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Patrocina

Auspician
FOTOS PRIMERA JORNADA DE
MEDICINA CARDIORESPIRATORIA
DR. ALBERTO
MONTOYA
ESPAÑA

CHARLAS

1. Técnica y tips para una correcta auscultación


cardiopulmonar, aprendemos los sonidos principales

2. Enfoque diagnóstico y terapéutico de miocardiopatía


arritmogénica, el holter es imprescindible
3. ¿Es tan frecuente la hipertensión pulmonar como creemos?

4. Colapso traqueal, tratamiento médico y quirúrgico en perros


5. Neumonía una grave enfermedad respiratoria. Abordaje
clínico,diagnóstico y tratamiento

6. No todos los gatos que respiran mal tienen asma.


Como no equivocarnos

7. Sincopes cardiogénicos y su diagnóstico diferencial


8. Manejo de tos crónica en perros. Uso de broncodilatadores
José Alberto Montoya-Alonso, DMV, MsC, MA,
Bi-PhD

Licenciado y Doctor en Veterinaria por la


Universidad Complutense de Madrid (UCM).
Doctor en Medicina por la Universidad de Las
Palmas de Gran Canaria (ULPGC).
Especialista universitario en Obesidad,
Especialista en bienestar animal y en salud
animal. Acreditado en Medicina interna y
cardiología en pequeños animales y Máster
Universitario en Innovación Educativa y
Evaluación de Programas Formativos por la
Universidad Nacional a Distancia (UNED)

Catedrático de medicina y cirugía animal del


Departamento de Patología Animal, donde ha
sido su director, en la Facultad de Veterinaria de
Las Palmas de Gran Canaria. Responsable del Servicio de Medicina
Veterinaria y del grupo de investigación de Clínica veterinaria e
investigación terapéutica del Instituto Universitario de Investigaciones
Biomédicas y Sanitarias de la ULPGC. Coordinador del Programa de
Doctorado de Investigación en Biomedicina. Académico electo de la Real
Academia de Ciencias Veterinarias de España (RACVE)

Ha sido presidente del grupo de Especialistas en cardiología y aparato


respiratorio (GECAR) de la Asociación Española de Especialistas en
Pequeños Animales (AVEPA), pertenece a la junta directiva de la
European Society of dirofilariosis and Angiostrongylosis. Pertenece a la
European Society of Veterinary Cardiology a la Academy of Veterinary
Cardiology y a la European Society of Veterinary and Comparative
Nutrition

Obtuvo el Eitan Bogin Prize de la International Society of Animal Clinical


Biochemistry (ISACB) en 2004. Es Premio a la Excelencia docente de la
Universidad de Las Palmas de Gran Canaria y fue Veterinario del año en
2007. Ha obtenido el I, II y III Premio laboratorios Boehringer de la
RACVE.

Ha dirigido 22 tesis doctorales y múltiples, suficiencias investigadoras


tesinas, trabajos fin de grado, y trabajos fin de master
Es profesor invitado de varias universidades extrajeras.
Ha participado como profesor y coordinador en más de 270 cursos, talleres,
seminarios, etc. de formación continuada y especialización para clínicos
veterinarios en España, Portugal y América.

Ha presentado más de 400 trabajos en congresos nacionales e


internacionales. Ha dirigido y participado en proyectos y contratos de
investigación suscritos con diferentes organismos públicos y privados en el
campo de la medicina veterinaria y humana.
Ha participado en la organización de más de 60 eventos científicos
Ha publicado más de 130 artículos científicos en revistas nacionales e
internacionales (en un 75% indexados) y editado, publicado y/o participado
en más de 20 libros.
Es miembro del comité científico y del comité editorial de más de 25
publicaciones biomédicas indexadas.
PROCEDURES PRO h CARDIOLOGY h PEER REVIEWED

The Basic
Cardiology
Examination
Wendy W. Mandese, DVM
Amara H. Estrada, DVM, DACVIM (Cardiology)
University of Florida

A thorough physical examination is valuable for diagnos- mitral valve disease and cardiac overload in dogs). Car-
ing heart disease and should include extensive examina- diac changes secondary to hypertension include myxo-
tion of all body systems. matous mitral valve disease, left atrial enlargement, or
left ventricular hypertrophy.2
General Appearance
Weight loss is common in patients with advanced car- Oral Examination
diac disease. In one study, >50% of dogs with dilated Pale mucous membranes can indicate shock or anemia,
cardiomyopathy experienced cardiac cachexia (ie, loss and hyperemic or injected mucous membranes can indi-
of lean body mass).1 Low body weight and failure to cate infection or polycythemia. Cyanosis occurs pri-
grow normally can also be signs of congenital cardiac marily in patients with cardiac defects that result in
disease in pediatric patients. right-to-left shunting, such as reverse patent ductus
arteriosus, atrial septal defect, and ventricular septal
Ocular Examination defect. Other health conditions, such as severe hypo-
Enlarged retinal vessels, retinal hemorrhage, or retinal thermia or severe respiratory disease, can also cause
detachment often indicates systemic hypertension, cyanosis. In differential cyanosis, the lower extremities
which can be primary (ie, idiopathic) or secondary to and vulva/prepuce appear cyanotic but the upper
conditions such as renal or cardiac disease, hyperadre- extremities and oral mucous membranes are pink and
nocorticism, diabetes mellitus, pre-eclampsia, and well oxygenated.3
hyperthyroidism. In patients with inconclusive labora-
tory results, echocardiography can be used to identify Several congenital cardiac defects are associated with dif-
underlying heart conditions that cause hypertension ferential cyanosis, but it is most commonly seen with a
(eg, hypertrophic cardiomyopathy in cats, myxomatous reverse patent ductus arteriosus. Periodontal disease

May 2017 cliniciansbrief.com 91


PROCEDURES PRO h CARDIOLOGY h PEER REVIEWED

should be assessed and noted, as secondary more likely to have audible crackles; crackles
cardiac complications (eg, endocarditis) are can also be auscultated in patients with pul-
possible if severe periodontal disease is not monary hypertension, bronchitis, and pneu-
addressed.4 monia. Muffled lung sounds can indicate
pleural effusion. Wheezes are associated with
Tracheal Palpation allergic airway disease, bronchitis, and col-
Tracheal palpation should be performed on lapsing trachea.
all coughing dogs. Small-breed dogs more
prone to myxomatous mitral valve disease Heart Rate
are also more prone to a collapsing trachea. Stress and anxiety associated with the veteri-
In both of these conditions, cough can occur nary environment can markedly increase a
during exercise or excitement5 and may be patient’s heart rate. Waiting for a patient’s ini-
caused by tracheal disease, even if a murmur tial arrival excitement to subside and asking
is present. Coughing can be heard with the client to be present during examination
tracheitis or tracheobronchitis and can be can help the clinician obtain a normal heart
caused by bacterial or viral infection or rate. The client can also be asked to obtain the
environmental allergens. patient’s resting heart rate at home. If an
arrhythmia is present, the type (eg, tachyar-
Respiratory Rate/Effort rhythmia, bradyarrhythmia) should be noted
Respiration should be evaluated when the and the nature characterized.
patient is calm. Clients can be trained to take
respiratory rates at home, especially while the Pulse
patient is sleeping. Several phone apps are Pulse pressure can be decreased or increased
available to make it easy for clients to obtain or have an altered configuration. Decreased
accurate readings. One study suggested that pulse pressure may be seen in patients with
most dogs and cats without cardiac disease or dilated cardiomyopathy, aortic or pulmonic
with well controlled heart disease will have a stenosis, heart failure, hypovolemia, or
resting respiratory rate of <30 breaths/min at shock. Increased pulse pressure can occur
home.6 Increased respiratory effort can indi- because of excitement and/or pain or hyper-
cate upper airway disease (effort occurs trophic cardiomyopathy.8 Dogs with aortic
during inspiration) or lower airway disease regurgitation commonly have a bounding
(effort occurs during expiration). pulse. Bounding pulses can also be felt in
patients with patent ductus arteriosus,
Lung Sounds severe bradycardia, hyperthyroidism, fever,
Abnormal lung sounds are most common in or anemia.
patients with primary respiratory disease.
Lung sounds also may be abnormal in patients Alterations in pulse conformation also may
with secondary respiratory conditions such as occur. Dogs with severe subaortic stenosis
pulmonary edema and pleural effusion. Aus- can have a weak pulse or a pulse pressure
cultation of the lungs is not a sensitive means that increases more slowly and peaks later
of detecting pulmonary edema or pleural effu- during systole (ie, pulsus parvus et tardus).
sion in dogs and cats, and many patients have Conversely, dogs with mitral regurgitation
pulmonary edema with no auscultatory abnor- commonly have a brisk pulse that rises more
malities other than increased bronchovesicu- rapidly in systole and lasts a shorter time.
lar sounds.7 Patients with severe pulmonary Other pulse abnormalities include pulsus par-
edema resulting in free fluid in the airways are adoxus and pulse deficits. Pulsus paradoxus is

92 cliniciansbrief.com May 2017


an increase in pulse pressure on expiration opathy. The presence of an S3 or S4 is referred
and a decrease on inspiration. This occurs to as a diastolic gallop. When a diastolic gallop
normally but is exaggerated in cardiac tam- is present, further evaluation is warranted.
ponade. Pulse deficits can occur with cardiac
tachyarrhythmias in which beats occur so Systolic clicks are found in dogs with chronic
rapidly that the ventricle does not have time valvular disease and originate from vibra-
to fill with an adequate amount of blood tions that occur when chordae tendineae and
before ejection (eg, fast atrial fibrillation, the mitral leaflets suddenly resist further
ventricular premature beats).7 Pulse should stretching and protrude into the left atrium.10
always be monitored while performing car- Muffled heart sounds may indicate the pres-
diac auscultation to detect pulse deficits. ence of pericardial or pleural effusion.

Blood Pressure Arrhythmias


Obtaining a systolic blood pressure using a Sinus arrhythmia is common in dogs, espe-
Doppler is a relatively simple procedure. To cially in patients who are relaxed and have a
obtain the most accurate reading, blood pres- lower heart rate. The heart rhythm is faster
sure should be measured in a quiet, calm envi- on inspiration and slower on expiration.
ronment with the client present, if possible. When the patient becomes more excited or
Proper technique, including appropriate cuff active, the sinus arrhythmia is often no lon-
width (ie, 40% of the circumference of the ger heard. Sinus arrhythmia does not always
limb or tail) is integral to obtaining an accu- correspond to respiration and can occur with
rate measurement. A minimum of 3 measure- other causes of increased vagal tone (eg, GI
ments should be obtained, and the variability disease).11 Pulses should be palpated in con-
between measurements should be <20%.9 junction with auscultation to determine if
pulse deficits are present. Sinus arrhythmia
Heart Sounds was previously thought to be uncommon in
The first heart sound (S1) is produced by clos- cats, but a 2009 study determined that
ing of the mitral and tricuspid valves. S1 is relaxed cats in their home environment can
loudest over the mitral valve area and is have frequent sinus arrhythmia.12
louder, longer, and lower pitched than the
second heart sound (S2). S2 is produced by Common abnormal rhythms include:
closing of the pulmonic and aortic valves. h Premature beats with pulse deficits: Asso-

S2 is shorter and higher pitched than S1. ciated with atrial and ventricular prema-
ture complexes. Can occur in bursts or be
The third heart sound (S3) is not usually heard sustained
during auscultation of healthy small animals, h Irregularly irregular rhythm: Associated

and its presence indicates myocardial failure. with atrial fibrillation. Has been described
The sound is generated during the period of as “shoes in a dryer”
rapid filling in early diastole when the ventri- h Slow arrhythmia with intermittent

cles suddenly resist expansion. pauses: Heard in patients with AV block or


sinus arrhythmia
The fourth heart sound (S4) originates from the h Persistent tachycardia or persistent bra-

vibration generated by cardiac structures when dycardia: Clients should be informed that
the atria contract. It can be a normal finding in an abnormality in heart rate and/or rhythm
giant-breed dogs and large animals or be asso- requires additional testing to determine
ciated with advanced hypertrophic cardiomy- the cause.

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PROCEDURES PRO h CARDIOLOGY h PEER REVIEWED

h Murmurs: Caused by turbulence disturbing h Intensity


the normal laminar flow of blood, which • Murmurs are graded on a scale of 1 to 6.
most often is caused by dysfunctional valves This scale can be subjective and may vary
or septal defects. Can also have physiologic between observers.
causes because of patient size, athletic abil- – Grade 1/6: Softest murmur audible. May
ity, or underlying noncardiac disease pro- only be heard in a quiet room after listen-
cesses (eg, fever, anemia)13 ing for several minutes. May not be audi-
ble to all observers, and may be transient
Characterization of murmurs is based on – Grade 2/6: Soft but more easily heard.
several criteria: Often focal over one valve only
h Timing in the cycle: A systolic murmur – Grade 3/6: Prominent and easily heard.
occurs between S1 and S2 and is common in May radiate to other areas
small animals. A diastolic murmur occurs – Grade 4/6: Loud and radiates widely. Not
between S2 of one beat and S1 of the follow- accompanied by a palpable thrill
ing beat and is uncommon in small ani- – Grade 5/6: Loud and accompanied by a
mals. A continuous murmur can be heard palpable thrill
throughout the cardiac cycle (Table 1). – Grade 6/6: Loud, accompanied by a pal-
h Location: Location or point of maximal pable thrill, and can be heard with the
intensity (PMI) refers to the valve area at stethoscope barely touching the thorax
which the murmur is heard loudest. Recog- • Innocent murmurs are soft, systolic,
nition of the PMI can help identify the spe- heard best at the mitral or aortic valves,
cific cardiac abnormality (Table 2; Figures and often low-grade (grade 1). They do not
1-5, page 96). radiate. They are often auscultated in
young puppies and kittens and usually
disappear by 3 to 4 months of age.
• Physiologic murmurs are soft and usually
TABLE 1 of low intensity (grade 1-2). PMI is at the
heart base in the area of the outflow tracts
(aortic and pulmonic area). These murmurs
COMMON PATHOLOGIC CAUSES
OF MURMURS BASED ON TIMING7 typically resolve with resolution of the
underlying disease. They may also be heard
in otherwise healthy animals that are deep
chested and/or athletic. They do not indi-
Murmur Type Pathologic Cause
cate any underlying cardiac disorder that
can be identified by chest radiography or
Systolic murmur Atrioventricular valve regurgitation
echocardiography and are common in ani-
Left-to-right shunt
Increased flow (hyperthyroidism) mals with anemia and occurs as a result of
Aortic or pulmonic stenosis changes in blood viscosity.
Ventricular septal defect/atrial septal defect h Character: Most murmurs have character-
(often not audible) istic sounds on auscultation:7
Diastolic murmur Aortic regurgitation • Harsh or regurgitant: Mimicked by placing
Pulmonary regurgitation the back of the tongue close to the roof of
Mitral stenosis the mouth and blowing out forcefully. Heard
Endocarditis in patients with ventricular septal defects
and atrioventricular valve insufficiency
Continuous murmur Patent ductus arteriosus
• Blowing: Mimicked by blowing air with

94 cliniciansbrief.com May 2017


TABLE 2

LOCALIZATION OF MURMURS IN COMMON CARDIAC LESIONS7

Condition Left Base Right Base Left Apex Right Apex Right Sternum

Mitral regurgitation Systolic PMI (+/- Systolic referred)

Tricuspid regurgitation Systolic PMI

Aortic regurgitation Diastolic PMI +/- Diastolic (Diastolic referred)

Aortic stenosis Systolic PMI +/- Systolic +/- Systolic

Pulmonic stenosis Systolic PMI

Ventricular septal defect +/- Systolic (often not heard) Systolic PMI

Atrial septal defect +/- Systolic (often not heard)

Tetralogy of Fallot Systolic PMI +/- Systolic

Patent ductus arteriosus Continuous PMI

moderate force through slightly parted sympathetic tone and usually increases as
lips. Often heard in patients with aortic or heart rate increases. The murmur can disap-
pulmonic insufficiency pear entirely when sympathetic stimulation
• Machinery: Sounds like the wind blowing abates and heart rate slows. A murmur may
through a tunnel. Most often heard in be audible on initial auscultation and may
patients with patent ductus arteriosus soften or disappear as the patient relaxes
• Systolic clicks: High frequency sounds during the examination.
heard over the left apex that may indicate
mitral valve disease Hypertrophic cardiomyopathy and systolic
• Crescendo-decrescendo: An ejection mur- anterior motion of the mitral valve are the
mur most common in patients with atrial most common diagnoses in cats with mur-
septal defects and aortic or pulmonic murs caused by heart disease.14-16 Because
stenosis benign murmurs and murmurs caused by car-
diac disease are dynamic and audibly indis-
Heart murmurs are present in approximately tinguishable, further evaluation is warranted
one-third of apparently healthy adult cats.14-16 when a murmur is detected.17
The intensity of these murmurs can vary with
Abdominal Palpation
Visit cliniciansbrief.com/cardiac-library to Ascites and/or liver enlargement may be
hear a collection of heart sounds associated present in patients with right-sided heart PMI = point of
maximal intensity
with clinical diagnoses. failure.

May 2017 cliniciansbrief.com 95


PROCEDURES PRO h CARDIOLOGY h PEER REVIEWED

STEP-BY-STEP
CARDIAC AUSCULTATION

Cardiac auscultation is best performed in a quiet


room with a standing patient. In anxious dogs, pant-
ing sounds can be mistaken for murmurs. Manually
close the dog’s mouth for a short time during auscul-
tation and give panting breaks as needed. Purring in
cats can also be mistaken for a murmur. Distract the
cat with a toy or change the position or location of
the patient to stop purring.

STEP 1
Place the stethoscope over the left cardiac apex
d FIGURE 3 Postmortem photograph of the right side of
(location of ventricles) and base (location of pul-
the heart in the thoracic cavity. A = aortic valve, RA = right
monary and aortic outflow tracts), right cardiac atrium, RV = right ventricle, T = tricuspid valve. Photo courtesy
apex and base, the length of the sternum, and the of Dr. Lisa Farrina, University of Florida College of Veterinary
thoracic inlet. Medicine Department of Pathology

d FIGURE 1 Position of cardiac apex and base in a left canine d FIGURE 4 Canine left thorax. A = aortic valve, LA = left atrium,
thorax. Illustrations by Ally Mandese and used with permission LV = left ventricle, M = mitral valve, P = pulmonic valve

d FIGURE 2 Canine right thorax. A = aortic valve, RA = right d FIGURE 5 Postmortem photograph of the left side of the
atrium, RV = right ventricle, T = tricuspid valve heart in the thoracic cavity. A = aortic valve, LA = left atrium,
M = mitral valve, P = pulmonic valve

96 cliniciansbrief.com May 2017


STEP 2 Conclusion
Cardiac abnormalities can be identified
Auscultate each heart valve at its PMI (Table 3). during a basic cardiac examination that
includes obtaining a complete history and
TABLE 3 performing a thorough physical examination
and simple diagnostics. Creating a list of dif-
STETHOSCOPE PLACEMENT ferential diagnoses based on the information
FOR CARDIAC EXAMINATION gathered during the cardiac examination can
help the clinician make informed decisions
about the appropriate next diagnostic or
Valve Point of Maximal Intensity therapeutic step. n

Mitral Left 5th intercostal space at costochondral junction

Tricuspid Between right intercostal spaces 3-5 just above


costochondral junction

Pulmonic Between left intercostal spaces 2-4 just above sternum PMI = point of maximal intensity

Aortic Within left intercostal space 4-5 just above costrochondral


junction See page 98 for references.

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PROCEDURES PRO h CARDIOLOGY h CONTINUED FROM PAGE 97

References
1. Freeman LM, Rush JE, Kehayias JJ, et al. Nutrition alterations 10. Kvart C, Häggström. Heart sounds and murmurs in dogs
and the effect of fish oil supplementation in dogs with heart and cats. In: Kvart C, Häggström J. Cardiac Auscultation &
failure. J Vet Intern Med. 1998;12(6):440-448. Phonocardiography in Dogs, Horses and Cats; 2002. Accessed
2. Davies C, Shell L. Systemic hypertension. In: Davies C, on Veterinary Information Network, April 18, 2017.
Shell L, eds. Common Small Animal Medical Diagnoses: An 11. Kittleson MD. Specific arrhythmias. In: Kittleson MD, Kienle RD,
Algorithmic Approach. Saunders; 2002. Accessed on Veterinary eds. Small Animal Cardiovascular Medicine. Maryland Heights,
Information Network, April 18, 2017. MO: Mosby Elsevier; 2005. Accessed on Veterinary Information
3. Kittleson MD. Diagnosis. In: Kittleson MD, Kienle RD, eds. Small Network, April 18, 2017.
Animal Cardiovascular Medicine. Maryland Heights, MO: Mosby 12. Hanås S, Tidholm A, Egenvall A, Holst BS. Twenty-four hour
Elsevier; 2005. Accessed on Veterinary Information Network, Holter monitoring of unsedated healthy cats in the home
April 18, 2017. environment. J Vet Cardiol. 2009;11(1):17-22.
4. Glickman LT, Glickman NW, Moore GE, Goldstein GS, Lewis HB. 13. Kvart C, Häggström J. Heart sounds and murmurs in dogs and
Evaluation of the risk of endocarditis and other cardiovascular cats: physiological flow murmurs. In: Kvart C, Häggström J.
events on the basis of the severity of periodontal disease in Cardiac Auscultation & Phonocardiography in Dogs, Horses and
dogs. J Am Vet Med Assoc. 2009;234(4):486-494. Cats; 2002. Accessed on Veterinary Information Network, April
5. Tappin SW. Canine tracheal collapse. J Small Anim Pract. 18, 2017.
2016;57(1):9-17. 14. Paige CF, Abbott JA, Elvinger F, Pyle RL. Prevalence of
6. Porciello F, Rishniw M, Ljungvall I, Ferasin L, Haggstrom J, cardiomyopathy in apparently healthy cats. J Am Vet Med
Ohad DG. Sleeping and resting respiratory rates in dogs and Assoc. 2009;234(11):1398-1403.
cats with medically-controlled left-sided congestive heart 15. Wagner T, Fuentes VL, Payne JR, McDermott N, Brodbelt D.
failure. Vet J. 2016;207:164-168. Comparison of auscultatory and echocardiographic findings
7. Kittleson MD, Kienle RD. Physical exam. In: Kittleson MD, in healthy adult cats. J Vet Cardiol. 2010;12(3):171-182.
Kienle RD, eds. Small Animal Cardiovascular Medicine. 16. Nakumura RK, Rishniw M, King MK, Sammarco CD. Prevalence
Maryland Heights, MO: Mosby Elsevier; 2005. Accessed on of echocardiographic evidence of cardiac disease in
Veterinary Information Network, April 18, 2017. apparently healthy cats with murmurs. J Feline Med Surg.
8. Ware WA. Clinical manifestations of cardiac disease. In: Nelson 2011;13(4):266-271.
RW, Couto CG, eds. Small Animal Internal Medicine. 5th ed. St. 17. Côté E, Manning AM, Emerson D, Laste NJ, Malakoff RL,
Louis, MO: Elsevier; 2014:6. Harpster NK. Assessment of the prevalence of heart murmurs
9. Ferasin L. How to measure blood pressure. Presented at: in overtly healthy cats. J Am Vet Med Assoc. 2004;225(3):384-
British Small Animal Veterinary Congress; 2011. Accessed on 388.
Veterinary Information Network, April 18, 2017.

TALKING POINTS h CONTINUED FROM PAGE 85

References
1. Freeman LM, Chandler ML, Hamper BA, Weeth LP. Current dogs and cats, and retail raw meat pet food in the Manawatu,
knowledge about the risks and benefits of raw meat-based New Zealand. Zoonoses Public Health. 2016. doi: 10.1111/
diets for dogs and cats. J Vet Intern Med. 2013;243(11):1549- zph.12323
1558. 10. Stiver L, Frazier KS, Mauel MJ, Styer EL. Septicemic
2. Weese JS. Worms & Germs Blog. http://www. salmonellosis in two cats fed a raw meat diet. J Am Anim
wormsandgermsblog.com Hosp Assoc. 2003;39(6):538-542.
3. Chengappa MM, Staats J, Oberst RD, Gabbert NH, McVey S. 11. Morley PS, Strohmeyer RA, Tankson JD, et al. Evaluation of
Prevalence of Salmonella in raw meat used in diets of racing the association between feeding raw meat and Salmonella
greyhounds. J Vet Diagn Invest. 1993;5(3):372-377. enterica infections at a Greyhound breeding facility. J Am Vet
4. Joff DJ, Schlesinger DP. Preliminary assessment of the risk of Med Assoc. 2006;228(10):1524-1532.
Salmonella infection in dogs fed raw chicken diets. Can Vet J. 12. Centers for Disease Control and Prevention. Human
2002;43(6):441-442. salmonellosis associated with animal-derived pet treats—
5. Finley R, Reid-Smith R, Ribble C, Popa M, Vandermeer M, United States and Canada, 2005. MMWR Morb Mortal Wkly
Aramini J. The occurrence and antimicrobial susceptibility of Rep. 2006;55(25):702-705.
salmonellae isolated from commercially available canine raw 13. Finley R, Reid-Smith R, Weese JS. Human health implications
food diets in three Canadian cities. Zoonoses Public Health. of Salmonella-contaminated natural pet treats and raw pet
2008;55(8-10):462-469. food. Clin Infect Dis. 2006;42(5):686-691.
6. Nemser SM, Doran T, Grabenstein M, et al. Investigation of 14. Pitout JD, Reisbig MD, Mulvey M, et al. Association between
Listeria, Salmonella, and Toxigenic Escherichia coli in various handling of pet treats and infection with Salmonella enterica
pet foods. Foodborne Pathog Dis. 2014;11(9):706-709. serotype newport expressing the AmpC beta-lactamase,
7. Strohmeyer RA, Morley PS, Hyatt DR, Dargatz DA, Scorza CMY-2. J Clin Microbiol. 2003;41(10):4578-4582.
AV, Lappin MR. Evaluation of bacterial and protozoal 15. Cavallo SJ, Daly ER, Seiferth J, et al. Human outbreak
contamination of commercially available raw meat diets for of Salmonella typhimurium associated with exposure to
dogs. J Am Vet Med Assoc. 2006;228(4):537-542. locally made chicken jerky pet treats, New Hampshire, 2013.
8. Weese JS, Rousseau J, Arroyo L. Bacteriological evaluation Foodborne Pathog Dis. 2015;12(5):441-446.
of commercial canine and feline raw diets. Can Vet J. 16. Fauth E, Freeman LM, Cornjeo L, Markovich JE, Janecko N,
2005;46(6):513-516. Weese JS. Salmonella bacteriuria in a cat fed a Salmonella-
9. Bojanić K, Midwinter AC, Marshall JC, Rogers LE, Biggs PJ, contaminated diet. J Am Vet Med Assoc. 2015;247(5):525-530.
Acke E. Isolation of Campylobacter spp. from client-owned

98 cliniciansbrief.com May 2017


CARDIOMIOPATÍA ARRITMOGÉNICA DEL BÓXER

Laín García y J. Alberto Montoya-Alonso

Facultad de Veterinaria

Universidad de Las Palmas de Gran Canaria

ESPAÑA

 Premio al mejor artículo científico divulgativo veterinario del año


2016, que concede la Real Academia de Ciencias Veterinarias de
España (RACVE) perteneciente al Instituto de España.

Resumen:

El objetivo de este artículo es dar a conocer una cardiomiopatía


relativamente habitual en los perros de raza Bóxer llamada cardiomiopatía
arritmogénica del ventrículo derecho. Se trata de una enfermedad hereditaria
asociada a una serie de mutaciones genéticas que provocan un proceso
degenerativo del miocardio con infiltración fibro-adiposa principalmente en el
ventrículo derecho. Es una enfermedad de tipo eléctrico por lo que, en fases
iniciales no se detectan alteraciones en la radiografía o la ecocardiografía. El
signo clínico más habitual es la presencia de síncopes e intolerancia al
ejercicio, aunque a veces el primer síntoma puede ser una muerte súbita. Se
diagnostica a partir de antecedentes familiares, signos clínicos, alteraciones
en el electrocardiograma y/o registro Holter (complejos ventriculares
prematuros (CVP) derechos), tests genéticos y/o biopsia del miocardio. Esta
última normalmente se realiza post mortem. El fármaco de elección para
reducir el número de CVP es el sotalol. La reducción en el número de
arritmias no implica una reducción del riesgo de muerte súbita. El pronóstico
es más favorable en pacientes jóvenes que no presenten síncopes.

Introducción
1
La cardiomiopatía arritmogénica del Bóxer (en inglés arrhythmogenic right
ventricular cardiomyopathy, ARVC) es una miopatía primaria hereditaria que
afecta principalmente al ventrículo derecho. Consiste en un proceso
degenerativo del miocardio donde se produce una infiltración fibroadiposa y
una atrofia de los miocitos. Esta miopatía predispone a la aparición de
arritmias, muerte súbita, fallo congestivo derecho, etc…Varios estudios han
demostrado que esta patología es muy similar a la cardiomiopatía
arritmogénica ventricular derecha de humanos.

Tanto las arritmias como otras alteraciones electrolíticas pueden detectarse


incluso antes de que aparezcan alteraciones histológicas o disfunción
ventricular. La progresión de la enfermedad no sigue un proceso continuo
sino que se alternan periodos de estabilidad con periodos donde aparecen
arritmias de forma más recurrente. En medicina humana se ha constatado
que ciertos factores ambientales como el ejercicio intenso o procesos que
cursan con inflamación pueden predisponer a la progresión de la
enfermedad. En fases avanzadas, la cardiomiopatía del ventrículo derecho o
la progresión de la afectación hacia el ventrículo izquierdo pueden provocar
la presencia de fallo cardíaco derecho o biventricular. Suele detectarse más
habitualmente en pacientes jóvenes y atletas, los cuales pueden sufrir
muerte súbita asociada a fibrilación ventricular. Se sospecha que estagrave
arritmia puede estar relacionada con apoptosis aguda e inflamación reactiva
de los miocitos.

La cardiomiopatía arritmogénica del Bóxer es una enfermedad hereditaria


genética de transmisión autosómica dominante que se manifiesta en edad
adulta. En humana se ha constatado que existen más de 1400 variantes en
12 genes relacionados con esta cardiomiopatía. De éstas, solamente 411
variantes se han confirmado como patológicas siendo la significancia del
resto todavía desconocida.

Presentación clínica y diagnóstico

2
La presentación clínica de esta patología se puede clasificar en tres posibles
categorías en cuanto al cuadro clínico:

1, perros asintomáticos con arritmias ventriculares ocasionales;

2, perros con taquiarritmias, síncopes e intolerancia al ejercicio;

3, perros con disfunción sistólica miocárdica, insuficiencia cardíaca


congestiva y evidencia de dilatación ventricular izquierda; esta tercera
categoría presenta una incidencia mucho menor respecto a las anteriores.

El motivo principal de visita son los episodios sincopales. El examen físico


suele ser normal, aunque en ocasiones el primer signo clínico es la muerte
súbita del animal. Se pueden auscultar arritmias, y en los pacientes con fallo
sistólico detectarse soplos de regurgitación mitral y tricúspide, edema
pulmonar, taquipnea, crepitaciones pulmonares, ascitis y pulso yugular
positivo.

Recientemente se han desarrollado tests genéticos de diagnóstico que son


capaces de identificar algunas variantes de alteraciones genéticas asociadas
a la patología (http://www.ncstatevets.org/genetics/boxerarvc/). De todos
modos, normalmente el diagnóstico se realiza a partir de la combinación de
varios factores como los antecedentes familiares, la presencia de síncopes o
intolerancia al ejercicio, la detección de extrasístoles ventriculares o
taquicardia ventricular principalmente de morfología derecha, y sobre todo a
partir del estudio anatomopatológico del miocardio.

En la mayoría depacientes afectados el examen físico es completamente


normal. En ocasiones se puede auscultar la presencia de latidos prematuros.
En caso de auscultar un soplo hay que tener en cuenta que los perros de
raza Bóxer pueden presentar soplos fisiológicos debido a su anatomía
cardíaca, o bien estar asociados a una estenosis aórtica. Los pacientes con
ARVC no suelen presentar soplos excepto en la forma donde existe
disfunción sistólica.

Las radiografías suelen ser normales excepto si existe fallo sistólico con
insuficiencia cardíaca congestiva. Normalmente no se aprecian alteraciones

3
estructurales o hemodinámicamente significativas en la ecocardiografía, no
obstante, en algunos casos, se puede detectar dilatación y cierto grado de
disfunción ventricular derecha. En los pacientes de categoría 3 puede haber
también fallo sistólico ventricular izquierdo (dilatación ventricular, fracción de
acortamiento disminuida, etc…) y fallo cardíaco congestivo.

En el electrocardiograma (ECG) suelen aparecer complejos ventriculares


prematuros (CVP) derechos (morfología similar a los bloqueos de rama
izquierda) en las derivaciones I, II y III. Las arritmias se pueden clasificar en
4 grados según su gravedad:

1, CVP simples aislados (ver Figura 1);

2, Bigeminismo, trigeminismo o ambos;

3, parejas ventriculares, tripletes o ambos;

4, fenómeno de R en T, taquicardia ventricular o ambos (ver Figura 2).

Figura 1. Electrocardiograma con un complejo ventricular prematuro derecho


aislado.

4
Figura 2. Taquicardia ventricular paroxística derecha.

De todos modos, el ECG tiene ciertas limitaciones a la hora de detectar


arritmias ya que a menudo se presentan de forma intermitente a lo largo del
día y por lo tanto esta prueba complementaria de diagnóstico solamente
permite analizar un breve período de tiempo de pocos minutos. Por lo tanto
el ECG presenta una buena especificidad pero una baja sensibilidad.

La presencia de CVP en el ECG es motivo suficiente para recomendar el


estudio mediante registro Holter de 24 horas. El registro Holter es el método
de elección para detectar arritmias de naturaleza intermitente ya que permite
periodos de evaluación mucho más largos y en un entorno habitual para el
paciente, sin el estrés que puede padecer cuando acuden a la consulta (ver
Figura 3).

5
Figura 3. Bóxer tras la colocación del dispositivo Holter.

Algunos criadores utilizan esta prueba para realizar un screening de sus


animales y detectar pacientes enfermos asintomáticos. Se han descrito
diferentes sistemas de gradación en cuanto a la gravedad de la enfermedad
en función del recuento de CVP (ver Tabla 1) (ver Figura 4).

6
Figura 4. Registro Holter. Presencia de complejos ventriculares.

Análisis del registro Holter según el recuento de complejos ventriculares


prematuros y episodios de taquicardia ventricular

Holter clase 1 <1000 CVPs simples/24h


Holter clase 2 >1000 CVPs simples /24h
Holter clase 3 <1000 CVPs simples /24h, parejas, tripletes, TV
Holter clase 4 >1000 CVPs simples /24h, parejas, tripletes, TV
TV clase I <200 TV en 24 horas
TV clase II >200 TV en 24 horas
CVP clase A <10000 CVPs en 24 horas
CVP clase B >10000 CVPs en 24 horas

CVPs, complejos ventriculares prematuros; TV, taquicardia ventricular

Tabla 1. Clasificaciones a partir del registro Holter para Bóxers con cardiomiopatía
arritmogénica.

Es importante destacar que, en ocasiones, el registro Holter en un paciente


con ARVC puede no ser concluyente ya que en un estudio realizado con
Bóxer se vio que diariamente existe una variabilidad de hasta el 83% en el
número de CVP que se generan. En tal situación se puede realizar un
segundo estudio Holter o bien antes descartar otras posibles causas de
síncope.

A nivel macroscópico la mayoría de los pacientes presentan un corazón de


aspecto normal, aunque a veces se puede detectar dilatación del ventrículo
derecho o incluso del izquierdo.

7
Estudios realizados a nivel microscópico han determinado que en los Bóxer
afectados existe una importante pérdida de la estructura miocítica del
ventrículo derecho debido a la presencia de infiltrados adiposos o fibro-
adiposos (ver Figura 5). Estos infiltrados también se han detectado en ambos
atrios y en el ventrículo izquierdo. La cantidad de infiltrados en el ventrículo
derecho resultó significativamente mucho mayor en pacientes afectados en
comparación con el grupo control.

Figura 5. Histopatología. Detalle de infiltrados adiposos en ventrículo derecho.

En algunos pacientes afectados se han identificado zonas de miocarditis con


infiltrados linfocíticos multifocales, así como evidencias histológicas de
apoptosis en los miocitos del ventrículo derecho. Algunos investigadores
consideran que los patrones adiposo y fibroadiposo constituyen una
situación clínica evolutiva de la enfermedad mediada por la presencia de
miocarditis, la cual en una fase inicial (forma adiposa) provoca un daño a
nivel miocítico que evoluciona al segundo estadio de la enfermedad (forma
fibroadiposa) debido al efecto reparador sobre el daño ocasionado.

En cuanto a la utilización de marcadores de daño miocárdico se ha visto que


existen niveles elevados de troponina cardiaca I (cTnI) sérica en Bóxer con
ARVC. Se cree que la elevación de los niveles séricos de cTnI se debe a la

8
miocitolisis, atrofia miocárdica y degeneración de las fibras musculares que
presentan los perros afectados. Otros estudios demuestran que la
concentración del marcador péptido natriurético cerebral (BNP) no puede
utilizarse como indicador de ARVC en Bóxer ya que no existe una diferencia
significativa entre animales enfermos y sanos.

Tratamiento

La mayoría de perros afectados no desarrollan disfunción sistólica ni fallo


cardiaco por lo que el tratamiento consiste básicamente en utilizar
antiarrítmicos ventriculares. En pacientes asintomáticos se debe iniciar el
tratamiento deforma inmediata si aparecen más de 1000 CVP en 24 horas, si
hay episodios de taquicardia ventricular, o si se detecta el fenómeno de R en
T. Los pacientes con síncopes o intolerancia al ejercicio idealmente deberían
empezar a medicarse tras haber realizado el registro Holter de 24 horas. En
algunos casos, si los síncopes son frecuentes o se detecta taquicardia
ventricular en el ECG es preferible iniciar el tratamiento lo antes posible.

El objetivo del tratamiento consiste en controlar la frecuencia de aparición de


arritmias malignas y prevenir el riesgo de muerte súbita. Se han descrito
diferentes protocolos antiarrítmicos en perros con ARVC, así como la
implantación de desfibriladores cardio-versores.

Tanto en medicina humana como en veterinaria el antiarrítmico de elección


en pacientes con cardiomiopatía aritmogénica del ventrículo derecho es el
sotalol. Se trata de un beta-bloqueante no selectivo de clase III que es muy
eficaz en la reducción del recuento de arritmias y no suele generar un efecto
pro-arrítmico. La administración de sotalol (1.5-3.5 mg/kg/12h) o bien la
combinación de mexiletina (5-8 mg/kg/8h) junto a atenolol (0.3-0.6
mg/kg/12h) son las pautas terapéuticas más eficaces. Tras 2-3 semanas de
tratamiento se debe realizar un segundo Holter para valorar la eficacia del
fármaco y descartar un efecto proarrítmico del mismo. Se considera que la
medicación está ejerciendo un efecto terapéutico si se observa una
reducción del 85% como mínimo en el número de CVP.También se ha

9
demostrado la eficacia de los ácidos grasos omega-3 presentes en aceites
de pescado como tratamiento para reducir el recuento de arritmias
ventriculares en Bóxer con cardiomiopatía arritmogénica.

Pronóstico

Ningún tratamiento probado es capaz de reducir la incidencia de síncopes ni


el riesgo de muerte súbita. Así mismo, en un estudio retrospectivo realizado
con una población de 62 Bóxer se vio que no había diferencias
estadísticamente significativas según el tratamiento farmacológico
administrado.

En cuanto al pronóstico algunos perros fallecen a consecuencia de una


arritmia grave sin mostrar signos clínicos previamente. Por lo tanto, la
ausencia de signos clínicos no significa que no exista riesgo de muerte
súbita. Mientras algunos pacientes con un número anormal de ectopias
nunca desarrollarán signos clínicos, otros con el mismo grado de afectación
pueden progresar y desarrollar arritmias más graves. En cuanto al tiempo
medio de supervivencia, es superior en perros jóvenes (p<0,001), y en
pacientes sin síncopes (p=0,012) [365 días en Bóxer con síncopes versus
693 días en Bóxer sin síncopes]. Además, la probabilidad de fallecer antes
de un año a partir del momento de diagnóstico es 4,8 veces superior en
perros con síncopes. Por lo tanto, el mejor pronóstico es para pacientes
jóvenes sin presencia de síncopes.

Referencias bibliográficas

1. Avramides D, Protonotarios N, Asimaki A, et al. Arrhythmogenic Right


Ventricular Cardiomyopathy/Dysplasia. Hellenic J Cardiology (2011) 52,
452-461.

10
2. Basso C, Fox PR, Meurs KM, et al. Arrhythmogenic Right Ventricular
Cardiomyopathy Causing Sudden Cardiac Death in Boxer Dogs. A New
Animal Model of Human Disease. Circulation (2004) 109, 1180-11.

3. Baumwart RD, Meurs KM, Atkins CE, et al. Clinical, echocardiographic


and electrocardiographic abnormalities in Boxers with cardiomyopathy
and left ventricular systolic dysfunction: 48 cases (1985-2003). J Am Vet
Med Assoc (2005) 226, 538-541.

4. Caro-Vadillo A, García-Guasch L, Carretón E, et al. Arrhythmogenic right


ventricular cardiomyopathy in Boxer dogs: a retrospective study of
survival. Vet Record (2013). doi: 10.1136/vr.100937.

5. Hariu CD, Carpenter D. Arrhythmogenic right ventricular cardiomyopathy


in Boxers. Compendium: continuing Education for Veterinarians (2010) pp:
E2-E7.

6. Meurs KM, Spier AW, Wright NA, et al. Comparison of the effects of four
antiarrhythmic treatments for familial ventricular arrhythmias in Boxers. J
Am Vet Med Assoc (2002) 221, 522-527.

7. Meurs KM. Boxer dog cardiomyopathy: an update. Vet Clin N Am Small


Anim Pract (2004) 34, 1235-1244.

8. Meurs KM, Lahmers S, Keene BW. Characteristics of ARVC Boxer with


sudden death. Proceedings of the ACVIM Forum. Denver, USA. June 15-
18 2011, p 649.

9. Nelson OL, Lahmers S, Schneider T, et al. The Use of an Implantable


Cardioverter Defibrillator in a Boxer Dog to Control Clinical Signs of
Arrhythmogenic Right Ventricular Cardiomyopathy. J Vet Intern Med
(2006) 20, 1232–1237.

11
10. Palermo V, Stafford Johnson MJ, Sala E, et al. Cardiomyopathy in Boxer
dogs: A retrospective study of the clinical presentation, diagnostic findings
and survival. Journal of Veterinary Cardiology (2011) 13, 45-55.

11. Smith CE, Freeman LM, Rush JE, et al. Omega-3 Fatty Acids in Boxer
Dogs with Arrhythmogenic Right Ventricular Cardiomyopathy. J Vet Intern
Med (2007) 21, 265–273.

12
Paper

Paper
Arrhythmogenic right ventricular
cardiomyopathy in boxer dogs: a retrospective
study of survival
A. Caro-Vadillo, L. García-Guasch, E. Carretón, J. A. Montoya-Alonso, J. Manubens

The aim of the present study was to retrospectively evaluate survival in a population of
62 boxer dogs with arrhythmogenic right ventricular cardiomyopathy (ARVC), without left
ventricular systolic failure, based on the following factors: age at diagnosis, presence of
syncopal episodes, Holter arrhythmia classification and administered treatment. Medical
records of boxer dogs with a diagnosis of ARVC between 2000 and 2010 were reviewed.
Results showed that median survival time (MST) was longer in younger ARVC dogs than in the
older ones P<0.001). MST was statistically different (P=0.012) between dogs with syncope
(365 days) and dogs without syncope episodes (693 days), the probability of death within
a year being 4.8 times greater in dogs with syncope (95% CI 1.48 to 15.99) than in dogs
without syncope. Regarding Holter classification results, MST was 547.5 days in Holter
class-2 dogs and 365 days in Holter class-4 dogs (P=0.030). There were no differences
regarding treatment options; MST was 365 days (95% CI 193.615 to 536.4) in the sotalol
group, 365 days (95% CI 92.86 to 637.14) in the mexiletine plus atenolol group, and 547.50
days (95% CI 170.45 to 924.55) in the procainamide group (P=0.383). According to this study,
the best prognosis is for the younger boxer dog without syncope. There were no differences in
survival times in relation to the different treatment options used.

