often severe, but rarely specific.
A. Anorexia, depression, fever
B. Vomiting, possibly GI hemorrhage with melena,
hematemesis
C. Jaundice, hepatic encephalopathy
Diagnosis
I. ALT and AST are consistently elevated within hours of the
insult.
A. May reach levels 30 to 50 times the reference range
B. Often fall to lower levels with a few days
C. Poor correlation of elevation with severity of injury
II. Changes in ALP are dependent on the type of injury.
A. More severe elevations with cholestatic processes
B. Mild elevations typical in first days of hepatic necrosis
C. Often elevated longer than ALT
D. Persistent elevations from continued cholestasis, reac-
tive biliary hyperplasia, or hepatic regeneration
III. Hyperbilirubinemia: more severe with periportal necrosis
IV. Hepatic biopsy to identify primary hepatic diseases
Treatment
I. Treat any primary disease.
II. The need for IV fluid therapy is dependent on the under-
lying condition and the severity of clinical signs and
dehydration.
CHAPTER 37 | Diseases of the Hepatobiliary System 429
A. Crystalloid solutions that do not contain lactate are
recommended.
B. Supplement with dextrose to provide a 2.5% or 5%
solution, depending on serum glucose levels.
C. Potassium chloride supplementation is instituted.
1. Give 0.3 to 0.5 mEq/kg/hr in IV fluids to animals
with severe hypokalemia.
2. Give 16 to 36 mEq/L in IV fluids to animals with
normokalemia and on a maintenance rate of fluids
(40 to 60 mL/kg/day).
III. Antioxidants may be beneficial.
A. d-Alpha-tocopheryl-1000-polyethylene glycol succinate
(Liqui-E; TwinLab, New York N.Y.) is given at 25 IU/kg
PO BID.
B. SAMe (Denosyl) is given at 20 mg/kg PO SID on an
empty stomach.
C. Silymarin
1. Drug of choice for amanita mushroom poisoning
2. Dose: 25 to 50 mg/kg PO SID for dogs and cats
IV. Supportive care for complications of acute hepatic failure
includes the following:
A. Treat hepatic encephalopathy, as discussed earlier.
B. Treat cerebral edema with mannitol (0.5 to 1 g/kg IV
BID to TID) and with elevation of the head, but treat-
ment is rarely successful.
C. Treat coagulopathies with fresh frozen plasma (5 to
10 mL/kg IV, repeated as needed to normalize coagula-
tion profile) or fresh whole blood if anemic (10 to
20 mL/kg IV).
D. Treat hypotension initially with IV crystalloid fluid
therapy, but severe hypotension that fails to respond
may be treated with the following:
1. Hydroxyethyl starch 10 to 20 mL/kg IV bolus fol-
lowed by 1 mL/kg/hr IV
2. Dopamine 2 to 10 mg/kg/min IV constant rate
infusion (CRI)
3. Dobutamine 5 to 20 mg/kg/min IV as CRI (dog) or
0.5 to 2 mg/kg/min IV as CRI (cat)
E. Pulmonary edema is poorly responsive to therapy.
1. Furosemide 2 to 4 mg/kg IV TID to QID may be
tried.
2. Supplement with oxygen via nasal cannula or oxygen
cage.
F. Use antibiotics (e.g., ampicillin, ampicillin, enrofloxacin,
cefoxitin) to prevent secondary infections.
G. Manage GI hemorrhage with famotidine.
V. Traumatic rupture rarely requires surgical intervention.
A. Stabilize the animal, providing blood products as
needed.
B. Only intervene surgically if bleeding seems uncon-
trollable.
Monitoring of Animal
I. Prognosis is good with acute hepatic injury (e.g., toxin,
trauma, brief hypoxia) if fulminant hepatic failure does
not develop.
II. The development of cerebral edema, pulmonary edema,
profound coagulopathy (prothrombin time and partial
430 SECTION 5 | Digestive System

