PEMICU 1 BLOK KGD

Vivian Saputra
405140126
LI
1. MM. Shock (+ Algoritma)
2. MM. Akut Abdomen (peritonitis, apendisitis, hernia strangulata & inkarserata,
intussusepsi, invaginasi)
3. MM. GI Bleeding (upper & lower)
4. MM. Upper GI Bleeding (Mallory Weiss Tear, Gastroduodenal erosion,
neoplasma, vaskular ektasi, peptic ulcer, stress ulcer)
SHOCK
 Shock
 is defined by the presence of multisystem end-organ hypoperfusion.
 Clinical indicators include
 Reduced mean arterial pressure (MAP)
 tachycardia
 Tachypnea
 cool skin and extremities
 acute altered mental status
 oliguria.
 Hypotension is usually  though not always present.
 Since the MAP is the product of cardiac output and systemic vascular resistance (SVR)，
reductions in blood pressure can be caused by decreases in cardiac output and/or SVR.
Shock
HYPOVOLEMIC SHOCK
 results either from the loss of RBC mass and plasma from hemorrhage or
from the loss of plasma volume alone due to extravascular fluid
sequestration or GI, urinary, and insensible losses.
 The signs and symptoms of nonhemorrhagic hypovolemic shock are the
same as those of hemorrhagic shock, although they may have a more
insidious onset.
 The normal physiologic response to hypovolemia is to maintain perfusion
of the brain and heart while attempting to restore an effective circulating
blood volume.
HYPOVOLEMIC SHOCK
 DIAGNOSIS
 Hypovolemic shock is readily
diagnosed when there are sign of
hemodynamic instability & the source
of vol loss is obvious
 example of hypovolemic shock : even
after acute hemorrage ,hb &
hematocrit valued do not change until
compensatory fluid shifts have
occurred /exogenous fluid is
administred
 it is essential to distinguish between
hypovolemic & cardiogenic shock
because both forms are associated
with reduced CO & compenatory
sympathetic mediated response (
characterized : tachycardia & elevated
SVR)
 The finding of cardiogenic shock :
jugular venous distention ,rales & S3
gallop distinguish it from hypovolemic
shock
 Septic shock
 Sepsis with hypotension (arterial blood pressure <90 mmHg systolic, or 40 mmHg less than
patient's normal blood pressure) for at least 1 h despite adequate fluid resuscitation.
or
 Need for vasopressors to maintain systolic blood pressure ≥90 mmHg or MAP ≥70 mmHg.

Etiology
 Respiratory infection was most common (64%)
 Microbiologic results were positive in 70% of individuals considered infected; of the isolates :
 62% were gram -negative bacteria (Pseudomonas species and Escherichia coli were most
common)
 47% were gram positive bacteria (Staphylococcus aureus was most common)
 19 % were fungi (Candida species).
Treatment
1.Oxigenation
2.Fluid Therapy
3.Vasopresor & Inotropic
4.Bicarbonat
5.Nutrition
NEUROGENIC SHOCK
 Interruption of sympathetic vasomotor Treatment involves a simultaneous
input after a high cervical spinal cord
injury, inadvertent cephalad migration
of spinal anesthesia, or devastating
head injury  neurogenic shock.
 In addition to arteriolar dilation,
venodilation causes pooling in the
venous system decreases venous
return and cardiac output.
 The extremities are often warm, in
contrast to the usual sympathetic
vasoconstriction induced coolness in
hypovolemic or cardiogenic shock.
approach to the relative hypovolemia
and to the loss of vasomotor tone.
Excessive volumes of fluid may be
required to restore normal
hemodynamics if given alone.
Once hemorrhage has been ruled out,
norepinephrine or a pure α adrenergic
agent (phenylephrine) may be
necessary to augment vascular
resistance and maintain an adequate
MAP.
 Hemorrhagic Shock
 Hemorrhage is the most common cause of shock in trauma patients.
 Hemorrhage is defined as an acute loss of circulating blood volume.
 The classification of hemorrhage into four classes based on clinical signs is a useful tool for
estimating the percentage of acute blood loss :
 Class I hemorrhage  is exemplified by the condition of an individual who has donated a
unit of blood.
 Class II hemorrhage  is uncomplicated hemorrhage for which crystalloid fluid
resuscitation is required.
 Class III hemorrhage  is a complicated hemorrhagic state in which at least crystalloid
infusion is required and perhaps also blood replacement.
 Class IV hemorrhage  is considered a preterminal event; unless very aggressive measures
are taken, the patient will die within minutes.
factors profoundly alter the classic hemodynamic response to an acute loss of circulating blood
volume