Introduction the early phase, individuals are often asymptomatic but can be at risk
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a famil- of sudden cardiac death. Later, individuals present with symptomatic
ial primary myocardial disease in the boxer dog characterised by the arrhythmias, and right ventricular morphological abnormalities in
progressive replacement of ventricular myocardium (primarily right conventional imaging (Azaouagh and others 2011).
ventricular myocardium) with fatty or fibrofatty tissue which leads to These changes are frequently associated with inflammatory infil-
right ventricular failure, arrhythmias and sudden cardiac death (Meurs trates, which probably play a major part in triggering life-threatening
and others 1999, 2011, Basso and others 2004, 2009, Meurs 2004, arrhythmias. Whether the inflammatory cells are a reaction to cell
2005, Baumwart and others 2005, Hariu and Carpenter 2010, Nakao death (either necrosis or apoptosis) or the consequence of infective
and others 2011, Palermo and others 2011). or immune mechanisms is not known. The role of inflammation
Several researchers have demonstrated that this disease has strik- in ARVC in human beings is unresolved, although inflammation
ing similarities to a human myocardial disease called ARVC (Basso may contribute to disease progression (Azaouagh and others 2011,
and others 2004). Pinamonti and others 2011).
In human beings, arrhythmias and other electrocardiographic Disease progression may result in biventricular heart failure (HF).
abnormalities can be present before histological evidence of myocytes The progressive loss of the right ventricular myocardium can impair
degeneration or clinical presence of right ventricular dysfunction. In the function of the right ventricle and lead to severe pump failure.
When ARVC involves the ventricular septum and the left ventricle,
congestive HF occurs (Azaouagh and others 2011, Pinamonti and
Veterinary Record (2013) doi: 10.1136/vr.100937 others 2011).
Electrical impulse could be interfered with by the fibrofatty
A. Caro-Vadillo, DVM, PhD, de Gran Canaria, Las Palmas de Gran replacement, and this is the cause of ventricular arrhythmias in
Faculty of Veterinary Medicine, Canaria, Arucas, Gran Canaria, Spain human beings. It has been described that the disease progression is
Medicina y Cirugía Animal, University not a continuous process; there are periodic bursts and stable phases.
E-mail for correspondence:
Complutense of Madrid, Madrid, Spain This disease deterioration can be clinically silent in most patients, but
aliciac@vet.ucm.es
L. García-Guasch, DVM, PhD, sometimes the patients suffer life-threatening arrhythmias. It has been
J. Manubens, DVM, Provenance: Not commissioned; described that different environmental factors, exercise or inflamma-
Department of Cardiology and externally peer reviewed tion, might facilitate disease progression. Young people and athletes
Respiratory, Hospital Veterinari Molins, with asymptomatic ARVC can suffer instantaneous sudden death due
Accepted December 18, 2012
Barcelona, Spain to ventricular fibrillation (VF). VF in these patients, is most likely to
E. Carretón, DVM, be related to acute myocyte death and reactive inflammation. In older
J. A. Montoya-Alonso, DVM, PhD, patients with ARVC, VF seems to be infrequent, who more often
Internal Medicine, Faculty of Veterinary have haemodynamically stable ventricular tachycardia (VT) (Basso
Medicine, University of Las Palmas and others 2009, Pinamonti and others 2011).
Paper

ARVC in boxer dogs is a familial disease apparently inherited as an cases (Bonagura and Luis Fuentes 2000, Cunningham and others
autosomal dominant trait (Meurs and others 1999). It is an adult-onset 2008, Boon 2011).
myocardial disease. Harpster described three forms of the disease: Thus, the dogs included in the present study represent the cat-
concealed, overt and myocardial dysfunction. Affected dogs can have egory 1 and category 2 forms of Harpster’s boxer cardiomyopathy
many different presentations ranging from being totally asymptomatic classification (Harpster 1983).
to sudden cardiac death. It is not clear if these forms represent a con- In this study, a modification of the Holter ventricular arrhythmia
tinuum of the disease, especially the two first forms (Harpster 1983). classification defined by Palermo and others (2011), has been used as
Clinically, the disease is characterised by the development of ven- detailed in Table 1.
tricular tachyarrhythmias. The concealed form is characterised by an Dogs with echocardiographic signs of mitral valve disease, con-
asymptomatic dog with occasional ventricular premature complexes genital heart disease (Ebstein anomaly, atrial septal defect), myocar-
(VPCs). The VPCs usually show a left bundle branch configuration. dial failure due to supraventricular tachycardia (with normal myo-
The overt form is characterised by VT and syncope or exercise intol- cardial function after control of the tachyarrhythmia), pulmonary
erance. The last group developed myocardial systolic dysfunction hypertension or systemic disease with secondary cardiac effects (eg,
(Harpster 1983, Kraus and others 2002, Meurs 2004). hypothyroidism, renal failure) were excluded. A basic blood analysis
Diagnosis of cardiomyopathy is based on a combination of factors was performed to rule out metabolic causes of arrhythmia (eg, anae-
including the presence of syncopal events, ECG and/or Holter abnor- mia, hypokalaemia, hypoxia). Abdominal ultrasonography was per-
malities, echocardiographic findings and a family history of disease formed in some cases as abdominal masses may cause ventricular
(Meurs and others 1999, Smith 2011). arrhythmias.
Treatment considerations usually focus on the use of ventricu- Dogs were classified in different groups according to the number
lar antiarrhythmics. Antiarrhythmic drugs may be prescribed in of VT episodes per day, number of VPCs per day, presence of syn-
an attempt to decrease the number of VPCs and the complexity cope, age at diagnosis and Holter classification as shown in Table 1.
of the arrhythmia. Boxer dogs with ARVC are always at risk of sud- Administered treatments were sotalol (Sotapor, Brystol-Myers Squibb)
den death, so treatment may be useful in preventing this (Meurs and at 1.5–3.5 mg/kg/12 hours orally, mexiletine (Mexitil, Boehringer
others 2002, Meurs 2005, Prosek and others 2006, Thomason and Ingelheim) plus atenolol (Tenormin, AstraZeneca) at 5–8 mg/kg/8 hours
others 2008, Basso and others 2009, Hariu and Carpenter 2010, +0.3–0.6 mg/kg/12hours orally, or procainamide (Biocoryl, Grupo
Avramides and others 2011, Azaouagh and others 2011, Smith 2011). Uriach) at 20–26 mg/kg/8 hours orally.
A reduction in VPCs has been demonstrated with several treat- The clinical progress of each dog was ascertained by telephone
ment protocols including: sotalol, procainamide and a combination interview with the owner. The interviews were conducted by spe-
of mexiletine plus atenolol, both in human (Basso and others 2009, cifically trained senior students, and the results were recorded in an
Friedman and others 2010, Markel and others 2010, Smith 2011, electronic questionnaire. The questionnaire consisted of questions
Avramides and others 2011, Azaouagh and others 2011) and in vet- with a definite number of possible answers, most commonly yes/no.
erinary medicine (Meurs and others 2002, Meurs 2005, Prosek and The interviewer was not blinded to the clinical status of the dog at
others 2006, Gelzer and others 2010). the initial examination. The owner was asked if the dog was dead or
Although several studies have been reported in boxer dogs with alive. If the dog was dead, the owner was asked if the dog had been
ARVC, they failed to provide consistent data regarding the risk stratifi- euthanased or died spontaneously, reasons for euthanasia, and, in case
cation of the disease. However, Palermo and others did look at survival of spontaneous death, the possible causes, including cardiac-related
in a group of boxer dogs with mainly the myocardial dysfunction and sudden death, presence of syncope, or progression of HF were probed.
left ventricular enlargement form of the disease, which were excluded Cardiac-related death was defined as death occurring because of pro-
from this study (Palermo and others 2011). Therefore, the aims of this gression of clinical signs of HF. Dogs that were euthanased because of
study were to retrospectively evaluate survival time in a population of refractory HF, were scored as cardiac-related deaths. In this study, sud-
boxer dogs with ARVC, without left ventricular systolic failure, based den death was defined as death occurring during sleep or activity such
on the following factors: age of diagnosis, presence of syncopal epi- as running, or within two hours after the dog showed sudden signs of
sodes, Holter arrhythmia classification and administered treatment, as HF (dyspnea). Sudden death was regarded as cardiac-related if no other
well as to identify long-term prognostic predictors in a large cohort of cause of death was obvious.
patients with ARVC, specifically focusing on the prognostic impact Data regarding the death was recorded, and survival time was
of Holter class and other clinical parameters. measured from the date of first presentation. Whether the dog’s death
was due to cardiac-related causes (spontaneous death, euthanasia) was
Materials and methods taken into consideration.
Medical records of client-owned boxer dogs referred to the Hospital In this study of survival, we considered only cardiac-related
Veterinario Clínico Complutense (Madrid, Spain), Hospital Clínico deaths, and patients who suffered a non-cardiac death were not includ-
Veterinario Universidad Las Palmas de Gran Canaria (Gran Canaria ed in the study.
island, Spain) and Hospital Veterinari Molins (Barcelona, Spain),
between January 2002 and October 2010 in which a diagnosis of Statistical analysis
ARVC had been made, were reviewed by just one author. The owners The Kaplan-Meier method and plot time to event curves were used to
were informed, and all of them signed an informed consent. estimate survival. Survival time differences were assessed by log Rank
The study was approved by the ethical committee of the
Veterinary Medicine Service of Las Palmas de Gran Canaria
University, and was carried out in accordance with the current TABLE 1: Holter classification, ventricular tachycardia
European legislation on animal protection. classification and ventricular premature complex grading
The diagnosis inclusion criteria included presence of more than for the boxer dog with ARVC included
1000 VPCs in 24 hours Holter recording and normal left ventricular Holter classification, ventricular tachycardia classification and ventricular prema-
chamber on echocardiographic examination. Some dogs also present- ture complex graduation
ed syncope or exercise intolerance and/or VPCs with increased com- Holter class 1 <1000 single VPCs/24 hours
plexity (couplets, triplets) and/or VT. The left ventricular chamber Holter class 2 >1000 single VPCs/24 hours
was considered to be normal when left ventricular systolic and diastol- Holter class 3 <1000 single VPCs/24 hours, couplets, triplets, VT
ic diameters, indexed to body surface area were less than 2.91 cm/m2 Holter class 4 >1000 single VPCs/24 hours, couplets, triplets, VT
VT class I <200 runs/24 hours
and 4.35 cm/m2, respectively. These echocardiographic criteria to
VT class II >200 runs/24 hours
include or exclude dogs in the present study are the same described by VPCs class A <10000/24 hours
Bonagura and Luis Fuentes (2000). These particular indexes are very VPCs class B >10000/24 hours
similar to the indexes included in Cunningham and others (2008).
VT, ventricular tachycardia; VPCs, ventricular premature complexes
Fractional shortening in this group was superior to 25 per cent in all
Paper

A B
1,0 1,0

0,8 0,8

Accum survival
Accum survival
a.(MST=693 days)
0,6 0,6
c.(MST=620 days)

0,4 0,4

b.(MST=15 days)
0,2 0,2
d.(MST=187 days)

0,0 0,0
0 500,0 1000,0 1500,0 2000,0 0 500,0 1000,0 1500,0 2000,0
Days Days

C D
1,0 1,0

0,8 0,8
Accum survival

Accum survival
0,6 e.(MST=547 days) 0,6
g.(MST=693 days)

0,4 0,4

0,2 0,2
f.(MST=365 days)
h.(MST=365 days)

0,0 0,0
0 500,0 1000,0 1500,0 2000,0 0 500,0 1000,0 1500,0 2000,0
Days Days

FIG 1: Kaplan-Meier survival curves in boxer dogs with arrhythmogenic right ventricular cardiomyopathy (ARVC) according to:(A)
ventricular tachycardia (VT) classification. a, Kaplan-Meier survival curve in ARVC dogs, VT class I. b, Kaplan-Meier survival curve in ARVC
dogs, VT class II. (B) ventricular premature complex (VPC) classification. a, Kaplan-Meier survival curve in ARVC dogs, VPC class A. b,
Kaplan-Meier survival curve in ARVC dogs, VPC class B. (C) Holter classification. a, Kaplan-Meier survival curve in ARVC dogs, Holter class
2. b, Kaplan-Meier survival curve in ARVC dogs, Holter class 4. (D) Presence or absence of syncope. a, Kaplan-Meier survival curve in ARVC
dogs without syncope. b, Kaplan-Meier survival curve in ARVC dogs with syncopal episodes

test. The cross-tabs, Fisher’s exact test and odds ratio were used to esti- There was a significant association between survival and the
mate risk of death within a year. A Cox regression multivariable analy- number of VPCs in 24 hours Holter monitoring (P=0.01) with a MST
sis (stepwise method for variable selection) was done. A P value <0.05 of 620 days (mean 706) in dogs with VPCs class A (<10.000/24 hours)
was considered significant. The statistical analyses were performed vs 182 days (mean 360) in dogs with VPCs class B (>10.000/24 hours)
using a commercially available software program: SPSS V.19.0. Table 2, Figure 1B.
There was a significant association between survival and Holter
Results class (P=0.03) with a MST of 547 days (mean 799) in dogs with
A total of 62 boxer dogs of both sexes met the inclusion criteria for the Holter class 2 vs 365 days (mean 485) in dogs with Holter class 4 Table
study. Males were over-represented (63 per cent (39/62) male, 37 per cent 2, Figure 1C.
(23/62) female; ratio 1.7:1). The mean age of presentation was 7.7 years There was a significant association between survival and syncope
old (min: three years, max: 12.2 years). The most common presenting (P=0.012), with a MST of 693 days (mean 445) in dogs without syn-
clinical sign was syncope in 68 per cent (42/62) of the boxer dogs, where- cope vs 365 days (mean 805) in dogs with syncope Table 2, Figure 1D.
as exercise intolerance was present in 24 per cent (15/62) of the dogs. There was a significant association between survival and age at
Twenty-four hours Holter monitoring was performed in all the dogs initiation of treatment (P<0.001) with a MST of 1460 days in dogs
included. The morphology of VPCs was consistent with a right ven- younger than four years at treatment initiation vs 620 days in dogs
tricular origin (left bundle branch block pattern). The majority of dogs between four and eight years and 292 days for dogs older than eight
76 per cent (47/62) were Holter class 4 (>1000 VPCs in 24 hours, with years Table 2 Figure 2.
increased complexity (couplets, triplets) and/or VT. The mean±sd of the There were no differences in survival between males (MST of 457
VPCs in the 62 dogs was 8748.66±7178.975 (min: 1129; max: 21869). days) and females (MST of 650 days) (P=0.345).
The mean±sd of the VT episodies in the 62 dogs was 186.18±341730 There were no differences with regards to survival, among the three
(min: 0; max: 2347). treatment options used (P=0.383), with a MST of 365 days (95% CI
According to inclusion criteria, echocardiography findings were 193.615 to 536.4) (mean 475) for sotalol treatment, a MST of 365 days
normal in 100 per cent of the dogs prior to treatment. (95% CI 92.86 to 637.14) (mean 595) for mexiletine plus atenolol
Median survival time (MST) was 365 days (mean±sd: 561±62.6), treatment and a MST of 547 days (95% CI 170.45 to 924.55) (mean
min: 7 days, max:1971 days for the complete group of patients. 632) for procainamide treatment Table 2.
There was a significant association between survival and VT class The probability of death within a year (odds ratio), of dogs with
(P<0.001), with a MST of 693 days (mean 748) in dogs with VT class VT class II is 20 times greater (95% CI 4 to 99.5; P<0.001) than in the
I (<200 runs/24 hours) vs 15 days (mean 169) in dogs with VT class II group of dogs with VT class I. The probability of death within a year,
(>200 runs/24 hours) Table 2, Figure 1A. of dogs with VPCs class B is 5.43 times greater (95% CI 1.79 to 16.46;
Paper

TABLE 2: Mean and sd of the days of survival in the different groups of boxer dogs with ARVC
MEAN±sd (days)

Age at treatment <4 years 4–8 years >8 years


n=5 n=30 n=27 P<0.001
1262.9±317.7 657.26±81.6 324.31±62.9
Treatment options Sotalol mexiletine+atenolol Procainamide
n=23 n=21 n=18 P=0.564
474.82±394.7 594.8±561 631.9±533.2
Syncope Yes No
n=42 n=20 P=0.012
805.22±129.7 444.86±62.3
Holter class Class 2 Class 4
n=15 n=47 P=0.03
798.66±169.5 485.29±59.6
VT class I II
n=42 n=20 P<0.001
747.6±73.6 169±50
VPCs class A B
n=36 n=26 P=0.01
706.3±82.7 360±82

ARVC, arrhythmogenic right ventricular cardiomyopathy; VT, ventricular tachycardia

P=0.004) than in the group of dogs with VPCs class A. The prob- Mean age at presentation was similar to that reported by Palermo
ability of death within a year, of dogs with Holter class 4 is 2.47 times and others (2011), by Harpster (1983), by Basso and others (2004) and
greater than in dogs with Holter class 2, however, this result was not by Baumwart and others (2005).
statistically significant (95% CI 0.73 to 8.3; P=0.235). The probability The most common clinical sign detected in the present study was
of death within a year, of dogs with syncope is 4.875 times greater syncope (68 per cent of boxer dog). It would be reasonable to suggest
(95% CI 1.48 to 15.99; P=0.013) than in dogs without syncope. that syncope, in this study, is associated with ventricular arrhyth-
The hazard ratio, for the complete duration of the study, calculat- mias. The presence of VT episodies and bradycardias as causes of
ed by Cox proportional hazard multivariable analysis, for VT was 4.8 syncope, coexisting in boxer dogs has been described (Thomason and
(95% CI 2.63 to 8.99; P<0.001). There were no other variables (VPC, others 2008). No evidence of bradycardia was found in the 24 hours
presence/absence of syncope, Holter class) statistically significant for Holter recordings in this study, therefore, in these patients syncope
this Cox proportional stepwise method. should be the result of rapid VT. In the present study, a significant
The hazard ratio, for one year, calculated by Cox proportional risk of death within the first year after the diagnosis in dogs with
hazard multivariable analysis, for VT was 6.05 (95% CI 2.92 to 12.51; syncope versus dogs without syncope has been found. In human
P<0.001). There were no other variables (VPC, presence/absence of patients presenting with syncope for which a diagnosis is not made,
syncope, Holter class) statistically significant for this Cox proportional the likelihood of sudden death is low, other studies would suggest
stepwise method. this is also the case in dogs (Barnett and others 2011). It is useful to
consider the deaths recorded in this study in the light of other studies
Discussion that have been completed which report typical life expectancies of
Boxer dog cardiomyopathy in Spain seems to progress in the same different dog breeds. Eichelberg and Seine (1996), reported an over-
way as the disease in other countries, although some differences have all life expectancy of 10 years based on a sample of 9248 dogs. On
been described between different families of boxer dogs (Palermo and that basis, it might be considered that boxer dogs presenting with
others 2011). collapse, syncope or exercise intolerance are more likely to suffer a
The signalment for the dogs in this study was similar to the premature death.
descriptions in previous publications. Males were over-represented The fact that boxer dogs with ARVC and syncope live for a short-
(Harpster 1983, 1991, Baumwart and others 2005, Meurs and others er time, has been proved in the present study; the probability of death
2011, Palermo and others 2011). within a year is 4.875 times greater for dogs with syncope.

1,0
0-4 years
4,1-8 years
8,1-12 years

0,8
Accum survival

a.(MST=1460 days)
0,6

b.(MST=620 days)
0,4

0,2
c.(MST=292 days)

0,0

0 500,0 1000,0 1500,0 2000,0


Days

FIG 2: Kaplan-Meier survival curves in the different groups of boxer dogs with arrhythmogenic right ventricular cardiomyopathy (ARVC)
according to age of initial diagnosis. (a) Kaplan-Meier survival curve in ARVC dogs younger than four years old. (b) Kaplan-Meier survival
curve in ARVC dogs between four and eight years old. (c) Kaplan-Meier survival curve in ARVC dogs older than eight years
Paper

The presence of frequent VT episodes was associated negatively mic drug (Friedman and others 2010). In human beings, another class
with survival in our study, unlike the findings reported by Palermo III antiarrhythmic drug, amiodarone, was associated with a poor
and others (2011). In human beings, VT is an independent and nega- long-term outcome (Pinamonti and others 2011). However, in another
tive predictor of mortality (Basso and others 2009). In this report, it study, amiodarone had superior efficacy in preventing ventricular
has been found that VT means a high risk of death within one year. arrhythmias (Marcus and others 2009).
It is probable that VT degenerates into VF leading to sudden death in Mexiletine is an orally available class Ib antiarrhythmic drug
the dogs used in this study. The number of VT episodes was the only similar to lidocaine; mexiletine which inhibits fast sodium channels
variable associated with a statistically significant hazard ratio risk of and reduces arrhythmias in canine in vitro models of repolarisation
death. This was probably due to the fact that the total number of abnormalities with triggered activity as well as in human beings with
VPCs and syncope episodes are closely related to the number of VT long QT wave syndrome. Previous antiarrhythmic drug studies in
episodes. boxer dogs found mexiletine to be effective for reduction of VT when
Similarly, the presence of a greater number of VPCs involved a combined with atenolol, with minimal proarrhytmic effects. Atenolol
high risk of death. Although the cut-off value to define the normal alone did not significantly reduce the number of VPCs and arrhyth-
number of VPCs in boxer dog is not determined, it is unusual to have mia grade (Meurs and others 2002). The administration of β-blockers
ventricular ectopy. It has been suggested that a small number of VPCs can aggravate or precipitate bradycardia-related syncope (Thomason
could be normal, especially in older dogs (Palermo and others 2011). and others 2008). However, in this study, a worse prognosis in the
In the present study, a negative correlation between number of VPCs group of dogs treated with either sotalol or atenolol plus mexiletine in
and survival time has been found. comparison with the procainamide group has not been found.
MST was significantly longer in the younger group of dogs at Potential benefits of combination therapy of sotalol with mexile-
the time of diagnosis. ARVC, although genetically determined, is tine have been shown in human clinical trials as well as in German
an acquired and progressive disease which shows an age-related pen- shepherd dogs with inherent ventricular arrhythmias (Prosek and oth-
etrance both in human beings and dogs (Meurs 2005, Basso and oth- ers 2006, Gelzer and others 2010, Smith 2011). This combination has
ers 2009, Avramides and others 2011, Smith 2011). In human beings, not been used in this study.
VF is the mechanism of instantaneous sudden death in young people Procainamide is a class Ia antiarrhytmic drug that affects normal
and athletes with ARVC, and VF is most likely related to a phase and abnormal tissues, with conduction-slowing and vasodilatory
of disease progression, due to acute myocytes death and reactive properties. In human beings, it has been recommended for haemo-
inflammation. dynamically stable ventricular and atrial arrhythmias with preserved
The reason why a better prognosis has been observed in younger ventricular function (Markel and others 2010). Although in some
dogs may be that VF is rare in older patients with long-lasting ARVC situations, procainamide could not eliminate VT, the heart rate is
(Basso and others 2009). In accordance with the results of the present decreased improving haemodynamic stability. The incidence of proar-
study, dogs that lived longer are less prone to sudden death. Despite rhythmia in dogs treated is not known. Although procainamide did
the hypothesis that in dogs the disease progresses over time, the natu- not induce significant reduction in VPCs, it is less expensive than
ral history of boxer dog cardiomyopathy requires further study. So, sotalol and sometimes this justifies its use.
even though this disease seems to be progressive in nature, according As mentioned above, none of the treatment protocols were related
to Harpster, in this report a better survival in younger dogs is found. to survival time. Although proven efficacy in ventricular arrhythmia
Another reason besides lack of evidences of inflammatory response for the treatment protocol used (Meurs and others 2002, Gelzer and
could be that early treatment (drug and restriction of vigorous exer- others 2010, Azaouagh and others 2011, Smith 2011) may be another
cise) was able to slow down the progression of the disease (Basso and factor which could have influenced the survival as neurocardiogenic
others 2009). More studies are needed to clarify this point. bradycardia as inducer of VT or VF (Thomason and others 2008),
It has been described that striatin genotype was significantly asso- progression of the disease to another form or proarrhythmia effects
ciated with sudden death at an earlier age than dogs without sudden of the antiarrhytmic drug used. However, this study detects a direct
death which live longer (Meurs and others 2011). In the present study, relationship in the number and complexity of VPCs and the risk of
genetic studies, to corroborate this possibility as the reason for longer sudden death, therefore, the ability of a treatment to alter the arrhyth-
MST in the younger dogs, were not carried out. mia could have an impact on survival.
Treatment is aimed mainly at the prevention and management According to other studies, the administration of fish oil could
of malignant arrhythmias and sudden death. Different antiarrhyth- decrease ventricular arrhythmia and the risk of sudden death in boxer
mic regimes to treat ARVC in dogs have been described (Meurs and dogs with ARVC (Smith and others 2007). This has not been used in
others 2002) as well as a successful use of an implantable cardiovert- this study.
er-defibrillator in boxer dogs (Nelson and others 2006). Differences In conclusion, MST was significantly longer in young boxer dogs,
between survival times in relation to the treatment options used were in dogs without syncopal episodes and in the VT class I group. As
not found in the current study. The drug chosen for an individual ani- regards therapeutic options, there were no statistically significant dif-
mal is usually selected on the basis of a combination of factors, includ- ferences in MST between the three groups.
ing clinical experience, adverse effects, ease of administration and cost As far as the probability of death within the first year after diagno-
of the drug. In human beings, sotalol proved to be highly effective sis is concerned, this risk is doubled for a cohort of dogs with syncope
in patients with ARVC, and inducible as well as non-inducible VT. and VPCs more than 10000 per day, and six times more for dogs with
D,l-sotalol is a non-selective β-blocker with class III antiarrhythmic VT episodes over 200 per day.
properties. Its antiarrhythmic efficacy has been demonstrated both
in boxer dogs with spontaneous VT as well as human patients with Limitations
VT that were refractory to class I antiarrhythmics (Meurs and others This was a retrospective cohort study with a fixed sample size and
2002, Avramides and others 2011). was susceptible to bias, confounding and incomplete power to detect
The reason for the selection of a β-blocker as a ventricular more modest, yet still clinically important, survival associations.
antiarrhythmic is its effect in modulation of the autonomic nerv- Because of the retrospective nature of the study, most of the dogs
ous system that could be involved in the development of VT. An had not subsequently undergone cardiac evaluations, so we cannot
excitement or exercise trigger for VT in boxer dogs has been reported establish a progression from arrhythmia to other forms of left ven-
(Meurs and others 2011). Patients being treated with sotalol or other tricular dysfunction.
antiarrhythmic drugs that block potassium channels may have an Another limitation was the absence of postmortem examinations
acceptable degree of QT prolongation or develop marked lengthening to assert the final diagnosis of the dogs. Genetic characterisation was
of the QT interval and even torsades de pointes. Such incidents can not available; therefore, potential differences in clinical features and
usually be attributed to development of excessive bradycardia, electro- prognosis impact of different genetic substrates cannot be ascertained.
lyte abnormalities, a decline in renal function, initiation of a new drug In addition, in this study, only clinical and Holter parameters at enrol-
that affects cardiac repolarisation, or metabolism of the antiarrhyth- ment have been analysed since the onset of the disease in the single
Paper

patient is unknown; that kind of evaluation was performed at differ- HARPSTER, N. (1983) Boxer cardiomyopathy. In: Current Veterinary Therapy VIII. Ed.
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HARPSTER, N. (1991) Boxer cardiomyopathy: a review of the long-term benefits
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cardiography with pace-mapping comparison. Journal of Veterinary Internal Medicine 16,
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Arrhythmogenic right ventricular


cardiomyopathy in boxer dogs: a
retrospective study of survival
A. Caro-Vadillo, L. García-Guasch, E. Carretón, et al.

Veterinary Record published online January 12, 2013


doi: 10.1136/vr.100937

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ENFERMEDADES CARDIORRESPIRATORIAS DE PEQUEÑOS ANIMALES

Actualización en hipertensión
pulmonar arterial en perros.
Conceptos básicos
Bernardo Serrano Parreño, DVM.
Elena Carretón Gómez, DVM, MSc, PhD.
J. Alberto Montoya-Alonso, DVM, MSc, MA, PhD.
Servicio de Medicina Veterinaria.
Facultad de Veterinaria de la Universidad de Las Palmas de Gran Canaria
alberto.montoya@ulpgc.es

La hipertensión pulmonar se define como un aumento de la presión arterial diastólica


y/o sistólica de la arteria pulmonar.
La fisiopatología de la hipertensión arterial pulmonar es compleja y multifactorial. Ésta
se produce por una disfunción endotelial que conduce a un desequilibrio de agentes
vasoactivos con predominio de la vasoconstricción.
La clasificación clínica de los pacientes con hipertensión pulmonar se basa
en la causa subyacente de la misma, mientras que la clasificación funcional
agrupa a los pacientes en clases según la gravedad de los signos clínicos
producidos por la hipertensión pulmonar.
Una vez identificada la causa primaria de la hipertensión pulmonar, el trata-
miento es fundamentalmente farmacológico mediante la administración de
fármacos que ayuden a reducir la presión de la arteria pulmonar y la carga
sobre el ventrículo derecho, con el fin de reducir la sintomatología, mejorar
la calidad de vida y el tiempo de supervivencia. Los principales síntomas aso-
ciados a esta patología son disnea, intolerancia al ejercicio, tos y síncopes.

70 Canis et Felis Número 133 - Abril 2015


Actualización en hipertensión pulmonar arterial en perros. Conceptos básicos

INTRODUCCIÓN
La hipertensión pulmonar (HTP) se define como un aumento de la presión
arterial diastólica y/o sistólica a nivel de la circulación pulmonar. De manera
más específica, la HTP puede definirse como sistólica cuando la presión ar-
terial pulmonar sistólica es superior a 30 mm Hg, o bien diastólica cuando
la presión arterial pulmonar diastólica es superior a 15 mm Hg. Aunque es
posible determinar estas presiones de manera directa a través de cateterismo
cardiaco del lado derecho, este procedimiento requiere sedación o anestesia,
siendo un procedimiento invasivo, no exento de riesgo para la vida del animal
y económicamente no accesible para veterinarios y clientes. De forma alter-
nativa, la presión arterial pulmonar puede valorarse mediante ecocardiografía
transtorácica evaluando de forma subjetiva algunas alteraciones, tales como
la dilatación de la arteria pulmonar y de las cámaras derechas, y el análisis
mediante Doppler de la regurgitación de la válvula tricúspide y de la valvular
pulmonar. La HTP puede presentarse como una enfermedad tanto de origen
primario como secundario. Entre las posibles etiologías, se incluyen: 1- pato-
logías que causen aumento de presión en atrio izquierdo, como endocardiosis
mitral y cardiomiopatía dilatada, 2- patologías que supongan sobrecarga de
volumen a nivel de circulación pulmonar, como defectos del septo interven-
tricular o conducto arterioso persistente, 3- patologías que cursen con un
aumento de la resistencia vascular, causada por enfermedades obstructivas
o por oclusión de la circulación pulmonar, como pudiera ser un tumor de
base cardiaca, 4- patologías pulmonares crónicas. En medicina veterinaria, el
incremento de presión a nivel de atrio izquierdo es causa más común de HTP
(45% de los casos).

FISIOPATOLOGÍA
La fisiopatología de la HTP arterial es compleja y multifactorial. Ésta se pro-
duce por una disfunción endotelial que conduce a un desequilibrio de agentes
vasoactivos (endotelina-1, óxido nítrico, prostaciclina, etc.), con predominio de
la vasoconstricción. Comprender los eventos y mecanismos en la constricción
y dilatación de los vasos pulmonares puede ayudar a un mejor enfoque pro-
nóstico y terapéutico del paciente. La hipoxia alveolar es una respuesta se-
cundaria a la vasoconstricción de los vasos pulmonares, la vasoconstricción
permite que la sangre sin oxígeno sea derivada hacia zonas del pulmón que se
encuentran más ventiladas mejorando la ventilación-perfusión. Inicialmen-
te es una respuesta fisiológica favorable pero en condiciones crónicas puede
conducir a HTP.

CLASIFICACIÓN CLÍNICA
Se ha propuesto una clasificación de la HTP basada en la presentación clínica
y las opciones de tratamiento.

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Clase clínica I: Hipertensión arterial pulmonar


Incluye pacientes con enfermedad vascular arteriolar pulmonar. En seres hu-
manos la forma más común es la idiopática. Aunque se ha descrito HTP idiopá-
tica en perros, se trata de una presentación poco habitual; no obstante, existen
referencias de pacientes con HTP en los que no ha podido identificarse una cau-
sa determinada. En perros, las causas más comunes de HTP clase I incluyen
enfermedades congénitas y dirifilatiosis cardiopulmonar.

Clase clínica II: Hipertensión venosa pulmonar


Los pacientes englobados en esta categoría desarrollan una HTP secundaria
a cardiopatías que afectan el lado izquierdo del corazón. Debido a un aumento
de presión en el atrio izquierdo, se produce una elevación en la presión venosa
pulmonar, lo que puede provocar la aparición de edema pulmonar e hipoxia,
así como una HTP reactiva.
Cuando la presión venosa pulmonar excede de 25 mmHg, la presión arterial pul-
monar aumenta en un intento por mantener el flujo sanguíneo pulmonar pero
finalmente se desarrolla hipertrofia arteriolar. La enfermedad cardiaca del lado
izquierdo es la causa más frecuente de HTP, tanto en seres humanos como en
perros. Aunque menos usual, se ha descrito HTP clase II tanto en seres humanos
como en perros con miocarditis y distensión atrial secundaria a fibrilación atrial.

Clasificación clínica III: Enfermedad pulmonar o hipoxia


La HTP también puede ser secundaria a enfermedad pulmonar primaria o
hipoxia crónica. Las enfermedades respiratorias relacionadas más a menudo
con HTP clase III en personas son la enfermedad pulmonar obstructiva cró-
nica, enfermedad intersticial pulmonar y el trastorno respiratorio del sueño.
En perros se asocia a fibrosis pulmonar, neumonía, enfermedad traqueo-
bronquial y neoplasias. Debido a una predisposición racial, hasta 40% de los
WestHighland White Terriers con enfermedad pulmonar intersticial crónica
presentan cierto grado de HTP.

Clase clínica IV: Enfermedad tromboembólica


La HTP clase IV es producida por el desarrollo de trombos o émbolos. En hu-
manos, la obstrucción de la arteria pulmonar se relaciona con tromboembolis-
mos, tumores y cuerpos extraños. En perros, el tromboembolismo pulmonar
se asocia a la presencia de anemia hemolítica inmunomediada, neoplasias,
neuropatías y enteropatías perdedoras de proteínas, hiperadrenocorticismo,
sepsis y traumatismo. Dada la posibilidad de émbolos por gusanos, la diri-
filatiosis cardiopulmonar canina puede incluirse también en esta categoría.

Clase clínica V: Otras causas


La HTP clase V comprende causas diversas de HTP. En personas, la clase V
incluye trastornos que de manera indirecta alteran el flujo sanguíneo cardiaco
(p. ej. policitemia vera primaria), enfermedades granulomatosas y enferme-

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dades que conducen a la destrucción del parénquima pulmonar. En medicina


veterinaria se ha documentado en muy pocas ocasiones; sin embargo, proba-
blemente la situación más habitual sea aquella que cursa con compresión de
la vasculatura pulmonar (por ejemplo, tumores de base cardiaca).

CLASIFICACIÓN FUNCIONAL
Mientras que la clasificación clínica se basa en la causa subyacente de la HTP,
la clasificación funcional agrupa a los pacientes según la gravedad de los sig-
nos clínicos producidos por la HTP.

Clase funcional I
Esta clase incluye pacientes con HTP que no sufren intolerancia al ejercicio y
que pueden ejercitarse sin signos de disnea, fatiga, dolor torácico o síncope.

Clase funcional II
Los pacientes de la clase II no presentan síntomas en reposo pero muestran
una leve disnea, intolerancia al ejercicio, dolor torácico o síncope al realizar
algún tipo de actividad física.

Clase funcional III


La HTP de estos pacientes produce limitaciones notables en el desarrollo de
actividad física y manifiestan intolerancia al ejercicio, disnea, fatiga, dolor to-
rácico y síncopes incluso durante actividad física muy leve; sin embargo, du-
rante el reposo no presentan sintomatología.

Clase funcional IV
Esta clase terminal incluye pacientes con HTP que son incapaces de desa-
rrollar ningún tipo de actividad física, de manera que cualquier ejercicio físico
desemboca en una intensa sintomatología. Estos pacientes son sintomáticos
incluso en reposo y además presentan insuficiencia cardiaca derecha.

DIAGNÓSTICO
1. PRESENTACIÓN CLÍNICA Y EXAMEN FÍSICO
Las alteraciones más frecuentemente observadas durante la auscultación
son un soplo cardiaco por insuficiencia mitral y/o tricuspídea, y un desdobla-
miento de S2, el cual se relaciona normalmente con el cierre de las cúspides
de las válvulas aórtica y pulmonar. También se puede auscultar crepitaciones
pulmonares o sonidos pulmonares broncovesiculares aumentados. Los sín-
tomas a los que con mayor frecuencia hace referencia el propietario son tos,
disnea, letargia, episodios sincopales, intolerancia al ejercicio, ascitis y ciano-
sis. La HTP se presenta con mayor frecuencia en razas pequeñas y en perros
de edad mediana y geriatras.

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2. PRUEBAS DE LABORATORIO

Debe obtenerse un perfil analítico básico para determinar alteraciones hema-


tológicas y serológicas así como un urianálisis. Se recomienda realizar sero-
logía para dirifilatiosis ya que ésta es una de las enfermedades más comunes
relacionadas con HTP en zonas endémicas.

Los hallazgos laboratoriales más comunes suelen ser leucocitosis moderada


(provocado por grandes trombos pulmonares), eritrocitos nucleados (que es
un potencial indicador de hipoxia) y policitemia, además de eosinofilia, baso-
filia, monocitosis y anemia no regenerativa en pacientes con dirifilatiosis. A
su vez puede cursar con trombocitopenia secundaria a coagulación intravas-
cular diseminada, como hallazgo en pacientes con tromboembolismo agudo.
En presencia de grandes trombos pulmonares, pueden aparecer leucogra-
mas inflamatorios y, en caso de tromboembolismo pulmonar, es de utilidad
la determinación plasmática de dímero-D. En el desarrollo de insuficiencia
cardíaca derecha, se puede desarrollar hipoalbuminemia si se produce ascitis
debido a la congestión hepática.

Se han descrito elevaciones de NT-proBNP (péptido natriurético secretado por


el miocardio en respuesta al aumento de la distensión) en pacientes con HTP
precapilar, y con HTP de moderada a severa, respecto a perros no hipertensos
o con HTP leve. También se ha observado una fuerte correlación positiva entre
la presión arterial sistólica estimada por el pico de regurgitación tricuspídea y
las concentraciones plasmáticas de NT-proBNP. Además, el incremento de la
troponina I cardiaca, como biomarcador de lesión miocárdica, se ha asociado
a menores tiempos de supervivencia en pacientes.

3. ELECTROCARDIOGRAFÍA

El electrocardiograma no es una prueba específica para diagnóstico o evalua-


ción de la HTP. Cuando aparecen alteraciones evaluables mediante esta técnica,
se desarrollan de forma secundaria a la enfermedad subyacente; puede obser-
varse una desviación del eje eléctrico hacia la derecha o dextroeje por cardio-
megalia derecha, arritmias supraventriculares o ventriculares asociado a enfer-
medad cardiaca izquierda, o bien bradiarritmias y bloqueos atrioventriculares
por un aumento del tono parasimpático ocasionado por enfermedad pulmonar.

4. RADIOGRAFÍA

En muchas ocasiones las radiografías torácicas son normales, no siendo pa-


tognomónicas de la enfermedad. No suelen ser específicas para el diagnóstico
de HTP pero se pueden evidenciar cambios que lo sugieran, dependiendo de la
causa subyacente de hipertensión pulmonar. Dentro de estos cambios se en-
cuentran cardiomegalia generalizada, cardiomegalia derecha y/o dilatación de
la arteria pulmonar (Figura 1). Cuando la HTP es secundaria a enfermedad
valvular mitral crónica se aprecian signos de insuficiencia cardiaca derecha,

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Actualización en hipertensión pulmonar arterial en perros. Conceptos básicos

junto a los hallazgos típicos de la cardiopatía izquierda (elevación de la tráquea


y compresión bronquial, aumento de tamaño de la silueta de atrio y ventrículo
izquierdo, dilatación de venas pulmonares, áreas de edema intersticial-alveo-
lar, etc.) a los que pueden asociarse patrones radiológicos compatibles con
bronquitis crónica, bronquiectasia, fibrosis pulmonar o colapso traqueobron-
quial. En los casos de síndrome de Eisenmenger, los pulmones parecen hipo-
perfundidos y la arteria pulmonar principal y las arterias lobares proximales
se encuentran dilatadas. En los casos de dirifilatiosis, con frecuencia la radio-
grafía torácica muestra arterias pulmonares dilatadas y tortuosas, dilatación
de las arterias lobares, dilatación y brusca terminación de las arterias pulmo-
nares periféricas (más evidente en los lóbulos caudales), cambios alveolares e
intersticiales, dilatación de ventrículo derecho con infiltrados pulmonares co-
rrespondientes a hemorragias o edema y, con menos frecuencia, efusión pleu-
ral y áreas de consolidación pulmonar y atelectasia (Figuras 2a y b).

Figura 1: Estudio radiográfico de silueta cardiaca en proyección dorso ventral (DV), con signo de
agrandamiento de cámaras derechas (signo de D invertida) y patrón hipervascular arterial y arteria
pulmonar dilatada.

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Figura 2: (a) Estudio radiográfico de silueta cardiaca en proyección dorso ventral (DV) de un perro
con Dirifilatiosis donde se aprecia cardiomegalia, dilatación del tronco pulmonar y arterias pulmo-
nares y arterias lobares aumentadas. (b) Estudio radiográfico latero-lateral derecho en el que se
observa un patrón vascular e intersticial con aumento de la silueta cardiaca principalmente de las
cámaras derechas.

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Actualización en hipertensión pulmonar arterial en perros. Conceptos básicos

5. ECOCARDIOGRAFÍA
La ecocardiografía es la técnica de elección para diagnosticar HTP, ya que
permite medir de manera no invasiva la presión y velocidades de flujo, visua-
lizar cambios de remodelación en cámaras cardiacas, y determinar la función
cardiaca relacionada a cambios por HTP.
La determinación de la velocidad máxima de regurgitación de la válvula tricús-
pide es el método ecocardiográfico más comúnmente empleado para diagnos-
ticar HTP, aunque no siempre es detectable. En ausencia de elevaciones en la
postcarga derecha asociada a alteraciones congénitas, como por ejemplo una
estenosis pulmonar, un pico de velocidad de regurgitación tricuspídea mayor a
2.8 m/s se considera anormal e indicativo de HTP (Figuras 3a y 3b).

a b

Figura 3a: Vista de cuatro cámaras en corte paraesternal longitudinal izquierdo, donde se aprecia
insuficiencia tricuspídea mediante Doppler color.
Figura 3b: Doppler contínuo con velocidades de regurgitación tricuspídea superiores a 2,7 m/s (imagen
cedida por H. V. Molins).

En ausencia de obstrucción del tracto de salida del ventrículo derecho, la


presión sistólica ventricular derecha es una estimación de la presión arterial
pulmonar sistólica y, por tanto, puede ayudar a identificar y a clasificar la HTP.
La presión arterial pulmonar sistólica tiene rangos que van desde los 15 a 25
mmHg en perros sanos, sin embargo, ésta puede incrementarse en ciertas
condiciones fisiológicas, como puede ser habitar a elevada altitud o en perros
de trabajo con elevada masa muscular. Las HTP se clasifica desde leve (30-50
mmHg), moderada (50-80 mmHg) a grave (>80 mmHg).
La presencia de insuficiencia pulmonar permite evaluar la presión arterial
pulmonar diastólica. La insuficiencia pulmonar ocurre en diástole y permite
diferenciar la presión de arteria pulmonar-ventrículo derecho. Esta medida es
útil en caso de que la regurgitación tricuspídea no sea evidente. La velocidad
de la insuficiencia pulmonar de 2.2 m/s o más o un gradiente de presión de 19

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mmHg o mayor es sugerente de HTP (Figura 4). Aun así, el flujo de regurgita-
ción pulmonar puede no estar presente en todos los pacientes con HTP.

Figura 4: Doppler color y espectral de arteria pulmonar con presencia de jet regurgitante dias-
tólico.

Los pacientes con HTP tienen mayor postcarga ventricular derecha, por lo que las
dimensiones de las cámaras derechas pueden ser normales o bien pueden pre-
sentarse dilatadas de forma leve a grave (Figura 5). Se puede apreciar cierto grado
de hipertrofia ventricular derecha y dilatación del ventrículo derecho, movimiento
septal paradójico y aplanamiento del septo interventricular debido a una sobrecar-
ga de presión ventricular derecha (Figura 6).Normalmente también se identifica
dilatación de la arteria pulmonar en pacientes con HTP (Figura 7). El diámetro nor-
mal de la arteria pulmonar principal en relación a la aorta en el corte paraesternal
derecho a nivel de la base en eje corto es de 0.98 (relación PA/Ao). En los casos
de infección por dirifilatiosis pulmonar los parásitos se visualizan en la arteria
pulmonar o en las cavidades derechas como dos líneas paralelas hiperecoicas.

Figura 5: Corte pa-


raesternal longitudinal
derecho de cuatro
cámaras, en el que se
observa dilatación de
las cámaras derechas
en relación al ventrícu-
lo izquierdo y aurícula
izquierda.

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Actualización en hipertensión pulmonar arterial en perros. Conceptos básicos

Figura 6: El aplana-
miento septal es uno
de los parámetros
subjetivos en modo B
que pueden sugerir un
aumento de presión
en cámaras derechas
secundario a hiperten-
sión pulmonar.

Figura 7: Dilatación
de la arteria pulmonar
principal. En la imagen
se aprecia un marcado
incremento en la ratio
pulmonar: aorta.

Otros parámetros, como los perfiles de velocidad de flujo sistólico en el Doppler


espectral de la arteria pulmonar, pueden ser de utilidad en el diagnóstico. En
pacientes con presión arterial pulmonar normal, se registra un perfil tipo I, con
velocidades de aceleración y desaceleración iguales produciendo una apariencia
simétrica. Conforme aumentan las presiones arteriales pulmonares, se registra
un perfil asimétrico debido a una rápida aceleración inicial y a una velocidad pico
temprana. Este perfil asimétrico sucede como resultado de una mayor tasa de
aumento en las presiones vasculares pulmonares y se le conoce como perfil tipo
II. Los perfiles tipo II se relacionan con HTP leve a moderada. En casos graves hay
una rápida aceleración con una velocidad pico inicial y una muesca sistólica me-
dia también presente, a lo cual se le conoce como perfil tipo III. La muesca sistóli-
ca indica flujo sanguíneo inverso, secundario a presiones vasculares pulmonares
elevadas y presenta un 80% de sensibilidad y especificidad para diagnosticarla.

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Otras medidas que se han uti-


lizado para ayudar al diagnós-
tico de HTP en perros son los
tiempos de intervalo ventricu-
lar sistólico, como es el tiempo
de aceleración (TA), tiempo de
eyección (TE), la relación TA/
TE, así como el periodo de pre-
eyección (PPE) (Figura 8). Estos
valores reflejan cambios en la
carga de ventrículo derecho de-
mostrándose que una relación
TA/TE igual o inferior de 0.31, y
un valor de TA igual o inferior a
0.58 ms son predictivos de HTP.
Estos cambios pueden ayudar
en el diagnóstico cuando otros
hallazgos clínicos lo sugieran y
no se detecte la medida Doppler
Figura 8: Perfil Doppler de flujo sistólico de arteria de regurgitación tricuspídea.
pulmonar con mediciones de tiempo de acelera-
La excursión sistólica del anillo
ción, desaceleración, de eyección y período de pre-
eyección. (Imagen cedida por H. V. Molins). plano tricuspídeo (TAPSE) es un
parámetro ecocardiográfico que
ha sido desarrollado en humanos
para evaluar la función sistólica de ventrículo derecho. Éste mide el desplaza-
miento apical de la porción lateral del anillo de la válvula tricúspide durante
la sístole desde el modo M. En pacientes con HTP, los valores de TAPSE por
debajo de los rangos de referencia se asocian a una disminución de la función
sistólica ventricular derecha y se relaciona a una alta mortalidad. El TAPSE se
mide en modo M a nivel del aspecto lateral del anillo de la válvula tricúspide
mediante el corte paraesternal izquierdo de cuatro cámaras (Figura 9).

TRATAMIENTO
Una vez se ha podido identificar y tratar la causa subyacente de la HTP, se puede
completar el tratamiento utilizando medicamentos para ayudar a reducir la pre-
sión arterial pulmonar y la carga sobre el ventrículo derecho con el fin de mejorar
los signos clínicos como la intolerancia al ejercicio, la disnea, la tos, y reducir los
episodios de síncopes para mejorar la calidad de vida y el tiempo de supervivencia.