thromboplastin time exceeding test limits), portal hyper- NEOPLASIA

tension, and refractory hypotension are grave prognostic
indicators. See Table 37-2.
III. The prognosis for survival is dependent on the primary
disease condition or etiology. TRAUMA
1. Blue-green algae poisoning is routinely fatal.
2. Most infectious causes have a good prognosis with Extrahepatic Biliary Tract Rupture
early treatment.
Definition
It is a tear in the gallbladder, cystic duct, hepatic ducts, or
VASCULAR DISEASES common bile duct with secondary leakage of bile into the
abdomen.
Acquired Por tosystemic Shunt
Causes
Definition I. Blunt force trauma (e.g., automobile crash, cow kick)
I. Various vascular communications can develop near the II. Penetrating abdominal injury (e.g., gunshot)
kidneys that connect the portal and systemic circulation. III. Infectious cholecystitis
II. They may develop from preexisting but nonfunctional IV. Gallbladder mucocele
communications. V. Cholelithiasis
III. They are associated with any disease that causes portal Pathophysiology
hypertension.
I. Bile duct ruptures almost always arise from blunt force
Causes trauma.
I. Hepatic arteriovenous fistula A. Most common site of rupture is the common bile duct
II. Noncirrhotic portal hypertension distal to the last hepatic duct.
III. Cirrhosis B. Second most common site is at the junction of the
IV. Hepatic fibrosis common bile duct and duodenum.
V. Postligation of congenital PSS C. The cystic duct is rarely ruptured by trauma.
VI. Any disease resulting in portal hypertension: cirrhosis, II. Gallbladder rupture almost always occurs from non-
idiopathic hepatic fibrosis, portal vein thrombosis traumatic causes.
III. Leakage of bile results in focal or diffuse peritonitis.
Pathophysiology
Clinical Signs
I. Portal hypertension stimulates the opening of alternative
I. Abdominal pain
vascular communications.
II. Abdominal distension
II. Development of HE is the same as for congenital PSS.
III. Vomiting, anorexia
Clinical Signs IV. Icterus
I. Dependent on underlying disease condition Diagnosis
II. Signs of HE I. Hyperbilirubinemia and elevated liver enzymes occur.
II. Abdominal radiographs may show focal or diffuse loss of
Diagnosis
detail consistent with free abdominal fluid.
I. Diagnostic tests are typically directed toward the primary III. Abdominal ultrasonography may identify the etiology (e.g.,
hepatic disease. mucocele), and the gallbladder may appear empty in cases
II. Multiple tortuous vessels are identified near the kidney of ductal rupture.
on ultrasonography. IV. Evaluation of fluid obtained on abdominocentesis or diag-
III. Rectal portal scintigraphy confirms the presence of a shunt nostic peritoneal lavage documents the presence of bile.
and is usually suggestive of acquired PSS.
IV. Direct visualization during laparotomy is needed in some Differential Diagnosis
cases. I. Acute hepatitis
II. Ruptured splenic mass
Treatment III. Gastric perforation
I. Treat the underlying disease condition. IV. Pancreatitis
II. Treat HE, if present. V. Peritonitis from other causes: see Chapter 38
III. Ligation of an acquired PSS is not recommended
A. An acquired PSS is a necessary adaptive process (in Treatment and Monitoring
portal hypertension) to prevent congestive enteropathy I. Surgical correction is required.
and ascites. A. Ruptured common bile duct: duct repair, cholecysto-
B. Ligation results in immediate postoperative death. jejunostomy
 CHAPTER 37 | Diseases of the Hepatobiliary System 431