 These factors include:

 Patient’s age
 Severity of injury, with special attention to type and anatomic location of
injury
 Time lapse between injury and initiation of treatment
 Prehospital fluid therapy
 Medications used for chronic conditions
 Initial management of shock hemorragic

 The basic management principle is to  D: Disability – neurologic examination

stop the bleeding and replace the  E: Exposure – complete examination
volume loss.
 Gastric Dilatation-Decompression In
 The physical examination is directed unconscious patients, gastric distention
toward the immediate diagnosis of life- increases the risk of aspiration of
threatening injuries and includes gastric contents, which is a potentially
assessment of the ABCDEs fatal complication
 A & B : Airway & breathing  Urinary Catheterization
 C: Hemorrhage control priorty is to  Vascular access line
stop the bleeding ,not to calculate the  Initial fluid therapy
volume of fluid lost !
www.researchgate.net/figure/234120899_fig1_Flowchart-of-initial-management-of-traumatic-
hemorrhagic-shock-In-the-acute-phase-of
 Cardiogenic shock
 Cardiogenic shock (CS) is
characterized by systemic
hypoperfusion due:
 severe depression of the cardiac index
(<2.2 [L/min] & sustained systolic
arterial hypotension (<90 mmHg)
despite an elevated filling pressure
(pulmonary capillary wedge pressure
[PCWP] > 18 mmHg)
 Circulatory failure bsed on cardiac
dysfunction may be caused :primary  Reduced coronary perfusion
myocardial failure ( most commonly
secondary to acute myocardial
infarction),cardiomyopathy
/myocarditis ( less frequently)
 Depression of myocardial contractility
 usuallay due to ischemia results in
reduced cardiac output & arterial
blood pressure hypoperfusion of the
myocardium & further ischemia &
depression of CO
 Systolic myocardial dysfuntion
reduces SV & together with diastolic
dysfunction  leads to elevated LV
end-diastolic pressure & PCWP
worsening ischemia & progressive
myocardial dysfunction
 Inflammatory cytokinesmay
contribute to CS
 Diagnosis