1. Análogos de la prostaciclina
La prostaciclina es un agente vasodilatador, inhibidor de la actividad plaqueta-
ria y que presenta efectos antiproliferativos. Entre los análogos de la prostaci-
clina se encuentran el epoprostenol, treprostinil, y el iloprost. El epoprostenol y
trepostinil se administran por vía intravenosa, el treprostinil puede administrar-

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Actualización en hipertensión pulmonar arterial en perros. Conceptos básicos

Figura 9: Medición del TAPSE. Modo M a nivel del aspecto lateral del anillo de la válvula tricúspide
visto en el corte apical de cuatro cámaras por la ventana paraesternal izquierda centrado en el
ventrículo derecho.

se por vía subcutánea y el iloprost puede ser administrado vía inhalatoria. En


humanos, estos medicamentos mejoran la sintomatología y la supervivencia.
Los efectos secundarios a su administración incluyen anemia, trombocitopenia,
hipotensión y síntomas gastrointestinales. Se ha observado que estos fármacos
son eficaces a nivel experimental en el tratamiento de la HTP canina pero aún
no hay evidencias clínicas publicadas. Dado su elevado coste económico, su
administración al paciente veterinario resulta impracticable.

2. Antagonistas de la endotelina
Es posible reducir la presión arterial pulmonar al antagonizar las acciones
de la endotelina 1. Los antagonistas de la endotelina más comunes incluyen
bosentán, sitaxsentan y ambrisentan. En humanos, estos medicamentos ad-
ministrados vía oral han demostrado mejorar la intolerancia al ejercicio, la
presión arterial pulmonar y la resistencia pulmonar. El bosentán se ha eva-
luado en perros de forma experimental; en estos pacientes, el bosentán fue
eficaz y redujo el remodelamiento vascular, mejoró la función miocárdica y
redujo el remodelamiento ventricular. Estos medicamentos, aunque menos
caros que los análogos de la prostaciclina, se consideran prohibitivos por su
coste en pacientes veterinarios y aún no se han llevado a cabo pruebas clíni-
cas en pacientes con HTP no inducida experimentalmente.

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3. Óxido nítrico y nitratos


El óxido nítrico es un vasodilatador administrado por vía inhalatoria, mientras
que el dinitrato de isosorbide y el mononitrato de isosorbide son vasodilata-
dores de administración vía oral. En humanos, los nitratos son prescritos por
sus efecto vasodilatador frente a la isquemia miocárdica, teniendo un valor
limitado en el tratamiento de la HTP. Estos medicamentos no son utilizados
de manera común en medicina veterinaria a causa de sus efectos colaterales
potencialmente graves. La L-arginina, precursor del óxido nítrico, ha sido ad-
ministrada en humanos con HTP observándose una mejora en las concentra-
ciones de óxido nítrico y ocasionando vasodilatación.

4. Inhibidores de la fosfodiesterasa 5
Hay varios inhibidores de la fosfodiesterasa 5 (PDE-5, por sus siglas en inglés)
incluyendo al sildenafil, tadalafil y vardenafil. Estos medicamentos inhiben de
manera específico a la PDE-5, la cual se encuentra en concentraciones elevadas
en los vasos pulmonares. La PDE-5 degrada al monofosfato de guanosina cíclico
(cGMP), de forma que cuando la PDE-5 es inhibida, las concentraciones de cGMP
aumentan y se promueve la vasodilatación. En humanos, los inhibidores de PDE-5
causan vasodilatación arterial pulmonar pero hay diferencias sutiles entre las tres
sustancias con respecto al inicio y duración de acción, el grado de reducción de la
resistencia vascular pulmonar y la habilidad para revertir la hipertrofia cardiaca.
El sildenafil es un inhibidor de la PDE-5 de corta duración. Se ha evaluado en
el tratamiento de la HTP canina y ha demostrado reducir la presión arterial
pulmonar, mejorar la calidad de vida y aumentar el tiempo de supervivencia.
En algunos pacientes presenta algunos efectos secundarios gastrointestina-
les y, aunque es un producto relativamente caro, puede ser accesible para
la mayoría de los propietarios. Se considera el fármaco de elección para el
tratamiento de la HTP en perros. La dosis recomendada de sildenafil es de 1
a 3 mg/kg por vía oral cada 8 a 12 horas.
El pimobendan y el levosimendan son fármacos de mecanismo dual; ejercen
efectos inotrópicos positivos relacionados con la sensibilización al calcio, así
como efectos vasodilatadores mediados por la inhibición de la PDE-3. Desde
el punto de vista clínico, el pimobendan ha demostrado mejorar la HTP se-
cundaria a enfermedad degenerativa de la válvula mitral (clase clínica II).

PRONÓSTICO
Los cambios estructurales que se producen a nivel pulmonar y que dan lugar
a la HTP son irreversibles. Por lo tanto, según la respuesta al tratamiento ad-
ministrado en función a la patología causante de la HTP, el pronóstico variará y
será más favorable o desfavorable a corto y medio plazo. A largo plazo, el pro-
nóstico siempre debe ser reservado. Éste suele ser peor en aquellos pacientes
con HTP secundaria a una patología pulmonar crónica, en comparación a los
casos secundarios a incrementos de presión en el lado izquierdo del corazón.

82 Canis et Felis Número 133 - Abril 2015


Actualización en hipertensión pulmonar arterial en perros. Conceptos básicos

BIBLIOGRAFÍA
1. ATKINSON, K. J., FINE, D. M., THOMBS, L. A., GORELICK, J. J. & DURHAM, H. E. 2009. Evaluation of
Pimobendan and N-Terminal Probrain Natriuretic Peptide in the Treatment of Pulmonary Hypertension
Secondary to Degenerative Mitral Valve Disease in Dogs. Journal of Veterinary Internal Medicine, 23, 1190-1196.
2. BACH, J. F., ROZANSKI, E. A., MACGREGOR, J., BETKOWSKI, J. M. & RUSH, J. E. 2006a. Retrospective
evaluation of sildenafil citrate as a therapy for pulmonary hypertension in dogs. Journal of veterinary
internal medicine, 20, 1132-1135.
3. CHIAVEGATO, D., BORGARELLI, M., D’AGNOLO, G. & SANTILLI, R. A. 2009. Pulmonary Hypertension
in Dogs with Mitral Regurgitation Attributable to Myxomatous Valve Disease. Veterinary Radiology &
Ultrasound, 50, 253-258.
4. FLEMING E. Pulmonary hypertension. Compend Contin Educ Vet 2006;28:720–30.
5. GLAUS, T. M., SOLDATI, G., MAURER, R. & EHRENSPERGER, F. 2004. Clinical and pathological charac-
terisation of primary pulmonary hypertension in a dog. Vet Rec, 154, 786-89.
6. JOHNSON, L., BOON, J. & ORTON, E. 1999. Clinical characteristics of 53 dogs with Doppler-derived
evidence of pulmonary hypertension: 1992-1996. J Vet Intern Med, 13, 440-7.
7. KELLIHAN, H. B. & STEPIEN, R. L. 2010. Pulmonary hypertension in dogs: diagnosis and therapy. Vet
Clin North Am Small Anim Pract, 40, 623-41.
8. KELLIHAN, H. B. & STEPIEN, R. L. 2012. Pulmonary hypertension in canine degenerative mitral valve
disease. J Vet Cardiol, 14, 149-64.
9. KELLUM HB, STEPIEN RL. Sildenafil citrate therapy in 22 dogs with pulmonary hypertension. J Vet Intern
Med 2007;21(6):1258–64.
10. KIM, H., YUNG, G. L., MARSH, J. J., KONOPKA, R. G., PEDERSEN, C. A., CHILES, P. G., MORRIS, T. A.
& CHANNICK, R. N. 2000. Endothelin mediates pulmonary vascular remodelling in a canine model of
chronic embolic pulmonary hypertension. European Respiratory Journal, 15, 640-648.
11. MCLAUGHLIN, V. V., ARCHER, S. L., BADESCH, D. B., BARST, R. J., FARBER, H. W., LINDNER, J. R.,
MATHIER, M. A., MCGOON, M. D., PARK, M. H. & ROSENSON, R. S. 2009. ACCF/AHA 2009 Expert Consensus
Document on Pulmonary HypertensionA Report of the American College of Cardiology Foundation Task
Force on Expert Consensus Documents and the American Heart Association Developed in Collaboration
With the American College of Chest Physicians; American Thoracic Society, Inc.; and the Pulmonary
Hypertension Association. Journal of the American College of Cardiology, 53, 1573-1619.
12. MONTOYA, A. J.-A. & CARRETÓN, E. 2012. Dirifilatiosis pautas de manejo clínico, Barcelona, España,
Multimedica Ediciones Veterinarias.
13. OYAMA, M. A. & SISSON, D. D. 2004. Cardiac Troponin-I Concentration in Dogs with Cardiac Disease.
Journal of veterinary internal medicine, 18, 831-839.
14. PARADIES, P., SPAGNOLO, P. P., AMATO, M. E., PULPITO, D. & SASANELLI, M. 2014. Doppler echocar-
diographic evidence of pulmonary hypertension in dogs: a retrospective clinical investigation. Veterinary
Research Communications, 38, 63-71.
15. QUINN, R. L. & WILLIAMS, J. G. 2011a. Canine pulmonary hypertension Part 1: An in-depth review of its
pathophysiology and classifications. Veterinary Medicine, 6, 454-9.
16. QUINN, R. L. & WILLIAMS, J. G. 2011b. Canine pulmonary hypertension, Part 2: Diagnosis and treatment.
Veterinary Medicine, 6, 26-36.
17. SCHOBER, K. & BAADE, H. 2006. Doppler echocardiographic prediction of pulmonary hypertension in
West Highland white terriers with chronic pulmonary disease. J Vet Intern Med, 20, 912-20.
18. SERRES, F., CHETBOUL, V., GOUNI, V. & AL, E. 2007. Diagnostic Value of Echo-Doppler and Tissue Doppler
Imaging in Dogs with Pulmonary Arterial Hypertension. J Vet Intern Med, 21, 1280-89.
19. SILVA, A. C., OBERLENDER, G., MANTOVANI, M. M., MUZZI, R. A. L., PEREIRA, L. J. & ZANGERONIMO, M.
G. 2014. Efficacy of sildenafil therapy for pulmonary hypertension in dogs: a systematic review. Archivos
De Medicina Veterinaria, 46, 277-287.
20. SIMONNEAU, G., GATZOULIS, M. A., ADATIA, I., CELERMAJER, D., DENTON, C., GHOFRANI, A., SANCHEZ,
M. A. G., KUMAR, R. K., LANDZBERG, M., MACHADO, R. F., OLSCHEWSKI, H., ROBBINS, I. M. & SOUZA,
R. 2013. Updated Clinical Classification of Pulmonary Hypertension. JACC, 62, 34-41.
21. STEPIEN, R. 2009. Pulmonary arterial hypertension secondary to chronic left-sided cardiac dysfunction
in dogs. J Small Anim Pract, 50, 34-43.

Número 133 - Abril 2015 Canis et Felis 83


CONSULTANT ON CALL h CARDIOLOGY h PEER REVIEWED

Pulmonary
Hypertension From
a Non-cardiologist
Perspective
Elizabeth Rozanski, DVM, DACVIM (Small Animal),
DACVECC
Tufts University

PROFILE Genetic Implications


h There are no known genetic influences.
Definition h Certain dog breeds may be likely to develop
h Pulmonary hypertension (PHTN) is an mitral valve disease (MVD), which may
increase in pulmonary arterial pressures result in PHTN, and West Highland white
(PAP). terriers (Westies) are considered at PHTN appears
• Normal systolic PAP is <25 mm Hg. Clini- increased risk for pulmonary fibrosis that to be recognized
cal signs of PHTN are typically seen at may lead to the development of secondary more frequently
>50 mm Hg. PHTN.2 with more
• In dogs with severe signs (eg, syncope), widespread
pressures close to 100 mm Hg are Incidence & Prevalence availability of
common.1 h Unknown, but PHTN appears to be recog- echocardiography.
• Clinical signs may be common with higher nized more frequently with more wide-
pressures. spread availability of echocardiography.
h Geographic distribution is worldwide; the
Systems presence of heartworm disease will increase
h The cardiopulmonary system is primarily the likelihood of PHTN, and high altitude
affected, but with severe PHTN, limited (>2000 m, about 6560 ft) may worsen PTHN.3 MVD = mitral valve disease
cardiac output affects the entire patient PAP = pulmonary arterial
by causing exercise intolerance, respiratory Signalment pressure

distress, and syncope. h Dogs are much more commonly affected PHTN = pulmonary
hypertension
than cats.

February 2016 cliniciansbrief.com 85


CONSULTANT ON CALL h CARDIOLOGY h PEER REVIEWED

intolerance are the most common signs.


• Some dogs have cough associated with
CATEGORIES OF CANINE PULMONARY HYPERTENSION4
either MVD or chronic pulmonary disease.
PHTN is classified into 5 categories in humans. Some veterinarians use the h There are no specific history and clinical

human classification model (below); others prefer to categorize cases as signs that clearly signify PHTN.
primary (rare) and secondary. Regardless, suspicion or documentation h Westies with pulmonary fibrosis or dogs
of PHTN should prompt a complete patient evaluation for underlying with heartworm disease should prompt
medical disease resulting in PHTN. specific concern for PHTN.
1. Pulmonary arterial hypertension, including idiopathic, congenital
heart disease, some connective tissue disorders, and, in developing Physical Examination
countries, schistosomiasis h A split or, less commonly, loud S2 is classi-
2. Left-sided heart failure, the most common cause of PHTN in humans cally appreciated on cardiac auscultation,
and in dogs as is mild-to-moderate tachycardia.
h Other possible abnormalities include signs
3. Chronic pulmonary disease (eg, pulmonary fibrosis, chronic bronchitis);
of right-sided heart failure (eg, jugular
also considered common in dogs
venous distension, hepatomegaly, ascites).
4. Chronic pulmonary thromboembolism

5. Miscellaneous, which includes various other causes (eg, polycythemia, DIAGNOSIS


vasculitis). Heartworm disease, which is common in dogs, may lead to
the development of PHTN. Definitive Diagnosis
h The gold standard in humans for diagnosis
of pulmonary arterial hypertension is a
right-heart catheterization for direct
h Westies are more commonly affected by assessment of pressure; although this
pulmonary fibrosis, which may lead to is possible in dogs and cats, it is rarely
secondary PHTN, than other breeds.2 performed.
h Can affect any age but tends to occur in h In veterinary medicine, PHTN is most com-

older patients.1 monly inferred by echocardiography.


h Both sexes are equally affected.1 • Echocardiography may provide an esti-
mate of PAP based on the speed (m/sec) of
Risk Factors the tricuspid or pulmonary regurgitant jet.
h Advancing age and/or presence of • Echocardiography is also useful to iden-
long-standing MVD or chronic pulmonary tify structural changes in the heart,
disease including paradoxical septal motion,
enlarged right heart, and a volume-
Pathophysiology underloaded (small) left heart.
h Depends on the underlying cause but • From the clinician’s standpoint, echocardi-
includes increasing pressures associated ography should be considered the most
with chronic pulmonary venous hyperten- useful method to document PHTN (Figure 1).
CT = computed sion or chronic pulmonary disease.
tomography
• In congenital heart disease, there may be Differential Diagnosis
MVD = mitral valve
disease primary arterial disease; with thrombotic h Before an echocardiogram, other differen-
PAP = pulmonary disease, there is occlusion to blood flow. tials include mitral valve disease with con-
arterial pressure gestive heart failure and other cardiac
PHTN = pulmonary History & Clinical Signs disease (eg, pericardial effusion with tam-
hypertension
h Respiratory distress, syncope, and exercise ponade, dilated cardiomyopathy), upper

86 cliniciansbrief.com February 2016


airway disease, or pneumonia.
h With syncope, differential diagnoses may

include seizure or arrhythmia.


h After echocardiographic confirmation of

PHTN, the focus should shift to identifying


the cause of PHTN.

Laboratory Findings
h Laboratory testing is typically unremark-
able unless there is underlying systemic
disease, including heartworm disease.
h Hypercoagulable conditions may lead to

pulmonary thromboembolism.
• Hypercoagulability may be difficult to
1A
detect on routine laboratory testing.
h NT pro-BNP, while emerging as a useful

marker in cardiac disease, is typically ele-


vated in PHTN and may inadvertently result
in treatment for congestive heart failure,5
which may or may not be present.
h Higher doses of furosemide may result in

worsening syncope in dogs with PHTN


without left-sided cardiac disease.

Imaging
h Echocardiography is the most definitive
diagnostic imaging.
h Thoracic radiographs are useful for evalua- 1B
tion but may underestimate the severity of
the PHTN.
d Echocardiographic Doppler study documenting high tricuspid
• However, it may be possible to appreciate regurgitant velocity consistent with pulmonary hypertension.
right-sided enlargement (reverse “D”) The modified Bernoulli equation [change in pressure = 4 ×
or pulmonary arterial enlargement (regurgitant velocity)2] may be used to estimate the systolic
(Figure 2, next page). PAP. In the example shown, the tricuspid regurgitant velocity
h Computed tomography (CT) and, particu- is 4.1 m/sec; thus, estimated PAP is 67 mm Hg.
larly, CT-angiography is useful to evaluate
lung parenchyma and to determine if pul-
monary thromboembolism is present.
h Abdominal ultrasonography is helpful to

evaluate the patient for other underlying


conditions and to evaluate the hepatic
vessels (Figure 3, page 89).
Laboratory testing is typically
unremarkable unless there is
Postmortem Findings
h Postmortem findings may reflect the
underlying systemic disease,
underlying cause. including heartworm disease.

February 2016 cliniciansbrief.com 87


CONSULTANT ON CALL h CARDIOLOGY h PEER REVIEWED

Medical
h Oxygen is administered if patient is
severely affected and sildenafil (1-3 mg/kg
orally 2 to 3 times a day) is the most com-
monly used medication.
h Even in patients without pulmonary throm-

boembolism as an underlying cause, vascu-


lar stasis may lead to an increased risk for
thrombotic disease, but the role of antico-
agulant therapy in patients with PHTN
2A remains unclear.
Fluid therapy is h Dogs with inflammatory lung disease may

contraindicated benefit from glucocorticoids; those with


in most cases of heart failure benefit from standard therapy
PHTN because with furosemide, pimobendan, and
angiotensin-converting enzyme (ACE)
of volume
inhibitors.
overload of the
h Fluid therapy is contraindicated in most
right side of
cases of PHTN because of volume overload
the heart. of the right side of the heart.
h Sildenafil may be the most useful specific

drug for PHTN.


h Other drug therapy may be warranted by

the underlying condition.

Contraindications
h Nitrates (eg, nitroglycerin) are contraindi-
cated in dogs receiving sildenafil.

2B h Furosemide may result in worsening of

cardiac output and is not indicated in dogs


that do not have concurrent left-sided
d Lateral and VD thoracic radiographs of a
congestive heart failure.
dog with PHTN, showing mild right-sided
enlargement of the heart and enlarged
Precautions/Interactions
pulmonary arteries (arrows).
h Anesthesia is considered high-risk in dogs
with severe PHTN.
• Procedures should only be performed
TREATMENT
when the benefit outweighs the risk and
Inpatient vs Outpatient ideally with a veterinary anesthesiologist.
h Decisions should be based on the stability
of the patient. Nutritional
ACE = angiotensin-
converting enzyme h Severely affected animals benefit from h Maintenance of a normal body condition is
PHTN = pulmonary inpatient oxygen therapy, as oxygen is a a goal.
hypertension potent pulmonary vasodilator. h Some dogs experience loss of appetite and
PAP = pulmonary h Mildly affected patients may be treated at may require coaxing to eat adequate
arterial pressure
home. amounts.

88 cliniciansbrief.com February 2016


Activity
h Activity should be limited based on degree
of patient’s comfort.
h Excessive exertion should be avoided.

• In moderately-to-severely affected dogs,


exercise should be limited.
–Smaller patients may be carried up and
down stairs.

Client Education
h Client education is important, as PHTN is a
severe condition that tends to progress
over time. 3
Alternative Therapy d Abdominal ultrasound image documenting enlarged hepatic
h None proven; fish oil supplementation may vessels consistent with right-sided heart failure.
be considered to decrease inflammation
and help decrease platelet adhesion

FOLLOW-UP

Patient Monitoring
h Monitoring should include evaluation for
worsening respiratory distress or exercise At-Home Treatment
intolerance. h Exercise should be restricted.
h Recheck echocardiography may be useful h Treat for primary condition, if identified.
to monitor changes in PAP, although pul- • Sildenafil, possibly pimobendan
monary pressures may not correlate with h Anticoagulants are likely warranted in

clinical signs. humans, and possibly in dogs.


• Changes in right ventricular motion and h Home oxygen therapy, if possible.

left ventricular filling are good at assess-


ing response, but tricuspid regurgitation Future Follow-Up
and perfusion index gradients rarely h Recheck regularly; monitor for develop-
change substantially. ment of right-sided heart failure or azote-
mia secondary to low cardiac output.
Complications h Ascites may be drained as needed for

h PHTN is a progressive disease, and cardio- patient comfort.


pulmonary failure is the most likely ulti-
COST KEY
mate outcome.
IN GENERAL
h Most dogs are euthanized for humane rea- $ = up to $100
sons associated with respiratory distress, Relative Cost
$$ = $101–$250
syncope, or heart failure. h $$$-$$$$$: Diagnosis of PHTN with echo-
cardiography alone is $$$; if CT or other
$$$ = $251–$500
h Sudden death is possible.

h Concurrent administration of nitrates may imaging is pursued, costs will increase to $$$$ = $501–$1000
be associated with severe hypotension and $$$$$. $$$$$ = more than
should be avoided. h Sildenafil is expensive for daily use. $1000

February 2016 cliniciansbrief.com 89


CONSULTANT ON CALL h CARDIOLOGY h PEER REVIEWED

VETORYL® CAPSULES
(trilostane)
5 mg, 10 mg, 30 mg, 60 mg and 120 mg strengths
Adrenocortical suppressant for oral use in dogs only.

BRIEF SUMMARY (For Full Prescribing Information,


see package insert.)

Prognosis h Other methods of prevention have not


CAUTION: Federal (USA) law restricts this drug to
use by or on the order of a licensed veterinarian.
h Prognosis is fair; some dogs with less been established. DESCRIPTION: VETORYL Capsules are an orally
profound signs will do well for h If possible, affected dogs should not active synthetic steroid analogue that blocks
production of hormones produced in the adrenal
months to perhaps a year; badly live at high altitudes and should not cortex of dogs.

affected dogs may not survive to hos- vacation in the mountains. INDICATION: VETORYL Capsules are indicated for
the treatment of pituitary- and adrenal-dependent
pital discharge. • Air travel should be avoided in hyperadrenocorticism in dogs.
h Dogs with mild-to-moderate PHTN affected dogs. CONTRAINDICATIONS: The use of VETORYL
associated with MVD often do quite Capsules is contraindicated in dogs that have
demonstrated hypersensitivity to trilostane. Do not
well, and the development of PHTN is Future Considerations use VETORYL Capsules in animals with primary
hepatic disease or renal insufficiency. Do not use in
not a particularly ominous sign in h Improved awareness may open up pregnant dogs. Studies conducted with trilostane in
laboratory animals have shown teratogenic effects
these dogs. therapeutic options such as treatment and early pregnancy loss.
h As in all diseases, owner expectations with endothelin receptor antagonists WARNINGS: In case of overdosage, symptomatic
and decisions influence survival treatment of hypoadrenocorticism with
(eg, bosentan) or with tyrosine kinase corticosteroids, mineralocorticoids and intravenous
times. inhibitors, which have been used with fluids may be required. Angiotensin converting
enzyme (ACE) inhibitors should be used with caution
some success in humans (although, to with VETORYL Capsules, as both drugs have
aldosterone-lowering effects which may be additive,
Prevention and Management date, no evidence exists in dogs). impairing the patient’s ability to maintain normal
electrolytes, blood volume and renal perfusion.
h Heartworm preventive therapy is • These drugs are expensive and may Potassium sparing diuretics (e.g. spironolactone)
should not be used with VETORYL Capsules as
warranted for all dogs in endemic have significant side effects. n both drugs have the potential to inhibit aldosterone,
regions. increasing the likelihood of hyperkalemia.

HUMAN WARNINGS: Keep out of reach of children.


Not for human use. Wash hands after use. Do not
empty capsule contents and do not attempt to divide
the capsules. Do not handle the capsules if pregnant
or if trying to conceive. Trilostane is associated with
teratogenic effects and early pregnancy loss in
laboratory animals. In the event of accidental
References Brown AJ, Davison E, Sleeper MM. Clinical efficacy
of sildenafil in treatment of pulmonary arterial ingestion/overdose, seek medical advice immediately
1. Kellihan HB, Stepien RL. Pulmonary hyper- hypertension in dogs. JVIM. 2010;24(4):850-854. and take the labeled container with you.
tension in dogs: diagnosis and therapy. Vet Clin
North Am Small Anim Pract. 2010:40(4):623-641. Chiavegato D, Borgarelli M, D’Agnolo G, Santilli RA. PRECAUTIONS: Hypoadrenocorticism can develop
Pulmonary hypertension in dogs with mitral at any dose of VETORYL Capsules. A small
2. Glaus TM, Hässig M, Baumgartner C, Reusch CE. regurgitation attributable to myxomatous percentage of dogs may develop corticosteroid
Pulmonary hypertension induced in dogs by valve disease. Vet Radiol Ultrasound. 2009:50(3): withdrawal syndrome within 10 days of starting
hypoxia at different high-altitude levels. Vet Res 253-258. treatment. Mitotane (o,p’-DDD) treatment will reduce
Commun. 2003;27(8):661-670. adrenal function. Experience in foreign markets
Johnson L, Boon J, Orton EC. Clinical suggests that when mitotane therapy is stopped, an
3. Schober KE, Baade H. Doppler characteristics of 53 dogs with Doppler-derived interval of at least one month should elapse before
echocardiographic prediction of pulmonary evidence of pulmonary hypertension: 1992- the introduction of VETORYL Capsules. The use of
hypertension in West Highland white terriers 1996. J Vet Intern Med. 1999;13(5):440-447. VETORYL Capsules will not affect the adrenal tumor
with chronic pulmonary disease. J Vet Intern itself. Adrenalectomy should be considered as an
Med. 2006;20(4):912-920. Rush JE, Keene BW, Fox PR. Pericardial disease in option for cases that are good surgical candidates.
the cat: A retrospective evaluation of 66 cases. The safe use of this drug has not been evaluated in
4. Ryan JJ, Thenappan T, Luo N, et al. The WHO JAAHA. 1990;26:39-46. lactating dogs and males intended for breeding.
classification of pulmonary hypertension: A
case-based imaging compendium. Pulm Circ. Serres FJ, Chetboul V, Tissier R, et al. Doppler
echocardiography-derived evidence of ADVERSE REACTIONS: The most common adverse
2012;2(1):107-121. reactions reported are poor/reduced appetite,
pulmonary arterial hypertension in dogs with
5. Kellihan HB, Mackie BA, Stepien RL. NT-proBNP, vomiting, lethargy/dullness, diarrhea, elevated liver
degenerative mitral valve disease: 86 cases enzymes, elevated potassium with or without
NT-proANP and cTnI concentrations in dogs (2001-2005). JAVMA. 2006:229(11):1772-1778.
with pre-capillary pulmonary hypertension. elevated sodium, elevated BUN, decreased Na/K
Stepian RL, Whitely NT, Dubielzig RR. Idiopathic or ratio, weakness, elevated creatinine, shaking, and
J Vet Cardiol. 2011;13(3):171-182. renal insufficiency. Occasionally, more serious
mesothelioma-related pericardial effusion:
clinical findings and survival in 17 dogs studied reactions, including severe depression, hemorrhagic
diarrhea, collapse, hypoadrenocortical crisis or
retrospectively. Small Anim Pract. 2000:
Suggested Reading 41(8):342-347.
adrenal necrosis/rupture may occur, and may result
in death.
Arita S, Arita N, Hikasa Y. Therapeutic effect of
low-dose imatinib on pulmonary arterial
hypertension in dogs. Can Vet J. 2013;54(3):
255-561.

Distributed by:
Dechra Veterinary Products
7015 College Boulevard, Suite 525
MVD = mitral valve disease Overland Park, KS 66211

VETORYL is a trademark of
PHTN = pulmonary hypertension Dechra Ltd. © 2015, Dechra Ltd.
NADA 141-291, Approved by FDA

90 cliniciansbrief.com February 2016


ASK THE EXPERT h RESPIRATORY MEDICINE h PEER REVIEWED

Common
Pulmonary
Diseases in Dogs
Douglas Palma, DVM, DACVIM (SAIM)
The Animal Medical Center
New York, New York

YOU HAVE ASKED ... ance. Depending on cause and nonrespi-


ratory involvement, nonspecific clinical
What should I know about signs (eg, lethargy, inappetence, weight
loss) may be present. Many patients may
common canine pulmonary
have a mixed pattern of breathing char-
diseases? acterized by increased inspiratory and
expiratory effort, as the disease pro-
cesses may involve concurrent airway
THE EXPERT SAYS ...
obstruction and altered lung compliance.
Pulmonary disease is a common cause of Therefore, a pure restrictive (decreased
respiratory signs in dogs. A thorough tidal volume, increased respiratory rate)
history and examination help localize or obstructive (increased expiratory
the pulmonary parenchyma rather than effort) pattern of breathing is often not
other parts of the respiratory system. observed.
Signalment, clinical onset and progres-
sion, geographic location, and additional The following are pulmonary diseases
organ involvement can help prioritize frequently encountered in dogs.
differential diagnoses.
Pneumonia
Patients with pulmonary disease may Bacterial Pneumonia
exhibit coughing, increased respiratory Pneumonia may be community-acquired
rate, dyspnea, and/or exercise intoler- (ie, characterized by bronchopneumonia

October 2016 cliniciansbrief.com 77


ASK THE EXPERT h RESPIRATORY MEDICINE h PEER REVIEWED

CDV = canine distemper


in a dog with a history of being housed in Aspiration pneumonia is more common
virus the community) or secondary to altered in older patients. Clinical history is
CIV = canine influenza pulmonary defenses, aspiration, or important to help identify potential
virus
hematogenous infection. underlying causes. The most commonly
EB = eosinophilic
bronchopneumopathy reported causes of aspiration pneumonia
PCR = polymerase chain Community-acquired pneumonia is in dogs include esophageal disease, vom-
reaction most common in young dogs and in dogs iting, neurologic disorders, laryngeal
RT-PCR = reverse with recent exposure to kennels or shel- disease, and postanesthetic aspiration.3
transcription
polymerase chain ters.1 Exposure to other dogs makes Bor- Opportunistic infections complicate the
reaction
detella bronchiseptica most common, but initial aspiration event. A mixed popula-
other opportunistic pathogens may be tion of bacteria with an anaerobic popu-
involved.1 Streptococcus zooepidemicus, lation is common. Aspiration pneumonia
another emerging bacterial pathogen, is is typically characterized by a distribu-
associated with development of hemor- tion to the most dependent lung lobe (ie,
rhagic pneumonia.2 right middle). However, distribution to
any lung or multiple lungs is possible.4
Although respiratory signs may be pres-
A ent, many older patients are clinically
silent; pneumonia must be considered in
dogs with nonspecific signs of lethargy,
inappetence, and/or fatigue.

Dogs with bacterial pneumonia are typi-


cally presented with acute-onset cough-
ing, lethargy, inappetence, and/or
respiratory distress. An inflammatory
leukogram and pyrexia, although com-
mon, are not always present. Radiographs
may reveal an interstitial-to-alveolar
pattern with a cranioventral distribution
(Figure 1). Atypical distributions can also
B occur.5

Culture-directed therapy is ideal; how-


ever, empiric treatment with knowledge
of common organisms is reasonable.6
Multidrug-resistant organisms are more
common following recent antibiotic
exposure.7,8

Viral Pneumonia
Viral pneumonia is generally associated
with canine distemper virus (CDV) or
canine influenza virus (CIV). Emerging
d FIGURE 1 (A) Bronchopneumonia. Cranioventral distribution of alveolar disease
with air bronchograms. (B) A patchy distribution can be observed on the lateral viral pathogens (eg, canine pantropic
projection. The changes overlying the heart may be missed in subtle cases. coronavirus, canine pneumovirus) have

78 cliniciansbrief.com October 2016


recently been described.9 Canine herpes-
virus can, albeit rarely, induce intersti-
tial pneumonia.10,11

CDV should be suspected in poorly vacci-


nated dogs with multiorgan involvement.
Dogs with CDV may have exhibited only
respiratory signs before developing char-
acteristic nonrespiratory signs.12 Radio-
graphs may reveal a diffuse interstitial
pattern (Figure 2). Diagnosis is sup-
ported by compatible clinical signs and
complementary diagnostic testing (ie,
real-time reverse transcription poly- d FIGURE 2 CDV pneumonia with a diffuse interstitial pattern confirmed by
merase chain reaction [RT-PCR], serol- multisystemic signs, urine RT-PCR, and necropsy
ogy, CSF pleocytosis). Conjunctival
scraping and tissue-based immunohisto-
chemistry may confirm diagnosis.

CIV may involve the pulmonary paren-


chyma and is often complicated by
opportunistic bacteria. Patients typi-
cally are presented with lethargy,
anorexia, nasal discharge, and cough-
ing. PCR of the nasal cavity or orophar-
ynx within 3 to 5 days of infection may
confirm organism presence. Patients
with clinical signs lasting longer than
5 days may require serologic testing.13
d FIGURE 3 Eosinophilic bronchopneumopathy. Note the heavy, patchy
Fungal Pneumonia bronchointerstitial pattern.
The incidence of fungal disease varies
widely by geographic region. Dogs with buminemia, hyperglobulinemia, nonre-
fungal pneumonia are generally young generative anemia, and monocytosis;
and exhibit signs of generalized illness hypercalcemia and eosinophilia are less
(eg, lethargy, weight loss, pyrexia, common. An inflammatory leukogram
decreased appetite). Many patients with may be observed. Radiographs often
pulmonary involvement do not show show a miliary pattern and may show
respiratory signs; coughing and respira- hilar lymphadenopathy. A combination
tory distress are most common among of serologic and antigen testing may sup-
those that do.14-16 Additional organ sys- port diagnosis. Cytology or tissue histo-
tems (eg, dermatologic, GI, ocular, mus- pathology may identify the organism.18-21
culoskeletal) may be affected.17
Eosinophilic Bronchopneumopathy
Blood testing is somewhat nonspecific. Eosinophilic bronchopneumopathy
Common abnormalities include hypoal- (EB) is an idiopathic inflammatory

October 2016 cliniciansbrief.com 79


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hypersensitivity disorder associated ment for pneumonia, have peripheral


with acute onset coughing, gagging, eosinophilia, or have uncharacteristi-
retching, and/or respiratory distress. cally severe diffuse bronchointersitial
Radiographs may reveal a diffuse bron- patterns; further diagnostic investiga-
chointerstitial pattern or alveolar dis- tion is indicated to confirm eosino-
ease (Figure 3, previous page). Patients philic inflammation and rule out other
with EB have airway cytology support- causes. Treatment with corticosteroids
ive of eosinophilic inflammation and is often successful; however, relapse
are negative for parasitic testing. can occur after dose tapering.22

EB’s acute nature, occurrence in young Pulmonary Edema


animals, and radiographic findings Noncardiogenic and cardiogenic edema
EB = eosinophilic may mimic pneumonia. EB should be are common causes of pulmonary paren-
bronchopneumopathy
suspected in patients that fail treat- chymal changes in dogs.

A C

B D

d FIGURE 4 (A & B) Congestive heart failure. Note the left-sided cardiomegaly, pulmonary venous
congestion, and interstitial pulmonary pattern. Edema is not exclusively perihilar. (C & D) Noncardiogenic
edema with bilateral, symmetrical caudodorsal distribution without venous congestion or cardiomegaly

80 cliniciansbrief.com October 2016


Cardiogenic edema is caused by
increased hydrostatic pressure and is
readily diagnosed by thoracic radio-
graphic documentation of left-sided
cardiomegaly, pulmonary venous conges-
tion, and a patchy interstitial or alveolar
pattern (frequently perihilar). Echocar-
diographic evaluation may support diag-
nosis.23 Natriuretic peptides may provide
additional insight in differentiation
between congestive heart failure and
other causes of respiratory distress (Fig-
ure 4). Plasma B-type natriuretic peptide
has been shown to have discriminatory
d FIGURE 5 Crenosoma vulpis (ie, lungworm). Note the patchy, unstructured
value in dogs; however, some degree of
interstitial densities. Larvae were recovered on bronchoscopy.
overlap exists between groups.24

Noncardiogenic edema is a low-pressure


edema characterized by increased blood patchy interstitial or alveolar infiltrates
vessel permeability. Seizures, electrocu- (Figure 5).28 Bullae may occasionally be
tion, strangulation or upper airway appreciated in association with some
obstruction, local pulmonary disease, infections (eg, Paragonimus kellicotti).29-31
and systemic inflammatory response
syndrome (ie, acute respiratory distress Peripheral eosinophilia is not always
syndrome) are the most commonly present with infection. Eosinophilic
reported causes.25,26 inflammation on airway cytology sup-
ports diagnosis. Identification of larvae
Thorough clinical history and physical or oocysts via fecal testing (eg, Baer-
examination are necessary to identify mann technique, fecal centrifugation)
potential underlying causes. Careful or airway sampling confirms diagno-
auscultation of the upper airways is sis.32 False-negative results can occur;
important. Radiographs often reveal any patient with eosinophilic bronchitis
bilateral, caudodorsal interstitial, and/ should be treated empirically. An
or alveolar disease. Radiographic pro- extended course of fenbendazole (ie,
gression can occur for as long as 48 2 weeks) is generally recommended to
hours.27 treat most pulmonary worms.

Lungworms Lung Lobe Torsion


Lungworms may cause bronchitis and Spontaneous lung lobe torsion occurs in
pneumonia. Chronic coughing is the dogs (most commonly pugs and Afghan
most common clinical sign. Acute-onset hounds33), can occur in any lung lobe,
exercise intolerance and/or respiratory and may be secondary to pleural effusion
distress may also be seen. or thoracic surgery. The right middle
lung lobe is overrepresented in deep-
Radiographic evaluation can vary from chested dogs; the left cranial lung lobe
a diffuse bronchointerstitial pattern to is overrepresented in pugs.33,34

October 2016 cliniciansbrief.com 81


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Nonspecific illness and respiratory signs Pulmonary neoplasia may, on occasion,


may be appreciated. Leukocytosis, left have a more diffuse nature. This is com-
shift, and pyrexia may be present.34 mon with pulmonary lymphoma40 and
Radiographs often reveal an alveolar pat- is sometimes seen with carcinoma
tern, trapped gas (vesiculated), and/or (author experience). Pulmonary lym-
pleural effusion. Bronchial malposition- phoma can have a rapid clinical course
ing is uncommon (Figure 6).35 Confirma- and mimic acute disorders. A diffuse,
tion via ultrasonography, bronchoscopy, unstructured interstitial pattern is typi-
and/or CT is recommended.36,37 Pleural cally appreciated. Additionally, bron-
fluid varies widely in gross and cytologic chointerstitial, alveolar, and nodular
appearance. Although nonspecific, the patterns may be observed (Figure 7).40
presence of pleural fluid, alveolar disease,
and acute respiratory signs is suggestive. Diagnosis of pulmonary lymphoma
Immediate lung lobectomy is warranted. requires airway cytology, pulmonary
fine-needle aspiration, and/or confirma-
Pulmonary Neoplasia tion on nonpulmonary samples.41
Radiographs usually reveal structured
interstitial densities within pulmonary Carcinoma frequently causes anorexia
parenchyma.38 These lesions may repre- and weight loss and should be consid-
sent primary or metastatic lesions. Clin- ered in older patients with refractory
ical signs are typically absent, although pneumonia.42
coughing is most common. Acute respi-
ratory signs may occur secondary to Pulmonary Embolism
generation of pleural effusion or bleed- Pulmonary embolism (PE) should be
ing from a lesion (ie, hemangiosarcoma suspected in dogs with acute respiratory
metastasis). Depending on the extent of signs, hypoxemia, and minimal radio-
PAH = pulmonary
arterial hypertension disease, anorexia, lethargy, and weight graphic changes. More common disor-
PE = pulmonary loss may be appreciated.39 ders should be ruled out. Radiographic
embolism

A B

d FIGURE 6 (A & B) Lung lobe torsion. Note classic vesicular pattern associated with gas trapping and pleural effusion. Bronchial attenuation
or displacement is subtle and often absent.

82 cliniciansbrief.com October 2016


findings vary from normal to patchy/
wedge-shaped alveolar/interstitial infil- A
trates. Pulmonary oligemia may be
appreciated in some patients (Figure 8,
next page).

Diagnostics should focus on document-


ing a predisposing hypercoagulable
state and attempting to confirm throm-
bosis. d-dimers, contrast angiography,
echocardiography, nuclear medicine,
and thoracic CT may indicate PE.43-45
Microvascular thrombosis may only be
documented on necropsy. However, no
test can reliably rule out PE; therefore,
treatment must be considered for B
patients in which the condition is sus-
pected. Optimal management has not
been described; however, anticoagulant
therapy is standard in human patients.
Thrombolytic therapy is standard in
humans with massive pulmonary throm-
boembolism (hemodynamically unsta-
ble). Recently, subpopulations of
submassive pulmonary thromboembo-
lism (hemodynamically stable) have
benefitted from thrombolytic therapy.46
Optimal thrombolytic protocols have not
been designed for dogs or cats. d FIGURE 7 (A) Pulmonary lymphoma with a diffuse, patchy bronchointerstitial
pattern confirmed on bronchoalveolar lavage and peripheral lymph node
aspiration. (B) Pulmonary carcinoma with a diffuse, severe bronchointerstitial
Pulmonary Arterial Hypertension pattern confirmed on bronchoalveolar lavage and postmortem examination.
Pulmonary arterial hypertension (PAH) Note: Pulmonary and hilar lymphadenopathy are not always present.
may be a primary vascular disorder or
secondary to cardiac disease, pulmonary
disease, or pulmonary embolism. The breath, exercise intolerance, collapse,
most commonly cited causes of PAH in syncope, right-sided congestive heart
dogs include chronic acquired valvular failure [rare]). Coughing is common and
disease, pulmonary disease, pulmonary is often associated with secondary causes
overcirculation, and heartworm dis- of PAH.52 Radiographic features and
ease.47-52 Primary pulmonary hyperten- physical examination results generally
sion has been described in dogs in reflect the underlying disease process;
association with a pulmonary arteriopa- rarely, pulmonary edema may be
thy53 and a primary pulmonary veno- observed.55 Investigation may be war-
occlusive condition.54 Patients may be ranted in at-risk patients (ie, patients
subclinical or may show signs of hypoxia with diffuse crackles, West Highland
(eg, weakness, fatigue, shortness of terriers with pulmonary fibrosis).

October 2016 cliniciansbrief.com 83


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Documentation of PAH can be performed Interstitial Lung Diseases


indirectly with echocardiography.56,57 Interstitial lung diseases are an uncom-
Direct pulmonary arterial measurement mon cause of respiratory disease in gen-
is rarely performed. PAH often contrib- eral. The most common interstitial lung
utes to signs with any chronic cardiopul- disease is idiopathic pulmonary fibrosis,
monary disease; thus, screening is which occurs most commonly in West
recommended. Phosphodiesterase type Highland terriers.62 Because of the
V inhibitors (eg, sildenafil,49,50,58 tadala- interstitial location of interstitial lung
fil59), pimobendan,60 and imatinib61 may diseases, histopathology is required for
be considered, depending on cause. definitive diagnosis.63 Common signs
include exercise intolerance, labored
breathing, syncope, and weakness.64
Coughing is typically not present.
Examination may reveal crackles,
fatigue, cyanosis, and a restrictive
breathing pattern.

Radiographs may reveal a diffuse,


unstructured interstitial pattern (Fig-
ure 9). Subtle changes in interstitial
opacity may go unnoticed despite severe
histologic disease.62

Thoracic CT may provide strong support


with a characteristic diffuse “ground
glass” appearance.65 This remains non-
d FIGURE 8 Pulmonary embolism confirmed on
necropsy. Note the right caudal lung field specific, however, and may be caused by
oligemia, which signifies vascular occlusion. other conditions. Additional supportive
diagnostics may include bronchoalveolar
lavage biomarkers (eg, endothelin-1)66 as
well as echocardiography to document
secondary pulmonary hypertension.

Additional Disorders
Other pulmonary conditions in dogs
include atypical infections (eg, Mycobac-
terium spp, protozoal),67,68 traumatic
injuries (eg, pulmonary contusions,
near-drowning), and inhaled irritants
(eg, pneumonitis, smoke). It is important
to note that the lungs may represent a
manifestation of systemic disease (eg,
leptospirosis, acute respiratory distress
d FIGURE 9 Idiopathic pulmonary fibrosis with a
diffuse bronchointerstitial pattern. Idiopathic
syndrome, anaphylaxis, transfusion-
PAH = pulmonary arterial
pulmonary fibrosis was confirmed on lung related acute lung injury). n
hypertension
biopsy.
See page 105 for references.