TA BL E 37-2

Hepatic Neoplasia
TUMOR TYPE ULTRASONOGRAPHIC FEATURES TREATMENT AND PROGNOSIS

Hepatocellular carcinoma
or adenoma
Bile duct carcinoma
Lymphoma
Biliary cystadenoma
(cats only)
Hemangiosarcoma
(primary and metastatic)
Metastatic carcinoma
Insulinoma (metastatic)
Mast cell disease (metastatic)
FeLV, Feline leukemia virus.
Inhomogeneous echogenicity, either diffuse
or circumscribed
Multifocal with mixed echogenicity
Generalized hyper- or hypoechogenicity
Focal or multifocal nodules of varying
echogenicity
Focal or multifocal cystic lesions within the liver
Solitary, circumscribed mass with cavitary
lesions or multiple hypoechoic nodules
Multifocal hypoechoic nodules or diffuse
inhomogeneity, target lesions
Not routinely identified
Diffuse hyperechogenicity, hypoechoic nodules
Surgical resection if restricted to a single lobe
Poor prognosis for carcinoma
Surgical resection if restricted to a single lobe
Poor prognosis
Treatment same as for generalized lymphoma
Fair prognosis for 1 year survival
Grave prognosis if animal in liver failure
Poor prognosis if cat is FeLV positive
Excellent prognosis if surgically resectable
Fair prognosis for 1-2 year survival if not
resected
Surgical resection of solitary mass, followed by
chemotherapy
Poor prognosis for 6-month survival
No therapy
Grave prognosis
Surgical removal of visible metastatic lesions
Management of primary tumor
Good prognosis for 1 year survival
Chemotherapy
Fair prognosis for 1 year survival

B. Ligation of ruptured hepatic ducts
C. Cholecystectomy for gallbladder rupture
II. See treatment of peritonitis is Chapter 38.
III. Prognosis is dependent on the site of rupture.
A. Excellent for rupture of gallbladder and common bile
duct distal to cystic duct
B. Variable depending on ease of repair for ruptures of
common bile duct proximal to cystic duct
C. Fair to good when bile peritonitis is present
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 Caso clínico 5
III parte de X

“LUCAS”
Cocker Spaniel
Macho no castrado, 12 kg

Plan diagnóstico
El problema que hay que abordar primero es el motivo por el que
viene el animal: vómitos y melena

El que tenga el hígado más pequeño de lo normal puede que le

problemas digestivos o no, pero hace un año que lo
diagnosticaron y se mantiene con medicacion protectora.

El soplo ha sido un hallazgo en la exploración que todavía no le

da problemas (tos, intolerancia al ejercicio, disnea...)

Plan diagnóstico
Descartar presencia cuerpo extraño/obstrucción
Confirmar/descartar microhepatia y comprobar si
le da problemas
¿CÓMO descartamos cuerpo extraño? PIENSA
Con una radiografía simple vemos si existe o no cuerpo extraño o
imagen de obstrucción.

Félix García

¿Aprecias algo?
 ¿Se observa alguna imagen
compatible con cuerpo extraño/
obstrucción?

Félix García
 ¿Se observa alguna imagen
compatible con cuerpo extraño/
obstrucción?

No existe imagen compatible con cuerpo

extraño. Tampoco se observa distensión
de las asas intestinales, por lo que no es
compatible con obstrucción.

Félix García
En la radiografía laterolateral realizada al principio, también se
puede valorar el tamaño del hígado.

Félix García
 En la radiografía laterolateral realizada al principio, también se
puede valorar el tamaño del hígado.

Félix García

El hígado es más pequeño de lo normal

¿Qué otra prueba realizarías para estar seguro de que no es un

problema gastrointestinal primario (neoplasia,
inflamatorio,obstructivo)?
 Caso clínico 5
IV parte de X

“LUCAS”
Cocker Spaniel
Macho no castrado, 12 kg

En la radiografías no veías nada, pero

debes cerciorarte que estás en lo cierto
ECOGRAFÍA

Félix García
ECOGRAFÍA

Félix García

En la ecografía de abdomen se observa un asa intestinal con la

pared engrosada, con contenido y la sombra acústica típica de la
existencia de un cuerpo extraño
Se ha confirmado mediante ecografía la existencia de un cuerpo
extraño intestinal. Está claro que no siempre que no se vea en una
radiografía hay que descartarlo por completo.