 focused history & physical examination • Tachypneu,Cheyne –stokes respiration &

should be performed， blood specimens jugular venous distention
sent to the laboratory & (ECG) and chest x- • Weak apical pulse & soft S1 & S3 gallop
ray obtained • Laboratory finding :
 CLINICAL FINDING • WBC is typically elevated with a left shift
• Most patients have dyspnea and appear pale • Renal function is initially unchanged ( but
，appre hensive & diaforetic & mental BUN & creatinine rise progressively)
status may be altered. • Hepatic transminase markelyd elevated
• The pulse is typically weak and rapid， due to liver hypoperfusion
often in the range of 90- 110 beats/min or • Lactic acid level is elevated
severe bradycardia due to high-grade heart • Arterial blood gas : may demonstrated
block may be present hypoxemia & anion gap metabolic acidosis
• Systolic BP is reduced (<90 mmHg or >/30 • Cardiac marekr ,creatine phosphokinase &
mmHg below baseline) with a narrow pulse troponin I & T : markely elevated
pressure (<30 mmHg
 Diagnosis
 ECG  Pulmonary arterhy cateterization
 In CS due to acute MI with L V failure,Qtheir use is generally recommended
waves and/ or >2-mm ST elevation in for measurement of filling pressure &
multiple leads or left bundle branch cardiac output to confirm the diagnosis
block are usually present. & to optimize the use of IV fluid
 Chest roentgenogram  chest x ray  Left heart catherization & coronary
shows pulmonary vascular congestion & angiography  Measurement of L V
often pumonary edema ,the heart size pressure and definition of the coronary
is usually normal when CS result from a anatomy provide useful information
1st MI and are indicated in most patients with
 Echocardiogram doppler mapping CS complicating MI.
demonstrates a left-right shunt in ps
with VSR
 Treatment
 General measure
 initial therapy : aimed at maintaining
adequate systemic & coronary perfusion by
raising systemic BP with vasopressor &
ajusting volume status to a level that
ensures optimum LV filling pressure
 Vassopressor  Norepinephrine is a potent
vasoconstrictor a n d inotropic
 stimulant that is useful for patients with
CS,NE should be started at a dose of 2-4
microgram/min & titrated upward
 If systemic perfusion /systolic pressure cannot
be maintained at > 90 mmHg with a dose of
15 microgram/min ( it is unlikely that further
increase will be beneficial)
 Dopamin : varying hemodynamic effect
based on the dose at low doses ( -< 2
microgram/kg /min)dilates the renal
vascular bed
 At moderate dose (2-10 microgram/kg /min)  it
has + chronotropic & inotropic effect ( as
consequence of beta adrenergic receptor
stimulation
 At higeher doses : vasoconstrictor effect ( result
from alfa receptor stimulation)
 Dobutamin : synthetic sympathomimetic
amine with + inotropic action & min +
chronotropic activity at a low doses ( 2.5
microgram /kg /min)
NORMAL HEMODYNAMIC PARAMETERS
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topics.php?paction=showTop
icSeg&topic_id=121&seg_id=
2377
http://www.ebmedicine.net/topics.php?paction=showTopicSeg&topic_id=121&seg_id=2377
AKUT ABDOMEN
STRANGULATED HERNIA
HERNIA
 An abdominal wall hernia is defined as an abnormal protrusion of peritoneal
contents through a fascial defect in the abdominal wall.
 Hernias are classified by anatomic location, hernia contents, and the status of
those contents (e.g., reducible, strangulated, or incarcerated)
 A hernia is called reducible when the hernia sac itself is soft and easy to
replace back through the hernia neck defect.
 A hernia is incarcerated when it is firm, often painful, and nonreducible by
direct manual pressure.
 Strangulation  develops as a consequence of incarceration and implies
impairment of blood flow (arterial, venous, or both).

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

STRANGULATED HERNIA
 A strangulated hernia presents as severe, exquisite pain at the hernia
site, often with signs and symptoms of intestinal obstruction, toxic
appearance, and, possibly, skin changes overlying the hernia sac.
 A strangulated hernia is an acute surgical emergency.

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

HERNIA
DIAGNOSIS
 CBC, serum chemistries, and urinalysis  routinely ordered but are of
minimal value in the evaluation.
 Plain abdominal radiography is generally nondiagnostic of an abdominal wall
hernia unless the patient has a complication such as a bowel obstruction,
pneumatosis intestinalis or pneumoperitoneum.
 CT is the test of choice for evaluation of an abdominal wall hernia as it
provides accurate detail of the abdominal wall and hernia contents.