84 cliniciansbrief.com October 2016


ASK THE EXPERT h RESPIRATORY MEDICINE h CONTINUED FROM PAGE 84

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for the diagnosis of blastomycosis. J Vet Intern Med.
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Community-acquired infectious pneumonia in
puppies: 65 cases (1993-2002). J Am Vet Med Assoc. 21. Hage CA, Knox KS, Davis TE, Wheat LJ. Antigen detec-
2007;230(10):1493-1497. tion in bronchoalveolar lavage fluid for diagnosis of
fungal pneumonia. Curr Opin Pulm Med. 2011;17(3):
2. Priestnall S, Erles K. Streptococcus zooepidemicus: an 167-171.
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22. Clercx C, Peeters D, Snaps F, et al. Eosinophilic
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features of cardiogenic pulmonary edema in dogs with
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15. Clinkenbeard KD, Cowell RL, Tyler RD. Disseminated enhanced ultrasound findings in three dogs with
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Med Assoc. 1988;193(11):1443-1447. 37. Seiler G, Schwarz T, Vignoli M, Rodriguez D. Computed
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1998;213(5):658-664. 38. Barrett LE, Pollard RE, Zwingenberger A, Zierenberg-
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19. Arceneaux KA, Taboada J, Hosgood G. Blastomycosis St. Louis, MO: Elsevier; 2004;508-516.
in dogs: 115 cases (1980-1995). J Am Vet Med Assoc. 40. Geyer NE, Reichle JK, Valdés-Martínez A, et al.
1998;213(5):658-664. Radiographic appearance of confirmed pulmonary

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lymphoma in cats and dogs. Vet Radiol Ultrasound. of 53 dogs with Doppler derived evidence of pul-
2010;51(4):386-390. monary hypertension: 1992-1996. J Vet Intern Med.
41. Hawkins EC, Morrison WB, DeNicola DB, Blevins WE. 1999;13(5):440-447
Cytologic analysis of bronchoalveolar lavage fluid from 48. Pyle RL, Abbott J, MacLean H. Pulmonary hyperten-
47 dogs with multicentric malignant lymphoma. J Am sion and cardiovascular sequelae in 54 dogs. Int J Appl
Vet Med Assoc. 1993;203(10):1418-1425. Res Vet Med. 2004;2(2):99.
42. Bertazzolo W, Zuliani D, Pogliani E, Caniatti M, Bussa- 49. Bach JF, Rozanski EA, MacGregor J, et al. Retrospective
dori C. Diffuse bronchiolo-alveolar carcinoma in a dog. evaluation of sildenafil citrate as a therapy for pul-
J Small Anim Pract. 2002;43(6):265-268. monary hypertension in dogs. J Vet Intern Med. 2006;
43. LaRue MJ, Murtaugh RJ. Pulmonary thromboembo- 20(5):1132-1135.
lism in dogs: 47 cases (1986-1987). J Am Vet Med Assoc. 50. Kellum HB, Stepien RL. Sildenafil citrate therapy in 22
1990;197(10):1368-1372. dogs with pulmonary hypertension. J Vet Intern Med.
44. Goggs R, Benigni L, Fuentes VL, Chan DL. Pulmo- 2007;21(6):1258-1264.
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45. Johnson LR, Lappin MR, Baker DC. Pulmonary throm- with pulmonary arterial hypertension. J Vet Intern Med.
boembolism in 29 dogs: 1985-1995. J Vet Intern Med. 2007;21(6):1280-1289.
1999;13(4):338-345. 52. Kellihan HB, Stepien, RL. Pulmonary hyperten-
46. Nakamura S, Takano H, Kubota Y, Asai K, Shimizu W. sion in dogs: diagnosis and therapy. Vet Clin North Am
Impact of the efficacy of thrombolytic therapy on the Small Anim Pract. 2010;40(4):623-640.
mortality of patients with acute submassive pulmo- 53. Zabka TS, Campbell FE, Wilson DW. Pulmonary arte-
nary embolism: a meta-analysis. J Thromb Haemost. riopathy and idiopathic pulmonary arterial hyperten-
2014;12(7):1086-1095. sion in six dogs. Vet Pathol. 2006;43(4):510 -522.
47. Johnson L, Boon J, Orton EC. Clinical characteristics 54. Williams K, Andrie K, Cartoceti A, et al. Pulmonary

PRACTICE MARKETPLACE h CONTINUED FROM PAGE 107

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108 cliniciansbrief.com October 2016


CAUTION: Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian.
Description:
NexGard® (afoxolaner) is available in four sizes of beef-flavored, soft chewables for oral administration to dogs and puppies
according to their weight. Each chewable is formulated to provide a minimum afoxolaner dosage of 1.14 mg/lb (2.5 mg/
kg). Afoxolaner has the chemical composition 1-Naphthalenecarboxamide, 4-[5- [3-chloro-5-(trifluoromethyl)-phenyl]-4,
5-dihydro-5-(trifluoromethyl)-3-isoxazolyl]-N-[2-oxo-2-[(2,2,2-trifluoroethyl)amino]ethyl.
Indications:
NexGard kills adult fleas and is indicated for the treatment and prevention of flea infestations (Ctenocephalides felis), and
the treatment and control of Black-legged tick (Ixodes scapularis), American Dog tick (Dermacentor variabilis), Lone Star tick
(Amblyomma americanum), and Brown dog tick (Rhipicephalus sanguineus) infestations in dogs and puppies 8 weeks of age
veno-occlusive disease: a newly recognized cause of and older, weighing 4 pounds of body weight or greater, for one month.
severe pulmonary hypertension in dogs. Vet Pathol. Dosage and Administration:
NexGard is given orally once a month, at the minimum dosage of 1.14 mg/lb (2.5 mg/kg).
2016;53(4):813-822.
Dosing Schedule:
55. Kellihan HB, Waller KR, Pinkos A, Steinberg H, Bates Body Afoxolaner Per Chewables
Weight Chewable (mg) Administered
ML. Acute resolution of pulmonary alveolar infiltrates 4.0 to 10.0 lbs. 11.3 One
in 10 dogs with pulmonary hypertension treated with 10.1 to 24.0 lbs. 28.3 One
sidenafil citrate: 2005-2014. J Vet Cardiol. 2015;17(3):182- 24.1 to 60.0 lbs. 68 One
60.1 to 121.0 lbs. 136 One
191.
Over 121.0 lbs. Administer the appropriate combination of chewables
56. Johnson LR. Diagnosis of pulmonary hypertension.
NexGard can be administered with or without food. Care should be taken that the dog consumes the complete dose, and
Clin Tech Small Anim Pract. 1999;14(4):231-236. treated animals should be observed for a few minutes to ensure that part of the dose is not lost or refused. If it is suspected
that any of the dose has been lost or if vomiting occurs within two hours of administration, redose with another full dose. If
57. Johnson L, Boon J, Orton EC. Clinical characteris- a dose is missed, administer NexGard and resume a monthly dosing schedule.
tics of 53 dogs with Doppler-derived evidence of Flea Treatment and Prevention:
Treatment with NexGard may begin at any time of the year. In areas where fleas are common year-round, monthly
pulmonary hypertension: 1992-1996. J Vet Intern treatment with NexGard should continue the entire year without interruption.
Med. 1999;13(5):440-447. To minimize the likelihood of flea reinfestation, it is important to treat all animals within a household with an approved flea
control product.
58. Brown AJ, Davison E, Sleeper MM. Clinical efficacy of Tick Treatment and Control:
sildenafil in treatment of pulmonary arterial hyperten- Treatment with NexGard may begin at any time of the year (see Effectiveness).
sion in dogs. J Vet Intern Med. 2010;24(4):850-854. Contraindications:
There are no known contraindications for the use of NexGard.
59. Hori Y, Kondo C, Matsui M, et al. Effect of the phos- Warnings:
Not for use in humans. Keep this and all drugs out of the reach of children. In case of accidental ingestion, contact a
phodiesterase type 5 inhibitor tadalafil on pulmonary physician immediately.
hemodynamics in a canine model of pulmonary Precautions:
The safe use of NexGard in breeding, pregnant or lactating dogs has not been evaluated. Use with caution in dogs with a
hypertension. Vet J. 2014;202(2):334-339 history of seizures (see Adverse Reactions).
60. Atkinson KJ, Fine DM, Thombs LA, et al. Evaluation Adverse Reactions:
In a well-controlled US field study, which included a total of 333 households and 615 treated dogs (415 administered
of pimobendan and N-terminal probrain natriuretic afoxolaner; 200 administered active control), no serious adverse reactions were observed with NexGard.
peptide in the treatment of pulmonary hypertension Over the 90-day study period, all observations of potential adverse reactions were recorded. The most frequent reactions
reported at an incidence of > 1% within any of the three months of observations are presented in the following table. The
secondary to degenerative mitral valve disease in most frequently reported adverse reaction was vomiting. The occurrence of vomiting was generally self-limiting and of short
dogs. J Vet Intern Med. 2009;23(6):1190-1196. duration and tended to decrease with subsequent doses in both groups. Five treated dogs experienced anorexia during the
study, and two of those dogs experienced anorexia with the first dose but not subsequent doses.
61. Arita S, Arita N, Hikasa Y. Therapeutic effect of low- Table 1: Dogs With Adverse Reactions.
Treatment Group
dose imatinib on pulmonary arterial hypertension in
Afoxolaner Oral active control
dogs. Can Vet J. 2013;54(3):255-261. N1 % (n=415) N2 % (n=200)
62. Heikkila-Laurila HP, Rajamaki MM. Idiopathic Vomiting (with and without blood) 17 4.1 25 12.5
pulmonary fibrosis in West Highland white terriers. Dry/Flaky Skin 13 3.1 2 1.0
Diarrhea (with and without blood) 13 3.1 7 3.5
Vet Clin North Am Small Anim Pract. 2014;44(1):129-142.
Lethargy 7 1.7 4 2.0
63. Norris CR, Griffey SM, Walsh, P. Use of keyhole lung  Anorexia 5 1.2 9 4.5
biopsy for diagnosis of interstitial lung diseases in 1
Number of dogs in the afoxolaner treatment group with the identified abnormality.
dogs and cats: 13 cases (1998-2001). J Am Vet Med Assoc.
2
Number of dogs in the control group with the identified abnormality.
In the US field study, one dog with a history of seizures experienced a seizure on the same day after receiving the first
2002; 221(10):1453-1459. dose and on the same day after receiving the second dose of NexGard. This dog experienced a third seizure one week after
receiving the third dose. The dog remained enrolled and completed the study. Another dog with a history of seizures had
64. Reinero CR, Cohn LA. Interstitial Lung Diseases. Vet a seizure 19 days after the third dose of NexGard. The dog remained enrolled and completed the study. A third dog with a
Clin North Am Small Anim Pract. 2007;33(5):937-947. history of seizures received NexGard and experienced no seizures throughout the study.
To report suspected adverse events, for technical assistance or to obtain a copy of the MSDS, contact Merial at 1-888-637-
65. Johnson S, Corcoran BM, Wotton PR, Schwarz T, 4251 or www.merial.com/NexGard. For additional information about adverse drug experience reporting for animal drugs,
Sullivan M. Thoracic high-resolution computed contact FDA at 1-888-FDA-VETS or online at http://www.fda.gov/AnimalVeterinary/SafetyHealth.
Mode of Action:
tomographic findings in dogs with canine Afoxolaner is a member of the isoxazoline family, shown to bind at a binding site to inhibit insect and acarine ligand-gated
idiopathic pulmonary fibrosis. J Small Anim Pract. chloride channels, in particular those gated by the neurotransmitter gamma-aminobutyric acid (GABA), thereby blocking pre-
and post-synaptic transfer of chloride ions across cell membranes. Prolonged afoxolaner-induced hyperexcitation results in
2005;46(8):381-388. uncontrolled activity of the central nervous system and death of insects and acarines. The selective toxicity of afoxolaner
between insects and acarines and mammals may be inferred by the differential sensitivity of the insects and acarines’
66. Krafft E, Heikkila HP, Jespers P, et al. Serum GABA receptors versus mammalian GABA receptors.
and bronchoalveolar lavage fluid endothelin-1 Effectiveness:
In a well-controlled laboratory study, NexGard began to kill fleas four hours after initial administration and demonstrated >99%
concentrations as diagnostic biomarkers of canine effectiveness at eight hours. In a separate well-controlled laboratory study, NexGard demonstrated 100%
idiopathic pulmonary fibrosis. J Vet Intern Med. effectiveness against adult fleas 24 hours post-infestation for 35 days, and was ≥ 93% effective at 12 hours post-infestation
through Day 21, and on Day 35. On Day 28, NexGard was 81.1% effective 12 hours post-infestation. Dogs in both the treated
2011;25(5):990-996. and control groups that were infested with fleas on Day -1 generated flea eggs at 12- and 24-hours post-treatment (0-11
eggs and 1-17 eggs in the NexGard treated dogs, and 4-90 eggs and 0-118 eggs in the control dogs, at 12- and 24-hours,
67. Martinho AP, Franco MM, Ribeiro MG, et al. respectively). At subsequent evaluations post-infestation, fleas from dogs in the treated group were essentially unable to
Disseminated Mycobacterium tuberculosis infection produce any eggs (0-1 eggs) while fleas from dogs in the control group continued to produce eggs (1-141 eggs).
In a 90-day US field study conducted in households with existing flea infestations of varying severity, the effectiveness of
in a dog. Am J Trop Med Hyg. 2013;88(3):596-600. NexGard against fleas on the Day 30, 60 and 90 visits compared with baseline was 98.0%, 99.7%, and 99.9%, respectively.
68. Dubey JP, Lindsay DS, Lappin MR. Toxoplasmosis and Collectively, the data from the three studies (two laboratory and one field) demonstrate that NexGard kills fleas before they
can lay eggs, thus preventing subsequent flea infestations after the start of treatment of existing flea infestations.
other intestinal coccidial infections in cats and dogs. In well-controlled laboratory studies, NexGard demonstrated >97% effectiveness against Dermacentor variabilis, >94%
Vet Clin North Am Small Anim Pract. 2009;39(6): effectiveness against Ixodes scapularis, and >93% effectiveness against Rhipicephalus sanguineus, 48 hours post-infestation for
30 days. At 72 hours post-infestation, NexGard demonstrated >97% effectiveness against Amblyomma americanum for 30 days.
1009-1034. Animal Safety:
In a margin of safety study, NexGard was administered orally to 8 to 9-week-old Beagle puppies at 1, 3, and 5 times the
maximum exposure dose (6.3 mg/kg) for three treatments every 28 days, followed by three treatments every 14 days, for
a total of six treatments. Dogs in the control group were sham-dosed. There were no clinically-relevant effects related to
treatment on physical examination, body weight, food consumption, clinical pathology (hematology, clinical chemistries, or
coagulation tests), gross pathology, histopathology or organ weights. Vomiting occurred throughout the study, with a similar
incidence in the treated and control groups, including one dog in the 5x group that vomited four hours after treatment.
In a well-controlled field study, NexGard was used concomitantly with other medications, such as vaccines, anthelmintics,
antibiotics (including topicals), steroids, NSAIDS, anesthetics, and antihistamines. No adverse reactions were observed
from the concomitant use of NexGard with other medications.
Storage Information:
Store at or below 30°C (86°F) with excursions permitted up to 40°C (104°F).
How Supplied:
NexGard is available in four sizes of beef-flavored soft chewables: 11.3, 28.3, 68 or 136 mg afoxolaner. Each chewable size
is available in color-coded packages of 1, 3 or 6 beef-flavored chewables.
NADA 141-406, Approved by FDA
Marketed by: Frontline Vet Labs™, a Division of Merial, Inc.
Duluth, GA 30096-4640 USA
Made in Brazil.
®NexGard is a registered trademark, and TMFRONTLINE VET LABS
is a trademark, of Merial. ©2015 Merial. All rights reserved.
1050-4493-03
Rev. 1/2015

October 2016 cliniciansbrief.com 109


COLAPSO TRAQUEAL
J. Alberto Montoya Alonso
Medicina veterinaria
Facultad de Veterinaria
Universidad de Las Palmas de Gran Canaria
35413-Arucas (Las Palmas)

Resumen

En el colapso traqueal existe una reducción de la luz traqueal en cualquier

parte de su longitud. Habitualmente hay una disminución del diámetro dorso-

ventral que se traducirá en un alargamiento de la membrana traqueal dorsal.

Esta membrana dorsal ocupará un espacio en la luz traqueal con importancia

dentro del mecanismo del colapso. No se conocen las causas pero podría estar

ligado a un problema en el cartílago 1. Es muy frecuente observarlo en razas

miniatura. La sintomatología suele ser una dificultad en la inspiración y ataques

paroxísticos de tos definidos como“graznido de ganso”. El diagnóstico que

confirme el proceso será endoscópico y radiográfico. El tratamiento efectivo es

dificultoso ya que requiere la colocación de una prótesis endotraqueal o stent

“a medida”, tratamiento médico y una gran colaboración por parte del

propietario .

Definición

La tráquea es un conducto flexible que une las vías áereas altas (área nasal,

oral, faríngea y laringe) y bajas (bronquios y bronquiolos). Está formada por

anillos cartilaginosos en forma de “C” conectados por ligamentos anulares. La

parte abierta de estos anillos está completada por el músculo o membrana

traqueal dorsal.2

La situación de colapso es una reducción dinámica del diámetro de la luz


traqueal cervical y/o torácica.

La reducción del diámetro traqueal suele ser dorso-ventral y conlleva un

alargamiento de la membrana traqueal dorsal que será el causante del

colapso traqueal dinámico.

Etiología

Se desconoce aunque se han descrito problemas en la función de los

cóndrocitos que conducirá a defectos en el cartílago traqueal.

Hay una mayor incidencia de esta enfermedad en razas como el Yorkshire

Terrier, Caniche, Pomerania, Bichón Maltés,Pug, Chihuahua y, en general,

perros miniatura. Estos animales, una nutrición deficiente o factores

metabólicos pueden acabar con una alteración de la condrogénesis y del

metabolismo del cartílago.

Se pensó en una inervación deficiente de la membrana traqueal pero no se ha

demostrado.

En estudios realizados en la Universidad de Queensland durante dos años se

encontró que de 2780 perros el 0,5% presentaban esta patología. De 521

perros de raza miniatura el 2,7% (14 perros) tenían colapso traqueal. En

diversos estudios se ratificó que suelen ser perros de edad media (6-7 años).

Patología

La tráquea es una estructura de cierta flexibilidad pero que apenas cambia con

las variaciones de presión durante la respiración.

Inspiración. Cae la presión progresivamente de la glotis a los bronquiolos.


Habrá un aumento del flujo de aire hacia los pulmones.
Espiración. Las estructuras cartilaginosas de las paredes de las vías
respiratorias deberían evitar el colapso cuando aumente la
presión intrapleural.

Algunos animales afectados tienen una carencia de condroitín sulfato y


glucosaminoglicanos. Esto se traduce en una carencia de agua en la matriz del

cartílago y, por lo tanto, debilitamiento.El debilitamiento del cartílago facilita el

aplanamiento de la tráquea cervical en inspiración y al aplanamiento de las

vías respiratorias intratorácicas durante la espiración o durante la tos.

La obstrucción crónica da lugar a disnea y tos que induce a su vez laringo-

traqueo-bronquitis crónica. Estos trastornos unidos a otros concurrentes

(obstrucción de vías respiratorias altas, bronquitis crónica o insuficiencia

cardíaca crónica) pueden producir grave sintomatología. La obesidad agrava

más el proceso al alterarse la distensibilidad torácica y del diafragma, con lo

que asistiremos a una disminución en la expansión del pulmón en la inspiración

y a una tendencia evidente al colapso de las vías respiratorias.

Está descrita la intubación endotraqueal y las infecciones respiratorias como

Desencadenantes del cuadro.

Síntomas

El colapso cervical suele producir tos u obstrucción inspiratoria. El colapso

Intratorácico suele producirse durante la espiración y los signos suelen ser

más fuertes. Pueden coincidir ambos colapsos o no e incluso podemos

observar colapsos bronquiales sin que ocurran los traqueales.

Son frecuentes los ataques paroxísticos descritos como “graznido de ganso”.

Los signos pueden ser provocados por agitación, presión sobre la tráquea,

condiciones ambientales (elevada temperatura o humedad) o al comer o beber.

La tos puede acabar en vómito debido al intento de eliminar secreciones

acumuladas en las vías respiratorias.

Diagnóstico
. La exploración del animal:

- Perros de raza miniatura


- Ataques paroxísticos de tos en “graznido de ganso”, sobre todo en
agitación.
- Perros obesos
- Sensibilidad traqueal
- Traquea aplanada
- Ruidos inspiratorios y/o dificultad espiratoria a la auscultación

.Radiografías Torácicas en inspiración y espiración que nos ayudarán a ver los

posibles cambios dinámicos del colapso.

.Traqueobroncoscopia. Mediante este procedimiento podemos visualizar el

grado, la extensión y la gravedad del colapso. Es recomendable realizar en el

mismo procedimiento y lavado traqueobronquial que nos ayuden a realizar un

análisis citológico y un cultivo de las muestras recogidas.

La endoscopia de las vías respiratorias bajas es la técnica exploratoria indicada

y más útil para el estudio y diagnóstico de trastornos patológicos de dichas

vías, al proporcionar una visión directa y permitir al mismo tiempo obtener

muestras de tejidos, estructuras específicas o muestras de lavado. Esta prueba

es fundamental cuando queremos valorar anormalidades estructurales (colapso

traqueal), presencia de masas, comprobar el estado de las paredes de la

traquea y bronquios, observar la posible inflamación de las vías respiratorias,

presencia de exudados, torsiones lobares o la hemorragia pulmonar. También

es útil para recoger muestras para su análisis posterior.

Indicaciones de la traqueobroncoscopia:

 tos persistente
 expectoración
 hemoptisis
 lesión obstructiva
 aspiración de cuerpo extraño
 extracción de cuerpo extraño
 colapso traqueal
 lavados traqueales
 toma de exudados
 pólipos intraluminales
 diagnóstico de parasitosis
 tumores endotraqueales y endobronquiales
 toma de biopsias
 procesos infecciosos
 procesos crónicos

Esta contraindicada la realización de esta prueba en casos de disnea severa

por un proceso pulmonar o en casos de infección aguda del tracto respiratorio.

Para realizar la traqueobroncoscopia se pueden utilizar endoscopios

rígidos o flexibles. La broncoscopia se puede realizar con endoscopios rígidos

o flexibles dependiendo del tamaño de la tráquea. Los inconvenientes que nos

encontramos con estos aparatos son muchos, aparatos grandes no pueden ser

utilizados en animales pequeños y aparatos muy pequeños nos reducirán

mucho la ventana de imagen.

Lo ideal es utilizar anestesia inhalatoria, usando el tubo endotraqueal del

máximo grosor que nos permita un movimiento cómodo del endoscopio o un

sistema que comunique el oxígeno y anestésico a la tráquea a través del canal

de trabajo. Durante todo el procedimiento, el paciente debe ser monitorizado

(pulso, color de mucosas, tiempo de relleno capilar, frecuencia y calidad de

pulso y frecuencia respiratoria).

El endoscopio debe ser introducido a través de la laringe, evitando la

contaminación del mismo si queremos realizar toma de muestras. Una vez

dentro de la traquea, el ligamento traqueal (en posición dorsal), nos permite

situarnos. A nivel de la bifurcación de la traquea, se divisa la carina como un

delgado pilar. El bronquio derecho está más cerca de la traquea mientras que

el izquierdo forma un arco.

Cada bronquio se explora individualmente teniendo en cuenta que el


derecho es de más fácil exploración al encontrarse más cercano a la carina 3.

ANORMALIDADES TRAQUEO-BRONCOSCOPICAS DE LA TRAQUEA

Anormalidad Correlación clínica

Tráquea
Hiperemia, exceso de moco Inflamación
Mb. Traqueal redundante Colapso traqueal
Anillos aplanados Colapso traqueal
Estrechamiento uniforme hipoplasia traqueal
Estrechamiento trauma previo
Lesión en masa Anillo fracturado,
granuloma por c.e.,
neoplasias.

Tangner y Hobson propusieron un sistema de clasificación del colapso traqueal


según el grado de colapso2.observado en la traqueobroncoscopia.

Fig.1

Tratamiento

.Corticoesteroides

Para reducir la inflamación pero tienen el inconveniente que aumentan el jadeo

y el peso del animal.

.Broncodilatadores.

Pueden ir bien al disminuir la probabilidad del colapso respiratorio.

Teofilina 20 mg/kg/2 veces al día.

. Antibióticos.

Si es posible por cultivo del lavado traqueobronquial.

. Antitusivos.

Deben ser agentes potentes como el Butorfanol 0,5-1 mg/kg/2-4 veces al día.

.Tratar la insuficiencia cardíaca.


.Tratar la obesidad.

. Cambio de correa a arnés

. Evitar el calor, la humedad, la agitación y el estrés.

.Quirúrgico.

Se trata de la implantación de prótesis de anillo:

- Son pacientes muy pequeños por lo que es complicado.


- Puede producirse parálisis laríngea en un 20% de los casos.
- Hay un índice alto de complicaciones inmediatas a la cirugía.
- Hay un índice alto de complicaciones a medio y largo plazo.

. Stent endotraqueal.

Este puede ser un sistema rápido, eficaz y relativamente sencillo frente a otras

técnicas quirúrgicas (más agresivas) descritas para este fin.

Un stent es una red expansora del diámetro traqueal que se libera dentro de la

tráquea a través de un procedimiento endoscópico.

Una vez hemos medido la longitud del colapso, la longitud total de la tráquea y

el diámetro traqueal normal, seleccionaremos el modelo más apropiado para

nuestro paciente de aquellos que nos puedan suministrar los fabricantes de

Stent para humana. Es decir, realizaremos un estudio radiográfico y

endoscópico de la lesión, y consultando los distintos modelos existentes,

seleccionaremos aquel que expanda la zona estenosada, comprobando el

movimiento del stent y los posibles daños secundarios, haciendo controles a

los 30, 60 y 90 días.

Ventajas e inconvenientes de la técnica:

Ventajas:

 Rapidez
 Eficacia desde el primer momento
 Técnica no invasiva
 Fácil recolocación si se descoloca
 Fácil de comprobar radiológicamente
 Gran porcentaje de recuperación frente a otras técnicas
 Se puede extraer sin problemas secundarios

Inconvenientes:

 Descolocación
 Granuloma cicatricial post-stent
 Precio
 Dificultad de acceder al material por ser de humana (muchas
trabas legales)
 Rotura traqueal
 Hemorragias
J. Alberto Montoya-Alonso, Laín García-Guasch

ASMA BRONQUIAL FELINO


J. Alberto Montoya-Alonso, DVM, PhD, MSc, MA
Lain García-Guasch, DVM, PhD, MSc,
Facultad de Veterinaria de Las Palmas de Gran Canaria
35416- Arucas (Las Palmas)- ESPAÑA

El asma felino es una de las patologías respiratorias más frecuentes en gatos.


Consiste en una enfermedad inflamatoria crónica de las vías aéreas inferiores
(bronquios y bronquiolos) a menudo de causa no identificada. Suele afectar a
pacientes jóvenes o de mediana edad. Se ha observado cierta predisposición en
gatos siameses. Los signos clínicos típicos incluyen un cuadro de tos, estornudos,
intolerancia al ejercicio y distrés respiratorio agudo.

El tracto respiratorio dispone de ciertos mecanismos simples de defensa que


protegen a los pulmones de un agente nocivo externo. A partir de un estímulo
irritante o inflamatorio del epitelio respiratorio se produce:

- Inflamación y edema del epitelio bronquial.


- Hipertrofia e hiperactividad de la mucosa glandular con una mayor secreción
de moco.
- Contracción de la musculatura lisa bronquial.

Estos cambios comportan una reducción en el diámetro del tracto respiratorio, el


consiguiente incremento en la resistencia al paso de aire por las vías aéreas, y una
mayor inflamación que dará lugar a los signos clínicos.

La ley descrita por Poiseuille postula que el flujo de aire que circula a través del
bronquio es proporcional al radio elevado a la 4ª potencia (r4). Por lo tanto, siguiendo
esta ley, pequeños incrementos en el diámetro bronquial implicará una importante
mejoría en cuanto a los signos clínicos del paciente.

La obstrucción grave de las vías aéreas genera un estado de hiperinsuflación


pulmonar debido a la dificultad para exhalar completamente el aire. En ocasiones
tiene como consecuencia la dilatación permanente de las vías aéreas
(bronquiectasia) y una reducción en la elasticidad pulmonar (enfisema).

Por desgracia no existen signos clínicos ni ninguna prueba de laboratorio disponible


en la clínica rutinaria que sirva para diagnosticar que nuestro paciente presenta
asma bronquial felino.

El diagnóstico se realiza por eliminación tras descartar todas las posibles causas de
disnea aguda, estornudos y tos en gatos. El diagnóstico diferencial de un gato con

Asma bronquial felino-1


J. Alberto Montoya-Alonso, Laín García-Guasch

sospecha de asma bronquial debe incluir la bronquitis crónica, edema pulmonar o


secundario a insuficiencia cardiaca (es importante recordar que los fallos cardiacos
en gato no suelen dar tos), infecciones víricas, bacterianas o por Mycoplasma spp,
cuerpos extraños en vías aéreas (poco frecuente), parásitos del tracto respiratorio
como Paragonimus, Aelurostrongylus y Capillaria (poco frecuentes), infección por
Bordetella, enfermedades del parénquima pulmonar, derrame pleural, neumotórax,…
También hay que valorar si en el entorno del gato puede identificarse la presencia de
alergenos, polución ambiental, humo, aerosoles irritantes,…

Signos clínicos:

Los signos clínicos más frecuentemente asociados a un gato con asma incluyen
disnea, taquipnea, ortopnea, intolerancia al ejercicio, tos paroxística de grado medio
a moderado, y distrés espiratorio agudo. En los casos graves, debido a la
broncoconstricción suelen presentarse respirando con la boca abierta, con cianosis,
y en posición esternal con abducción de los codos (Imagen 1). Por desgracia estos
signos clínicos también se observan en pacientes cardiópatas descompensados.
Para determinar si los signos clínicos son de origen cardiaco, o bien secundarios a
un problema respiratorio es útil fijarse en la temperatura corporal. Los pacientes que
presentan un shock cardiogénico suelen estar hipodérmicos debido al bajo gasto
cardiaco, mientras que los gatos asmáticos sueles tener una temperatura corporal
normal. A diferencia de lo que ocurre en un gato asmático, un gato cardiópata no
suele presentar tos.

El examen físico debe realizarse sin generar ningún tipo de estrés. Puede ser
totalmente normal en reposo pero en ocasiones se observa una espiración forzada,
reflejo traqueal positivo, y se pueden auscultar sibilancias y crepitaciones. La
auscultación puede ser totalmente normal. Debido al atrapamiento de aire puede
identificarse una menor compresión de la caja torácica y un aspecto de tórax en
tonel.

En la bronquitis crónica el gato presenta una tos de aparición diaria de al menos dos
meses de duración y que no responde al tratamiento con broncodilatadores; en
cambio el asma, al ser una broncoconstricción aguda provoca una tos intermitente
que responde muy bien al tratamiento.

Radiografía:

Las radiografías pueden ser normales pero es habitual identificar evidencias de


engrosamiento de las paredes bronquiales (“donuts” y “vías de tren”) por la
inflamación (Imagen 2). Se puede observar un incremento en la radiolucencia
pulmonar sobre todo en los campos periféricos que indica la presencia de
atrapamiento de aire (“air trapping”), y un aplanamiento del diafragma debido a la

Asma bronquial felino-2


J. Alberto Montoya-Alonso, Laín García-Guasch

hiperinsuflación pulmonar. En un bajo porcentaje de los casos puede identificarse


atelectasia del lóbulo pulmonar medio derecho (Imagen 3). También en muy raras
ocasiones puede haber neumotórax o fracturas de costillas. A menudo se observa
aerofagia.

Analítica laboratorial:

El 20% de los gatos asmáticos presenta eosinofilia periférica, pero este hallazgo no
es específico ya que también se observa en pacientes sanos. También puede
asociarse a la presencia de parásitos intestinales, pulmonares, ectoparásitos o
filarias. Aunque es infrecuente, si el paciente presenta hipoxemia crónica puede
haber elevaciones en el hematocrito.

En el examen coprológico por flotación se debe buscar huevos de Paragonimus y


Capillaria; y mediante la cámara de Bareman larvas de Aelurostrongylus.

El examen citológico de la muestra obtenida por lavado broncoalveolar (BAL) suele


mostrar evidencias de inflamación de las vías aéreas ya que hay un incremento en el
número de eosinófilos y neutrófilos. Es complicado interpretar cultivos
bacteriológicos positivos ya que también se obtienen crecimientos a partir de
muestras de gatos sanos. En cambio se ha observado que el Micoplasma spp. crece
en el 25% de los cultivos de gatos asmáticos y no a partir de muestras de gatos
sanos.

Tratamiento

Tratamiento de emergencia:

Cuando un gato se presenta con un cuadro de distrés respiratorio agudo y grave


(con cianosis o respirando con la boca abierta), antes de realizar ninguna prueba de
diagnóstico se debe estabilizar al paciente reduciendo al mínimo el estrés. Se debe
administrar oxígeno al 40%-60% (mediante una cámara de oxigenación, incubadora,
flow-by,…) y un broncodilatador (terbutalina 0.01 mg/kg IM, IV, SC; Terbasmin®). Si
es posible, administrar también un broncodilatador inhalado. El de elección es el
albuterol (Ventolin®). Se trata de un β2-agonista de acción rápida muy efectivo en las
crisis agudas ya que relaja la musculatura bronquial e incrementa el diámetro de las
vías aéreas a los 5 minutos de haber sido administrado. Su efecto alcanza las 3-6
horas. La aminofilina tiene una actividad broncodilatadora menor que la terbutalina
por lo que no es un fármaco de primera elección.

A menudo es aconsejable sedarlo para poder manejarlo con mayor tranquilidad. El


tener que tomar esta decisión puede ser complicado ya que de entrada
desconocemos la causa del distrés respiratorio y pueden aparecer complicaciones

Asma bronquial felino-3


J. Alberto Montoya-Alonso, Laín García-Guasch

asociadas a los efectos secundarios de los fármacos administrados (sobre todo si se


trata de un paciente cardiópata). Se debe evitar el uso de fármacos y dosis que
puedan causar depresión respiratoria o que favorezcan a la aparición de arritmias. Si
no se dispone de un acceso acceso intravenoso y pensamos que puede ser un
paciente cardiópata, una buena combinación de fármacos es butorfanol (0.05-0.2
mg/kg) junto a midazolam (0.2-0.5 mg/kg) IM. Otra alternativa sería administrar
acepromacina (0.01-0.05 mg/kg) más ketamina (0.2 mg/kg) IM ya que la ketamina
tiene también potencialmente propiedades broncodilatadoras. Si se dispone de
acceso intravenoso se puede administrar igualmente la combinación de butorfanol
más midazolam, o también diazepam (5 mg/mL) más ketamina (100 mg/mL)
mezclados en proporción 1:1 y administrando 0.05-0.15 mL/Kg.

Lo esperable sería obtener una respuesta positiva en los primeros 30-45 minutos
con la consiguiente reducción de la frecuencia respiratoria y el esfuerzo espiratorio.
Si no responde favorablemente se debe volver a administrar el broncodilatador y
añadir una cortisona de acción rápida (dexametasona 0.25-2 mg/kg IV, IM). Si no
responde buscar otras causas de disnea y plantearse si es mejor intubar al gato y
realizar ventilación por presión positiva junto a la administración de oxígeno. En
cuanto sea posible realizar pruebas complementarias de diagnóstico (radiografías,
ecocardiografía, BAL,…) para descartar el resto de patologías.

Mediante pulsioximetría puede medirse el nivel de saturación de hemoglobina, que


debe mantenerse como mínimo al 92% ya que niveles menores de saturación se
correlacionan con una presión parcial de oxígeno arterial demasiado baja. Un nivel
de saturación inferior al 92% o bien una presión arterial de oxígeno por debajo de
75-80 mmHg indica un grado de hipoxemia de moderado a grave.

Pautas de terapia crónica:

En primer lugar, en caso de identificarlo, se debe eliminar la exposición al alergeno o


sustancia irritante responsable.

- Pacientes con crisis esporádicas:

En los pacientes en los que las crisis de disnea no ocurren de forma diaria se puede
administrar albuterol inhalado (Ventolin®) cada vez que el gato presente los signos
clínicos. En estos casos se presume que al no aparecer los síntomas de forma diaria
no existe suficiente inflamación de las vías aéreas como para administrar anti-
inflamatorios. Si la incidencia de aparición incrementa considerablemente se debe
plantear la necesidad de administrar una terapia más agresiva.

- Pacientes con crisis diarias:

Asma bronquial felino-4


J. Alberto Montoya-Alonso, Laín García-Guasch

En los pacientes que presentan síntomas de forma diaria pero que no tienen
dificultad respiratoria entre crisis las asmáticas, se puede administrar corticoides
inhalados como la fluticasona (Flixotide® de 220 μg) cada 12 horas, y tener
preparado albuterol (Ventolin®) para cuando tenga una cuadro asmático más fuerte.
Se puede observar cierta mejoría a las 24 horas de haber iniciado el tratamiento con
glucocorticoides inhalados, pero el máximo efecto no se alcanza hasta los 7-14 días.

Los gatos con cuadros asmáticos de grado moderado no presentan síntomas de


forma sostenida a lo largo de todo el día pero ya empiezan a tener una calidad de
vida algo peor. En estos casos se puede administrar fluticasona cada 12 horas,
albuterol cuando presente los episodios asmáticos, y prednisona a dosis de 1 mg/kg
PO cada 12 horas durante 5 días y posteriormente cada 24 horas durante 5 días
más. Tras 10 días de tratamiento con cortisona el paciente suele mejorar bastante y
se puede eliminar dicha medicación.

Cuando el paciente presenta síntomas clínicos en reposo la administración de


corticoides es el tratamiento más efectivo. Inicialmente se administra a dosis altas
(1-2 mg/kg bid PO durante 7-10 días) y a continuación se va reduciendo la
dosificación durante 2-3 meses. Se debe intentar pasar a corticoides inhalados,
aunque puede resultar caro y mal tolerado ya que el riesgo de efectos secundarios
es mucho menor en relación a la medicación administrada por vía oral. La
fluticasona (Flixotide®) se considera la formulación más potente y efectiva con el
mayor tiempo de acción y una mínima absorción a nivel sistémico. También es
necesario administrar albuterol (Ventolin®) cada 6-8 horas. Otro broncodilatador de la
misma familia es el salmeterol (Serevent®). Tarda unos 15-30 minutos en actuar pero
la duración de su efecto es mayor (> 12 horas). A diferencia del albuterol, éste no se
recomienda como tratamiento de elección en una crisis aguda sino como adyuvante
al tratamiento crónico con glucocorticoides. Algunos pacientes pueden necesitar
además una dosis mínima de cortisona vía oral, de mantenimiento, para controlar los
síntomas. En gatos que no toleran medicación vía oral se puede administrar acetato
de metilprednisolona a 10-20 mg/gato IM, SC cada 2-4 semanas.

En los gatos que no toleran la mediación mediante inhaladores se puede administrar


broncodilatadores agonistas β-adrenérgicos como la terbutalina (Terbasmin®) a
dosis de 0.625 mg PO bid. Los posibles efectos secundarios incluyen taquicardia,
nerviosismo e hipotensión. Otra opción son los derivados de las metilxantinas
(teofilina y aminofilina). Hasta hace unos años se podía administrar preparaciones
orales de larga duración (Theo-Dur®) a dosis de 20-25 mg/kg PO sid pero
actualmente se han retirado del mercado.

Los antibióticos no suelen administrarse ya que raramente los problemas


bronquiales en gatos se asocian a infecciones bacterianas del tracto respiratorio. Se
ha comprobado que a partir de muestras de BAL de gatos sanos se obtienen

Asma bronquial felino-5


J. Alberto Montoya-Alonso, Laín García-Guasch

resultados de cultivos falsamente positivos. La única excepción es en caso de


obtener crecimiento positivo de Mycoplasma spp en el cultivo ya que este
microorganismo no suele detectarse en cultivos de muestras tomadas de animales
sanos. Por ese motivo, se considera una buena opción administrar doxiciclina a
dosis de 10 mg/kg PO cada 24 horas hasta tener resultados del cultivo.

La serotonina es un mediador liberado por los mastocitos que interviene en el


proceso de contracción de la musculatura lisa bronquial. Estudios in vitro han
demostrado que la ciproheptadina posee un efecto antagonista de la serotonina. No
existen suficientes estudios in vivo publicados pero la dosis propuesta es de 1-4
mg/gato PO bid en gatos que no responden a la medicación con cortisona y
broncodilatadores. Los efectos secundarios incluyen letargia e incremento del
apetito.

Otros fármacos como la ciclosporina A, antagonistas de los receptores de


leucotrienos, anticuerpos anti-interleukinas, magnesio,… se han probado en humana
pero no hay suficientes estudios que demuestren su aplicación en veterinaria.

Pronóstico

La mayor parte de los gatos con problemas bronquiales responden bien a la terapia
pero el propietario debe ser consciente de que puede tratarse de una medicación
que tenga que administrarse de por vida para evitar recidivas.

Asma bronquial felino-6


Guideline and Recommendation
J Vet Intern Med 2017;31:279–294

Antimicrobial use Guidelines for Treatment of Respiratory Tract


Disease in Dogs and Cats: Antimicrobial Guidelines Working Group
of the International Society for Companion Animal Infectious
Diseases
M.R. Lappin, J. Blondeau, D. Boothe, E.B. Breitschwerdt, L. Guardabassi, D.H. Lloyd, M.G. Papich,
S.C. Rankin, J.E. Sykes, J. Turnidge, and J.S. Weese
Respiratory tract disease can be associated with primary or secondary bacterial infections in dogs and cats and is a com-
mon reason for use and potential misuse, improper use, and overuse of antimicrobials. There is a lack of comprehensive
treatment guidelines such as those that are available for human medicine. Accordingly, the International Society for Compan-
ion Animal Infectious Diseases convened a Working Group of clinical microbiologists, pharmacologists, and internists to
share experiences, examine scientific data, review clinical trials, and develop these guidelines to assist veterinarians in making
antimicrobial treatment choices for use in the management of bacterial respiratory diseases in dogs and cats.
Key words: Bronchitis; Pneumonia; Pyothorax; Rhinitis.