En la ecografía se valora también el estado del hígado, así como

el resto del abdomen, y se observa:
- inflitración hepática: focos ecogénicos 6 x 4 mm y alguno
hipoecogénico 6 x 6 mm
- epiplón reactivo
- intestinos bien estratificados, con peristaltismo

También podíamos haber dado un contraste

radiográfico, piensa que palpábamos algo
en el abdomen caudal
Se ha confirmado mediante ecografía la existencia de un cuerpo
extraño intestinal. Está claro que no siempre que no se vea en una
radiografía hay que descartarlo por completo.

En la ecografía se valora también el estado del hígado, así como

el resto del abdomen, y se observa:
- inflitración hepática: focos ecogénicos 6 x 4 mm y alguno
hipoecogénico 6 x 6 mm
- epiplón reactivo
- intestinos bien estratificados, con peristaltismo

Plan
Realización de analíticas sanguíneas
Hemograma
Bioquímica (especial antención en la función hepática)
 HEMOGRAMA Parámetros Resultados Referencia
Rec. eritrocit (x106/µg/dl) 9.6 5.5 - 8.5
C. hemoglobina (g/Dl) 17.4 12 - 18
Hto (%) 63 37 - 55
VCM (fl) 77 62 - 77
CCMH (g/dl) 34.7 33 - 37
HCM (pg) 24.6 21, 5 - 26,5
¿A qué puede ser
Rec. leucocitos 14920 6000 - 17000
debido el aumento
Fórmula leucocitaria % (x/µl)
de Hto y el rec. de
Linfocitos 6 895 500 - 4900
eritrocitos?
Monocitos 5 746 300 - 2500
Neutrof. segmentados 89 13279 3000 – 11500
Neutrófilos en banda 0 0 0 - 300
Eosinófilos 0.8 150 100 - 1500
Basófilos 0 0 0 - 200
Rec. Plaquetas (x 1000) 260 200 - 500
Rec. reticulocitos 0.2%
 Caso clínico 5
II parte de X

“LUCAS”
Cocker Spaniel
Macho no castrado, 12 kg

Haz lista de problemas y los diagnósticos

diferenciales de cada uno de ellos
 LISTA DE PROBLEMAS
Microhepatia
Soplo cardiaco
Vómitos crónicos y melena

Piensa bien en los diagnósticos diferenciales antes de

avanzar
 Diagnósticos diferenciales
o  Microhepatia
o  Hepatopatía crónica
o  Cirrosis
o  Shunt (extra, intrahepático)
o  Soplo cardiaco
o  Valvulopatía
o  Cardiomiopatía Dilatada
o  Vómitos crónicos y melena
o  Secundario problema hepático
o  Gastrointestinal primario
o  Cuerpo extraño/obstrucción
o  Inflamatorio
o  Neoplásico

¿Qué problema hay que abordar primero? Plan diagnóstico

 Caso clínico 5
I parte de X

“LUCAS”
Cocker Spaniel, 9 años.
Macho no castrado, 12 kg

Motivo de visita
Vómitos desde hace meses, esporádicos, biliosos
Esta mañana eran oscuros y además había diarrea
Anamnesis
Diagnóstico hace 1 año en otro veterinario de
microhepatia. En tratamiento con pienso hepático y
s-adenil-metionina (Denosyl®)
Vómitos desde hace meses, pero diferentes a los de
hoy
No descartan que se haya podido comer algo extraño.
No posibilidad de tóxicos
No poliuria/polidipsia
Diarreas desde hoy
Exploración física
Mucosas húmedas, hiperémicas, TRC < 1.5,
pulso periférico normal
Dolor a la palpación abdominal, se palpa masa
pequeña caudal.
Palpación rectal: melena
Auscultación: soplo III/IV sistólico izqdo
140 lpm, 30 rpm

Haz la lista de problemas