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

 STRANGULATED HERNIA
DIAGNOSIS  CT findings of a strangulated hernia
 Doppler US can detect the arterial flow to include :
the loop of bowel but is usually not  bowel wall thickening,
sensitive enough to detect venous flow and  extraluminal fluid,
cannot detect lymphatic flow.  marked fat stranding,
 Color Doppler flow  can help differentiate  Engorged mesenteric vessels
between an incarcerated or strangulated suggesting vascular compromise.
hernia.
 CT allows visualization of bowel and
omentum protruding through the
peritoneum.
 An incarcerated hernia can be identified
by fat stranding around the hernia sac.
Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.
STRANGULATED HERNIA
TREATMENT
 If the hernia is easily reducible on physical examination  refer the patient for elective
outpatient surgical repair.
 If the hernia is exquisitely tender and is associated with systemic signs and symptoms,
such as intestinal obstruction, toxic appearance, peritonitis, or sepsis, then assume
hernia strangulation.
 Consult general surgery immediately.
 Administer broad-spectrum IV antibiotics, such as cefoxitin, provide fluid
resuscitation and adequate narcotic analgesia, and obtain preoperative laboratory
studies.
 If the hernia is incarcerated but the patient does not yet show signs of strangulation,
then make one or two attempts at reduction in the ED.

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.
ACUTE APPENDICITIS
 Acute Appendicitis: Pathogenesis
 Its etiology is still not completely understood
 Fecaliths, incompletely digested food residue, lymphoid hyperplasia, intraluminal
scarring, tumors, bacteria, viruses, and inflammatory bower disease have all been
associated with inflammation of the appendix and appendicitis
 Although not proven, obstruction of the appendiceal lumen is believed to be an
important step in the development of appendicitis
 In some cases, obstruction leads to bacterial overgrowth and luminal distension, with
an increase in intraluminal pressure that can inhibit the flow of lymph and blood in
some cases
 Then, vascular thrombosis and ischemic necrosis with perforation of the distal appendix
may occur
 Appendiceal fecaliths (or appendcicoliths) are found in approximately 50% of patients
with gangrenous appendicitis who perforeate but are rarely identified in those who have
simple disease
 When perforation occurs, the resulant leak may be contained by the omentum or oterh
surrounding tissues to form an abscess. Free perforation normally causes severe
peritonitis
Acute Appendicitis: Clinical Manifestations
 Non-spesific complaints occur first
 Patients may notice changes in bowel habits or malaise and vague,
perhaps intermittent crampy, abdominal pain in the epigastric or
periumbilical region
 The pain susequently migrates to the right lower quadrant over 12-24 h,
where it is sharper and can be difinitively localizes as transmural
inflmmation when the appendix irritates the parietal peritoneum
 Patients with appendicitis will most often observe that their nausea, if
present, followed the development of abdominal pain, which can help
distinguish them from patients with gastroenteritis, for example, where
nausea occurs first
Acute Appendicitis: Clinical Manifestations
Acute Appendicitis: Clinical Manifestations
 Patients with pelvic appendicitis are processes beside appendicitis or the
more likely to present with dysuria, presence of complications such as
urinary frequency, diarrhea, or perforation
tenesmus. They may only experience  Patients with appendicitis will be
pain in the suprapubic region on found to lie quite still to avoid
palpation or on rectal or pelvic peritoneal irritation caused by
examination movement, and some will report
 Patients with simple appendicitis discomfort caused by a bumpy car ride
normally only appear mildly ill with a on the way to the hostpital or clinic,
pulse and temperature that are coughing, sneezing, or other actions
usually only slightly above normal that replicate a Valsava maneuver