T his document contains guidelines for the treatment


of bacterial causes of feline upper respiratory tract
disease (URTD), canine infectious respiratory disease
Abbreviations:
CIRDC canine infectious respiratory disease complex
complex (CIRDC; previously known as canine infec- FCV feline calicivirus
tious tracheobronchitis or kennel cough complex), FHV-1 feline herpesvirus 1
bronchitis, pneumonia, and pyothorax that were final- PCR polymerase chain reaction
ized in 2016 by the Antimicrobial Guidelines Working URI upper respiratory infection
Group of the International Society for Companion URTD feline upper respiratory tract disease
Animal Infectious Diseases (www.iscaid.org). During
the development of the guidelines, other veterinary rec-
ommendations on antimicrobial treatment1–4 and corre- reviewed the literature and met in person to develop the
sponding guidelines for human medicine were initial draft of the guidelines. This was followed by a
evaluated, with consideration of the differences among number of revisions completed electronically in an
species.5,6 attempt to build consensus with the wording of each
The committee unanimously believes that there are recommendation within the Working Group. The
limitations in objective, published information relevant Working Group recommendations were then provided
to the treatment of bacterial respiratory diseases in dogs to all guidelines committee members who were asked to
and cats. Thus, the Working Group used a modification independently select whether they agreed, were neutral,
of the Delhi method for consensus building in the devel- or disagreed with a recommendation. A updated draft
opment of these guidelines.7 The Working Group of the document was then completed and provided to 6
experts in the field that were not members of the Work-
ing Group who were asked to rate each recommenda-
From the Colorado State University, Fort Collins, CO (Lappin); tion by means of the same system. For those
University of Saskatoon, Saskatoon, SK (Blondeau); Auburn
recommendations that received any “disagree” votes
University, Auburn, AL (Boothe); North Carolina State University,
Raleigh, NC (Breitschwerdt, Papich); University of Copenhagen, from the 17 total reviewers (Working Group and out-
Copenhagen, Denmark (Guardabassi); Royal Veterinary College, side reviewers), the percentage distribution of all review-
London, UK (Lloyd); University of Pennsylvania, Philadelphia, PA ers and appropriate comments are presented.
(Rankin); University of California, Davis, CA (Sykes); Ontario As with all guidelines, the antimicrobial use guideli-
Veterinary College, Guelph, ON (Weese); and the The Women’s nes for the treatment of bacterial respiratory tract infec-
and Children Hospital, Adelaide, SA, Australia (Turnidge). tions in dogs and cats should be interpreted as general
An overview of the guidelines was presented at the 2016 American
College of Veterinary Internal Medicine Forum, Denver, Colorado.
recommendations that are reasonable and appropriate
Corresponding author: M.R. Lappin, Colorado State University, for the majority of cases. The Working Group acknowl-
300 West Drake Road, Fort Collins, CO 80523; e-mail: mlappin@ edges the variability among cases and these guidelines
colostate.edu. should not be considered standards of care that must be
Submitted May 22, 2016; Revised September 5, 2016; followed in all circumstances. Rather, they should be
Accepted November 7, 2016. considered the basis of decision-making, with the poten-
Copyright © 2017 The Authors. Journal of Veterinary Internal tial that different or additional approaches might be
Medicine published by Wiley Periodicals, Inc. on behalf of the Ameri-
can College of Veterinary Internal Medicine.
required in some cases. Further, although these guideli-
This is an open access article under the terms of the Creative nes are designed as international guidelines that are
Commons Attribution-NonCommercial License, which permits use, appropriate for all regions of the world, the Working
distribution and reproduction in any medium, provided the original Group realizes that regional differences in antimicrobial
work is properly cited and is not used for commercial purposes. resistance rates, antimicrobial availability, prescribing
DOI: 10.1111/jvim.14627
280 Lappin et al

patterns, and restrictions on use of some agents exist. disease. The Working Group recommends that all cats
The user of this document is obligated to be familiar with suspected bacterial URI be evaluated for the pres-
with local and regional regulations that might restrict ence of feline leukemia virus antigen and feline immun-
use of certain antimicrobials listed in this document. odeficiency virus antibodies in serum in accordance
Diagnostic and treatment recommendations contained with the American Association of Feline Practitioners
in these guidelines are largely limited to those relating Retrovirus Panel Report.23 Although these retroviruses
to bacterial infection. do not cause respiratory disease directly, both have
been associated with lymphoma (which could cause
Feline Upper Respiratory Tract Disease URTD) and both can cause immunosuppression that
could predispose to severe viral and bacterial URIs.
Definitions and Causes Many diagnostic tests could be performed to assess for
evidence of primary or secondary bacterial URI (See the
Feline upper respiratory tract disease is a syndrome
Diagnosis of Chronic Bacterial Upper Respiratory Infec-
consisting of clinical signs that can include serous to
tion (>10 Days of Duration) section). It is the opinion
mucopurulent ocular and nasal discharges, epistaxis,
of the Working Group that there is limited benefit to per-
sneezing, and conjunctivitis.8–11 Clinical signs can be
forming cytology of nasal discharges to diagnose bacte-
acute (≤10 days) or chronic (>10 days). The term “up-
rial infection and guide the antimicrobial choice.
per respiratory infection (URI)” is reserved for cats
If nasal discharges are serous and lack a mucopuru-
with clinical signs of URTD that are directly associated
lent or purulent component, the Working Group
with one or more of the known pathogenic viral, bacte-
believes that antimicrobial treatment is not recom-
rial, or fungal organisms.
mended because of the likelihood of uncomplicated
It is believed that the majority of cats with acute clin-
viral infection.
ical signs of URTD have feline herpesvirus 1 (FHV-1)-
If acute bacterial URI is suspected based on purulent
or calicivirus (FCV)-associated URI. Some of the cats
or mucopurulent discharge, in the absence of evidence of
with viral infections can develop secondary bacterial
the cause of URTD based on history and physical exami-
infections.12–15 Staphylococcus spp., Streptococcus spp.,
nation findings, the Working Group recommends a per-
Pasteurella multocida, Escherichia coli, and anaerobes
iod of observation without immediate use of an
are organisms that are commonly cultured from the sur-
antimicrobial drug. This might vary in duration based on
face of the upper respiratory mucous membranes from
other clinical findings (See the Treatment of Suspected
healthy cats.16,17 However, several bacterial species,
Acute Bacterial Upper Respiratory Infection section). In
including Chlamydia felis, Bordetella bronchiseptica,
humans, antimicrobial treatment is recommended only if
Streptococcus canis, Streptococcus equi subspp. zooepi-
clinical signs have not improved after 10 days or have
demicus, and Mycoplasma spp., have been isolated or
worsened after 5–7 days.24 A more extensive workup for
detected by molecular techniques such as the poly-
an underlying cause can be postponed until after the per-
merase chain reaction (PCR) from cats with URTD
iod of observation, up to 10 days after the onset of clini-
without the presence of pathogenic viruses, suggesting a
cal signs if the cat develops chronic URTD.
primary role in some cats.16,18–22 The presence of puru-
Aerobic bacterial culture and antimicrobial suscepti-
lent or mucopurulent nasal or ocular discharges might
bility test results from nasal discharges are difficult to
increase the suspicion that primary or secondary bacte-
interpret because (1) some pathogenic organisms (eg,
rial infection is present, but there is no definite proof of
Chlamydia and Mycoplasma) cannot be cultured on
this association because viral or fungal agents can also
standard laboratory media and (2) positive culture
induce mucopurulent discharges.
might not be associated with bacterial infection due to
growth of commensal organisms. Thus, the Working
Diagnosis of Acute Bacterial Upper Respiratory Group recommends that aerobic bacterial culture and
Infection (≤10 Days Duration) antimicrobial susceptibility testing not be performed on
nasal secretions collected from cats with acute bacterial
For cats with signs of URTD of ≤10 days’ duration, URI.
a thorough history should evaluate in particular the Results from Mycoplasma spp. culture (or PCR
vaccination status, the presence or exposure to other assay), and molecular diagnostic procedures for FHV-1,
cats, whether cats are allowed outdoors, contact with a FCV, and C. felis are difficult to interpret in individual
shelter, kennel or veterinary hospital, health status of cats. Mycoplasma spp., FHV-1, FCV, and C. felis can
in-contact cats, health status of in-contact humans, be grown or amplified by molecular assays from both
exposure to dogs that might be boarded or have healthy or diseased cats, and vaccine strains of B. bron-
recently come from a shelter (possible increased risk of chiseptica, FHV-1, FCV, and C. felis can be detected by
infection by B. bronchiseptica), likelihood of foreign molecular diagnostic assays for varying periods of time
body contact (including house plants), and a history of depending on the vaccine type.25,26 When positive,
recent stress which is thought to reactivate FHV-1 molecular diagnostic tests for FCV, FHV-1, or C. felis
infection in some cats.17 Careful ocular, oral, and otic might be useful to support a diagnosis of infection in
examination to evaluate for other primary problems is the presence of suggestive clinical signs and the absence
indicated. Thoracic auscultation should be performed to of a history of recent vaccination. However, if an out-
evaluate for evidence of concurrent lower respiratory break of URI is suspected in populations of cats like
Respiratory Treatment Guidelines 281

Table 1. First-line antimicrobial options for bacterial respiratory infections in the dog and cat.
Infection Type First-Line Drug Options
Acute bacterial upper respiratory Doxycyclinea or amoxicillin per os (PO)
infection (URI) in cats
Chronic bacterial URI in cats Doxycycline or amoxicillin PO
Base the choice on C&Sb if available
Canine infectious respiratory disease complex Doxycyclinea or amoxicillin–clavulanate PO
(bacterial component)
Bacterial bronchitis (dogs or cats) Doxycyclinea PO
Base changes if needed on clinical responses and
C&S if available
Pneumonia in animals with extensive contact with Doxycyclinea PO
other animals that have no systemic manifestations Base changes if needed on clinical responses
of disease (ie, fever, lethargy, dehydration) and C&S if available
Pneumonia with or without clinical evidence of sepsisc Parenteral administration of a fluoroquinoloned and a
penicillin or clindamycine initially
Base oral drug choices to follow on clinical responses
and C&S results if available
Pyothorax (dogs or cats)b Parenteral administration of a fluoroquinoloned and a
penicillin or clindamycine initially combined with
therapeutic lavage initially
Base oral drug choices to follow on clinical responses
and C&S results if available
a
Minocycline has been substituted in some situations when doxycycline is unavailable or of greater expense. See Table 2 for dose recom-
mendations.
b
Culture and antimicrobial susceptibility testing = C&S.
c
For animals with clinical findings of life-threatening disease, the consensus of the Working Group was to administer dual agent treat-
ment parenterally with the potential for de-escalation of treatment and switch to oral drugs based on clinical responses and culture and
antimicrobial susceptibility testing. See Table 2 for dose differences by route and the text for further recommendations for oral or par-
enteral administration.
d
Enrofloxacin is often chosen as there is a veterinary product for parenteral administration and the drug has a wide spectrum against
Gram-negative organisms and Mycoplasma spp. There are other drugs with a wide spectrum against Gram-negative bacteria that can be
substituted based on antimicrobial susceptibility testing or clinician preference. See Table 2 for a discussion of how to administer enrofloxa-
cin and for other drug choices. Enrofloxacin should be administered at ≤5 mg/kg/24 h in cats to lessen risk of retinal degeneration. One
reviewer noted that IV ciprofloxacin could also be used; however, the other reviewers (94%) believed that enrofloxacin should be used as
labeled for veterinary use.
e
When enrofloxacin or other drugs with Gram-negative activity are administered parenterally to animals with life-threatening disease,
concurrent administration of other parenteral drugs with activity against anaerobes and Gram-positive bacteria is recommended. Common
choices include ampicillin or clindamycin. Which of these drugs to choose will depend on the most likely infectious agent suspected and
historical antimicrobial resistance in the geographical region. For example, Enterococcus spp. and Streptococcus spp. are more likely to be
susceptible to a penicillin, and Toxoplasma gondii and Neospora caninum are more likely to be susceptible to clindamycin. Cephalosporins
are generally not recommended for the treatment of anaerobic infections because of unpredictable activity and lack of evidence for their
efficacy. Please see the text for further discussion of other potential drug choices or combinations.

those in shelters, catteries, boarding facilities, or multi- If antimicrobial treatment is chosen for a cat with
ple cat households, these assays also might be indicated, acute bacterial URI, the optimal duration of treatment
particularly if severe clinical disease is occurring. If pos- is unknown and so this recommendation is based on
sible, several affected cats should be evaluated to experiences of the Working Group members that are
increase sensitivity and positive predictive value of the clinicians. The Working Group recommends empirical
assay results. administration of doxycycline (Tables 1 and 2) for 7–
10 days to cats with suspected acute bacterial URI as
Treatment of Suspected Acute Bacterial Upper the first-line antimicrobial option.27,28 The Working
Respiratory Infection Group believes that doxycycline is a good first choice
because it is well tolerated by cats; most B. bronchisep-
Some cats with mucopurulent nasal discharge main- tica isolates from cats are susceptible to doxycycline
tain normal appetite and attitude and experience spon- in vitro (by unapproved standards for testing), despite
taneous resolution of illness within 10 days without resistance to other agents such as beta-lactams and
antimicrobial treatment. The Working Group recom- sulfonamides,29–31 and doxycycline is effective in vivo
mends that antimicrobial treatment be considered for the treatment of cats with C. felis infections,27,32–34
within the 10-day observation period only if fever, and Mycoplasma spp. infections.35 Doxycycline is also
lethargy, or anorexia is present concurrently with effective for the treatment of a variety of chlamydial
mucopurulent nasal discharge. and mycoplasma infections in cats and other
282 Lappin et al

Table 2. Antimicrobial treatment options for respiratory tract infections in the dog and cat.
Drug Dose Comments
Amikacin Dogs: 15 mg/kg, IV/IM/SC, q24h Not recommended for routine use but might be useful for the
Cats: 10 mg/kg, IV/IM/SC, q24h treatment of multidrug-resistant organisms or if parenteral
enrofloxacin or ciprofloxacin are contraindicated. Potentially
nephrotoxic. Avoid in dehydrated animals and those with renal
insufficiency
Amoxicillin 22 mg/kg, PO, q12h Might be useful for the treatment of secondary bacterial URI
caused by Pasteurella spp. and Streptococcus spp., some
Staphylococcus spp. and many anaerobic bacteria. Ineffective
against beta-lactamase-producing bacteria, most Bordetella
bronchiseptica isolates, all Mycoplasma spp., and Chlamydia felis in
cats. One Working Group member supports the use of amoxicillin
q8h because of the short plasma half-life
Amoxicillin–clavulanate Dogs: 11 mg/kg, PO, q12h Used as a first-line option for secondary bacterial URI from
Cats: 12.5 mg/kg, PO, q12h Pasteurella spp., Streptococcus spp., methicillin-susceptible
(dose based on Staphylococcus spp. (including penicillinase-producing strains),
combination of many anaerobic bacteria, and most B. bronchiseptica isolates.
amoxicillin–clavulanate Ineffective against all Mycoplasma spp., and inferior to other drugs
for C. felis in cats. One Working Group member supports the use
of amoxicillin q8h because of the short plasma half-life
Ampicillin-sulbactam 20 mg/kg, IV, IM, q6–8h Used alone parenterally for cases with uncomplicated secondary
bacterial pneumonia (Gram-positive and anaerobic bacteria). Used
concurrently with another drug with wider Gram-negative activity
if life-threatening disease exists
Ampicillin sodium 22–30 mg/kg, IV, SQ, q8h Used parenterally for cases with uncomplicated secondary bacterial
pneumonia (Gram-positive and anaerobic bacteria). Used
concurrently with another drug with Gram-negative activity if life-
threatening disease exists
Azithromycin 5–10 mg/kg, PO, q12h day 1 Used for primary bacterial diseases (in particular Mycoplasma spp.)
and then q3 days (Longer and for pneumonia of undetermined etiology because the spectrum
intervals are not indicated) includes Toxoplasma gondii and Neospora caninum
Cefazolin 25 mg/kg, SQ, IM, IV, q6h Used parenterally for cases with uncomplicated secondary bacterial
pneumonia (Gram-positive and anaerobic bacteria). Used
concurrently with another drug with wider Gram-negative activity
if life-threatening disease exists. Ineffective against
B. bronchiseptica, Mycoplasma spp., and C. felis in cats, and
enterococci
Cefadroxil Dogs: 11–22 mg/kg, PO, q12h Used PO for secondary bacterial URI from Pasteurella spp., and
Cats: 22 mg/kg, PO, q24h some Staphylococcus spp. and Streptococcus spp., and many
anaerobic bacteria. Ineffective against B. bronchiseptica,
Mycoplasma spp., and C. felis in cats, and Enterococcus spp.
Resistance might be common in Enterobacteriaceae in some regions
Cefoxitin 10–20 mg/kg, IV, IM, q6–8h Used parenterally for cases with secondary bacterial pneumonia
(Gram-positive and anaerobic bacteria). Has a greater Gram-
negative spectrum than first-generation cephalosporins. Ineffective
against B. bronchiseptica, Mycoplasma spp., and C. felis in cats,
and Enterococcus spp
Cefovecin 8 mg/kg, SC, once. Can be repeated Might be effective for the treatment of secondary bacterial URI
once after 7–14 days caused by Pasteurella spp., some Staphylococcus pseudintermedius
and Streptococcus spp. Ineffective for B. bronchiseptica,
Mycoplasma spp., and C. felis in cats and Enterococcus spp.
Pharmacokinetic data are available to support the use in dogs and
cats, with a duration of 14 days (dogs) and 21 days (cats)
Cephalexin 22–25 mg/kg, PO, q12h See cefadroxil comments
Chloramphenicol Dogs: 50 mg/kg, PO, q8h Reserved for multidrug-resistant infections with few other options.
Cats: 50 mg/cat, PO q12h Effective for the primary bacterial pathogens, penetrates tissues
well, and has an excellent spectrum against anaerobes and so
might be considered for the treatment of pneumonia when the
owner cannot afford dual antimicrobial agent treatment.
Myelosuppression can occur, particularly with long-term treatment.
Owners should be instructed to wear gloves when handling the
drug because of rare idiosyncratic aplastic anemia in humans

(continued)
Respiratory Treatment Guidelines 283

Table 2 (Continued)

Drug Dose Comments


Clindamycin Dogs: 10 mg/kg, PO, SC, q12h Activity against most anaerobic bacteria, many Gram-positive
Cats: 10–15 mg/kg, PO, SC, q12h bacteria and some mycoplasmas. Not effective for most Gram-
negative bacteria and some Bacterioides spp.
Doxycycline 5 mg/kg, PO, q12h Used for dogs or cats with URI, CIRDC, or bronchitis that is likely
Or to be associated with B. bronchiseptica, Mycoplasma spp., and
10 mg/kg, PO, q24h C. felis (cats). An injectable formulation is available if parenteral
administration is needed. Either the hyclate or monohydrate salts
can be used. Can be used in kittens and puppies >4 weeks of age
without enamel discoloration
Enrofloxacin Dogs: 5–20 mg/kg PO, IM, IV q24h Active against most isolates of B. bronchiseptica, Mycoplasma spp.,
Cats: 5 mg/kg, PO, q24h and C. felis (cats) as well as many secondary Gram-negative and
Gram-positive bacteria. Practically no activity against Enterococcus
spp and anaerobic bacteria. Associated with risk of retinopathy in
cats and so do not exceed 5 mg/kg/d of enrofloxacin in this
species. All quinolones are associated with cartilage problems in
growing puppies and kittens. Enrofloxacin is not approved for
parenteral use in cats and is not soluble enough to be injected
directly. It can precipitate and can chelate with cations in some
fluid solutions. One Working Group member recommends never
with the 5 mg/kg dose in dogs because of likely induction of
resistant strains and 1 Working Group member does not
recommend the drug for cats because the 5 mg/kg dose might
induce resistance and higher doses can induce retinal degeneration
Gentamicin Dogs: 9–14 mg/kg, IV, q24h Not recommended for routine use but might be useful for the
Cats: 5–8 mg/kg, IV, q24h treatment of multidrug-resistant organisms or if parenteral
enrofloxacin is contraindicated. Potentially nephrotoxic. Avoid in
dehydrated animals and those with renal insufficiency
Imipenem–cilastatin 3–10 mg/kg, IV, IM q8h Reserve for the treatment of multidrug-resistant infections,
particularly those caused by Enterobacteriaceae or Pseudomonas
aeruginosa. Recommend consultation with a respiratory or infectious
disease veterinary specialist or veterinary pharmacologist before use
Marbofloxacin 2.7–5.5 mg/kg PO q24h Effective for the primary bacterial pathogens B. bronchiseptica,
Mycoplasma spp., and C. felis (cats) as well as many secondary
infections with Gram-negative and Gram-positive organisms.
Limited efficacy against Enterococcus spp. and anaerobic bacteria.
Available as an injectable solution in some countries
Meropenem Dogs: 8.5 mg/kg SC q12h Reserve for the treatment of multidrug-resistant infections,
Or 24 mg/kg IV q12h particularly those caused by Enterobacteriaceae or P. aeruginosa.
Cats: 10 mg/kg q12h, SC, IM, IV Recommend consultation with an infectious disease veterinary
specialist or veterinary pharmacologist before use
Minocycline Dogs: 5 mg/kg, PO, q12h Similar to doxycycline and can be used for dogs or cats with URI,
Cats: 8.8 mg/kg PO q24h or CIRDC, or bronchitis that is likely to be associated with
50 mg/cat PO q24h B. bronchiseptica, Mycoplasma spp., and C. felis (cats)
Orbifloxacin 2.5–7.5 mg/kg PO q12h for tablets See Marbofloxacin comments. The oral suspension is well tolerated
7.5 mg/kg, PO, q12h for the oral by cats
suspension in cats
Ormetoprim- 27.5 mg/kg, PO q24h in dogs See comments on trimethoprim–sulfonamide-containing products
sulfadimethoxine Note: dosing is based on total
sulfadimethoxine-ormetoprim
concentration (5 to 1 ratio)
Pradofloxacin 5.0 mg/kg PO q24h if tablets are Effective for the primary bacterial pathogens B. bronchiseptica,
used in dogs or cats Mycoplasma spp., and C. felis (cats) as well as many secondary
7.5 mg/kg PO q24h if oral infections with Gram-negative and Gram-positive organisms. In
suspension for cats is used contrast to other veterinary fluoroquinolones, pradofloxacin has
activity against some anaerobic bacteria. The drug is labeled in
some countries for the treatment of acute infections of the upper
respiratory tract of cats caused by susceptible strains of Pasteurella
multocida, Escherichia coli and the S. intermedius group (including
S. pseudintermedius). The use of pradofloxacin in dogs has been
associated with myelosuppression and is extra-label in North
America

(continued)
284 Lappin et al

Table 2 (Continued)

Drug Dose Comments


Piperacillin-tazobactam 50 mg/kg IV q6h for Antipseudomonal penicillin. Used for life-threatening pneumonia or
immunocompetent animals, pyothorax for the treatment of Gram-negative (including some
or 3.2 mg/kg/h CRI, after loading ESBL), Gram-positive and anaerobic bacteria. Ineffective for
dose of 3 mg/kg IV, for other Mycoplasma, T. gondii, and N. caninum
animals
Trimethoprim- 15 mg/kg PO q12h Generally avoided in respiratory tract infections that might involve
sulfamethoxazole, Note: dosing is based on total anaerobic bacteria (particularly pyothorax). Might be less effective
trimethoprim-sulfadiazine trimethoprim + sulfadiazine that other first-line choices for some primary bacterial pathogens
concentration other than Streptococcus spp. Concerns regarding adverse effects
exist (KCS, folate deficiency anemia, blood dyscrasias) in some
dogs, especially with prolonged treatment. If prolonged (>7 day)
treatment is anticipated, baseline Schirmer’s tear testing is
recommended, with periodic re-evaluation and owner monitoring
for ocular discharge. Avoid in dogs that might be sensitive to
potential adverse effects such as KCS, hepatopathy,
hypersensitivity, and skin eruptions, and owners of treated dogs
should be informed of the clinical findings to be monitored.

CIRDC, canine infectious respiratory disease complex; URI, upper respiratory infection.

mammalian host species. It also has activity against clavulanate potassium (amoxicillin–clavulanate) had
many opportunistic bacterial pathogens that are compo- apparent clinical responses in 1 study of shelter cats
nents of the normal microbiota of the respiratory tract. with acute bacterial URI and so this drug also could be
Of the 17 reviewers, 16 (94%) agreed with this Working considered as an alternative to doxycycline in regions
Group recommendation and 1 disagreed because there where a high prevalence of beta-lactamase-producing
is no breakpoint data for this antimicrobial for B. bron- organisms has been identified (eg, based on regional
chiseptica or other bacteria in cats and there are no antibiograms).44
pharmacokinetics, controlled clinical trials, susceptibility In 1 study of shelter cats with suspected bacterial URI,
data, or pharmacodynamic data on which to base the the injectable cephalosporin, cefovecin was inferior to
recommendation. doxycycline or amoxicillin–clavulanate.44 One limitation
Due to delayed esophageal transit time for capsules of this study was the lack of a negative control group.44
and tablets, cats are prone to drug-induced esophagitis Thus, it is the opinion of the Working Group that more
and resultant esophageal strictures.36,37 Although any evidence is needed before cefovecin can be recommended
table or capsule could cause this problem, doxycycline for the treatment of bacterial URI in cats (Table 2).
hyclate tablets and clindamycin hydrochloride cap-
sules have been reported most frequently to cause Monitoring Treatment of Suspected Acute Bacterial
problems.38–40 Thus, tablets and capsules should be given Upper Respiratory Infection
coated with a lubricating substance, followed by water,
administered in a pill treat, concurrently with at least Most cats with this syndrome will rapidly improve
2 mL of a liquid, or followed by a small amount of within 10 days with or without antimicrobial adminis-
food.37 Doxycycline formulated and approved for use in tration. If an antimicrobial drug was prescribed and
cats is available in some countries and should be used if was ineffective and bacterial infection is still suspected
available. The use of compounded suspensions of doxy- after the first 7–10 days of administration, the Working
cycline should be avoided because marketing of such for- Group recommends that a more extensive diagnostic
mulations is in violation with regulations in some workup should be offered to the owner. An alternate
countries, including the USA. In addition, compounded antimicrobial agent with a different spectrum should be
aqueous-based formulations of doxycycline are associ- considered only if the owner refuses a diagnostic
ated with a variable loss of activity beyond 7 days.41 workup and careful re-evaluation of the cat still sup-
Minocycline pharmacokinetics are now available for cats ports the presence of a bacterial infection without an
and this tetracycline should be evaluated further for effi- obvious underlying cause (see the Diagnosis of acute
cacy against infectious disease agents in cats.42 bacterial Upper Respiratory Infection section). Longer
The Working Group considers amoxicillin to be an duration of treatment might be required to clear the
acceptable alternate first-line option for the treatment carrier state of C. felis.33,34
of acute bacterial URI when C. felis and Mycoplasma
are not highly suspected. This is based on evidence that Diagnosis of Chronic Bacterial Upper Respiratory
cats administered amoxicillin for the treatment of sus- Infection (>10 Days of Duration)
pected secondary bacterial infections in shelter cats with
acute bacterial URI often have apparent clinical A more extensive diagnostic workup should be con-
responses.20,43 Cats administered amoxicillin and sidered for cats with URTD of >10 days of duration,
Respiratory Treatment Guidelines 285

particularly in the face of therapeutic failure after treat- Staphylococcus intermedius group.46 In 1 study of shel-
ment of suspected acute bacterial URI as described. ter cats, a pradofloxacin protocol was equivalent to
The diagnostic workup should be performed to eval- amoxicillin for the treatment of suspected bacterial
uate for other causes including Cuterebra spp. and fun- URI.20 The other veterinary fluoroquinolones (en-
gal diseases as well as noninfectious causes of URTD rofloxacin, orbifloxacin, and marbofloxacin [Table 2])
including allergic diseases, neoplasia, foreign bodies, have also been used by veterinarians to treat suspected
nasopharyngeal stenosis, oronasal fistulas, nasopharyn- feline bacterial URI.47 In the first study, all cats were
geal polyps, and trauma.8–11 Referral to a specialist is administered an antibiotic;20 a placebo control study
recommended if advanced imaging or rhinoscopy capa- evaluating pradofloxacin for the treatment of bacterial
bilities are not available. If other treatable causes of URI in cats has not been published to our knowledge.
URTD are not identified, The Working Group recom- Because of concerns about the emergence of, and ani-
mends that nasal lavage or brushings (for cytology, aer- mal and public health consequences of, resistance to flu-
obic bacterial culture and antimicrobial susceptibility oroquinolones and third-generation cephalosporins, the
testing, Mycoplasma spp. culture or PCR, and fungal Working Group recommends that these drugs should
culture) and nasal tissue biopsy for histopathological be reserved for situations where culture and susceptibil-
examination with or without cultures (if not evaluated ity results indicate potential efficacy and when other
by lavage) should be performed. Of the 17 reviewers, antimicrobial agents (eg, doxycycline, amoxicillin) are
16 (94%) agreed with the recommendation and 1 dis- not viable options. Moreover, there is no clinical evi-
agreed and stated that the results of nasal tissue cul- dence indicating that fluoroquinolones and third-genera-
tures in cats with chronic URTD are always impossible tion cephalosporins are superior to doxycycline and
to interpret. amoxicillin in the treatment of chronic bacterial URI in
In 1 study, nasal lavage specimens gave a higher cats.
sensitivity for bacterial growth than tissue biopsy Although azithromycin pharmacokinetics have been
specimens.45 However, as discussed previously, bacterial determined in cats,48,49 azithromycin and amoxicillin
culture results can be difficult to impossible to interpret protocols for the treatment of suspected bacterial upper
as bacteria can be cultured from the nasal cavity of respiratory tract infections in shelter cats were equiva-
healthy cats. For example, multidrug-resistant bacteria lent in 1 study where all cats were administered an
can colonize and be grown from the nasal passages in antibiotic.43 Azithromycin is also not as efficacious as
the absence of infection. The purpose of culture and doxycycline for the treatment of feline ocular chlamy-
susceptibility testing in cats with chronic bacterial URI diosis in a study in which all cats were administered an
is usually to identify the antimicrobial susceptibility of antibiotic.33 Thus, the Working Group recommends
severe secondary bacterial infections that occur sec- that azithromycin should be reserved for situations
ondary to an untreatable underlying cause (eg, idio- when chlamydiosis is not likely and when other antimi-
pathic inflammatory rhinitis). Antimicrobial treatment crobial agents (eg, doxycycline, amoxicillin) are not
of these cats might provide relief from severe clinical viable options. Of the 17 reviewers, 16 (94%) agreed
signs, but it should be recognized that these cats will with this recommendation. One reviewer commented
continue to be predisposed to opportunistic infections, that there is evidence that azithromycin treatment in
often with antimicrobial-resistant bacteria. Therefore, people produces therapeutic benefits for infections of
use of antimicrobials should be limited to those cats the respiratory tract via mechanisms that are not attrib-
with severe clinical signs. uted to the antibacterial properties.49 However, at this
The Working Group recommends consultation with time, the Working Group does not advocate for the
an internal medicine specialist with expertise in infec- administration of azithromycin to animals only for its
tious disease, clinical pharmacologist, or clinical micro- disease-modifying properties or immunomodulatory
biologist before treating multidrug-resistant organisms effects.
(resistant to ≥3 drug classes) isolated from nasal lavage If Pseudomonas aeruginosa is isolated in pure or
cultures. nearly pure culture and believed to be the cause of a
secondary infection, extensive flushing of the nasal cav-
Treatment of Chronic Feline Bacterial Upper ity under anesthesia should be performed to remove
Respiratory Infection loculated secretions. Although use of drug combinations
(such as a fluoroquinolone combined with a beta-lactam
In cats with chronic bacterial URI, the antimicrobial [Table 2]) has been recommended to treat P. aeruginosa
agent should be selected on the basis of culture and infections because of the tendency of this organism to
antimicrobial susceptibility test results if available. If an rapidly develop resistance, monotherapy with a fluoro-
organism with resistance against a previously prescribed quinolone is accepted for the treatment of P. aeruginosa
antimicrobial agent is identified and the clinical otitis/osteomyelitis in human patients, unless resistance
response is poor, an alternate drug should be substi- is encountered.50,51 Regardless of whether monotherapy
tuted (Table 2). or combination treatment is chosen, the Working
Pradofloxacin is a veterinary fluoroquinolone that is Group recommends that antimicrobials be selected on
approved in some countries for the treatment of acute the basis of culture and susceptibility testing and that a
infections of the upper respiratory tract caused by clinical microbiologist, clinical pharmacologist, or inter-
susceptible strains of P. multocida, E. coli and the nal medicine specialist with expertise in infectious
286 Lappin et al

disease be consulted before initiating treatment. Of the Monitoring Treatment of Chronic Bacterial Upper
17 reviewers, 15 (88%) agreed with this recommenda- Respiratory Infection
tion and 2 were neutral (12%).
Optimal duration of the treatment of chronic bacte- Because results of bacterial culture and antimicrobial
rial URI in cats with no other underlying disease is susceptibility testing from specimens collected from the
unknown. The consensus of the Working Group was to nasal cavity are difficult to interpret, monitoring the
administer the chosen antimicrobial for at least 7 days efficacy of treatment of cats with suspected chronic bac-
and if the drug is tolerated and showing a positive clini- terial URI is usually based on clinical signs of disease.
cal effect, the drug should be continued as long as there
is progressive clinical improvement and for at least Canine Infectious Respiratory Disease Complex
1 week past clinical resolution of nasal disease or pla-
Definition and Causes
teau in response to treatment. However, the Working
Group acknowledges that stopping treatment sooner The clinical syndrome associated with CIRDC is gen-
might also be effective in some cats. erally characterized by an acute onset of cough with or
If mucopurulent discharge with or without sneezing without sneezing. Nasal and ocular discharges can also
recurs after treatment in a cat that has had a thorough occur depending on the infectious agent that is
diagnostic evaluation, the previously effective antimicro- involved. Fever is uncommon but might be present. The
bial agent is usually prescribed empirically again, for at viruses that have been implicated include canine aden-
least 7–10 days, to assess for the treatment response. ovirus 2, canine distemper virus, canine respiratory
The Working Group recommends avoidance of coronavirus, canine influenza viruses, canine her-
repeated empirical treatment on a regular basis when- pesvirus, canine pneumovirus, and canine parainfluenza
ever possible. However, some cats with suspected virus.55–59 Bacteria implicated as primary pathogens in
chronic bacterial URI require such an approach to les- this complex include B. bronchiseptica, S. equi sub-
sen clinical signs of disease even though clinical cure is species zooepidemicus, and Mycoplasma spp.55,59–63
never achieved. The Working Group believes there is Dogs with canine distemper virus infection often have
currently no known optimal protocol for repeated diarrhea and can have mucopurulent ocular and nasal
empirical treatment for chronic URI in cats. Evidence discharge that might be confused with mucopurulent
from the human infectious disease literature shows discharges caused by primary bacterial pathogens.
organisms cultured from patients within 3 months of Because of its significance to the health of other dogs
primary treatment had a higher likelihood of resistance and for prognosis, the possibility of underlying distem-
to the treatment drug or class used. As such, some res- per virus infection should always be considered in
piratory treatment guidelines in human medicine recom- young dogs with mucopurulent ocular and nasal dis-
mend a different drug (or drug class) if used within charges, even when other signs of distemper are absent.
3 months of the initial treatment.52 Until further data Infection with S. equi subspecies zooepidemicus should
are available, the Working Group recommends use of be suspected if cases of acute hemorrhagic pneumonia
the previously effective antimicrobial drug with switch or sudden death are reported.64
to a different drug class or a more active drug within Co-infections with multiple respiratory pathogens are
the class if treatment is ineffective after a minimum of common in dogs with CIRDC and each of the agents
48 hours. Collection of specimens for culture and sus- can be harbored by dogs with no clinical signs. Vaccines
ceptibility is recommended if neither of these are available for some of the causes of CIRDC in some
approaches is successful. countries and include canine parainfluenza virus, canine
There is no evidence to support the use of topical adenovirus 2, canine distemper virus, H3N8 canine
(intranasal) antiseptic or antimicrobial administration influenza virus, H3N2 influenza virus, and B. bron-
for the treatment of acute or chronic bacterial URI. chiseptica. With the exception of canine distemper virus,
However, topical administration of 0.9% saline solu- the immunity induced by vaccination does not prevent
tion is believed to have has a mild mucolytic effect and colonization and shedding of the organisms and clinical
might be effective in clearing nasal secretions in some signs of disease can develop in vaccinated dogs (2011
cats. AAHA Canine Vaccination Guidelines; www.aahanet.
Many cats with chronic URTD have complete diag- org). However, morbidity is generally decreased in vac-
nostic evaluations performed and the only finding is lym- cinates compared with dogs that are not vaccinated
phocytic–plasmacytic or mixed inflammation identified when exposed to the pathogens.
on histopathological evaluation without a known under-
lying cause (idiopathic feline rhinosinusitis). Although Diagnosis of Bacterial Causes of CIRDC
chronic infection with respiratory viruses has been specu-
lated to play a role in this disease, the true underlying eti- A thorough history and physical examination should
ology remains enigmatic.16,22 Although there was no be performed on all dogs with suspected CIRDC. Many
association among Bartonella spp. test results among cats diagnostic tests could be performed to assess for evi-
with and without URTD in shelters in 1 study or with dence of primary or secondary bacterial CIRDC. It is
chronic rhinosinusitis in another study, additional the opinion of the Working Group that there is limited
research is required to ascertain the role of Bartonella benefit to performing cytology of nasal discharges to
spp. in feline chronic rhinosinusitis.53,54 diagnose bacterial infection and guide the antimicrobial
Respiratory Treatment Guidelines 287

choice. Aerobic bacterial culture and antimicrobial sus- unknown and the 7–10-day recommendation was based
ceptibility testing, Mycoplasma spp. culture (or PCR on the clinical experiences of the Working Group. Of
assay), and molecular diagnostic procedures for canine the 17 reviewers, 15 (88%) agreed with this recommen-
parainfluenza virus, canine adenovirus 2, canine distem- dation and 2 disagreed. One reviewer stated that if there
per virus, canine respiratory coronavirus, canine influ- is no evidence of pneumonia and the case is not at high
enza viruses, canine herpesvirus, pneumovirus, risk of pneumonia (brachycephalic, collapsing airways;
B. bronchiseptica, and Mycoplasma spp. (or M. cynos immunosuppressed), antimicrobial treatment is not indi-
alone) can be performed. However, each of these organ- cated at all. The other dissenting reviewer disagreed
isms can be grown or detected by molecular methods with the recommendation because there is no break-
from healthy and diseased dogs and vaccine strains of point data for doxycycline for B. bronchiseptica or
the organisms can be amplified by molecular diagnostic Mycoplasma spp. in dogs and so whether the agents are
assays.65 Molecular assays might also be of limited sen- truly susceptible to the drug is unknown.
sitivity by the time dogs are presented for examination Additional antimicrobial susceptibility data for sec-
because viral shedding rates tend to peak very early in ondary bacterial agents like Pasteurella spp., Streptococ-
disease. Thus, these tests are generally not recom- cus spp., Staphylococcus spp., and anaerobes are
mended by the Working Group for single cases with needed. For Pasteurella spp. and Streptococcus spp.,
typical clinical presentations, no evidence of pneumonia, amoxicillin is usually adequate, whereas strains of Sta-
and when high-risk populations (eg, breeding kennels) phylococcus spp. are usually susceptible in vitro to
are not involved. amoxicillin–clavulanic acid. Thus, these antimicrobials
If an outbreak of CIRDC is suspected in populations are considered by the Working Group to be alternate
of dogs like those in shelters, breeding kennels, board- first-line antimicrobials for the treatment of secondary
ing facilities, or multiple dog households, molecular bacterial infections in this syndrome if treatment with
assays might be indicated, along with bacterial culture doxycycline fails or is not possible (eg, it is not well tol-
and serological testing for viral pathogens, particularly erated). However, it should also be recognized that
if poor response to treatment or severe clinical disease some B. bronchiseptica isolates and all mycoplasmas are
is occurring. If possible, specimens from respiratory resistant to amoxicillin–clavulanate. Of the 17 reviewers,
discharges should be collected from several affected 13 (77%) agreed, 3 reviewers (18%) disagreed, and 1
dogs and assayed individually to increase sensitivity reviewer was neutral (6%). Reviewers that provided
and positive predictive value and necropsy should negative comments were concerned that because the
be performed if there are fatalities. If clinical signs concentrations of beta-lactams in bronchial secretions
consistent with pneumonia develop, a more extensive are unknown for dogs and cats, the use of these drugs
diagnostic evaluation is indicated (See the Pneumonia could be ineffective if tracheobronchitis without pneu-
in Dogs and Cats section). monia was present. Another concern was that use of
amoxicillin–clavulanate more likely selects for resistance
Treatment of Suspected Bacterial Canine Infectious phenotypes of clinical concern (eg, methicillin resistance
Respiratory Disease Complex in staphylococci).
Inhalational aminoglycoside treatment has been anec-
The majority of cases of CIRDC are currently dotally mentioned as beneficial for the management of
believed to be viral in etiology and so antimicrobial dogs with B. bronchiseptica-associated CIRDC. How-
administration is often not indicated. Most dogs with ever, in the absence of controlled studies for safety or
clinical signs of CIRDC including mucopurulent nasal efficacy, the Working Group does not recommend this
discharge maintain normal appetite and attitude and treatment protocol for dogs with suspected bacterial
might resolve spontaneously within 10 days without CIRDC.
antimicrobial treatment. The Working Group recom-
mends that antimicrobial treatment be considered Monitoring Treatment of Bacterial Canine Infectious
within the 10-day observation period only if fever, Respiratory Disease Complex
lethargy, or inappetence is present together with mucop-
urulent discharges. This disease syndrome is usually self-limited or
If bacterial CIRDC is suspected in dogs with mucop- responds quickly to antimicrobial treatment. Thus, pri-
urulent nasal discharge, fever, lethargy, or inappetence mary or repeated diagnostic tests are rarely needed
but no clinical evidence of pneumonia (eg, crackles or unless pneumonia is suspected. Bacterial culture is not
wheezes on thoracic auscultation), the Working Group recommended after successful treatment. Canine infec-
recommends administration of doxycycline empirically tious respiratory disease complex has not been associ-
for 7–10 days as the first-line antimicrobial option ated with chronic upper respiratory disease in the dogs.
(Table 1). Doxycycline is believed to have clinical activ- Most dogs with bacterial CIRDC have clinical signs
ity against Mycoplasma. As in cats, doxycycline is well that resolve quickly and so if the first drug chosen is
tolerated by dogs and isolates of B. bronchiseptica from ineffective and bacterial disease is still suspected after
dogs are typically susceptible in vitro to doxycy- the first 7 days, the Working Group recommends that a
cline.60,66 However, the susceptibility testing studies more extensive diagnostic workup should be considered
used an unapproved standard. Optimal duration of before considering use of other drug classes like fluoro-
treatment for dogs with bacterial causes of CIRDC is quinolones or azithromycin.
288 Lappin et al

Bacterial Bronchitis in Dogs and Cats to obtain materials for Mycoplasma spp. culture and
aerobic bacterial culture and antimicrobial susceptibil-
Definition and Causes ity testing. Mycoplasma PCR assay results do not
always correlate with those of culture and might reflect
Inflammation of the bronchi in dogs and cats is asso-
oral contamination.71 Specimens obtained by bron-
ciated with many different conditions including inhaled
choscopy are most accurate for diagnosis, but collec-
irritants; infections by bacteria, viruses, Dirofilaria
tion of specimens by other methods like tracheal
immitis, respiratory parasites (tissue migration of Toxo-
washing is acceptable if diffuse disease is present and
cara canis); pharyngeal or esophageal dysfunction; and
bronchoscopy is not available, not affordable or of too
allergies.67 Acute inflammation of the bronchi can occur
great a risk to the animal. The results of analysis of
secondary to the primary infectious disease agents dis-
bronchoalveolar lavage and brush specimens are not
cussed in the acute and chronic URI in cats section and
always in agreement.72
in CIRDC section. In general, the clinical manifesta-
The presence of neutrophilic inflammation, intracellu-
tions, diagnostic plan, and treatment plan are as
lar bacteria, and positive bacterial culture with charac-
described in those sections. However, some dogs and
teristic radiographic findings suggests primary or
cats infected with the primary bacterial pathogens
secondary bacterial bronchitis. However, the trachea is
B. bronchiseptica and Mycoplasma spp. can develop
not sterile in normal dogs and low numbers of bacteria
chronic bronchitis or bronchopneumonia.68 In addition,
cultured in the absence of cytological evidence of intra-
dogs and cats with other inflammatory diseases of the
cellular bacteria might not imply bacterial infection.
bronchi or anatomic defects of the larynx and trachea
(eg, laryngeal paralysis, collapsing airways) might
develop secondary bacterial bronchitis. The source of Treatment of Suspected Bacterial Bronchitis
those bacteria is thought to be the natural oral micro-
While waiting for results of culture and antimicro-
biota. Thus, the same bacteria described for secondary
bial susceptibility testing, the Working Group recom-
bacterial URI in cats and secondary bacterial CIRDC
mends either no antimicrobial treatment or, if the
in dogs might be associated with bronchitis. However,
clinical disease is severe, empirical administration of
many dogs with chronic bronchitis do not have large
doxycycline for 7–10 days (Tables 1 and 2). The use of
numbers of bacteria cultured after bronchoalveolar
doxycycline is recommended based on its in vitro activ-
lavage and so the syndrome is not always associated
ity against B. bronchiseptica isolates from dogs and
with bacterial infection.69,70
cats,31,66,73 reports of positive clinical responses to
doxycycline in cats with respiratory Mycoplasma infec-
Diagnosis of Suspected Bacterial Bronchitis tions, and a low rate of adverse effects.74,75 Of the 17
reviewers, 16 (94%) agreed with this Working Group
The primary clinical manifestation of bacterial recommendation and 1 disagreed because there is no
bronchitis in dogs and cats is cough, with or without breakpoint data for this antimicrobial drug for these
signs of respiratory distress. Dogs or cats with bacteria in dogs. Depending on the clinical and labora-
chronic cough, with or without prior evidence of URI tory testing results, antimicrobial treatment is contin-
or CIRDC should have a full physical examination ued, initiated, or modified based on antimicrobial
performed, which should include thorough tracheal susceptibility testing with the drug that is selected
and thoracic auscultation. Thoracic radiographs being one believed to penetrate the blood bronchus
should be made on full inspiration to evaluate for barrier based on data from other species. If a positive
pulmonary and cardiac changes that could be associ- response is obtained in the first 7–10 days, treatment
ated with cough. In dogs, radiographs should include should be continued to 1 week past resolution of clini-
the cervical and intrathoracic trachea and both inspi- cal signs of disease. Optimal duration of treatment for
ratory and expiratory radiographs can be performed this syndrome is unknown and so this recommendation
to identify collapsing airways. Alternately, fluoroscopy was based on the experiences of the clinicians on the
is available in some veterinary clinics for diagnosis of Working Group. Dogs that fail to respond to antimi-
collapsing airways. Some dogs and cats with bacterial crobial treatment are likely to have primary chronic
bronchitis have radiographic evidence of thickened (noninfectious) bronchitis.
bronchi, but others have normal radiographs even Most veterinary microbiology laboratories do not
though inflammation exists on cytology of airway report antimicrobial susceptibility results for Myco-
washings. Computed tomography can also be used plasma spp. and this genus can be difficult to culture.
to determine the extent of disease. Other causes of Thus, the antimicrobial choices for dogs with suspected
bronchial inflammation should be explored (D. immitis or proven Mycoplasma-associated bronchitis are often
serology, fecal flotation, fecal sedimentation, Baer- made empirically. Doxycycline or minocycline is com-
mann test, laryngeal function evaluation) as indicated monly used by veterinarians for this syndrome and is
by the history. likely to have a therapeutic effect for pets with sus-
If radiographic evidence of bronchial disease is pre- pected Mycoplasma spp. bronchitis.68,76 Veterinary fluo-
sent or suspected based on clinical findings, airway roquinolones and azithromycin are other drugs that
washings for cytological examination are indicated to might be effective for the treatment of Mycoplasma spp.
determine the type of inflammation that is present and infections.
Respiratory Treatment Guidelines 289

Monitoring Treatment of Bacterial Bronchitis bacterial culture, and antimicrobial susceptibility and
Mycoplasma spp. culture is recommended.
If bronchitis is associated with Mycoplasma spp. or Culture and susceptibility testing should be recom-
B. bronchiseptica, clinical resolution might be obtained mended to the client and performed before starting
with 1 course of antimicrobial treatment. In some cases, antimicrobial drug treatment, provided that the animal is
prolonged antimicrobial treatment might be needed. In sufficiently stable; however, antimicrobial treatment
the event that another primary cause of inflammation should not be unduly delayed. Although no controlled
such as allergic bronchitis exists and secondary bacterial data are available for dogs and cats, the clinical opinion
infections are occurring, recurrent treatment might be of the Working Group is that antimicrobial treatment
required. Controlling inflammation associated with the should be initiated as soon as possible and within
primary disease syndrome might also lessen recurrence 1–2 hours if clinical signs of sepsis exist.
of secondary bacterial bronchitis.77 Repeated thoracic In addition, not all cases of aspiration pneumonia
radiographs can be taken to follow bronchial changes, require antimicrobial treatment, because clinical disease
but this is of limited sensitivity. In some cases, repeated might be primarily or solely chemical pneumonitis from
cytology and culture might be indicated. aspirated materials. Anaerobic bacteria are sometimes
associated with pneumonia, particularly if there is a his-
tory of aspiration, or grass awn foreign bodies are pre-
Pneumonia in Dogs and Cats sent. However, some commercial laboratories have
Definition and Causes difficulty culturing these agents and most do not pro-
vide antimicrobial susceptibility data; thus, antimicro-
Inflammation of the lungs (pneumonia) can occur bial agents with an anaerobic spectrum are often
after a variety of insults. In dogs and cats, although included for the treatment of bacterial pneumonia in
uncommon, primary bacterial pneumonia can occur dogs and cats when anaerobic culture is not available
after infection with B. bronchiseptica, Mycoplasma or likely to be reliable.
spp., S. equi zooepidemicus, S. canis, and Yersinia In cases with probable aspiration pneumonia, multi-
pestis.61–64,68,78–80 Of 65 puppies <1 year of age with ple bacteria are often cultured making it difficult to
“community acquired” pneumonia in the United States, determine which is involved with continued inflamma-
49% were infected with B. bronchiseptica.80 Dogs with tion. Care should also be exercised when interpreting
B. bronchiseptica infection were younger and had more the significance of few or rare organisms, mixed culture,
severe disease than dogs from which other bacteria were or presence of possible airway contaminants such as
cultured. Most cases of bacterial pneumonia in dogs coagulase-negative staphylococci or Bacillus spp. If an
and cats are secondary to other primary inflammatory endoscope is used to collect a lavage specimen, the pos-
events like viral infections or aspiration of oral, esopha- sibility of endoscope-related contamination should also
geal, or gastric contents during vomiting or regurgita- be considered, particularly when unusual species such
tion (commonly associated with megaesophagus), after as Serratia or Stenotrophomonas are isolated.88
aspiration because of pharyngeal or laryngeal function The Working Group recommends consulting with a
abnormalities, during anesthesia recovery, and after clinical microbiologist or specialist with expertise with
inhalation of foreign bodies.81–83 In addition, bacterial infectious diseases or pulmonology for interpretation of
pneumonia can develop in the presence of immunodefi- culture and antimicrobial susceptibility results from
ciency syndromes. Secondary bacterial pneumonia endotracheal or bronchoalveolar lavage specimens. Fif-
potentially could develop as a result of other pulmonary teen reviewers (88%) agreed, 1 disagreed (6%), and 1
or airway diseases like neoplasia, ciliary dyskinesia, (6%) was neutral to this Working Group recommenda-
bronchiectasis, and collapsing airways. tion. The person that disagreed believes that a consulta-
Common organisms isolated from dogs and cats with tion is only needed for difficult cases.
lower respiratory disease include E. coli, Pasteurella Because bacterial pneumonia is often associated with
spp., Streptococcus spp, B. bronchiseptica, Enterococcus an underlying disease process, attempts to identify and
spp., Mycoplasma spp., S. pseudintermedius and other manage current problems should be made. In cats and
coagulase-positive Staphylococcus spp., and Pseu- dogs that have life-threatening bacterial pneumonia or
domonas spp.78–80,84–87 are oxygen dependent, airway sampling might not be
feasible. Although more data are required to clarify the
Diagnosis of Bacterial Pneumonia usefulness of blood cultures (aerobic and anaerobic) in
animals with severe pneumonia, it is the consensus
Dogs and cats that develop cough that is associated opinion of the Working Group to consider blood cul-
with fever, lethargy, inappetence, or tachypnea should tures in these animals before starting empirical antimi-
be evaluated for the presence of pneumonia by a full crobial drug treatment as an alternative way to obtain
physical examination, complete blood cell count, and isolates for targeted antimicrobial susceptibility to guide
thoracic radiographs. If clinicopathologic findings and long-term management. Empirical antimicrobial treat-
thoracic radiological findings (alveolar lung disease) ment should not be delayed in an effort to stabilize
support a diagnosis of bacterial pneumonia, collection affected animals and obtain a pre-antimicrobial airway
of a transtracheal, endotracheal, or a bronchoalveolar sample. Thirteen reviewers (82%) agreed, 3 were neutral
lavage specimen for cytologic examination, aerobic (18%), and 1 (6%) disagreed with this Working Group
290 Lappin et al

recommendation. The primary comment was that blood Group recommendation. The primary comments were
culture for this purpose in children is known to be that the risk of not treating a case was greater than the
insensitive and false-positive results can be obtained.89 perceived benefit of withholding treatment or that oral
medications could be adequate for this syndrome. How-
Treatment of Suspected Bacterial Pneumonia ever, if megaesophagus or other esophageal motility dis-
orders exist, parenteral administration of the
The Working Group discussed whether antimicrobial antimicrobial drug is indicated.
treatment should be delayed while waiting until the If clinical findings in dogs or cats with pneumonia
results of culture and antimicrobial susceptibility testing suggest the existence of sepsis (eg, injected mucous
are available. However, as not all clients can afford the membranes, hypoglycemia), the Working Group recom-
diagnostic procedures and pneumonia can be a life- mends concurrent parenteral administration of either
threatening disease, the consensus opinion was to pro- enrofloxacin or marbofloxacin (available in injectable
vide empirical antimicrobial treatment while waiting for form in some countries) combined with a drug with
test results with potential for de-escalation of treatment Gram-positive and anaerobic spectra until bacterial cul-
based on antimicrobial susceptibility testing. While hos- ture and antimicrobial susceptibility testing results
pitalized, parenteral antimicrobial treatment is generally return. In 1 study, most bacteria from the lower airways
recommended by the Working Group for the treatment of dogs with respiratory disease were susceptible to
of animals with pneumonia, regardless of the severity of enrofloxacin.91 Other drugs for parenteral use with a
disease. Once the animal is discharged, treatment can Gram-negative spectrum might be indicated in lieu of
be continued by means of the oral route. It is the opin- enrofloxacin based on culture and antimicrobial suscep-
ion of the Working Group that doxycycline is a reason- tibility testing (Table 2). The Working Group states
able empiric choice for dogs or cats with mild that common options for Gram-positive and anaerobic
pneumonia that is suspected to be from infection with bacteria include ampicillin or clindamycin administered
B. bronchiseptica or Mycoplasma spp. (eg, the animal is parenterally (Table 2). Which of these drugs to choose
from a shelter or boarding environment) and no other while waiting on antimicrobial susceptibility test results
systemic signs of disease like fever, dehydration, will depend on the most likely infectious agent sus-
lethargy, or respiratory distress are present. This is pected, previously prescribed antimicrobials (if any),
based on the known susceptibility of these organisms to and historical antimicrobial resistance in the geographi-
doxycycline (see Section on Canine Infectious Respira- cal region. Fourteen reviewers (82%) agreed and 3
tory Disease Complex) and published case reports of (18%) disagreed with this Working Group recommen-
successful treatment with doxycycline (Table 2).74,75,78 dation. The primary comment was that if Bacteroides
Fifteen reviewers (88%) agreed and 2 (12%) disagreed spp. were present, clindamycin could be ineffective and
with this Working Group recommendation. One that metronidazole could be considered another option.
reviewer stated that they doubted that pneumonia Drugs that could be administered PO for outpatient
would be present without fever and if pneumonia exists, treatment of bacterial pneumonia should be selected on
it should be treated with bactericidal drugs. The other the basis of culture and antimicrobial susceptibility
dissenting reviewer commented on the lack of break- results for organisms isolated from the lower airways,
point data for doxycycline and the bacteria from dogs de-escalating whenever possible. If culture and antimi-
and cats as well as the concern that doxycycline might crobial susceptibility testing was not performed, the
not penetrate into the extracellular fluids of the lungs. antimicrobial drug class or classes that were initially
Azithromycin is used by some veterinarians empiri- prescribed and associated with clinical response is/are
cally in dogs with uncomplicated pneumonia, but the chosen for continued oral treatment.
Working Group believes that data supporting this rec- Inflammatory responses to bacterial pneumonia
ommendation are lacking. increase pulmonary pathology. Thus, glucocorticoids are
Streptococcus equi subspecies zooepidemicus strains used concurrently in some human patients with bacterial
isolated from dogs are susceptible to penicillin, amoxi- pneumonia.92,93 However, it was the consensus opinion
cillin, and ampicillin. Administration of amoxicillin– of the Working Group that further data are needed from
clavulanate is unnecessary if this organism is suspected dogs and cats before a definitive recommendation can be
because streptococci are not known to produce made in regard to the use of systemic or inhaled gluco-
beta-lactamases.90 corticoids, which have the potential to contribute to
Not all dogs or cats with acute aspiration pneumonia adverse outcomes due to immunosuppression.
have a bacterial infection. However, aspirated bacteria
can cause infection secondary to the chemical inflamma- Monitoring Treatment of Bacterial Pneumonia
tion associated with aspiration. If the dog or cat is
acutely affected and has no evidence of systemic sepsis, The current recommendation in most veterinary text-
the Working Group believes that either no treatment or books is to treat bacterial pneumonia for 4–6 weeks,
parenteral administration of a beta-lactam antimicrobial but evidence to support this duration of treatment in
like ampicillin, ampicillin-sulbactam, or the first-genera- either cats or dogs is lacking. Although such lengthy
tion cephalosporin cefazolin might be sufficient courses of antimicrobial treatment might be necessary
(Table 2). Thirteen reviewers (82%) agreed, 3 were neu- for some animals with severe pulmonary involvement or
tral (18%), and 1 (6%) disagreed with this Working those with immunodeficiency syndromes, it is the
Respiratory Treatment Guidelines 291

consensus opinion of the Working Group that shorter Treatment of Pyothorax in Dogs and Cats
courses of appropriate treatment, such as those used to
treat pneumonia in humans, might be effective in some The Working Group recommends that treatment of
situations. In the face of insufficient data supporting a pyothorax include IV fluid administration and critically,
shorter course of treatment, the Working Group recom- drainage of pus after placement of chest tubes with
mends re-evaluation of animals with pneumonia no intermittent or preferably continuous suction with or
later than 10–14 days after starting treatment. At that without lavage.96–103 Surgical debridement might be
point, decisions to extend treatment should be based on required in some cases. Sixteen reviewers (94%) agreed,
clinical, hematological, and radiographic findings. Addi- and 1 (6%) disagreed with this Working Group recom-
tional studies evaluating durations of treatment that are mendation. The primary comment was that evidence
shorter than 4–6 weeks are required. supporting the definitive need for thoracic lavage was
lacking. However, based on lack of data supporting its
use, the Working Group does not recommend adminis-
Pyothorax in Dogs and Cats tration of antimicrobial drugs into the pleural space.
Definition and Causes The Working Group recommends the combination of
parenteral administration of enrofloxacin or mar-
In cats with pyothorax, the bacteria isolated from bofloxacin (when available in parenteral form) with a
thoracic fluid are most commonly a mixture of oropha- penicillin or clindamycin combined with therapeutic
ryngeal anaerobes including Fusobacterium, Prevotella, drainage of the pleural space with or without lavage for
Porphyromonas, Bacteroides, Peptostreptococcus, the initial treatment or canine and feline pyothorax
Clostridium, Actinomyces, and Filifactor villosus. Pas- pending the results of culture and antimicrobial suscepti-
teurella spp, Streptococcus spp., and Mycoplasma spp. bility testing. Sixteen reviewers (94%) agreed and 1 (6%)
have also been isolated.94–97 Less commonly, Staphylo- disagreed with this Working Group recommendation.
coccus spp., Gram-negative bacteria other than Pas- The primary comment was that pradofloxacin adminis-
teurella, and organisms such as Nocardia spp. and tered PO as a single drug could be effective if available.
Rhodococcus equi have been isolated. Wounds resulting Treatment with an antimicrobial drug with activity
from cat fights and URI are risk factors for pyothorax against anaerobes should be continued regardless of cul-
in cats.97 ture results because fastidious anaerobic bacteria could
Bacteria isolated from dogs with pyothorax are most be present. If combination treatment was initiated and
commonly mixed anaerobes (Prevotella spp., Peptostrep- the bacterial isolates are susceptible to both drugs in
tococcus spp., Propionibacterium acnes, Clostridium spp., the initial treatment regime, then either of the treatment
Bacteroides spp., Fusobacterium spp.) and Enterobacte- drugs could be discontinued. If organisms are grown
riaceae, especially E. coli and Klebsiella pneumo- that are resistant to one of the drugs and clinical
niae.94,98–100 Streptococcus canis, Staphylococcus spp, improvement is not noted, that antimicrobial agent
Enterococcus spp., Corynebacterium spp., Bacillus spp., should be discontinued. A second drug to which the iso-
Trueperella (formerly Arcanobacterium) pyogenes, Pas- late is susceptible should be substituted if the animal
teurella, Acinetobacter, Capnocytophaga spp., Enterobac- has not responded sufficiently. If organisms are grown
ter spp., Stenotrophomonas maltophila, Aeromonas that are resistant to both antimicrobials or clinical evi-
hydrophila, Achromobacter xylosoxidans, Serratia mar- dence of improvement is not evident, antimicrobial
cescens and Pseudomonas spp. Actinomyces spp. and to treatment should be changed to a drug to which the
a lesser extent Nocardia spp. and Streptomyces spp. organisms are susceptible in vitro. Fifteen reviewers
have been implicated in canine pyothorax.99 Pyothorax (88%) agreed, 1 was neutral (6%), and 1 (6%) dis-
in dogs commonly results from migrating plant foreign agreed with this Working Group recommendation. The
bodies or trauma but can also result from bite wound dissenting reviewer stated that mixed culture results can
inoculation.94,98–103 be difficult to interpret and so if the animal’s clinical
condition improves on the first therapeutic regimen,
Diagnosis of Pyothorax in Dogs and Cats changes should not be made.
Consultation with a specialist is recommended when
Thoracic radiographs should be made to evaluate for multidrug-resistant organisms are isolated. In all situa-
the presence of lung consolidation in the dog or cat tions, the clinical condition must be considered when
after therapeutic thoracocentesis. A pleural fluid speci- interpreting culture results, and continuing apparently
men should be submitted for cytologic analysis, aerobic effective treatment despite in vitro resistance is recom-
bacterial culture, and antimicrobial susceptibility test- mended because of the potential that the offending
ing, as well as culture for anaerobic bacteria and Myco- organism was not isolated.
plasma spp. (cats) if available. Performance of Gram
stain and acid-fast stains might provide addition infor-
mation. Detection of actinomycetes and Mycoplasma
Monitoring Treatment of Pyothorax
spp. requires specialized growth conditions and pro- It has been recommended that cats with pyothorax
longed incubation, and so the laboratory should be be treated for a minimum of 3 weeks and ideally 4–
informed that Actinomyces spp., Nocardia spp., or 6 weeks.97,101 Additional research is required to deter-
Mycoplasma spp. are differential diagnoses. mine whether shorter periods of antimicrobial drug
292 Lappin et al

treatment might be adequate. Serial thoracic radiogra- http://www.fecava.org/sites/default/files/files/DSAVA_Antibiotic


phy might be useful to determine whether antimicro- Guidelines%20-%20v1-1_3(1).pdf. Accessed December 8, 2016.
bial treatment needs to be continued, although further 4. Swedish Veterinary Association. Guidelines for the clinical
study is also required to determine whether persistent use of antimicrobials in the treatment of dogs and cats, 2009.
Available at: www.svf.se. Accessed December 8, 2016.
radiographic abnormalities correlate with the need for
5. Lionel A, Mandell LA, Richard G, et al. Infectious Diseases
additional antimicrobial drug treatment. At a mini- Society of America/American Thoracic Society consensus guideli-
mum, follow-up radiography should be performed for nes on the management of community-acquired pneumonia in
10–14 days after starting treatment and at completion adults. Clin Infect Dis 2007;44:27–72.
of treatment. If the pyothorax persists or reoccurs 6. Bradley JS, Byington CL, Shah SS, et al. The management
after cessation of antimicrobials, repeated thoracocen- of community-acquired pneumonia in infants and children older
tesis should be performed for cytological assessment than 3 months of age: Clinical Practice Guidelines by the Pediatric
and for culture and antimicrobial susceptibility testing. Infectious Diseases Society and the Infectious Diseases Society of
America. Clin Infect Dis 2011;53:325–376.
7. Murphy MK, Black NA, Lamping DL. Consensus develop-
Conclusions ment methods, and their use in clinical guideline development.
Health Technol Assess 1998;2:1–88.
The Working Group emphasizes the need for addi- 8. Allen HS, Broussard J, Noone KM. Nasopharyngeal dis-
tional prospective studies to evaluate different treat- eases in cats: A retrospective study of 53 cases (1991–1998). J Am
ments and treatment durations in dogs and cats with Anim Hosp Assoc 1999;35:457–461.
bacterial respiratory diseases so that more accurate rec- 9. Henderson SM, Bradley K, Day MJ. Investigation of nasal
ommendations can be made. For the same purpose, disease in the cat-a retrospective study of 77 cases. J Feline Med
research is needed to develop standard practices for col- Surg 2004;6:245–257.
10. Demko JL, Cohn LA. Chronic nasal discharge in cats: 75
lection of clinical specimens and interpretation of cul-
cases (1993–2004). J Am Vet Med Assoc 2007;230:1032–1037.
ture results. 11. Quimby J, Lappin MR. Feline focus: Update on feline
upper respiratory diseases: Introduction and diagnostics. Compend
Acknowledgments Contin Educ Vet 2009;31:554–564.
12. Helps CR, Lait P, Damhuis A. Factors associated with
The Working Group thanks the following individuals upper respiratory tract disease caused by feline herpesvirus, feline
for a prepublication review of the document and for calicivirus, Chlamydophila felis and Bordetella bronchiseptica in
providing votes to be used with the panel recommenda- cats: Experience from 218 European catteries. Vet Rec
tions; Leah Cohn (University of Missouri), Joshua 2005;156:669–773.
Daniels (The Ohio State University), Eleanor Hawkins 13. Bannasch MJ, Foley JE. Epidemiologic evaluation of multi-
(North Carolina State University), Steve Holloway ple respiratory pathogens in cats in animal shelters. J Feline Med
(Advanced PetCare Australia), Lynelle Johnson Surg 2005;7:109–119.
(University of California, Davis), and Carol Reneiro 14. Di Martino B, Di Francesco CE, Meridiani I. Etiological
investigation of multiple respiratory infections in cats. New Micro-
(University of Missouri).
biol 2007;30:455–461.
Grant support: The work was supported by the Inter- 15. Veir JK, Ruch-Gallie R, Spindel ME, et al. Prevalence of
national Society for Companion Animal Infectious Dis- selected infectious organisms and comparison of two anatomic
eases (ISCAID; www.iscaid.org). sampling sites in shelter cats with upper respiratory tract disease.
Conflict of Interest Declaration: Jane Sykes serves as J Feline Med Surg 2008;10:551–557.
Associate Editor for the Journal of Veterinary Internal 16. Johnson LR, Foley JE, De Cock HE. Assessment of infec-
Medicine. She was not involved in review of this manu- tious organisms associated with chronic rhinosinusitis in cats.
script. M.G. Papich has received consulting fees, J Am Vet Med Assoc 2005;227:579–585.
research support, and gifts from Bayer and Zoetis, 17. Quimby J, Lappin MR. Update on feline upper respiratory
who are sponsors of some of the antibiotics recom- diseases: Condition-specific recommendations. Compend Contin
Educ Vet 2010;32:1–10.
mended in this manuscript. He receives royalties from
18. Welsh RD. Bordetella bronchiseptica infections in cats.
a book (published by Elsevier) that was the source of J Am Anim Hosp Assoc 1996;32:153–158.
dosages listed in this paper. 19. Binns SH, Dawson S, Speakman AJ, et al. Prevalence and
Off-label Antimicrobial Declaration: This document risk factors for feline Bordetella bro nchiseptica infection. Vet Rec
describes off-label antimicrobial use in multiple sections. 1999;144:575–580.
20. Spindel ME, Veir JK, Radecki SV. Evaluation of prad-
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SÍNCOPE CARDIOGÉNICO EN EL PERRO
Montoya, J.A.
Medicina interna veterinaria
Facultad de Veterinaria de Las Palmas de Gran Canaria
35416- Las Palmas
alberto.montoya@ulpgc.es

Definición y clasificación
El síncope cardiogénico consiste en una pérdida súbita, aguda,
transitoria y reversible de la consciencia debida a la restricción del
flujo sanguíneo cerebral, como consecuencia de un rápido descenso
del gasto cardiaco y es un síndrome que acompaña a muchos procesos
cardiovasculares.

El gasto cardiaco depende de forma directa de dos factores: el


volumen sistólico y la frecuencia cardiaca. Cuando los síncopes se
producen por una disminución del volumen sistólico se denominan
mecánicos u obstructivos; cuando lo que se modifica es la frecuencia
cardiaca se denominan eléctricos o arrítmicos.

Etiología
Los síncopes mecánicos están producidos por: miocardiopatías
(dilatada e hipertrófica) y miocarditis, taponamientos cardiacos y
pericarditis constrictivas; valvulopatías y endocardiopatías restrictivas
así como endocarditis bacterianas. Hay que mencionar los asociados
a Dirofilaria immitis, a neoplasias cardiacas como el quemodectoma y
el hemangiosarcoma, a cuadros de hipertensión sistémica o pulmonar
grave o a defectos cardiacos congénitos (estenosis pulmonar o aórtica
y ductus arterioso persistente). Sin embargo, la causa más frecuente
de la presentación de síncopes mecánicos es la descompensación de
cuadros de insuficiencia cardiaca congestiva.

Los síncopes eléctricos se producen por arritmias y pueden


ser taquiarrítmicos y bradiarrítmicos (estos últimos también
denominados síncopes de Stokes-Adams). Tanto las taquiarritmias
supraventriculares (extrasístoles y taquicardias supraventriculares,
flúter y fibrilación atrial), como las ventriculares pueden generarlos.
También las bradiarritmias (bradicardia sinusal, paro sinusal y

1
bloqueos A-V de 2º y 3º grado) y el síndrome del seno enfermo se
asocian a la aparición de este cuadro.

En la mayoría de las ocasiones y en función de la alteración


cardiovascular primaria los cuadros sincopales son de origen
electromecánico.

Patogenia
El gasto cardiaco debe cubrir las necesidades orgánicas en cada
momento y esto se consigue mediante mecanismos compensadores
cardiovasculares que dirigidos por el sistema nervioso autónomo
modifican y adaptan en cada momento el volumen sistólico y la
frecuencia cardiaca.

Cuando una disminución brusca y severa del gasto cardiaco


implican un fallo en el riego sanguíneo cerebral suficiente se
provoca el síncope, que se explica debido a que el metabolismo
cerebral depende en su totalidad de la perfusión de oxígeno aportado
por la sangre.

En los casos de síncopes obstructivos, hay una causa


mecánica que dificulta u obstaculiza la eyección del flujo sanguíneo
durante la sístole, o bien provoca una disminución de la capacidad
de llenado diastólico de los ventrículos. Generalmente, los síncopes
de este grupo, suelen ir asociados a aumentos súbitos del gasto
cardiaco a los que el corazón no puede responder.

En los síncopes arrítmicos lo que se produce es una alteración


eléctrica cardiaca y cuando la frecuencia cardiaca se altera, por un
aumento o por una disminución, surge una brusca reducción del
gasto cardiaco que puede provocar la insuficiencia cardiaca aguda.
Estas arritmias pueden desencadenar también alteraciones a nivel de
la perfusión coronaria y de la funcionalidad miocárdica,
favoreciendo aún más la aparición del síncope.
Los síncopes taquiarrítmicos, son de esfuerzo o de estrés y en
ellos lo que se produce es un aumento de la frecuencia cardiaca, que
paradójicamente, no se acompaña de un incremento del gasto
cardiaco, porque se produce un acortamiento de los periodos
diastólicos (periodos de llenado ventricular) que genera una
disminución del volumen sistólico y por tanto del gasto cardiaco.

2
Las bradiarritmias severas, también originan un brusco
descenso el gasto cardiaco como consecuencia de que se sobrepasan
los límites del incremento compensatorio del volumen diastólico
ventricular y del volumen total. Este tipo de síncopes pueden
desencadenarse por dos situaciones: *disminuciones severas de la
frecuencia; y/o *bloqueos del impulso, sobre todo en los casos de
bloqueos atrio-ventriculares completos o incompletos, donde el
impulso no es transmitido a los ventrículos, y éstos dejan de
contraerse durante un periodo de tiempo variable.

Sintomatología
La sintomatología que aparece en los pacientes incluye, por lo
general: mucosas pálidas, bradicardia, hipotensión, debilidad, pulso
yugular y/o filiforme. En los de origen mecánico pueden auscultarse
soplos y cambios de los ruidos cardiacos (alteraciones de la
intensidad, desdoblamientos y/o galopes).

Dependiendo de la duración del déficit de riego cerebral,


aparecen nuevos síntomas más o menos intensos. Si tiene una
duración menor de 10 segundos solamente se produce una
disminución parcial de los reflejos y aturdimiento con debilidad
muscular y/o temblores, pudiendo pasar, incluso, desapercibido para
el dueño. Cuando dura más de 20 segundos el animal presenta pérdida
de consciencia, respiración sincopada y convulsiones. Con una
duración superior al medio minuto aparecen convulsiones más
intensas y relajación de esfínteres. Si el síncope dura más de 3-4 min.
, el animal puede morir o recuperarse parcialmente quedando secuelas
graves en el sistema nervioso central.

En la mayoría de los casos la recuperación suele ser rápida,


aunque después del ataque puede aparecer taquicardia, agitación,
congestión de mucosas, nauseas y vómitos, alteraciones de la visión y
emisión de sonidos extraños. El propietario suele referir que el animal
pasa un tiempo nervioso, asustado y confuso. Si el ataque ha sido muy
prolongado el paciente puede presentar un estado somnoliento,
relajado, adinámico y semicomatoso durante unas horas.

3
Diagnóstico
Es muy importante realizar una historia clínica completa para
orientar el problema, ya que en muy pocos casos tendremos ocasión
de presenciar un ataque y, además, la información de los propietarios
suele ser escasa y poco exacta.

La anamnesis incluirá los datos referentes a edad, raza, sexo,


peso, tipo de alimentación, vacunaciones, desparasitaciones y
padecimientos anteriores.

En cuanto a las características de los ataques se debe conocer el


momento de presentación; sus relaciones con el ejercicio, el estrés, la
comida y la administración de fármacos; la forma de presentación,
frecuencia, duración e intensidad de los mismos. Es importante que el
propietario realice la descripción completa del ataque incluyendo la
fase prodrómica, el ataque propiamente dicho y el comportamiento
del paciente después del mismo.

Se debe realizar un completo examen general y una exploración


cardiológica completa que incluya radiología, electrocardiografía y
ecocardiografía y medida de las presiones arteriales. Unas pruebas
laboratoriales, que incluyan al menos: hematología completa y
determinaciones de proteínas séricas, glucosa, urea, creatinina, ALT,
gamma-GT, calcio, potasio, y análisis coproparasitológico son
necesarias para descartar otras causas potenciales de convulsiones en
el perro, y a menudo es difícil diagnosticar un síncope cardiogénico.

Diagnóstico diferencial
Los datos recogidos de la anamnesis, exploración y técnicas
complementarias permiten evaluar el estado del paciente y orientar al
clínico hacia un diagnóstico certero. Sin embargo, hay que realizar un
diagnóstico diferencial entre este proceso y otras alteraciones que
pueden presentar una sintomatología similar (Tabla nº 1), como son:
enfermedades nerviosas, alteraciones pulmonares, anemias e
hipovolemias, enfermedades metabólicas (hipoglucemia, síndrome de
Addison, diabetes mellitus), alteraciones electrolíticas, enfermedades
musculares, afecciones renales o hepáticas y, en perros jóvenes,
parasitosis masivas; y que deben tenerse en cuenta a la hora de
investigar la etiología del episodio y aplicar el tratamiento adecuado.

4
Tratamiento
La primera norma a tener en cuenta es que el síncope en sí no
debe tratarse, sino que hay que tratar la causa primaria.

Los síncopes mecánicos puros son siempre consecuentes a una


alteración cardiovascular grave, por lo que nosotros recomendamos
instaurar una pauta de tratamiento integral de la insuficiencia cardiaca
establecida (diuréticos, vasodilatadores, inótropos positivos, dieta
hiposódica). En caso de instaurar tratamiento sintomático, este podría
encaminarse básicamente a mejorar el gasto cardiaco, empleando
medidas hipertensoras como la administración de soluciones: salina
fisiológica, ringer o ringer-lactato por vía IV rápida, junto con dosis
bajas de diazepam en caso que existan convulsiones.

En lo que respecta a los síncopes eléctricos taquiarrítmicos


hay que conocer el tipo de arritmia que está produciendo el síncope,
así como su causa, para administrar el tratamiento específico. Así en
las supraventriculares los fármacos de elección son los digitálicos, los
beta-bloqueantes o los bloqueantes del canal del calcio. En las
ventriculares se emplean lidocaina, procainamida, mexiletina,
bloqueantes del canal del calcio y beta-bloqueantes.

En los síncopes bradiarrítmicos debe realizarse inicialmente


una prueba de estimulación con atropina. Para ello, se administra
atropina a dosis de 0.04 mg/kg. por vía intramuscular, después
durante 30 minutos, se debe mantener monitorizado al animal o
realizar un E.C.G. cada 5 minutos. Si existe respuesta se puede
intentar el tratamiento con agentes vagolíticos como atropina,
propantelina o glicopirrolato. Dado que la atropina tiene numerosos
efectos secundarios, que estos tratamientos son muy prolongados y
que su administración es compleja (la vía oral es difícil debido al
sabor amargo del preparado y la administración parenteral es molesta
para el animal), no constituye el fármaco de elección a largo plazo y
es preferible el empleo de beta-simpaticomiméticos.

Si no encontramos respuesta a la atropina el pronóstico se


agrava y debemos realizar la prueba de estimulación con isoproterenol
(igual que la de atropina pero empleando 0.01 mg/kg. IM); si es
positiva podemos emplear en el tratamiento los agentes beta-

5
adrenérgicos como isoproterenol, orciprenalina, hexoprenalina,
terbutalina o teofilina.

Si el animal no responde ni a la prueba de la atropina ni a la del


isoproterenol, el único tratamiento posible es la implantación de un
marcapasos. No obstante hemos encontrado casos de baja respuesta al
isoproterenol con buena calidad de vida y supervivencia prolongada
empleando simpaticomiméticos.

Como hemos citado, es frecuente encontrar cuadros de etiología


electromecánica en los que el tratamiento debe ser mixto, intentando
mantener al animal con un gasto cardiaco suficiente para evitar la
presentación de los síncopes.

6
1. ORIGEN METABOLICO
 Hepatoencefalia.
Insuficiencia hepática-cirrosis
Shunt porto-cava
 Azotemia
Insuficiencia renal
 Hipoglucemia
Parasitosis intestinales masivas
Insulinoma
Hipoglucemia funcional (perros de caza)
Estrés
Idiopática (razas “toy” 6-12 semanas de vida)
Glucosuria renal
Síndrome de malaabsorción intestinal
Septicemia
Hipoglucemia pre- y posparto
 Diabetes mellitus
 Hipocalcemia
Lactación
Enfermedad renal crónica
Hiperparatiroidismo
Ejercicio muy intenso
 Hipomagnesemia
 Hipercaliemia
Hipoadrenocorticismo
Retención urinaria
Cetoacidosis
 Hiperlipemia

2. ORIGEN TOXICO Y YATROGENICO


 Plomo
 Etilenglicol
 Estricnina
 Organoclorados
 Organofosforados
 Hidralacina, acepromazina

3. ORIGEN NERVIOSO
 Neoplasias cerebrales
 Encefalitis
 Malformaciones congénitas
Hidrocefalia
Lisencefalia
 Traumatismo craneal
 Edema cerebral
 Congestión y hemorragia cerebrales
 Epilepsia esencial

4. OTRO ORIGEN
 Alteraciones respiratorias
Hipoxemia
Síncope tusígeno
Derrame pleural
 Hipertermia
 Reacciones de hipersensibilidad y alergia
 Enfermedades hematológicas

TABLA 1. DIAGNOSTICO DIFERENCIAL DE SÍNCOPES


CARDIOGÉNICOS EN EL PERRO

7
FARMACO DOSIS VIA
Atropina (Sulfato) 0.02-0.04 mg/kg. IV, SC, PO
Dexametasona 2-4 mg/kg/día IV
Diazepam 1-2 mg/kg. IV
Glicopirrolato 0.002-0.01 mg/kg. IV, IM
Hexoprenalina 0.05 mg/kg/8-12 h. IV, IM, SC, PO
Isoproterenol 0.01 mg/kg/6-8-12 h. IV, IM, SC
Midazolam 0.11 mg/kg. IV,IM
Orciprenalina 1 mg/kg/8-12 h. PO
Propantelina 11-2 mg/kg/8-12 h. PO
Teofilina 10 mg/kg/8-12 h. PO
Terbutalina 1,25-5 mg/animal/8-12 h. PO

TABLA 2: FARMACOS UTILIZADOS EN EL TRATAMIENTO DEL SINCOPE


CARDIOGENICO

8
9
BRONQUITIS CRÓNICA CANINA: Enfoque práctico
J. Alberto Montoya-Alonso, DVM, PhD, MSc, MA
Elena Carretón, DVM, MSc
Facultad de Veterinaria de Las Palmas de Gran Canaria
35416- Arucas (Las Palmas)- ESPAÑA
amontoya@dpat.ulpgc.es

Definición:

Presencia de tos crónica y pertinaz durante un período igual o superior a dos meses
consecutivos. Se asocia a modificaciones irreversibles de las vías aéreas. El proceso original o
causa subyacente no se ha identificado.

Numerosos autores coinciden en destacar el período mínimo de la persistencia de la tos en 2


meses, ya que este dato tiene importantes derivaciones para el clínico debido a que la bronquitis
crónica no puede ser diagnosticada sin descartar cuidadosamente otra enfermedad activa.

Afecta a perros y gatos a partir de 8 años sin predisposición de raza o sexo. Sin embargo, se ha
observado una mayor predisposición en gatos siameses y en perros de razas pequeñas como
Caniche, Pequinés, Pomeranian. Probablemente afecte el modo de vida urbano que hace que los
animales estén inhalando humo de coches. Dichas razas también están predispuestas a padecer
colapso traqueal y valvulopatía mitral con compresión del tronco bronquial principal.

Etiología:

Normalmente la causa no se descubre porque la enfermedad es detectable cuando aparecen los


signos clínicos en etapas avanzadas,

Procesos inmunomediados:
Hipersensibilidad a irritantes inhalados, contaminantes atmosféricos; ozono, dióxido de azufre,
humo de tabaco, polvo.
Factores genéticos

Procesos infecciosos:
o Micoplasma en gatos
o Bordetella bronchiséptica en perros, secundario a estados de inmunodeficiencia
o A su vez, las infecciones pueden ser secundarias a la propia bronquitis crónica, siendo
difícil establecer relación causa-efecto

Infestaciones parasitarias
o Oslerus osleri en perros.
o Capillaria aerophila ,Crenosoma vulpis, en gatos.
o Mammonogamus spp.
Otros procesos como la discinesia ciliar
Factores predisponentes a bronquitis crónica canina y felina.

Sintomatología

El cuadro clínico de esta enfermedad suele manifestarse con toses secas, más frecuentes por la
noche o a primeras horas de la mañana. Es frecuente que los propietarios confundan la tos con
vómitos si estas toses son en cuadros paroxísticos, más o menos intensos y con arcadas finales.
También pueden asociarlo con intentos del animal para expulsar algo “clavado” en la orofaringe.

Debemos por tanto realizar una cuidadosa anamnesis de manera que lleguemos a diferenciar un
cuadro de vómitos primario de un problema respiratorio con emesis secundaria refleja.

1
La tos puede ser más evidente tras algunos ejercicios físicos y después de periodos de excitación,
alegría o estrés. Un dato importante a tener en cuenta es que la sintomatología es variable en
función de la estación del año y de las condiciones meteorológicas de modo que suele empeorar
esta sintomatología durante la primavera y el otoño.

Otro síntoma que aparece con frecuencia es la disnea e incapacidad de adaptación a los cambios
bruscos de la temperatura ambiental.

En general la actitud del paciente suele ser normal y solo en raras ocasiones encontramos
pacientes deprimidos, anoréxicos o con pérdida de peso. Esta sintomatología es más frecuente en
los casos de bronquitis infecciosa.

Tos duradera de más de dos meses. Acompañada de


Anamnesis hipersecreción de moco por la noche e improductiva, seca y
áspera durante el día.
El animal empieza a demostrar intolerancia al ejercicio y la tos
aumenta después de realizarlo.

Lo normal es que estado general no esté afectado.


Examen físico Los pacientes suelen presentar sobrepeso
Disnea.
Auscultación Puede ser normal.
Espiración prolongada, sibilancias, aumento de los sonidos
broncovesiculares y crujidos.
Estertores espiratorios finales con respiración abdominal en
cuadros avanzados por el colapso traqueal.
Se puede observar un segundo tono cardíaco aumentado en
animales con hipertensión pulmonar secundaria

Sintomatología de la bronquitis crónica canina y felina.

Diagnóstico:

Podemos empezar a sospechar de bronquitis crónica cuando en la anamnesis nos revelen que el
animal presenta tos continuada diaria desde hace varias semanas, evidencia de moco excesivo y
además que el animal haya dado negativo a pruebas de detección de filarias y no presente signos
de insuficiencia cardiaca, neumonía u otras enfermedades respiratorias crónicas. Además
utilizaremos diversas técnicas diagnósticas:

1. Diagnóstico Radiológico:
Debemos tener en cuenta que puede darse un patrón bronquial normal, a pesar de observar unos
signos clínicos evidentes.
Nos resultará útil para descartar otras causas de tos crónica o descubrir complicaciones como
neumonía, bronquiectasia o enfermedad cardiaca.
Veremos, como signo específico, densidades o infiltrados periféricos debidos a la falta de drenaje
del moco.
Engrosamiento bronquial (con forma de buñuelos o raíles de tren) según la proyección verticales o
longitudinal con manguito peribronquiolar.
Las densidades intersticiales y peribronquiales en perros viejos son normales, muestran cambios
histológicos asociados a la edad.
La existencia de infiltraciones alveolares puede indicar coexistencia de bronconeumonía o edema
pulmonar.
Si observamos dilataciones saculares de los bronquios estaremos frente un hallazgo de
bronquiectasia secundaria a bronquitis crónica.
También es común un cuadro intersticial leve en bronquitis crónica.
Puede producirse secuestro de aire y como consecuencia observaremos los pulmones inflados,
por lo tanto aparecerá radiotransparencia y aplanamiento del diafragma por el empuje de los
pulmones contra éste.
En casos graves se observa bronquiectasia, neumonía y atelectasia.
En el gato pueden encontrarse atelectasias en el lóbulo medio derecho.

2
Si realizamos radiografías durante la espiración evidenciaremos el colapso en las grandes vías
aéreas
Además puede observarse cardiomegalia debido al cor pulmonale

2. Diagnóstico Broncoscópico:
Algunos autores recomiendan realizar broncoscopia para descartar otras enfermedades o cuando
el animal no responde al tratamiento.
Es útil para obtener muestras representativas de las vías aéreas profundas para citología y cultivo.
Observaremos de forma característica: mucosa eritematosa, engrosada, edematosa, contorno de
vías respiratorias irregular, colapso total o parcial de vías desde los bronquios principales hasta los
de tercer orden, sobre todo durante la espiración pasiva, se ven hileras o placas de moco denso.
La bronquiectasia también puede reconocerse con la broncoscopia
Pueden observarse proliferaciones polipoides o nodulares proyectadas hacia la luz bronquial.

3. Electrocardiograma:
-Arritmia sinusal respiratoria
-Marcapasos migratorios
-Ondas p pulmonares

4. Pruebas Laboratoriales:
Hemograma: Normalmente no se observa nada específico. No obstante, podemos observar
neutrofilia madura generada por el estrés, así como policitemia por la hipoxemia crónica. Anemia,
leucocitosis neutrofílica y desvío a la izquierda si hay una bronconeumonía secundaria.
Observaremos eosinofilia en procesos alérgicos o parasitarios, más común en los gatos

Bioquímica sérica: Suele ser inespecífica. Se recomienda realizar análisis antigénico para
dirofilariosis, sobre todo en perros que vivan en zonas endémicas.

Análisis fecal: Recomendable realizarlo para detectar gusanos pulmonares

Análisis de filarias

Análisis de orina

Análisis de gases en sangre arterial: Se registra hipoxemia, PaO2< 80mmHg en le 30% de


los casos. Hipercapnia poco frecuente, PaCO2> 40mmHg hallazgo serio de hipoventilación
asociado a trabajo respiratorio

Curva de volumen pulmonar:


o Relación tiempo espiración /tiempo inspiración alta, mayor o igual a 1,31.
o Flujo de aire al 25% del volumen corriente reducido por el estrechamiento o
colapso de vías.
o Desequilibrio en la ventilación/perfusión.

Estas pruebas se recomienda realizarlas para comprobar si el tratamiento es eficaz y el animal


va recuperando su función pulmonar.

5. Examen de líquido traqueobronquial:


El examen citológico nos revela: neutrófilos degenerados lo cuál nos indica infección
bacteriana o bronconeumonía, eosinófilos, signo de parasitismo, alergia o hipersensibilidad (tener
en cuenta parásitos cardíacos, muy comunes en gatos), pueden aparecer también macrófagos y
linfocitos así como hiperplasia de células epiteliales bronquiales.
Se debe hacer un cultivo del fluido traqueobronquial y un análisis de sensibilidad en perros con
diagnóstico de bronquitis crónica y que en sus radiografías y análisis broncoscópico se evidencie
bronquiectasia.
La presencia de un número pequeño de bacterias en un cultivo no necesariamente implica la
existencia de infección.
Para que los resultados de los cultivos traqueobronquiales y de las pruebas de sensibilidad sean
interpretados correctamente es necesario que las muestras sean recogidas de de las vías aéreas
bajas y no de la faringe.

6. Diagnóstico diferencial:
La bronquitis crónica se diagnostica basándonos en la exclusión clínica de otras enfermedades
respiratorias crónicas.

3
En perros, más de 60 procesos cursan con tos, ya que es el signo más evidente y el motivo de
consulta.

Tratamiento:

1. EDUCACIÓN DEL DUEÑO:


Advertirle de que su animal presenta lesiones irreversibles y por tanto el animal
se halla ante una enfermedad incurable. Explicarle el objetivo de la terapia que vamos a
aplicar.

2. TERAPIA DEL PACIENTE:

MEDIDAS CORRECTORAS Y DE MANTENIMIENTO:

1. Evitar el contacto del animal con: humo, polvo, limpia hogares, etc., porque pueden
provocar colapso traqueal, dando lugar a excitación y estrés en el paciente lo que le
provoca ataques de tos paroxística.

2. Dar al paciente pienso dietético para reducir peso, así se mejorará la ventilación y la
oxigenación arterial, y se reducirá el estrés del sistema cardiovascular.

3. Recomendar ejercicio ligero.

4. Oxigenoterapia si el animal sufre episodios de hipoxemia y bronconeumonía severas.

MEDIDAS PRINCIPALES: van encaminadas a:

1. Aliviar la inflamación y la obstrucción provocada por la hipersecreción de moco con


Antiinflamatorios y Broncodilatadores.

2. Controlar la tos siempre que esta sea improductiva, lo que es indicativo de que la
inflamación ya se está resolviendo con Antitusígenos.

3. Controlar la infección con Antibióticos, que deberán se de amplio espectro y


lipolíticos.

4. Hidratar las vías aéreas con nebulización.

5.

Glucocorticoides Prednisona o Dosis de inicio: 0.5-1mg/kg 10-14 Efectos


de acción corta. días/12h. Oral y parenteral. secundarios:
o Si remite la tos: reducir la dosis a la hepatomegalia,
mitad cada 10-14 días hasta el debilidad
mínimo que produce mejoría. muscular,
o Si no remite: combinación con disminución de
broncodilatadores como el las defensas,
Salbutamol inducción a la
obesidad.
Antiinflamatorios.

Broncodilatadores.
Los broncodilatadores de utilidad en la clínica de pequeños animales puede dividirse en tres
grandes grupos: Broncodilatadores directos, bases xánticas y anticolinérgicos, de los cuales,
desde el punto de vista terapéutico, solo interesan los dos primeros, ya que los anticolinérgicos,
como la atropina, tienen efectos secundarios no deseables en la mayoría de los casos.

4
Metilxantinas Teofilina Perros: 20 mg/kg/24h Puede producir efectos
secundarios como:
hiperexcitabilidad, taquicardia y
distrés gastrointestinal.
Reducir la dosis si se observa
mejoría.
Si no responde al tratamiento o
se sospecha de toxicidad, medir
la concentración plasmática de
Aminofilina teofilina 4,5h después de la
administración de teofilina de
liberación lenta y 1,5 h después,
Perros: 11 mg/kg/8h si es de liberación rápida.
Oxifilina

Se suele usar en perros Toys


en forma de elixir 14
mg/kg/8h.

Agonistas β2 Salbutamol Perros: 0.1 mg/kg /8h Si se aprecia mejoría


simpaticomiméticos reducir la dosis.
Clembuterol 0,6 ug/kg/12h
Procaterol 1 ug/kg/12h
Terbutalina 100 ug/kg/8h

Antitusívos
Los fármacos antitusívos como el dextrometorfano tienen un valor muy limitado y no son efectivos
en líneas generales. Los supresores narcóticos como la codeína, sí son más efectivos pero en
casos de complicaciones infecciosas pueden agravar el cuadro puesto que afectan de modo
negativo a los mecanismos de defensa normal facilitando el acumulo de secreciones respiratorias.

Hidrocodona 0.22mg/kg /6-12h, PO


Butorfanol 0.05-0,1mg/kg/6-8h, PO ó SC
Codeína 1-2mg/kg/6-12h PO.
Dihidrocodeína 0,5-1mg/kg /
Butamirato 0,1mg/kg/12h, PO.
Clorbutinol 0,5mg/kg/12h, PO.
Dextrometrofano 1-2mg/ kg /6-8h, PO.
Antitusívos

Fenobarbital 2-6mg/Kg /día/8-12h, PO


Perros: 0.05-0.01mg/kg, IV, IM o SC
0.55-2,2 mg/kg/6-8 h, PO
Acepromazina Gatos: 0,11-0,22 mg/kg, IV, IM o SC; 1,1-2,2
mg/kg/8-12h, PO
Tranquilizantes

5
Doxicilina 2.5-5 mg/kg /12 h. PO
Cloramfenicol 50mg/kg /8h. PO
Enrofloxacina 5-10mg/kg /12 h PO ó 20-40 La Enrofloxacina inhibe el
mg/kg7día PO metabolismo de la teofilina,
dando lugar a niveles tóxicos
en sangre. Reducir la dosis de
teofilina al 30%.
En infecciones severas: 15mg/kg /12h. PO
Cloramfenicol y Trimetropín-
sulfa

Clindamicina con 11mg/kg /12h. PO


Enrofloxacina o
Ciprofloxacina
Gentamicina nebulizada Aplicar con un nebulizador
desechable durante 10
minutos.
Antibióticos

Profilaxis y Prevención:

Se recomiendan controles rutinarios de parásitos como Filarias.


Mantener una higiene bucal regular para evitar la aspiración microbiana a las vías.
Evitar el contacto prolongado con los factores predisponentes citados, sobre todo los que sean de
carácter doméstico (humo de cigarro, limpiadores, polvo, etc.).

Lecturas Recomendadas:

Caro A: Enfermedades pulmonares obstructivas crónicas del perro y el gato. E. Montoya-Alonso


JA: Enfermedades respiratorias en pequeños animales. Buenos Aires, Inter-Médica, 2005, pp:121-
125.

Kuehn NF: Chronic Bronchitis in Dogs. En: King LG: Textbook of Respiratory Disease in Dogs and
Cats. Saunders, 2004, pp: 379-387.

Nielssen A & Taylor SM: Enfermedades de la vía respiratoria baja. En: Morgan RV, Bright RM &
Swartout MS: Clínica de pequeños animales. Sauders-Elsevier, 2.004, pp: 167-168.