 If the temperature is >38.3 C and if
there are rigors, the provider should
be concerned about other disease
Acute Appendicitis: Clinical Manifestations
Acute Appendicitis: Differintial Diagnosis
Acute Appendicitis: Laboratory Testing
 Laboratory testing does not identify patients with appendicitis but can
help the clinician work through the differintial diagnosis
 The white blood cell count is only mildly to moderately elevated in
approximately 70% of patients with simple appendicitis (with a
leukocytosis of 10,000-18,000 cells/uL). A left shift toward immature
PMN leukocytes is present in >95% of cases
 Serum amylase and lipase levels shoud be measured
 Urinalysis is indicated to help exclude genitourinary conditions that may
mimic acute appendicitis
Acute Appendicitis: Imaging
 Plain films of the abdomen are rarely helpful and so are not routinely
obtained unless the clinician is worried about other conditions such as
intestinal obstruction, perforated viscus, or ureterolithiasis
 USG findings suggesting the presence of appendicitis include wall
thickening, an increase appendiceal diameter, and the presence of free
fluid
 CT findings include dilation with wall thickening, a lumen that does not fill
with enteric contrast, and fatty tissue stranding or air surrounding the
appendix, which suggests inflammation
Acute Appendicitis: Treatment
 In the absence of contraindications, a patient who has a strongly
suggestive medical history and physical examination with supportive
laboratory findings should undergo appendectomy urgently
 If there is a mass representing a phlegmon or abscess, such patients are
best served by treatment with broad spectrum antibiotics, drainage if
there is an abscess >3cm in diameter, and parenteral fluids and bowel rest
 Laparoscopic appendectomy
 Postoperative complications are fever and leukocytosis. Continuation of
these findings beyong 5 days should rise concern for the presence of an
intraabdominal abscess
Peritonitisndicitis
Acute Peritonitis: Introduction
 Acute peritonitis, or inflammation of the visceral and parietal
peritoneum, is most often but not always infectious in origin, resulting
from perforation of a hollow viscus. This is called secondary peritonitis,
as opposed to primary or spontaneous peritonitis, when a spesific
intraabdominal source cannot be identified. In either instance, the
inflammation can be localized or diffuse
Acute Peritonitis: Etiology
 Infective organism
 Secondary peritonitis most commonly results from perforation of the
appendix, colonic diverticuli, or the stomach and duodenum
 Others: complication of bowel infarction or incarceration, cancer,
inflammatory bowel disease, and intestinal obstruction or volvulus
 Over 90% of the cases of primary or spontaneous bacterial peritonitis
occur in patients with ascites or hypoproteinemia (< 1 g/L)
 Aseptic peritonitis is most commonly caused by the abdnormal presence
of physiologic fluids like gastric juice, bile, pancreatic enzymes, blood, or
urine
Acute Peritonitis: Clinical Features
 The cardinal signs and symptoms of peritonitis are acute, typically severe,
abdominal pain with tenderness (diffuse/localized) and fever
 Bowel sounds are usually absent to hypoactive
 Most patients present with tachycardia and signs of volume depletion
with hypotension
 Laboratory testing typically reveals a significant leukocytosis, and
patients may be severely acidotic
 Radiographic studies may show dilation of the bowel and associated
bowel wall edema
Acute Peritonitis: Differential Diagnosis
Acute Peritonitis: Therapy And Prognosis
 Successful treatment depends on correcting any electrolyte
abnormalities, restoration of fluid volume and stabilization of the
cardiovascular system, appropiate antibiotic therapy, and surgical
correction of any underlying abnormalities
Esophageal Corrosive Lesion
 Esophageal Corrosive Lesion
 Caustics (strong acids and alkalis), when ingested, burn upper GI tract tissues,
sometimes resulting in esophageal or gastric perforation