6
FOTOS PRIMERA JORNADA DE
MEDICINA CARDIORESPIRATORIA
DR. LINA
SANZ
CHILE

CHARLAS

1. Abordaje clínico, diagnóstico y terapéutico del gato con tos

2. Patologías pleurales
3. Diagnóstico radiográfico de las principales urgencias
respiratorias felinas y caninas
Dra. Lina Sanz Aguirre
2018

Dra. Lina Sanz Aguirre


Instituto de Medicina Felina y
Centro Opción Felina
LA TOS
 REFLEJO PROTECTIVO
 ESTIMULACIÓN DE MECANORECEPTORES O
QUIMIORECEPTORES EN LA VÍA AÉREA
 BRONQUIOLOS Y ALVEOLOS NO TIENE
RECEPTORES ….. SI ENFERMEDAD PULMONAR
GENERA TOS ES POR EXTENSIÓN A VÍAS DE
MÁS DIÁMETRO

PROTOCOLO FRENTE A ANTECEDENTE DE TOS


 ASEGURARSE QUE ES TOS Y NO ARCADA,
VÓMITO, REGURGITACIÓN
 SUELEN SER ATAQUES PAROXÍSTICOS
 EN JÓVENES PREDOMINAN CAUSAS
INFECCIOSAS
 EN ADULTOS PREDOMINA ASMA (ORIENTALES
Y SIAMESES CON MÁS FRECUENCIA)
PROTOCOLO FRENTE A ANTECEDENTE DE TOS
 FRECUENCIA Y NATURALEZA DE LA TOS

 SUAVE Y PRODUCTIVA… ENFERMEDAD DE


PARÉNQUIMA

 SECA Y DURA … ENFERMEDAD DE VÍA AÉREA

PROTOCOLO FRENTE A ANTECEDENTE DE TOS


 INICIO Y DURACIÓN

 AGUDA … CUERPO EXTRAÑO INHALADO, ASMA,


TRAUMA, ENFERMEDAD INFECCIOSA

 CRÓNICA …. BRONQUITIS CRÓNICA, ASMA ,


NEOPLASIA
APROXIMACIÓN DIAGNÓSTICA
 AUSCULTAR LARINGE, TRÁQUEA Y CAMPOS
PULMONARES
 PALPACIÓN LARINGE Y TRÁQUEA
 PALPACIÓN Y RESISTENCIA DE TÓRAX
ANTERIOR

EXÁMENES COMPLEMENTARIOS
 SANGUÍNEOS NO DAN LA CAUSA PERO
APORTAN; INCLUYENDO TEST RETROVIRAL
 HIPERGLOBULINEMIA, NEUTROFILIA SUGIEREN
INFLAMATORIO E INFECCIOSO
 EOSINOFILIA SUGIERE PROCESO ALÉRGICO O
PARASITARIO
 ANEMIA REGENERATIVA SUGIERE ANEMIA –
HEMORRAGIA
 ERITROCITOSIS SUGIERE HIPOXIA CRÓNICA
TOS AGUDA
 PUEDE CONSIDERARSE TERAPIA EMPÍRICA
 EXAMEN NASOFARÍNGEO BAJO ANESTESIA
PARA CUERPOS EXTRAÑOS INHALADOS
 TRAQUEOSCOPÍA PARA CUERPOS EXTRAÑOS
EN TRÁQUEA
 ANTIMICROBIANOS SUELEN INDICARSE,
MÍNIMO 3 SEMANAS
 DOXICICLINA 10 MG/KG CADA 12 HORAS A 24 HORAS
***
 AZITROMICINA 5 – 10 MG /KG CADA 12 HORAS Y LUEGO
DOSIS MÁS BAJAS
 AMOXICILINA CON ÁCIDO CLAVULÁMICO

TOS CRÓNICA (mayor a 2 semanas)


 BRONQUITIS Y ASMA ES LO MÁS FRECUENTE
 SI SE PRESCRIBIRÁN CORTICOIDES DEBEN SER
SOLO INHALADOS MIENTRAS SE DEFINE EL
DIAGNÓSTICO
 DOXICICLINA POR MÍNIMO DE TRES SEMANAS
Y ANTIELMÍNTICOS SUELEN USARSE
 LIMPIEZA Y MANEJO DEL AMBIENTE
ASMA FELINA

 Limitación al flujo aéreo en la vía aérea baja que


resuelve espontáneamente o con medicación.
 Combinación de inflamación, mucus acumulado y
contracción del músculo liso bronquial
 Signos desde toses esporádicas a ahogo dramático
 Se reconoce en ocasiones como complejo asma /
bronquitis

ASMA FELINA

 Proceso crónico del árbol bronquial con


signología similar a la bronquitis crónica
 BRONQUITIS CRÓNICA : Genera toses a diario en
todos los casos; debe excluirse para el diagnóstico
de asma. Generada por dirofilaria, pneumonia,
parásitos pulmonares y neoplasia.
ASMA FELINA

 En humanos el asma se diagnostica por estudios


dinámicos que requieren cooperación.
 En ocasiones , entonces, no podemos distinguir
entre asma y bronquitis en felinos que tengan tos
como único signo

ASMA FELINA
 Felinos predispuestos a severo asma por
hiperreactividad bronquial:
 Mayor cantidad de músculo liso en pared
bronquial y ductos alveolares
 Mayor cantidad de cartílago elástico respecto al
hialino en bronquiolos
 Mayor cantidad de células globoides y glándulas
submucosas
 Mayor viscosidad mucus
 Mayor cantidad de mastocitos pulmonares
(serotonina!!!)
ASMA FELINA

 Ante cualquier noxa el epitelio respiratorio bajo se


hipertrofia, entra en metaplasia, se erosiona y
finalmente se ulcera.
 Las células caliciformes y glándulas submucosas se
hipertrofian y generan gran cantidad de mucus
viscoso
 Se infiltra la mucosa y submucosa bronquial con
células inflamatorias.
ASMA FELINA

 Signos serán tos, ruido respiratorio (resuello o


wheeze) y letargia por la limitación de la vía aérea
dada por mucus, edema y estrechamiento por
infiltrados.. En gatos se suma la broncoconstricción

ASMA FELINA

 Por las fórmulas de Bernouilli y Poiseuile- Hagen la


disminución en el diámetro genera incremento de la
velocidad y cae la presión.
 Un 50% de reducción luminal hace caer en 16 veces el
volumen de aire
 Degranulación de proteínas catiónicas desde
eosinófilos
ASMA FELINA

 La patogenia incluye la interacción entre linfocitos


T activados y eosinófilos (LBA)
 Son CD4 activados por aeroalergenos, liberan IL-5
la cual promueve eosinófilopoyesis, activación y
supervivencia de eosinófilos ( Perfil de citoquinas T
helper 2)

ASMA FELINA

 Los gatos generan:


 IgE alergeno – específicos, IgG e IgA en suero y
LBA alergeno – específicos
 Hiperreactividad en vía aérea
 Eosinofilia en vía aérea
 Perfil de citoquinas agudo T H - 2
ASMA FELINA

 Prevalencias:
 1% de población general
 5 a 15% en siameses

 Edad promedio 2 a 8 años para el inicio

ASMA FELINA
 Signología:
 Tos por la mayor sensibilidad de la vía aérea
 Resuellos por el paso de aire forzado por espacios
estenosados
 Cépitos por excesivo mucus, espiratorios
 Letargia
 Asintomáticos entre crisis los casos leves, no así los
severos.
ASMA FELINA

 Signología:
 Puede estimularse la tos por compresión de pared
toráxica.
 Disnea espiratoria obstructiva de leve a severa
(cianosis y boca abierta)
 Signos parten episódicos y luego se cronifican
 Signos frente al alergeno

ASMA FELINA

 Diagnóstico:
 Broncoconstricción reversible es pauta
 Aplicar terbutalina por inhalación o parenteral
(agonista β2) 0,01 mg/Kg i.m. y reevaluar en 5 a 10
minutos… es el único criterio aprobado de distinción
clínica entre BC y AF
 En su defecto …dexametasona 2 mg/Kg
ASMA FELINA

 Diagnóstico:
 Examen físico es irrelevante
 Baja condición corporal, cianosis, diestress, crépitos
en crónicos
 Por flotación y prueba Baermann excluir
Aelurostrongylus abstrusus o Eucoleus aerophila
(formalmente Capillaria aerophila)

ASMA FELINA

 Diagnóstico radiográfico:

 Radiografías normales o anormales


 Patrón bronquial con anillos y líneas de ferrocarril
 Hiperluscencia lobar por enfisema , con
aplanamiento diafragmático, redondeamiento de
ángulos lumbofrénicos y costofrénicos, ángulos
lumbofrénicos caudales al último par costa,
paralelismo costal
ASMA FELINA
 Diagnóstico radiográfico:

 Esternón convexo ventralmente, tórax biconvexo


lateralmente
 Colapso del lobo medio derecho en 15% de casos,
evidencia de atelectasia (orientación dorsoventral
en el árbol bronquial)
 Infiltrados y patrón miliar diseminado por
tapones mucosos y/o áreas atelectásicas.

ASMA FELINA
 Diagnóstico radiográfico:

 Radiografías NO distinguen de bronquitis crónica


 Radiografías similares a pneumonitis intersticial
, neoplasia y otros
 Radiografía se mantiene similar entre controles
!!!!
 Tomar tres a cuatro proyecciones
ASMA FELINA

 Broncoscopía:

 Raramente requerida!!!
 Procedimiento puede comprometer la vida en estos
casos
 Luego de 6 a 7 días de terapia agresiva que incluya
corticoides, si no existen cambios en la signología,
se prescribe con especialistas

ASMA FELINA
 Citología traqueobronquial:
 20 a 25% de eosinófilos en LBA son comunes en
gatos sanos
 Su presencia no indica alergia o parasitismo
 Macrófagos, neutrófilos se recolectan de sanos y
enfermos en igual cantidad…
 Obtenida por LBA o lavado transtraqueal

 No recomendado
ASMA FELINA

 Cultivo traqueobronquial:

 Parénquima sano NO es estéril


 Incluso Klebsiella y Pseudomonas desde gatos sanos
 Solo relevante Mycoplasma , que al igual que
algunos virus (VHF-1) degrada la endopeptidasa
neutra (que degrada sustancia P, proteína que
genera broncoconstricción y edema)

ASMA FELINA
 Diferenciales:

 Para el status asthmaticus es la falla cardíaca


congestiva izquierda por cardiomiopatía… muy
inusual
 Para lo crónico: toda otra pneumopatía que genera
tos : bronquitis crónica, dirofilarias, H1N1,
parásitos, neoplasia.
ASMA FELINA
 Terapia:

 Broncodilatador y antiinflamatorio es lo básico


 Disminuir de peso en CC alta
 Disminuir stress ambiental
 Fenbendazole (antígeno tratable) 50 mg/Kg/14 ds
 En Aelurostrongylus abstrusus también se puede
aplicar tópico imidacloprid / moxidectin

ASMA FELINA
 Terapia Corticoides:

 Es lo más efectivo a largo plazo


 Disminuye citoquinas
 Corticoides inhalatorios
 Con toses mayores a una crisis por semana 1 – 2
mg/Kg de prednisolona cada 12 horas por 5 a 7 días…
baja sostenida lenta en 2 meses y siempre seguir con
inhalatorio (propionato de futicasona Provent®)
ASMA FELINA
 Terapia Corticoides:

 Inyectable solo acetato de metilprednisolona


10 a 20 mg i.m. en gatos que no toleran otra
administración
 Cada 4 a 8 semanas
 Efectos adversos
ASMA FELINA

 Terapia Broncodilatadores:

 Usar agonistas de receptores β2 selectivos para evitar


efectos cardiovasculares.
 Sulfato de terbutalina
 Sulfato de albuterol

ASMA FELINA

 Terapia Broncodilatadores:

 Sulfato de terbutalina
 Relaja músculo liso bronquial, vascular y uterino
 Tabletas, jarabes, puff y parenteral (sc o im)
 0,01 mg /Kg i.m. en crisis (clínica u hogar)
 0,1 - 0,2 mg/Kg oral cada 8 horas
ASMA FELINA
 Terapia Broncodilatadores:

 Sulfato de terbutalina
 Frecuencia cardíaca alcanza los 240 lpm y respiratoria
baja un 50% cuando es efectiva
 Monitorear kalemia
 Cuidado con cardiomiopatía pre existente

ASMA FELINA

 Terapia Broncodilatadores:

 Sulfato de albuterol (salbutamol)


 Tabletas, jarabes y puff
 Solo usar el inhalador, con 90 µg por puff
ASMA FELINA

 Terapia Broncodilatadores:

 Metilxantinas
 Aminofilina no recomendada
 Teofilina 4 mg/Kg oral cada 8 a 12 horas. En
preparación de larga acción 25 mg/Kg cada 24 horas

ASMA FELINA

 Terapia Antitusivos:

 No indicados
 Tos es productiva
ASMA FELINA
 Terapia Mucolíticos:

 No se necesitan habitualmente
 Principales autores no lo usan
 Bromhexina 2 mg/Kg oral cada 12 horas por 7 a 10
días y bajar dosis a la mitad por 7 a 10 días más
 Acetilcisteína nebulizada, 5 a 10 mg/Kg por 30
minutos cada 12 horas (viene al 10 y 20%).. PERO
IRRITA

ASMA FELINA
 Terapia Espectorantes:
 No se utilizan
 Inducen vómito (guafenesin)

 Terapia Antibióticos:
 Más de 105 organismos por ml
 Basado en sensibilidad
 Doxiciclina con Mycoplasma en cualquier
concentración
ASMA FELINA
 Terapia Ciproheptadina:

 Antiserotónínico
 Solo en gatos que no responden a dosis máximas
de broncodilatadores y corticoides
 2 – 4 mg total PO cada 12 horas… depresión a las 24
horas y si hay efectos benéficos se ven luego de 4 a
7 días

ASMA FELINA
 Terapia Antileucotrienos:

 LTC4, LTD4, LTE4


 Generan hipersecresión de mucus, edema por
incremento de permeabilidad,
broncoconstricción y quemotaxis a eosinófilos y
PMN
 No hay evidencia fuerte de su beneficio en estos
casos
 Zafirlukast 1 a 2 mg/Kg/bid – Montelukast 0,5 – 1
mg/Kg/sod.
ASMA FELINA
 Tubos de inhalación:

 70% lo usan de inmediato, 20% requieren


acostumbrarse, 10% no lo tolerarán.
 Efectos óptimos en 1 a 2 semanas
 Preferir broncodilatador y corticoide por separado
 Flovent ® de 110 a 220 µg cada 12 horas

ASMA FELINA
 Recomendación Dr Phil Padrid:

 Solo tos : fluticasona 110 mcg bid (2 puff) y


albuterol bid (2 puff)
 Tos y despertar nocturno: fluticasona 220 mcg bid
, albuterol bid, prednisolona 1 mg/Kg/sod 5 ds
 Signos marcados: Igual al anterior con
prednisolona 1 -2 mg/Kg cada 12 horas, luego cada
24 y dosis descendientes
ASMA FELINA
 Recomendación Dr Phil Padrid:

 En emergencia
 Reposo, escasa manipulación
 Oxígeno 10 – 20 minutos
 Terbulatlina (o dexa) inyectable
 Esperar 5 – 10 minutos
 Terbutalina cada 30 minutos por 4 veces si es
necesario
 Luego mantención de caso grave.

PNEUMONIAS

 INFLAMACIÓN DEL PARÉNQUIMA


PULMONAR
 INFRECUENTE
 VARIADAS ETIOLOGÍAS
 BACTERIAS SUELEN SER SECUNDARIAS
PNEUMONIAS
 Bacterias patógenas incluyen:
 Escherichia coli
 Klebsiella
 Pasteurella (también primario)
 Pseudomonas
 Bordertella (también primario)
 Streptococcus sp
 Nocardia
 Actinomices

PNEUMONIAS

 Condiciones asociadas:
 Aspiración por esofagopatía o recuperación
anestésica
 Enfermedad metabólica como la pneumonitis
urémica, hiperadrenocorticismo y diabetes
mellitus
 Trauma contuso, penetrante o Cx
 Inmunosupresión por drogas, neoplasias o
retrovirus
 Infección preexistente
ANTECECENTES

 Pneumonia por Mycoplasma es infrecuente y


secuela de severa enfermedad del tracto
respiratorio alto
 Chlamidophila felis puede generarla en gatitos
 Casos parasitarios y protozoarios son frecuentes
 Casos fúngicos suelen ser por Criptococcus
neoformans

ANTECECENTES

 Pneumonitis virales por calicivirus en


gatitos o secundarias a FIV
 Se denomina pneumonitis intersticial
 Producto de algunas cepas muy patógenas
 Infrecuente
ANTECECENTES
 Micosis menos frecuentes (USA) incluyen:
 Blastomicosis
 Histoplasmosis
 Aspergilosis
 Candidiasis
 Aspergilosis
 Coccidiomicosis
▪ Tipo intersticial
▪ Testear FIV – FeLV
▪ Fluconazol, itrakonazol

PNEUMONIAS

 Signos:
 Tos infrecuente, puede ser productiva
 Disnea de predominio espiratorio
 Disnea restrictiva
 Fiebre
 Letargia y anorexia
 Halitosis
 Respirar con boca abierta
 Auscultación con crépitos, sibilancias, silencio
en consolidación
 Ocasionalmente descarga nasal y disneas mixta
BORDETELLA BRONCHIPSEPTICA

 Cocobacilo aerobio gram (-)


 Seroprevalencias de 24 a 79%
 Aislamientos de 3 a 11%
 Mayores prevalencias en gaterías, albergues o
múltiples gatos en casa
 Sin relación con agentes clásicos del complejo
respiratorio alto
 Stress de parto induce eliminación desde
orofaringe

BORDETELLA BRONCHIPSEPTICA

 Principal causa de pneumonia infecciosa


primaria
 Mayor prevalencia en menores de 10
semanas
 Afecta cilios, libera toxinas
 Depresión, disnea, cianosis, muerte
 Nódulos grises en necropsia y exudado
purulento al corte
BORDETELLA BRONCHIPSEPTICA

 Toxinas:
- Dermonecrótica: inflamación
- Citotoxina: cilioestasis
- Enzimática: altera fagocitosis
(PMN)

BORDETELLA BRONCHIPSEPTICA

 Inmunidad materna corta de 2-6 sem


 Importancia del perro y cerdo en la
epidemiología
 Terapia no suele eliminar el agente
 Puede ser zoonosis en
inmunocomprometidos o esplenectomizados
BORDETELLA BRONCHIPSEPTICA

 Cuadros altos orofaríngeos suelen limitarse


en 10-14 días
 Signos 5-6 días por la inflamación mediada
por citoquinas
 Algunos cronifican asintomáticos (41%)

BORDETELLA BRONCHIPSEPTICA

 Altamente contagiosa
 Lavado broncoalveolar o transtraqueal
 Cultivo dirigido en la orden
 Medio carbón – cefalexina
 Terapia según antibiograma
 Empírico : doxiciclina (10 mg/Kg/24 hr),
oxitetraciclina, enrofloxacino y otras
quinolonas. Algunas cepas amoxi –
clavulámico
BORDETELLA BRONCHIPSEPTICA

 Terapia clásica:
- Doxiciclina 10 mg/kg/24 hrs
con Prednisolona 1 mg/kg/24 hr por
10 días y 0,5 mg/kg por 10 días
- Nebulizaciones 14 días (3ml agua)
- NaCl
- Inhalaciones
Diseminan hasta 5 meses pos infección

BORDETELLA BRONCHIPSEPTICA

 Prevención:
 Disminuir hacinamiento
 Eliminar excretores orofaríngeos de
reproducción (hembras)
 Reducción stress
 Desinfectantes
 Vacunación Novibac Bb ®
Diagnóstico
pneumonia

 Examen clínico
 Radiografías (alveolar, bronquial, intersticial ,
nodular, consolidaciones; linfoadenomegalia
en micobacterias, hongos y linfoma)
 Neutrofilia con o sin D a I
 Neutropenia por secuestro
 Neutrófilos tóxicos

Diagnóstico
pneumonia

 Anemia NN en cronicidad
 Hipoxemia PaO2 menor a 80 mmHg o SPO2
menor al 90% - 92%
 Citología por aspiración percutánea, LTT, LBA
 Cultivo Bb, aerobios, anaerobios y hongos
 Test especiales
Diagnóstico diferencial
pneumonia

 Asma / bronquitis
 Pneumonia eosinofílica
 H5N1
 Linfoma pulmonar intersticial
 Neoplasia primaria (carcinoma broncogénico,
CCE) o metastásica

Aelurostrongylus abstrusus

 Nemátodo metastrongylidae
 Frecuente infestación
 Huésped: - babosa, caracol (intermedios)
- Roedores , aves, reptiles, anfibios
(paraténicos)
 Bronquiolitis y neumonia
 Adultos en alvéolos , bronquiolos y pequeñas
ramas de arteria pulmonar
Aelurostrongylus abstrusus

 Huevos pasan a L1 en alvéolos


 L1 deglutidas y salen con defecaciones
 Pueden sobrevivir meses
 Ingeridas por moluscos terrestres
 Gato ingiere caracoles, babosas o paraténicos
 Larva llega al pulmón por sangre o linfa en 24
h (L3 penetra digestivo)

Aelurostrongylus abstrusus

 Adulto macho 5 mm
 Adulto hembra 9 mm
 Larva en fecas de 3,6 mm con cola en S
 Prepatencia de 34 a 42 días
Aelurostrongylus abstrusus

 Se genera gran respuesta inflamatoria


 Casos asintomáticos autolimitantes en 3-4
meses (menos de 50 larvas)
 Tos es signo predominante
 Escaso compromiso sistémico … asma
 En ocasiones disnea
 Pneumonia intersticial y/o bronquitis –
bronquiolitis

Aelurostrongylus abstrusus

 Puede generar pleuritis con nódulos de 10 mm


 Infiltrados de linfocitos, macrófagos y
eosinófilos
 Genera hiperplasia e hipertrofia epitelial que
puede quedar como secuela , generalmente sin
impacto clínico
Aelurostrongylus abstrusus

 Radiografía muestra cambios 2 – 6 semanas


pos infección
 Cambios pueden ser severos incluyendo
patrones miliares
 Técnica de Baerman en fecas
 Citología pulmonar por punción , LTT, LBA

Aelurostrongylus abstrusus

 Terapia
 Febendazole 50 mg/kg/día por 10-20 días
- Ivermectina 0,4 mg/kg SC única
- Mebendazol 30 mg/kg/24 hr por 5 días
- Imidacloprid / moxidectina tópico
Dra. Lina Sanz Aguirre
2018
Dra. Lina Sanz Aguirre
2018

Dra. Lina Sanz Aguirre


Instituto de Medicina Felina y
Centro Opción Felina
 Aplicaciones de radiología simple y
contrastada, no intervencionista

 Muchas de las técnicas se van reemplazando


por TAC simple y contrastado, especialmente en
emergencias luego de estabilización

 “Radiografía de Urgencia”

 Ecografía y radiografía SON


COMPLEMENTARIAS … en tórax y
abdomen tener ambas
 Excepciones suelen involucrar tejido
óseo o mineralizaciones
 Las radiografías, excepto casos aislados,
pueden esperar
 Si se obtendrá ecografía… partirmos con
Radiografía
 Las radiografías DEBEN esperar

 CUANDO SE HABLA DE RADIOGRAFÍAS


NOS REFERIMOS A

ESTUDIOS RADIOGRÁFICOS
 Dos proyecciones en abdomen
 Pueden ser tres a cuatro en
gastrointestinal y estudio de masas
 Dos proyecciones en mediastino
 Cuatro proyecciones en broncoalveolar
y espacio pleural
Indicaciones
 Estudio de cavidad nasal y senos paranasales

 Estudio de cuello y tórax

 Estudio de tórax : 4 proyecciones para


broncoalveolar y espacio pleural

 Estudio de tórax : 2 proyecciones para mediastino en


general

Consideraciones
 Paciente estable que tolere manipulación
 Aprovechar su estado anestesiado / sedado
 Solo xilaxina altera en forma consistente
diagnósticos intra toráxicos
 Extremar simetría y adecuada técnica
 No olvidar pick de inspiración y centrado
 Controles en proceso broncoalveolar cada 12 a
28 horas (Morgan, 2009)
 Posterior a toracocéntesis.
HVS 2018

HVS 2018
Pneumomediastino
 Considerar en pacientes con distress respiratorio,
mala oxigenación y radiografía “sin grandes
cambios”
 Este diagnóstico DEBE BUSCARSE (Similar a TEP)
 Signos patognomónicos en LL
 Puede generar Pneumotórax pero no a la inversa
 Grave o crónico genera pneumoretroperitoneo

HVS 2018
Tromboembolismo pulmonar
 Buscar cada arteria para considerar su vena
vecina
 Ocasionalmente afecta a vasos lobares
principales
 Se evalúa todo el tórax y no solo los puntos de
observación oficiales
 No olvidar glomérulonefritis,
hiperadrenocorticismo, pancreatitis, PPIF, CID,
neoplasias
 Si existe arteritis deformante la única causa es
Dirofilaria

Vet praxis 2015


Vet praxis 2015

Vet praxis 2015


Efusión pleural
 Estudio de tres a CUATRO proyecciones
POSTERIOR a toracocéntesis bilateral
 Análisis de fluido citoquímico y de patología
imprescindible
 Test Rivalta obligatorio en felinos
 Signos patognomónicos (VD)
 Evaluar redondeamiento de márgenes de pleura
visceral
 Diferencias entre especies !!
SIGNOS RADIOGRÁFICOS
 FLUIDO ENCAPSULADO NO SE MODIFICA SEGÚN
DECÚBITO

 FLUIDO típico SE MODIFICA SEGÚN DECÚBITOS


 100 ML MÍNIMO EN RAZA MEDIANA
 50 ML PEQUEÑOS Y GATOS

HVS 2018
HVS 2018

Pneumotórax
 Signo patognomónico es mejor visualizado en V-
D
 Requiere buena técnica
 Se obtiene posterior a toracocéntesis bilateral
HVS 2018

Trauma esternal
 Luxacíón
 Luxofractura
 Diferenciar malformaciones congénitas
HVS 2018

HVS 2018
Masa mediastinal craneal
 Más frecuente en felinos que caninos
 Mayor generación de Sindrome de Claude
Bernard Horner en caninos que felinos (**)
 Raramente se mineraliza
 Tiene signo patognomónico
 Puede o no tener efusión pleural – mediastinal

HVS 2018
HVS 2018

Efusión mediastinal
 Buscar fisuras reversas o mediastinales
 Signo patognomónico en V-D o D-V
 Simetría necesaria
 Puede existir efusión pleural concomitante
Efusión en politrauma
 Importante la toracocéntesis previa
 Evaluación de pared costal, esternón, columna
toráxica, articulación escápulohumeral,
integridad de diafragma
 No siempre se logra simetría en trauma de pared
toráxica y/o pacientes inestables

HVS 2018
HVS 2018

Rotura diafragmática traumática


 Signo patognomónico en VD
 Requiere EXTREMA SIMETRÍA
 Se privilegia Llder, Llizq y DV
 Muchos signos comunes a otras patologías
HVS 2018

HVS 2018
Hemiparálisis de diafragma
 Confirmación RADIOGRÁFICA o fluroscópica
 Se confunde con Rotura Diafragmática
 Proyección DV o VD con signo patognomónico

HVS 2018
HVS 2018

Hipoplasia de tráquea
 Confirmación RADIOGRÁFICA
 Signo patognomónico
 Proyección L-L
 Suele coexistir con otros procesos
TASA TRAQUEOTORÁXICA
MEDICIÓN ENTRADA TORÁXICA:
Entre T1 y su ángulo cráneoventral y
Esternebra I a la altura de la porción más
craneal de la I costilla y llegando al punto de
menor espesor del manubrio

TASA TRAQUEOTORÁXICA
MEDICIÓN TRÁQUEA:
Perpendicular al eje mayor y a la altura
de intersección de la línea de la entrada
toráxica con el centro del lumen traqueal
TASA TRAQUEOTORÁXICA
0,21 +/- 0,03 RAZAS GENERALES,
MESO O LONGICEFÁLICOS
0,16 +/- 0,03 RAZAS BRAQUICEFÁLICAS
0, 13 +/- 0,038 BULL DOG INGLÉS
0,11 +/- 0,03 BULLDOG INGLÉS
(rango de 0,07 a 0,21)

TASA TRAQUEOTORÁXICA
Diámetro tráquea / esternebra a VII
cervical….
0,18 en DSH
0,20 en Persas
Diámetro tráquea / ancho tercio proximal
de III costilla
1,59 DSH
1,71 Persas
HVS 2018

HVS 2018
Masas que comprimen vía aérea
 Proyección L-L da más información
 Masas en cuello o mediastino
 Requieren de citología / biopsia

HVS 2018
HVS 2018

Cardiomegalia
 Conocer diferencias entre especies
 Se REQUIERE foco, simetría y pick de inspiración
 Evaluación cualitativa
 Evaluación cuantitativa
 En urgencia suele obtenerse luego del manejo
 Evaluación de fallo cardíaco congestivo derecho e
izquierdo
HVS 2018

HVS 2018
HVS 2018

HVS 2018
HVS 2018

HVS 2018
Colapso lobo medio derecho
 Pneumonia
 Torsión lobar
 Aspiración
 Asma felino
 Carcinoma broncogénico

Colapso lobo medio derecho


 Lineal o abultado en L-L
 Se aprecia en V.-D / D-V o existe shift
HVS 2018

Patrón alveolar
 Signo patognomónico
 El más fácil patrón de diagnóstico
 El más relevante patrón
HVS 2018

HVS 2018
Patología de esófago
 Siempre dos vistas
 Cuello y tórax
 VD da pronóstico
 LL con signos patognomónicos

HVS 2018
HVS 2018

HVS 2018
Bulla Pulmonar
 Diagnóstico en estudios simétricos
 Diferenciar de masa / asbceso

HVS 2018
HVS 2018

Contusión Pulmonar
 Falsos negativos primeras horas
 Patrones mixtos
 Evaluar pared toráxica y patrones concomitantes
 Dificultad con enfisema subcutáneo
HVS 2018

HVS 2018
Broncopatía
 Puede generar crisis respiratoria
 Bronquiectasia y enfisema son irreversibles
 Suele existir cambios en corazón derecho (cor
pulmonare)
 Suele existir hipertensíón

Dra. Lina Sanz Aguirre


2018
FOTOS PRIMERA JORNADA DE
MEDICINA CARDIORESPIRATORIA
DR. PAULO
MALLEA
CHILE

CHARLAS

1. Anestesia en el paciente cardiópata felino complicaciones


y su manejo

2. Tips en anestesia de paciente cardiópata canino geriatra


F e l i n e H y p e r t ro p h i c
C a rd i o m y o p a t h y :
An Update
Jonathan A. Abbott, DVM

KEYWORDS
 Feline  Hypertrophic cardiomyopathy
 Feline myocardial disease

INTRODUCTION/HISTORICAL PERSPECTIVE

Recently proposed classifications of human cardiomyopathies have emphasized the


etiology or molecular basis of myocardial disease.1,2 Although the cause of a few
specific breed-associated feline cardiomyopathies has been determined, feline
myocardial disease remains largely idiopathic.3,4 Accordingly, morphopathologic/
functional designations remain valid. Given that premise, cardiomyopathy can be
defined as a heart muscle disease that is associated with dysfunction.5 Hypertrophic
cardiomyopathy (HCM) is a disorder in which myocardial hypertrophy develops in the
absence of hemodynamic load or metabolic cause; it is morphologically characterized
by hypertrophy of a non-dilated ventricle.6–8 Feline HCM is a diagnosis of exclusion
that is valid when hypertrophy is echocardiographically evident in the absence of
disorders such as systemic hypertension or hyperthyroidism.
The recognition of cardiomyopathies, and specifically HCM, is recent. The clinical
characteristics of the entity that has become known as HCM were first described in
human patients during the late 1950s.9 The recognition of feline HCM occurred some-
what later. The association between feline cardiac disease and the occurrence of
systemic arterial thromboembolism was reported by Holzworth, but early reports of
thromboembolic phenomena do not specifically relate these events to heart muscle
disease.10,11 In 1970, Liu12 retrospectively evaluated the postmortem features of
acquired feline diseases that had resulted in congestive heart failure. Characteristic
pathologic findings of advanced feline HCM, including left ventricular hypertrophy
(LVH); left ventricular fibrosis; and left atrial dilation, were described but the term cardio-
myopathy was not used. The use of the term cardiomyopathy in reference to feline heart
disease seems to have first appeared in 1973.13 Later publications, including an issue of
this periodical from 1976, refer to feline cardiomyopathy and propose classifications of

Department of Small Animal Clinical Sciences, Virginia-Maryland Regional College of Veteri-


nary Medicine, Virginia Polytechnic Institute and State University, Duck Pond Drive, Blacksburg,
VA 24061-0442, USA
E-mail address: abbottj@vt.edu

Vet Clin Small Anim 40 (2010) 685–700


doi:10.1016/j.cvsm.2010.04.004 vetsmall.theclinics.com
0195-5616/10/$ – see front matter ª 2010 Elsevier Inc. All rights reserved.
686 Abbott

this entity.14 Tilley and Liu proposed the possibility that feline HCM might represent
a model of the human disease in 1980, and the echocardiographic features of feline
myocardial disease were defined later during that decade.15,16

ETIOPATHOGENESIS

It is now established that HCM in human beings is a genetic disease.8,17 Several


hundred distinct genetic mutations have been associated with HCM; genetic testing
together with pedigree analyses have demonstrated that these mutations are casually
related to the HCM phenotype.18–20 Although exceptions have recently been identi-
fied, causative mutations primarily affect genes that encode proteins that are incorpo-
rated into the contractile elements, or sarcomeres, of the myocyte.21
Among feline patients, familial occurrence of HCM has been observed in mix-breed,
Persian and American shorthair cats, and a mutation responsible for HCM in Maine
coon cats has been identified.3,22–24 The occurrence of HCM in Maine coon cats lack-
ing this mutation has been reported, suggesting that other causative mutations exist in
the gene pool of this breed or that there is a nongenetic cause of HCM in some Maine
coon cats. A genetic mutation associated with HCM in ragdoll cats also has been
recently identified.4 Although other etiologic factors cannot be excluded, available
evidence suggests that feline HCM probably has a genetic basis.
The precise mechanism by which genetic mutations lead to the development of
hypertrophy has not been established. It is thought that altered sarcomeric proteins
are responsible for myofiber dysfunction. Indeed, there are data acquired from in vitro
investigations that provide evidence of diminished contractile function in HCM despite
the finding that most affected patients have normal or enhanced ventricular
emptying.25,26 Why impaired systolic myocardial function should result in compensa-
tory hypertrophy has not yet been determined. Activation of signaling pathways asso-
ciated with trophic factors, such as angiotensin II, aldosterone, and insulin-like growth
factor, may ultimately be responsible for the development of hypertrophy.27,28
In human beings with HCM, the phenotypic expression of causative mutations is
highly diverse. The pathogenic potential of the various mutations is variable, but other
factors also determine the consequences of abnormal genotype. Indeed, family
members that share a causative mutation may differ markedly in clinical outcome
and severity of myocardial hypertrophy.20 It is likely that variable genetic expressivity
observed in human HCM is related to factors that include the pathogenic heteroge-
neity of causative mutations; the presence of genetic co-modifiers; and epigenetic
influences, possibly including the environment.20 It is possible that feline HCM shares
these features and, despite considerable progress, more complete characterization of
this disease will therefore present challenges.

EPIDEMIOLOGY

Population characteristics of feline HCM have been retrospectively evaluated.29,30 A


sex predisposition for males is consistent and the mean age at diagnosis is close to
6 years.29–31 Despite the fact that these data were obtained from referral populations,
a substantive proportion, between 33% and 55%, were subclinical (asymptomatic)
when the disease was identified.29–31 One of these investigations identified the admin-
istration of corticosteroids as a historical antecedent to the development of heart
failure.30 The association between administration of glucocorticoids and development
of heart failure in cats was also addressed in a separate retrospective investigation.32
The design of the latter study does not allow conclusions regarding causality, but
evidence was provided demonstrating that the development of heart failure
Feline Hypertrophic Cardiomyopathy 687

associated with glucocorticoid administrations is a distinct clinical entity; specifically,


patients that survive acute decompensation may have improved survival relative to
cats that have not received glucocorticoids.32
Disease prevalence and identification of physical findings that represent markers of
disease have been the focus of recent investigations.33–36 Most studies have used
a cross-sectional or retrospective study design, and therefore inferences regarding
the causes of HCM are limited. However, prevalence (the instantaneous disease
burden of a population) is potentially useful because it provides an a priori or pretest
probability of disease in specific populations. This information has clinical relevance
because it has a bearing on potential value of diagnostic screening and the interpre-
tation of diagnostic tests.
The prevalence of cardiac murmurs in a sample of 103 cats recruited for participa-
tion in a blood donor program in New England was reported to be 21%.33 Cats
included in this investigation were between 1 and 9 years of age and, in the opinion
of the pet owner, healthy. Murmurs were generally of low intensity and, in some
cats, the intensity of murmurs varied in association with changes in heart rate. Quan-
titative echocardiographic variables were not reported but left ventricular hypertrophy
or equivocal septal hypertrophy was identified in six of the seven cats that were echo-
cardiographically examined. Systemic arterial blood pressure was not reported so it is
possible that hypertrophy identified during this study was associated with systemic
disease and did not reflect HCM.
Of 42 healthy purebred Maine coon cats subject to screening examinations in
Scandinavia, only one had a cardiac murmur.34 And indeed, this murmur was
thought to be associated with pregnancy because it was not identified during
reexamination performed after queening. Echocardiographic evidence of LVH
was detected in 9.5% of these 42 cats. Reported follow-up data for some of these
cats provide indirect evidence that noncardiac disorders were not responsible for
the finding of LVH but blood pressure was not determined. Two cats that did not
have LVH had echocardiographic evidence of systolic anterior motion of the mitral
valve (SAM) suggesting an incipient or variant form of HCM. When these cats
were included in the affected group, the prevalence of echocardiographic findings
compatible with HCM was 14.3%.
Echocardiographic data obtained during pre-breeding evaluation of purebred cats
thought to be at risk for heritable heart disease have also been retrospectively evalu-
ated.35 Of 144 cats, the majority were Maine coon cats but sphinx, British shorthair,
Bengal, and Norwegian forest cats were also represented. Physical examination find-
ings were not reported but echocardiographic evidence of HCM was detected in 8.3%
of the cohort. In a recent investigation, the results of which have been presented in
abstract form but not yet published, 34% of 199 apparently healthy cats had murmurs
during at least one examination. Of cats with murmurs that were subject to echocar-
diographic examination, 50% had left ventricular hypertrophy.37
The author and colleagues recently reported the results of a community-based
echocardiographic survey of apparently healthy cats.36 One hundred three healthy
cats were recruited from the pet-owning population of a veterinary college in the
Southeastern United States. The echocardiographer was unaware of the physical find-
ings and subjects with noncardiac disorders, including systemic hypertension and
hyperthyroidism, were excluded. Of 103 cats, 16% had cardiac murmurs while at
rest, during routine auscultatory examination. Dynamic auscultation was also per-
formed during this study; the prevalence of murmurs in cats subject to a provocative
maneuver that consisted of lifting the cat quickly in the air, was 27%. Of cats that had
a murmur during dynamic auscultation, 46% did not have a murmur during routine
688 Abbott

auscultation. HCM was echocardiographically identified in 15% of the study popula-


tion, but of cats with HCM, only 33% had heart murmurs.
The echocardiographic criteria used for diagnosis of HCM in this study are relevant to
interpretation of the results. Two-dimensional echocardiography, not M-mode, was
exclusively used for evaluation of ventricular wall thickness. Systematic quantitative
assessment of wall thickness was made in short- and long-axis images. HCM was iden-
tified when any region of the left ventricular wall was equal to or exceeded 6 mm at end
diastole. This method is apt to be more sensitive than the use of M-mode echocardiog-
raphy for identification of hypertrophy. The majority of affected cats had mild and
segmental hypertrophy and none had atrial enlargement. The diagnostic criteria used
in this study were based on those that have been used for identification of HCM in
humans and similar to those used in a published veterinary investigation.31,38 The prev-
alence was seemingly high, but it is consistent with current understanding, as it is now
accepted that HCM in humans is a disease that has a broad spectrum of phenotypic
expression, occurs in a subclinical form, and is not inevitably associated with progres-
sion and poor outcome. To place the findings in perspective, the prevalence of HCM
characterized by diffuse hypertrophy or marked SAM was 4%.
The various reported estimates of murmur and disease prevalence likely differ
because of geographic variability and differences in methodology. However, it is clear
that cardiac murmurs are often detected in apparently healthy cats, that murmurs in
cats vary in intensity in association with environmental stimuli, and that the finding
of a cardiac murmur is not consistently associated with echocardiographic abnormal-
ities. The prevalence of mild, subclinical HCM in cats is probably close to 15%. HCM is
the most common genetic heart disease in humans and has a reported prevalence of
0.2%.38 Based on available data, the prevalence of HCM in cats is considerably
higher, but this is credible if it is accepted that clinical signs are not the inevitable
consequence of this disease. In humans, clinically evident HCM is rare.8,39,40 In
contrast, feline HCM is the disease most commonly responsible for heart failure in
this species. In clinical studies that have evaluated biomarkers in feline subjects
with respiratory distress, more than 50% of subjects with heart failure had
HCM.41,42 When echocardiographic case records are considered independent of clin-
ical signs, HCM is identified in approximately 30% of patients.43

PATHOPHYSIOLOGY OF HYPERTROPHIC CARDIOMYOPATHY


Diastolic Dysfunction
It has generally been accepted that diastolic dysfunction is the pathophysiologic
mechanism that is primarily responsible for the clinical manifestations of HCM. That
systolic function contributes prominently to cardiac performance is readily evident
but the importance of diastolic function is less obvious. Diastolic function (the ability
of the ventricle to fill at low pressure) is complex but depends on the energy-depen-
dent process of myocardial relaxation and mechanical properties of the ventricle
that determine chamber stiffness. In most patients with HCM, global systolic perfor-
mance is normal or hyperdynamic but delayed myocardial relaxation and diminished
ventricular compliance potentially result in elevated filling pressures when ventricular
volumes are normal or small.43 Rises in ventricular filling pressures can result in pulmo-
nary venous congestion and edema. Chronic elevation of ventricular filling pressures
contributes atrial enlargement.
Dynamic Left Ventricular Outflow Tract Obstruction
The phenomenon of dynamic left ventricular outflow tract (LVOT) obstruction (LVOTO)
has generated considerable interest and has been a subject of debate. Usually
Feline Hypertrophic Cardiomyopathy 689

dynamic, as opposed to fixed or anatomic, obstruction of left ventricular outflow results


from systolic motion of the mitral valve leaflets toward the interventricular septum
(IVS).17,31 Because the IVS represents the anterior boundary of the subvalvular LVOT
and because of the parallel anatomic arrangement of left ventricular inflow and outflow,
the displaced leaflets cause a mechanical impediment to ventricular ejection. As
a consequence, a systolic pressure gradient develops across the LVOT. Mitral valve
regurgitation usually accompanies SAM because the abnormal orientation of the valve
apparatus results in incomplete leaflet apposition during systole (Fig. 1). The cause of
SAM has been the subject of considerable speculation. The notion that SAM was a result
of the Venturi effect was initially favored.44 Venturi forces develop when narrowing of
a conduit results in the acceleration of flow and the development of a pressure gradient.
In the context of HCM, the development of lower systolic pressures distal to the site of
leaflet-septal apposition results in lift, or Venturi, forces that act perpendicular to flow,
pulling the mitral leaflets toward the septum. More recently it has been recognized that
SAM may begin in early systole, even before ejection, at a time when Venturi forces are
apt to be negligible.45 Current evidence suggests that the hydrodynamic pushing force,
or drag, is primarily responsible for anterior movement of the leaflets.44 Abnormal
geometry of the mitral valve apparatus, with or without structural abnormalities, likely
plays a predisposing role. In fact, in a canine model, experimental displacement of
the left ventricular papillary muscles toward the geometric center of the ventricle results

Fig. 1. Echocardiographic images obtained from a cat with hypertrophic cardiomyopathy.


Left ventricular outflow tract obstruction and mitral valve regurgitation caused by systolic
anterior motion of the mitral valve are evident. (A) Systolic right parasternal long-axis image
that includes the left ventricular outflow. Arrow indicates point of mitral leaflet-septal
contact. (B) M-mode image of the mitral valve. Arrow indicates point of mitral leaflet-septal
contact. (C) Systolic right parasternal long-axis image that includes the left ventricular
outflow with superimposed color Doppler map; there is caudally detected jet of mitral valve
regurgitation. Disturbed flow is evident within the subvalvular left ventricular outflow tract.
(D) Continuous-wave Doppler spectrogram of the left ventricular outflow tract. The peak
velocity exceeds 3 ms/s. There is late-systolic acceleration, which provides evidence of
dynamic obstruction.
690 Abbott

in SAM.46 It is probable that the cause of SAM is multifactorial. Abnormalities of the


mitral apparatus that result in chordal laxity together with hyperdynamic systolic perfor-
mance result in a substrate in which drag forces cause anterior displacement of the
mitral valve leaflets. SAM is not an intrinsic feature of HCM and has been observed in
other clinical and experimental scenarios in which there is absolute or relative redun-
dancy of the mitral leaflets or chordae in the setting of hyperdynamic systolic perfor-
mance.47 Therefore, echocardiographic identification of SAM is not necessarily
a specific echocardiographic marker of feline HCM but in most cases, it is finding
that is highly suggestive of the diagnosis. It is clinically relevant that the tendency to
develop SAM is load dependent and highly labile. Decreases in preload and afterload,
and increases in contractile state can all induce or augment SAM in susceptible individ-
uals. As a result, the pressure gradient and resulting heart murmur associated with SAM
can vary markedly during brief time intervals.
The clinical importance of SAM has been debated, and indeed whether or not SAM
results in actual obstruction was once questioned.48 It is now accepted that SAM not
only results in a systolic pressure gradient across the LVOT but also causes an imped-
iment to ventricular ejection.8 The pathophysiologic consequences of this obstruction
are reported to include increased wall stress.8,49 Wall stress, or the tension borne by
the ventricle, is determined by intracavitary pressure, chamber volume, and wall thick-
ness; it is directly proportional to the first two factors and inversely related to the last.
The prevalence of asymmetrical ventricular geometry in patients with HCM makes it
difficult to accurately define global wall stress and unsurprisingly, there are few
reported, relevant data. However, in one study of human patients with HCM, global
wall stress was not different when patients with obstructive and nonobstructive
HCM were compared.50 It is relevant that the supraphysiologic intraventricular pres-
sures in HCM develop during late systole. During this phase of the cardiac cycle,
ventricular wall thickness and radius are high and low, respectively, which are factors
that limit the development of high wall stress.
As increase in wall thickness can serve to normalize wall stress, and therefore, even
if wall stress is not increased in patients with HCM, the pressure gradient resulting
from SAM might be an additional stimulus for hypertrophy. Indeed there are observa-
tional data obtained from cohorts of human subjects with obstructive HCM who have
been subject to surgical treatment that decreases systolic pressure gradient that
suggest regression of hypertrophy.51 Still, it is difficult to reconcile the notion of
SAM as a cause of hypertrophy with the prevalence of asymmetric septal hypertrophy
in people with HCM. Presumably, if SAM were the cause of hypertrophy it would affect
the free wall and septum equally.50
Structural and functional coronary artery abnormalities are associated with HCM.
Intramural coronary arteries are narrowed because of medial hypertrophy and,
although there are inconsistencies in the published literature, perfusion abnormalities
have been associated with pressure gradients across the LVOT.52–55
The presence of dynamic LVOTO in human patients with HCM has been associated
with poor outcome and particularly with sudden unexpected death.49 This association,
however, has been questioned.56 The risk for poor outcome reported in one influential
publication was not statistically related to magnitude of pressure gradient. Instead, it
was simply the presence of obstruction at rest (treated as a yes/no binary variable) that
was associated with poor outcome.49 When this is considered in light of the marked
lability of pressure gradient in human HCM (a day-to-day change of as much as 32
mmHg can apparently reflect random variation) and the prevalence of LVOTO in
human beings that are subject to provocations, including exercise, it raises questions
regarding the association between LVOTO and poor prognosis.56–59
Feline Hypertrophic Cardiomyopathy 691

Ultimately, uncertainty persists. SAM is undoubtedly the cause of LVOTO obstruction


and mitral valve regurgitation, abnormalities that may be responsible for rises in filling
pressures, altered coronary perfusion, and therefore perhaps the development of
myocardial fibrosis. Furthermore, in human beings, clinical signs that are not responsive
to medical therapy and are associated with LVOTO are successfully treated by surgery.8
Still, it is possible that resting obstruction is a confounding variable that is associated with
malignant phenotype but is not the proximate cause of mortality. Although inherently
limited by the retrospective nature of the observations, it is interesting that SAM in feline
patients has been associated with better rather than worse survival.30,31 In the cat, the
effect of obstruction on clinically relevant end points, including morbidity and mortality,
is unclear and the suitability of SAM as therapeutic target can therefore be debated.

CLINICAL PRESENTATION

Feline HCM is usually identified when auscultatory findings, such as arrhythmias,


gallop sounds, or murmurs, are incidentally detected during routine veterinary exam-
inations or when clinical signs result from heart failure or embolism.29,30 In a few
affected cats, sudden unexpected death is the first clinical manifestation of the
disease. Respiratory distress related to pulmonary edema or sometimes, pleural effu-
sion, is the most common clinical manifestation of heart failure in feline HCM. Clinical
signs of feline heart failure typically have a sudden onset and, in contrast to canine
patients with heart failure, cough is rarely observed. In some cats with heart failure,
clinical signs of low cardiac output, including hypothermia and pre-renal azotemia
are observed. In cats, tachycardia is not consistently associated with heart failure
and in some cases, bradycardia is evident.
Murmurs in patients with HCM have been associated with SAM, which results in
LVOTO and mitral regurgitation (MR), as well as with MR caused by hypertrophic
remodeling and distortion of the mitral apparatus.43 It appears that murmurs in cats
with or without cardiomyopathy are commonly associated with dynamic and labile
phenomena. Fairly often, the intensities of murmurs heard in cats vary from moment
to moment. The lability of SAM no doubt accounts for this observation in some
cats. Additionally, dynamic right ventricular outflow tract obstruction has been identi-
fied as a cause of murmurs in healthy cats and cats with noncardiac disease.60 In an
echocardiographic survey of apparently healthy cats, the prevalence of cardiac
murmurs was 16%, of which only 31% had echocardiographically identified structural
heart disease.36 However, the Doppler finding of late-systolic acceleration of either
right or left ventricular outflow in apparently healthy cats was statistically associated
with the finding of a murmur independent of the presence of structural heart disease.
Some cats had late-systolic acceleration that was anatomically localized to the prox-
imal LVOT. Dynamic mid-LVOT obstruction perhaps related to sympathetic activation,
but not obviously associated with HCM, may therefore cause murmurs in some cats
that do not have structural cardiac disease. The statistical association between
murmurs and late-systolic acceleration of ventricular ejection was stronger when
provoked murmurs were included in the analysis.36 Auscultation and echocardiog-
raphy were performed by different examiners at different times so the association is
not necessarily causal, but it is plausible that sympathetic activation causes dynamic
outflow tract obstruction that explains some apparently physiologic feline murmurs.
Echocardiography
Feline HCM has been echocardiographically defined by end-diastolic measurements
of ventricular wall thickness that equal or exceed 6 mm.31 Hypertrophy is commonly
692 Abbott

asymmetric and in Maine coon cats with HCM, it is often the left ventricular posterior
wall and papillary muscles that are most affected.61 Ejection phase indices of left
ventricular systolic performance such as %fractional shortening are usually normal
or reflect hyperdynamic ventricular emptying. Left atrial size in cats with HCM is gener-
ally greater than in healthy cats, but left atrial enlargement is not an intrinsic feature of
the disease nor required for its diagnosis.62 However, left atrial size is a surrogate
measure of hemodynamic burden and left atrial enlargement has been associated
with poor outcome in people and cats with HCM.30,63 Furthermore, left atrial enlarge-
ment is a clinically important finding and is almost always present when clinical signs
of respiratory distress result from feline myocardial disease. As previously described,
SAM is commonly identified in cats with HCM and associated with SAM are Doppler
findings of a labile, late-systolic pressure gradient across the LVOT and usually
concurrent MR.
Progressive decline in systolic myocardial function is observed in some affected
cats and presumably this is caused by ischemia related to small vessel disease or
LVOTO.64 Feline myocardial disease sometimes defies simple classification even after
echocardiographic examination. Indeed, some examples of unclassified cardiomyop-
athy may represent progression of long-standing HCM. Restrictive cardiomyopathy
(RCM) is generally considered to be a distinct disorder, which is characterized by atrial
enlargement in association with normal, or nearly normal, ventricular wall thickness.
Although some forms of RCM may represent the sequela of endomyocardial fibrosis,
it is interesting that a restrictive phenotype has been documented in people who have
sarcomeric mutations that are known to result in HCM.65
Early echocardiographic descriptions suggested that outflow tract obstruction was
infrequently observed in feline HCM.16 However, more recent data suggest that the
prevalence is as high as 67%.31 This figure is considerably higher than that reported
from humans in which approximately 30% of the those affected manifested LVOT
obstruction at rest.59 However, current data suggest that the classification of obstruc-
tive and non-obstructive HCM may represent a false dichotomy. When human
subjects with HCM are echocardiographically evaluated immediately after exercise
or after provocations known to induce LVOTO, the proportion of those subjects that
have obstruction exceeds 60%.59,66,67 It is clear that the phenomenon of SAM is labile
and highly dependent on functional state. The high prevalence of SAM in cats might
reflect sympathetic activation associated with a ‘‘white-coat effect’’ in hospitalized
cats; in a sense all echocardiographic examinations of non-sedated cats are per-
formed in a state that is analogous to that immediately after exercise.

SCREENING FOR HCM

Recent interest in the epidemiology of feline heart disease raises questions regarding
screening for this disease. The cost-benefit ratio of screening for clinically occult
disease is favorable if an affordable test can identify a disease that is serious and treat-
able. Feline HCM, in its severe form, is undoubtedly serious and is clearly an important
cause of morbidity and mortality in cats. Unfortunately, there is little known of the
natural history of feline HCM; the rate at which subclinical HCM progresses to a clinical
stage and indeed, the proportion of subclinically affected patients that ultimately
develop clinical signs is not known. There is also little known regarding the efficacy
of treatment for HCM. Several therapeutic strategies intended to prevent the develop-
ment of congestion and the occurrence of embolism have been employed but none
systematically evaluated. For purebred cats with a known or presumed genetic basis
for HCM, screening can be justified because genetic counseling might reduce the
Feline Hypertrophic Cardiomyopathy 693

prevalence of disease in specific populations. The question of screening for HCM


might also be relevant for populations subject to elective procedures, such as dental
cleaning, that require anesthesia.
In apparently healthy cats, auscultation is an insensitive diagnostic marker of HCM,
meaning that few cats with subclinical HCM have murmurs. The positive predictive
value of a test (the proportion of individuals that have the disease among those that
have a positive test) is dependent on the prevalence of the disease. If the prevalence
of subclinical HCM is close to 15%, the positive predictive value of a murmur in appar-
ently healthy cats is only 31%. The negative predictive value of a cardiac murmur
might be more diagnostically useful; it can be anticipated that 87% of cats that do
not have murmurs do not have cardiomyopathy. In practical terms, echocardiographic
examination of outwardly healthy cats with heart murmurs is advisable, but it should
be recognized that many murmurs are apt to represent false positives; that is, echo-
cardiographic examination prompted by identification of a cardiac murmur will
disclose a sizable proportion of cats that are free of structural cardiac disease.
Echocardiographic screening, without regard to physical findings, for HCM can be
justified in populations subject to the development of familial HCM. Otherwise, the
cost of the examination might be excessive given the prevalence of the disease and
the lack of proven therapies. In the absence of a hypothetical and flawless molecular
or genetic test, there is no definitive, gold-standard test for HCM. Even postmortem
examination is likely to have diagnostic limitations given the interindividual variability
in cardiac mass among normal cats; the potential subjectivity of the examination; and
the fact that histologic abnormalities, such as myofiber disarray, are not necessarily
diffuse.68 Although the sensitivity and specificity of echocardiography for diagnosis
of HCM has not been evaluated, echocardiographic examination is, for all intents and
purposes, the gold standard. Even then, the accuracy of echocardiographic identifica-
tion of HCM depends on not only technical factors, including the experience of the
examiner, but also on the cut point of wall thickness that is used as the diagnostic crite-
rion. Many, but not all, clinical investigations of feline HCM have used an end-diastolic
wall thickness equal to or exceeding 6 mm as the primary diagnostic criterion.30,31,61
Provided metabolic and hemodynamic causes of hypertrophy are excluded, this
dimension (6 mm) likely represents a specific, but not necessarily sensitive, marker of
HCM. In fact, reference intervals defined by published normative echocardiographic
data have upper limits that are generally less than 5.5 mm and less than 5 mm for
two.43 The feline study that included the largest number of subjects suggests that
95% of healthy cats have septal and free wall dimensions that are less than 5.6
mm.69 Although it is not generally taken into account, end-diastolic ventricular wall
thickness is weakly related to body weight, which might be relevant to the evaluation
of exceptionally heavy cats. The results of studies of healthy Maine coon cats, a breed
which tends to have a large body size, refute this because unaffected individuals of this
breed have end-diastolic measurements of wall thickness that are similar to mixed-
breed cats.70 Indeed, statistical analysis of echocardiographic data obtained during
screening examinations of Maine coon cats suggests that 6 mm might be overly conser-
vative as a marker of ventricular hypertrophy. Evaluation of jackknife distances, which
statistically identify extreme observations or outliers, suggested the possibility that
a measurement of wall thickness that exceeds 5 mm is outside the normal range.34
Biomarkers, specifically B-type natriuretic peptide (BNP), have been evaluated as
screening strategies and this subject is more completely addressed in another article
by David J. Connolly elsewhere in this issue. Although differences in criteria used to
define the severity of HCM make the data difficult to interpret, the sensitivity of raised
BNP for the identification of subclinical HCM may be as high as 94% or even
694 Abbott

100%.71–73 However, sensitivity (the proportion of patients with the disease that have
a positive test) is an intrinsic feature of the test. In contrast, positive predictive value
is highly dependent on disease prevalence. Because of the dependence on preva-
lence, even a test with 95% sensitivity and 95% specificity has only a 77% positive
predictive value when prevalence is 15%. Because of this and other factors, the suit-
ability of BNP measurement as a screening test is uncertain at this time.74

THERAPY
Subclinical HCM
Optimally, it would be possible to identify patients that have a subclinical form of HCM
that is destined to worsen and to intervene in a way that would slow or prevent
progression of disease. Unfortunately, there is little known of the natural history of
feline HCM and as yet no published evidence that medical therapy can alter the course
of subclinical disease. The use of beta-blockers, such as atenolol, is often advocated
particularly in patients that have resting LVOTO, but the efficacy of this intervention
has not been determined. In cats, a causal relationship between LVOTO and poor
outcome has not been established, and as noted, retrospectively evaluated case
series have associated LVOTO with improved outcome in cats.30,31 However, the
latter argument must be viewed with circumspection. Cases of HCM associated
with LVOTO generally have murmurs and therefore are apt to be identified when
patients are subclinical. Furthermore, if progression to clinical disease is associated
with a decrease in systolic myocardial function, a notion for which there is some
evidence, cross-sectional or retrospective studies might associate poor outcome
with lack of LVOTO.75 The role of LVOTO is presently inconclusive. However, there
is evidence that beta-blockade may hasten the recurrence of pulmonary edema in
cats that have developed heart failure caused by HCM or RCM and, in the absence
of evidence to the contrary, this raises the possibility that beta-blockade might
harm cats with subclinical disease.76 The occurrence of pulmonary edema caused
by HCM is an objective marker that is a suitable inclusion criterion for clinical trials
but it is a factor without an established relationship to characteristics that might
predispose patients with HCM to adverse outcome in response to beta-blockade. If
beta-blockade does indeed harm cats that have developed edema, the absence of
data makes it impossible to determine precisely when, during the natural history of
HCM, patients are at risk for these adverse effects.
Because there are data that suggest a role for abnormal response to hormones in
the pathogenesis of HCM, the possibility that neuroendocrine modulating drugs might
favorably affect the natural history of the disease has been investigated.77,78 Evidence
obtained from studies of transgenic mice suggests that aldosterone may be relevant
to the pathogenesis of HCM insofar as spironolactone attenuates the development of
myocardial fibrosis and myofiber disarray.28 Based on these experimental findings,
there may be a role for the use of spironolactone in cats with cardiac disease.
However, relative to placebo, 4-months therapy with oral spironolactone did not alter
echocardiographic indices of diastolic function in a colony of Maine coon cats with
HCM.79 The same group also evaluated the effect of angiotensin-converting enzyme
inhibition.77 Maine coon cats with HCM but without heart failure were randomly
assigned to receive placebo or ramipril. Evidence that the circulating renin angiotensin
system was suppressed was presented, but despite this, echocardiographic and
magnetic resonance indices of myocardial mass and diastolic function were unaf-
fected. Given the genetic heterogeneity that probably exists in feline HCM, it is
possible that these agents or others might slow progression of HCM in other breeds
Feline Hypertrophic Cardiomyopathy 695

of cats. And of course, it is possible that longer duration of therapy and the evaluation
of clinically relevant outcome measures, such as time to onset of heart failure or
mortality, might have disclosed benefit. At this time, however, evidence that medical
therapy favorably alters the course of subclinical feline HCM is lacking.
Heart Failure
Other than furosemide, for which efficacy is assumed, there are no medical interven-
tions that have demonstrated efficacy in the management of feline heart failure.
Attempts to improve diastolic function have been made through interventions that
are thought to speed myocardial relaxation or slow heart rate. Diltiazem is a calcium
channel blocker that has been widely used in the therapy of feline HCM. The effect
of diltiazem on heart rate is modest.80 However, there is evidence to suggest that
this drug has a positive lusitropic effect; that is, it improves ventricular filling through
a salutary effect on myocardial relaxation.81 The presumed favorable effects of
beta-blockers on diastolic function are primarily indirect and result from decreases
in heart rate. In an open-label clinical trial, the effects of diltiazem, propranolol, and
verapamil on cats with pulmonary edema caused by HCM were compared. Of the
three, diltiazem was the most efficacious.81 However, this trial did not include a nega-
tive control in the form of a placebo group. Ace inhibition has also been used in the
management of heart failure due to feline HCM.82 These drugs are apparently safe
and the concern that vasodilation due to ACE inhibition might result in adverse effects
related to worsening LVOTO may not be valid.82 However, conclusive evidence of effi-
cacy is lacking.
The results of a multicenter, randomized, placebo-controlled trial that had been
designed to evaluate the relative efficacy of atenolol, diltiazem, and enalapril in feline
patients with congestive heart failure caused by HCM or RCM have been presented at
a national meeting, but not yet published.76 The primary outcome variable was time
until recurrence of congestive signs and none of the agents was superior to placebo
in this regard. Patients that received enalapril remained in the trial longer than those
receiving the alternatives, although this result was not statistically significant. Patients
receiving atenolol fared less well than did those in the placebo group.83 The finding
that atenolol may harm cats with pulmonary edema was possibly unexpected but is
consistent with the result of the only comparable study in which administration of
propranolol was associated with decreased survival.81 Based on the results of the
aforementioned randomized clinical trial,76 the use of enalapril together with furose-
mide seems a reasonable approach to the management of feline patients with conges-
tive heart failure caused by diastolic dysfunction.

PROGNOSIS/NATURAL HISTORY

Survival data obtained from retrospective evaluation of teaching hospital records have
been reported by two groups of investigators.29,30 Survival times for the entire study
samples were similar for both studies and were close to 700 days. Median survival
times of 92 days and 563 days were reported for patients with heart failure. The retro-
spective nature of the studies makes it difficult to interpret these differences but it
seems that patients with heart failure in general, fare poorly. However, both groups
of investigators reported median survival for subclinical HCM that was in excess of
3 years.29,30
Much of the early clinical literature that relates to HCM in human beings originated
from a small number of tertiary, HCM centers and was therefore subject to referral
bias. This bias contributed to the notion that HCM was generally associated with an
696 Abbott

ominous prognosis.8 It is now recognized that human HCM is a disorder that exhibits
a broad spectrum of severity. In fact, in a recent review, human HCM was described as
a ‘‘relatively benign disease’’; the finding that survival times of non-selected cohorts
are similar to those of the general population supports this view.20 Little is known of
the natural history of feline HCM. However, it is possible that referral bias has similarly
shaped perception of this disease and it may be that the feline disorder is also char-
acterized by genetic heterogeneity and a broad spectrum of phenotypic expression
that includes mild, non-progressive disease and lethal variants that cause congestive
failure, embolism, and death.

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700 Abbott

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ANESTHETIC MANAGEMENT OF SPECIFIC CARDIOVASCULAR DISEASES
Luisito S. Pablo, DVM, MS, DACVA
University of Florida, Gainesville, Florida

Small animal patients that need general anesthesia may have preexisting cardiovascular
diseases. To ensure oxygen delivery to the tissue, the cardiac output and oxygen content of the
blood should be optimized. Cardiac output is the product of stroke volume and heart rate.
Patients with cardiovascular diseases may have reduced cardiac output due to decreased stroke
volume. The determinants of stroke volume are preload, afterload, and myocardial contractility.
The hemodynamic goals for patients with cardiovascular diseases involve targeting these factors
with the ultimate objective of providing adequate cardiac output to the anesthetized patients.
The main objective of this presentation is to present the anesthetic management of
specific cardiovascular diseases. The cardiovascular conditions that will be discussed in this
presentation are the more commonly encountered problems in practice.

Dogs with Mitral Regurgitation (MR)


MR in dogs is due mainly to endocardiosis. The clinical consequences of mitral valve
endocardiosis are seen in elderly small-breed dogs. The anesthetic risk associated with MR
depends on its severity. Mild MR does not have hemodynamic consequence. Dogs with
untreated congestive heart failure will have the highest risk. Dogs being treated with an ACE
inhibitor and diuretics for congestive heart failure can be anesthetized but extreme care should be
taken. Anesthesia should not be performed in dogs with untreated congestive heart failure.
With MR, part of the left ventricular stroke volume is ejected through the incompetent
mitral valve into the left atrium. It creates a volume load on the left atrium and left ventricle
resulting in increased pressure in those chambers. With these increased pressures, the LA and LV
dilate and develop hypertrophy. Later in the disease process, the increased pressures will be
reflected back upon the pulmonary venous circulation and ultimately results in pulmonary
edema.
The hemodynamic goals for MR include: (1) reduce preload slightly to reduce regurgitant
flow (preload); (2) avoid acute increases in afterload; (3) maintain contractility; (4) avoid
bradycardia; (5) maintain sinus rhythm; and (6) do not increase myocardial oxygen requirement
by avoiding severe tachycardia and hypotension.
To accomplish the above mentioned goals, there are specific steps that can be done. Do
not overload the patient with fluids. Do not use fluid boluses to treat hypotension during
anesthesia. Fluid should be given at a lower rate of 3.0-5.0 ml/kg/hour. Those patients with
compensated CHF should receive fluid with lower sodium load like 2.5% dextrose and half-
strength LRS. Avoid sinus bradycardia. Maintain normal heart rate. Slight tachycardia is
acceptable. Atropine (0.02 mg/kg IV) or glycopyrrolate (0.01 mg/kg IV) should be given to
correct sinus bradycardia. Maintain myocardial contractility. Treat hypotension using beta-1
agonist like dobutamine or dopamine. Dobutamine and dopamine can be given at 5.0-10.0
μg/kg/min. Slight vasodilation is acceptable. Avoid peripheral vasoconstriction. Alpha2-agonists
should not be used in dogs with MR. Minimize excitement. Increased catecholamine release may
cause vasoconstriction.

452
Anesthetic Considerations
Premedication: Low dose of acepromazine is acceptable. This will reduce the afterload. It
will provide sedation and minimize catecholamine-induced dysrhythmias. It can be administered
at 0.01-0.02 mg/kg IM, SC. Opioids are indicated if there will be pain involved. Most opioids
maintain cardiac contractility. However, they may cause sinus bradycardia. An anticholinergic
(atropine or glycopyrrolate) can be added to the preanesthetic protocol if the patient has
preexisting bradycardia or if a relatively high dose of an opioid is used. The opioids that are
commonly used for premedication are morphine, hydromorphone, butorphanol, and
buprenorphine. These are the recommended dosages for the different opioids: (1) morphine: 0.2-
0.5 mg/kg IM, SC, (2) hydromorphone: 0.05-0.1 mg/kg IM, SC, (3) butorphanol: 0.2-0.4 mg/kg
IM, SC, and (4) buprenorphine: 0.01-0.02 mg/kg IM, SC. Benzodiazepines are acceptable
premedicants for MR. They produce minimal cardiopulmonary depression. They can produce
paradoxical agitation in dogs if given alone or with an opioid. Instead of sedation, the dog may
show restlessness and dysphoria. It is best to avoid the use of benzodiazepines in dogs that are
not depressed. Diazepam and midazolam are the two most commonly used benzodiazepines in
dogs. Midazolam is water soluble and can be administered IM, SC or IV. Diazepam is not water
soluble and when given IM will result in unpredictable absorption. These are the dosages for the
benzodiazepines: (1) diazepam: 0.2-0.4 mg/kg IV and (2) midazolam: 0.2-0.4 mg/kg IM, SC, IV.
Induction: Propofol is an acceptable choice for dogs with mitral regurgitation. It causes some
degree of vasodilation, which will be beneficial for this heart condition. When used in these
cases, it should be given slowly following premedication. The dose of propofol is 4.0 mg/kg IV;
half of the dose should be given over 40-60 seconds and the remaining dose is given to effect.
A combination of diazepam-ketamine or midazolam-ketamine can be used in MR. The
combination will result in transient sinus tachycardia. Ketamine, by itself, does not result in
significant increase in peripheral vascular resistance. Diazepam is given at 0.25 mg/kg IV and
ketamine at 5.0 mg/kg IV. Lower doses should be used in dogs that have profound sedation from
the premedicants and are depressed. Etomidate is the most heart-friendly induction agent.
However, it is still expensive. It is the drug of choice in patients with enlarged heart and showing
signs of congestive heart failure before presentation. The dose of etomidate is 0.5-1.0 mg/kg IV.
If etomidate is not available, a neuroleptanalgesic combination can be used. This combination
maintains myocardial function. Bradycardia may occur due to the opioid’s effect on the vagal
tone. Anticholinergic can be added to the protocol to prevent sinus bradycardia. The two most
common combinations used in practice are diazepam-hydromorphone and diazepam-fentanyl.
The doses for diazepam and hydromorphone are 0.25 mg/kg IV and 0.2 mg/kg IV, respectively.
When fentanyl is chosen, instead of hydromorphone, the dose is 10 ug/kg IV.
Maintenance: Anesthesia should be maintained with either isoflurane or sevoflurane.
Dogs that develop hypotension and tend not to respond to the positive inotrope should be
managed by “balancing” the anesthetic technique. A fentanyl CRI at 0.2-2 ug/kg/min can be
added to the inhalant administration. This will allow the use of the lower concentration of the
inhalant.
The drugs that need to be avoided in dogs with MR are xylazine, medetomidine,
dexmedetomidine, and phenylephrine (vasoconstrictor).
Postoperative: Provide external heat support. Hypothermia can result in increased oxygen
demand. Provide oxygen until the patient is ventilating adequately. Hypoventilation will result in
hypoxemia when breathing room air. Provide optimal recovery conditions. Minimize stress,
which can increase catecholamine release. Provide pain control when painful procedure is

453
performed. It is not recommended to give NSAID in patients with compensated congestive heart
failure.

Cats with Hypertrophic Cardiomyopathy


Many cats with hypertrophic cardiomyopathy may be asymptomatic. These cats can have
mild to severe left ventricular thickening. Cats with hypertrophic cardiomyopathy can live longer
than two years after a bout of pulmonary edema. Anesthesia should not be performed in cats with
definite signs of congestive heart failure due to hypertrophic cardiomyopathy.
Left ventricular myocardium thickens (concentric hypertrophy). This results in stiff
chamber. The basic problem in hypertrophic cardiomyopathy is the diastolic dysfunction of the
left ventricle. It is characterized by delayed or incomplete myocardial relaxation and reduced
compliance of the left ventricle. The stiff chamber leads to increased diastolic intraventricular
pressure and then left atrial enlargement. The increased pressure in left atrium will be transmitted
to the pulmonary veins and pulmonary edema will follow. Mitral regurgitation will develop as a
result of the distortional change in the mitral valve apparatus caused by the hypertrophy of the
left ventricle. In those cats with asymmetric hypertrophic cardiomyopathy, left ventricular
outflow obstruction can develop when the anterior leaflet of the mitral valve moves to contact
the septum during systole.
Hemodynamic goals for hypertrophic cardiomyopathy include: (1) maintain preload in
cats without congestive heart failure; (2) increase afterload, if possible; (3) do not increase
myocardial contractility; (4) maintain normal heart rate and avoid sinus tachycardia; (5) maintain
sinus rhythm; and (6) avoid increase in myocardial oxygen consumption. To accomplish these
goals, there are specific steps that should be considered. Adequate diastolic filling can be
accomplished by large ventricular volume and sinus rhythm. Increased contractility, reduced
afterload and preload will decrease the ventricular volume. Ketamine should be avoided because
it increases contractility and heart rate. It also increases the myocardial oxygen demand.
Acepromazine at the higher dose will cause vasodilation resulting in augmentation of the outflow
obstruction. Dysrhythmias should be controlled before anesthesia. Minimize stress and
excitement because of the catecholamine release that will increase heart rate and contractility.
The drugs (beta blocker or calcium channel blocker) being taken by the patient for hypertrophic
cardiomyopathy should be administered up to and including the day of anesthesia.

Anesthetic considerations
Premedication: Opioids are considered good choices because they have minimal effects on
myocardial contractility, preload and afterload. The opioids that are commonly used for
premedication are hydromorphone, morphine, methadone, butorphanol, and buprenorphine. The
premedicant doses for the opioids are as follows: hydromorphone (0.03-0.05 mg/kg IM SC),
morphine (0.1 mg/kg IM SC), methadone (0.1 mg/kg IM SC), butorphanol (0.2 mg/kg IM SC),
and buprenorphine: (0.01-0.02 mg/kg IM SC).
Benzodiazepines are also suitable for these cases. They produce minimal cardiopulmonary
depression. However, they can produce paradoxical agitation and restlessness in cats. To
minimize these side effects, midazolam or diazepam can be given with the IV induction agent.
Small amount of the induction agent is given first. The dose of midazolam or diazepam is given
next. The induction is completed with the primary induction agent given to effect. The dose for
diazepam and midazolam is 0.2-0.4 mg/kg. Diazepam is preferably given IV while midazolam
can be given by IM, SC, or IV route.

454
Medetomidine has been shown to eliminate outflow tract obstruction in cats with dynamic
left ventricular outflow obstruction. The dose used in the study is 20 ug/kg IM. It appears that
medetomidine or now dexmedetomidine may be used in cats with HCM that are not amenable to
physical restraint during examination.
Induction: The use of propofol in cats with hypertrophic cardiomyopathy is debatable. There
is a study that showed that it impairs regional myocardial function in ischemic myocardium. It
also causes peripheral vasodilation. If used, it should be given very slowly and with a
benzodiazepine. The calculated dose is 4.0 mg/kg IV; half of the dose should be given over 40-
60 seconds and the remaining dose is given to effect.
Etomidate is the most heart-friendly induction agent. However, it is very expensive. It is the
author’s drug of choice in patients with enlarged heart and had shown signs of congestive heart
failure before presentation. The dose is 0.5-1.0 mg/kg IV. Half of the calculated dose is given as
a slow bolus and the rest of the dose given to effect.
Neuroleptanalgesic combination is another option in cats with HCM. The combination
maintains myocardial function. Diazepam and hydromorphone are given at 0.25 mg/kg IV and
0.2 mg/kg IV, respectively. The fentanyl can replace the hydromorphone and is given at 10 ug/kg
IV.
Mask induction using sevoflurane or isoflurane should be avoided because of the stress and
excitement associated with this induction method. The outflow obstruction will be worse because
of the increased heart rate and myocardial contractility due to the sympathetic stimulation.
The drugs that should be avoided are high to moderate dose of acepromazine, ketamine,
atropine, glycopyrrolate, and thiopental.
Maintenance: Anesthesia should be maintained with either isoflurane or sevoflurane. Cats
that develop hypotension should be managed by administering phenylephrine CRI at 1-5
μg/kg/min. It is advisable to avoid dobutamine and dopamine. A fentanyl CRI at 0.2-2
μg/kg/min can be added to the inhalant administration. This will allow the use of the lower
concentration of the inhalant.
The patient should be monitored closely during anesthesia. The monitoring tools should
include pulse oximetry, blood pressure measurement, capnography, ECG, and temperature
probe.
Postoperative: The measures taken postoperatively will minimize mortality and morbidity in
these cases. Provide external heat support. Hypothermia can result in increased oxygen demand.
Provide oxygen until the patient is ventilating adequately. Hypoventilation will result in
hypoxemia when breathing room air. Minimize stress, which can increase catecholamine release.
Provide pain control when painful procedure is performed. It is advisable not to give NSAID in
patients with compensated congestive heart failure.

Dilated cardiomyopathy (DCM)


DCM is common in large-breed dogs. The main concerns in this condition are the
reduction in myocardial contractility and dysrhythmias. The hemodynamic goals these patients
that need anesthesia include: (1) maintain preload, (2) avoid increases in afterload, (3) maintain
or increase contractility, (4) maintain normal heart rate, (5) control dysrhythmias, and (6) do not
increase myocardial oxygen requirement by avoiding severe tachycardia and hypotension. These
goals are almost similar to those set for mitral regurgitation. Therefore, a detailed discussion of
the management of DCM is not included in these notes.

455
References
Clutton RE: Cardiopulmonary disease, in Seymour C, Gleed R (eds): Manual of Small Animal
Anaesthesia and Analgesia. Kingsley House, UK, British Small Animal Veterinary Association,
1999, pp155-181
Skubas N, Lichtman AD, Sharma A, et al: Anesthesia for cardiac surgery, in Barash PG, Cullen
BF, Stoelting RK (eds): Clinical Anesthesia (ed 5). Philadelphia, PA, Lippincott Williams and
Wilkins, 2006, pp 886-973

456
ANESTESIA EN
CARDIOMIOPATIA
HIPERTROFICA FELINA

INTRODUCCION
• Engrosamiento CONCENTRICO del miocardio
• Relajación Alterada
• Disfunción DIASTOLICA
• IDIOPATICA o SECUNDARIA
• Consecuencias Hemodinámicas
• Aumento Presión Atrial
• Regurgitación
• Edema Pulmonar
• LVOT (Aumentos FC o Velocidad de Flujo)
• Trombos en atrio por estasis o TEP

GC = FC X VS
MANEJO ANESTÉSICO
• Evaluación de acuerdo a SEVERIDAD
• Casos Subclínicos – poca relevancia hemodinámica

• Enfermedad LEVE, soplos y cambios estructurales menores podrían ser anestesiados con
diversas combinaciones de fármacos.
CONSIDERACION  Disociativos en Contexto de HTA es controversial…
AUMENTO estimulación simpática, FC, Contractilidad, Presión Arterial y trabajo
Cardiovascular , Consumo de O2 y LVOTO.
MANEJO ANESTÉSICO

• OBJETIVO PRINCIPAL INDEPENDIENTE DE SEVERIDAD

OPTIMIZAR PERFUSION Y MINIMIZAR DEMANDA DE OXIGENO MIOCARDICO.

MANEJO ANESTÉSICO - PREMEDIACIÓN


• Opiodes
• Acepromacina Controversial – Efecto Dosis dependiente
• Agonistas Alfa2  Contraindicados?
• Benzodiazepinas
MANEJO ANESTÉSICO - INDUCCION
• PROPOFOL
• ETOMIDATO
• FENTANILO – BENZODIAZEPINA
• CAJA CON ANESTESICOS INHALADOS
• KETAMINA ??

MANEJO DE HIPOTENSIÓN

• OPTIMIZACION DE FC Y RITMO ( Enfermedad leve vs grave – engrosamiento,


consumo y perfusión)
• CORRECCION DE CAM ADMINISTRADA
• FLUIDO TERAPIA Y VOLUMEN ( COLOIDES ??)
• INOTROPOS POSITIVOS??(consumo O2 – trabajo cardiaco - arritmogenicos)
• VASOPRESORES - Fenilefrina CRI at 1-5 μg/kg/min
Anestesia en
Enfermedad
Valvular

Introducción
Enfermedad mas común en el perro

Mitral dentro del top 3 enfermedades en el gato

dMVD, la forma mas común en el perro, 30% de perros geriátricos

Endocardiosis, enfermedad degenerativa valvular, degeneración


mixomatosa

Incompetencia valvular e incluso prolapso hacia el atrio

REFLUJO
Introducción

GC = FC X VS
Evaluación Pre anestésica

Soplo?

No todos los pacientes con enfermedad cardiaca se tratan igual

Historia detallada (antigua y actual)

Exámenes de Sangre y Orina

Examen Físico

Radiografías de Tórax

ECG

Presión Arterial
Documentar enfermedad
Determinar el riesgo
MANTENER
HOMEOSTASIS Y
PERFUSION TISULAR,
DO2 Y CORONARIA

Manejo Anestésico – Consideraciones Generales


Regurgitación
Mantener FC alta ?

GC = ↑FC X ↓VS Anticolinergicos ?

Opiodes ¡?

Control Hipotermia

GC = ↓ FC X VS
Manejo Anestésico – Inducción
Pacientes Estables
Ketamina ??

Propofol ??

Gases ??

Agonistas alfa 2 ?? Regurgitación

Acepromacina??

Manejo Anestésico – Inducción


Pacientes Inestables
En riego Significativo de Insuficiencia Cardiaca
Congestiva o que hayan tenido eventos de Congestión
o Arritmias
• Requieren Estabilización Previa
Control de Hipotensión
Control de Arritmias
Control Edema Pulmonar

• Chequeo Cardiorespiratorio
Rx Tórax
Ecocardiografía
ECG
Presión Arterial
Manejo Anestésico – Inducción
Pacientes Inestables
Objetivo Especifico : Evitar al Máximo los efectos Cardiodepresores de los
Agentes Inhalatorios

ANESTESIA BALANCEADA

Agonistas Alfa 2 ?
Opiodes ?
Benzodiacepinas ?
Conceptos generales y
Fisiología Cardiovascular
Aplicada a la Anestesia
de Cardiopatas Dr. Paulo Mallea V.
Dipl. Anestesia y Cuidados Intensivos
Cert FCCS – Cert ABCtrauma

Introducción
• Función Sistema Cardiovascular

• Entonces ¿ Enfermedad Cardiovascular ?

• Drogas Anestésicas - Mecanismos de acción – DO2

• Metas en Anestesia Cardiovascular


Entender Mecanismos Fisiológicos y Fisiopatológicos
Mecanismos de Acción de Fármacos
Soporte del Paciente
Herramientas de Monitorización
Fármacos

Fisiopatología

¿ Se Puede Predecir lo que ocurrirá con nuestro Paciente ?


Introducción – Riesgo Anestésico
Clasificación ACVIM
cardiopatías

Introducción – Riesgo Anestésico


Introducción – Riesgo Anestésico

Raza
+
+ ASA +
Temperamento Equipamiento
Introducción - Mortalidad
Valores de Mortalidad varian de acuerdo al lugar
Introducción - Mortalidad

Introducción - Mortalidad
Deshidratación
Azotemia

Luego…

Diuresis por Frío ↓ Flujo Renal


Hipervolemia Relativa ↓ TFG
↓ ADH Isquemia

↓ Actividad Enzimático
Metabólica

Mayor tiempo de
recuperacion Anestesica
ACIDOSIS RESPIRATORIA

Lactato

ACIDOSIS METABOLICA

Escalofríos

Provea Oxigeno

Tremores aumentan el VO2 hasta 500% !!!!


Perfusión y Entrega de Oxigeno

Perfusión y Entrega de Oxigeno


Perfusión y Entrega de Oxigeno

Presión Arterial Y Gasto Cardiaco

VS
VELOCIDAD EYECCION VI
RESITENCIA ARTERIAL
VISCOSIDAD SANGUINEA

VISCOSISDAD
COMPLIANCE ARTERIAL
DURACION DEL CICLO
CARDIACO
¿ Cuando tomar medidas ?

Causas Hipotensión
Evaluación Peri-Quirúrgica

• Diagnostico Cardiovascular
• Tratamientos Farmacológicos
• Cambios de dosis recientes
• Radiografias previas
• ECG
• Presion Arterial
• Ecocardiograma

Pacientes con enfermedad Grave


deben tener una evaluación máximo con
2 semanas de antigüedad

Evaluación Peri-Quirúrgica – Examen Físico


¿ SEDACION O ANESTESIA ?

¿ Entonces, que protocolo utilizo ?


TELEMEDICINA CARDIOIMAGEN

El servicio de telemedicina, requiere de una implementación básica para poder utilizar el servicio
en su totalidad, por ejemplo; electrocardiograma, equipo de radiografías, ecógrafo. Tener
conocimientos básicos en la obtención de imágenes, si no los tienes no te preocupes nosotros te
ayudamos con capacitación, tutoriales y material de estudio rápido y practico.

Si cuantas con uno o con todos estos equipos, estás en un muy buen momento de utilizar el
servicio en su totalidad, si aún no los tienes pero cuentas con algunos, no pasara mucho tiempo en
que te decidas complementar tu atención médica, entregar valor agregado a tus servicios.

Hoy en día con esta tecnología podemos diagnosticar el 80 % de los casos.

Estos métodos no sustituyen la atención médica presencial pero ayuda en toma de decisiones y
conducta terapéutica.

Beneficios del programa

Para el paciente/propietario:

 disminuye los costos en traslados e incomodidad en pacientes de tamaños grandes y


hospitalizados de difícil traslado.
 Aumenta la rapidez en toma de decisiones y resolución de casos.
 Evita viajes innecesarios.
 Reduce mortalidad. Muchos pacientes mueren a la espera de un especialista.

Para el médico veterinario/clínica:

 Mejora la atención de tus pacientes.


 Optimiza la formación académica, debido a que durante el uso del servicio es inevitable
no aprender sobre las enfermedades y tratamientos, y con el tiempo te darás cuenta que
cada vez puedes tomar decisiones que actualmente se te hacen complicados.
 No pierdas tiempo coordinando interconsultas, simplemente gana tiempo tomando
decisiones oportunas y resolutivas.
 Dale valor agregado a tu servicio, incrementa las ventas, fideliza a tus clientes y mejora tu
competitividad.
 Si estas lejos de los centros de especialidades, con este servicio podrás tener acceso a una
opinión especializada en corto tiempo.
 Mejora la visualización de tu clínica, cardioimagen generara campañas de marketing por
diversos medios en los cuales se promocionara la red de asociados por región, comuna o
país, de tal forma que los propietarios puedan acceder al servicio mediante tu clínica.
 Aumenta el número de clientes.
 Los integrantes de la red de diagnostico cardioimagen tendrán en un futuro acceso a
cursos de capacitación en área de medicina cardio-respiratoria a valores preferenciales e
incluso gratuitos.

Servicios: tele-radiografía, tele-electrocardiografía, tele-ecocardiografía, tele-consulta


(evaluación de casos clínicos completos), dando continuidad y seguimientos con los tele-
controles.
Los valores de los distintos servicios fueron pensados para que en tu clínica los
puedas vender a precio de mercado generando buen margen de utilidades. Sin embargo
tú decides los precios finales a propietarios.
El acceso al carro de compra es exclusivo para los médicos y clínicas asociadas,
resguardando la información económica.
Los casos estarán siempre respaldados en la nube, de esta forma podernos tener
siempre a disposición la información y poder dar continuidad a los casos.

COMO EMPEZAR.

FACIL !!! si ya tienes conocimientos en toma de imágenes ecográficas solo necesitas ver un
pequeño tutorial, revisar unos apuntes que nosotros entregamos y ya puedes comenzar a
utilizar el servicio ¡!!.

SI NO TIENES EXPERIENCIA EN ECOGRAFIA!!! Y estas comenzando en esta apasionante


área, no importa aprenderás rápido!!!!... te capacitamos!! En la obtención de las
imágenes necesarias para lograr una interpretación clínica. Como; la capacitación
consiste en la revisión de unos videos tutoriales simples y prácticos, lectura
complementaria resumida y seleccionada exclusivamente para que puedas avanzar rápido
y sin dificultad. Posteriormente terminamos la capacitación en nuestro centro con 2 días
de práctica clínica con casos reales y ya estás listo para comenzar a utilizar
TELEMEDICINA!!!
QUE COSTO TIENE: PRACTICAMENTE NO TIENE COSTO!!!, el valor de la capacitación es de
250.000 pesos que puedes cancelar con diferentes medios de pagos tarjetas de crédito,
webpay, cheques, o directamente en nuestra consulta con transbank. PERO POR QUE NO
TIENE COSTO!! TE ENTREGAMOS GRATIS LOS PRIMEROS 5 SERVICIOS DE EVALUACIÓN
DE CASOS CLINICOS que tienen un valor de mercado de 60-75 mil pesos. Por lo tanto tu
INVERSION está completamente recuperada.

Si tienes más consultas no dudes en contactarnos, estaremos felices de poder ayudar.


Whatsapp +56996219845

Me despido atentamente, un abrazo.

Nelson Pérez Ruiz MV. Director Cardioimagen.


DR. SEBASTIÁN
BUSTAMANTE
CHILE

CHARLAS

1. Parálisis laríngea...¿qué es esto?


Operar o no operar, esa es la cuestión
Parálisis laringea: Qué es esto?
Operar o no operar?
Sebastián Bustamante B.
Primero no cagarla más…

Primum non noxere


La verdadera sabiduría está en conocer nuestra propia
ignorancia
Parálisis Laringea
Falla de abducción de los aritenoides durante la
inspiración

Idiopática y secundaria a otras enfermedades, posible


polineuropatía

Sintomas: Tos, Estridor laringeo, tos inducida por ingesta


de alimentos o agua, cambio del ladrido e intolerancia al
ejercicio.

Diagnóstico directo por Laringoscopía


2 grandes grupos

Perros grandes y viejos: Promedio de


edad de 9 años en Labradores, Golden,
San Bernardo, Newfoundlands y Spaniel
Británico

Perros Jóvenes: Bouviers des Flandres,


Siberian Huskies, Bull Terriers y O.A.
> 30% de estos
pacientes
presentan
HipoT4
Diagnóstico

Laringoscopía PO

Laringoscopía transnasal

Ecolaringoscopía

Clínico

OJO PIOJO!!!
Movimiento paradojal de los aritenoides
Tratamiento

Quirúrgico: Unilateralización
aritenoídea, Bilateralización,
Laringectomía/Aritenoidectomía y
LaringoÞsura castellada.

Manejo mŽdico: AINES, Antitus’genos y


Broncodilatadores
Unilateralización Aritenoídea
Aritenoidectomía
LaringoÞsura

Comparación quirúrgica

Bilateralización……………. 67% de muerte

Laringectomía……………… 30%

Unilateralización……………….14%
Traqueostom’a deÞnitiva
Article

Long-term outcome of permanent tracheostomies in dogs: 21 cases


(2000–2012)
Lindsay L. Occhipinti, Joe G. Hauptman

Abstract — This retrospective study reports long-term outcome, survival, and complications in dogs which received
a permanent tracheostomy due to upper airway obstruction. Data were collected from medical records (n = 21) in
Table Association
1. over
2 institutions ofPatients
a 12-year period. diagnosis withuntil
were followed survival time (P causes
death, complications, = 0.09)
of death, and survival approached signif
times are reported. Major complications were reported in 50% of patients with 20% of patients receiving revision
surgery. The most common complications were aspiration pneumonia andMedian days surgery. Median
need for revision
not significant, su
Diagnosis
survival time was 328 days with 25% of patients surviving 1321 days or longer.(25th, 75th)
Some (26%) patients died acutely with shortest surv
at home at various times after surgery. Permanent tracheostomy is a viable procedure for patients with end stage
Brachycephalic airway
upper airway obstruction; syndrome
however, a subpopulation of patients suffers acute1062
death at(728, 1744)
various times after surgery, paralysis, severe l
which is thought to be due to airway obstruction.
Bilateral acquired laryngeal paralysis 91 (8, 329) cervical bite wou
Laryngeal
Résumé — neoplasia
Résultat à long terme des trachéostomies chez les chiens :1399 (760, 2037)Cette étudeof patients in each
21 cas (2000–2012).
Laryngeal
rétrospective collapse
présente les of undetermined
résultats, la survie et les origin
complications à long terme628 (320,
chez les chiens937)
qui ont subi une
Severe laryngospasm
trachéostomie permanente en raison d’une obstruction des voies respiratoires 22 (11, 32)données ont été In the present s
supérieures. Les
recueillies dans les dossiers médicaux (n = 21) de 2 institutions sur une période de 12 ans. Les patients ont été
Traumatic laryngeal collapse due to bite wounds 164 (82, 245)
suivis jusqu’à la mort à la suite de complications; les causes de décès et les temps de survie sont signalés. Des
patients, which is
Laryngeal
complicationsmalformation
majeures ont été signalées chez 50 % des patients et 20 %1760 (1645,
des patients ont 2006)
subi une reprisesurgery was requir
chirurgicale. Les complications les plus fréquentes étaient la pneumonie de déglutition et le besoin de reprise
chirurgicale. Le temps de survie moyen était de 328 jours avec 25 % des patients qui ont survécu 1321 jours oureported by Hedl
Table 2. Complications
plus. Certains anddeassociation
patients (26 %) sont morts with survival
façon aiguë à la maison in days
à divers moments après la chirurgie. Une
trachéostomie permanente est une intervention viable pour les patients ayant une obstruction des voies respiratoiresrequired revision
Positive median
de stade final. Cependant, une sous-population Negative
de patients sont décédés aiguë à divers moments après latoma, which was
median
de façon
chirurgie, que l’on croit attribuable à l’obstruction des voies respiratoires.
Factor (25th, 75th) (25th, 75th) (TraduitP-value par Isabelle Vallières)viously (3). Unlik
Muchas gracias por la oportunidad a Cardioimagen!!!

Y Muchas gracias por la atención!!!!

sebaveccs@gmail.com

agenda.vetera.cl@gmal.com

Sebabustamanteb en Instagram

Sebastián Ricardo Bustamante Bustamante


En Facebook.
Reconocimiento
Trayectoria

En el marco del curso se realizó un reconocimiento


a la trayectoria en el área cardiológica al Dr. Ramón Martínez.
Médico veterinario con dedicación a docencia y atención
clínica de la especialidad desde 1970.
Patrocina

Auspician
GRACIAS!