http://www.msdmanuals.com/professional/injuries-poisoning/poisoning/caustic-ingestion
 Causes
 Common acid-containing sources
include the following:
 Toilet bowl–cleaning products
 Automotive battery liquid
 Rust-removal products
 Metal-cleaning products
 Cement-cleaning products
 Drain-cleaning products
 Soldering flux containing zinc
chloride
http://emedicine.medscape.com/article/813772-
clinical#b3
 Common alkaline-containing sources
include the following:
 Drain-cleaning products
 Ammonia-containing products
 Oven-cleaning products
 Swimming pool–cleaning products
 Automatic dishwasher detergent
 Hair relaxers
 Clinitest tablets
 Bleaches
 Patfis
 Alkaline ingestions  liquefactive necrosis (a process that involves
saponification of fats and solubilization of proteins)
 Cell death  emulsification and disruption of cellular membranes.
 The hydroxide ion of the alkaline agent reacts with tissue collagen and causes
it to swell.
 Severe injury occurs rapidly after alkaline ingestion, within minutes of
contact.
 The esophagus is the most commonly involved organ with the stomach
much less frequently involved after alkaline ingestions.
 Tissue edema occurs immediately, may persist for 48 hours, and may
eventually progress sufficiently to create airway obstruction.

http://emedicine.medscape.com/article/813772-overview#a5
 Patfis
 Acid ingestion  coagulation necrosis  desiccation or denaturation of
superficial tissue proteins  formation of an eschar or coagulum
 This eschar may protect the underlying tissue from further damage
 the stomach is the most commonly involved organ following an acid ingestion
( due to some natural protection of the esophageal squamous epithelium)
 The eschar sloughs in 3-4 days and granulation tissue fills the defect.
 Acute complications include gastric and intestinal perforation and upper
gastrointestinal hemorrhage.

http://emedicine.medscape.com/article/813772-overview#a5
 Symptoms and sign
 Initial symptoms of caustic ingestion include drooling and dysphagia.
 In severe cases, pain, vomiting, and sometimes bleeding develop immediately
in the mouth, throat, chest, or abdomen.
 Airway burns may cause coughing, tachypnea, or stridor
 Swollen, erythematous tissue may be visible intraorally
 Esophageal strictures can develop over weeks, even if initial symptoms had
been mild and treatment had been adequate

http://www.msdmanuals.com/professional/injuries-poisoning/poisoning/caustic-ingestion
 Diagnosis
 Endoscopy
 Meticulous endoscopy is indicated to check for the presence and severity of
esophageal and gastric burns when symptoms or history suggests more
than trivial ingestion

http://www.msdmanuals.com/professional/injuries-poisoning/poisoning/caustic-ingestion
 Treatment
 Prehospital care
 Attempt to identify the specific product, concentration of active ingredients,
and estimated volume and amount ingested.
 Do not induce emesis or attempt to neutralize the substance by using a weak
acid or base
 Small amounts of a diluent may be beneficial if administered as soon as
possible after a solid or granular alkaline ingestion, to remove any particles
that are adhering to the oral or esophageal mucosa.
 Water or milk may be administered in small amounts.

http://emedicine.medscape.com/article/813772-treatment#d10
  Emergency departement care
 Airway control
 Because of the risk of rapidly developing airway edema, the patient’s airway and mental status
should be immediately assessed and continually monitored.
 Equipment for endotracheal intubation and cricothyrotomy should be readily available.
 Gastric emptying and decontamination
 Do not administer emetics because of risks of re-exposure of the vulnerable mucosa to the
caustic agent.
 In large-volume liquid acid ingestions, nasogastric tube (NGT) suction may be beneficial if
performed rapidly after ingestion
 Dilution
 May be beneficial for ingestion of solid or granular alkaline material if performed within 30
minutes after ingestion using small volumes of water.
 Because of the risk of emesis, carefully consider the risks versus benefits of dilution.
 Do not dilute acids with water; this would result in excessive heat production.

http://emedicine.medscape.com/article/813772-treatment#d10
Intussusception
 Intussusception
 Occurs when a portion of alimentary track is telescoped into a adjascent
segment.
 Common obstruction for 3 month – 6 years old
 60% occur < 1yo
 80% occur 24 month
http://eradiology.bidmc.harvard.edu/LearningLab/gastro/Daftary.pdf
http://eradiology.bidmc.harvard.edu/LearningLab/gastro/Daftary.pdf
 Palpitation on
abdomen

http://eradiology.bidmc.harvard.edu/LearningLab/gastro/Daftary.pdf
http://eradiology.bidmc.harvard.edu/LearningLab/gastro/Daftary.pdf
Diagnosis
 Clinical history &physical findings  suggestive of intussusception 
performed ultrasound.
 Screening ultrasounds for suspected intussusception increases the yield of
diagnostic/therapeutic enemas and reduces unnecessary radiation exposure
in children with negative ultrasound examinations
 Contrast enemas demonstrate a filling defect or cupping in the head of
the contrast media where its advance is obstructed by the
intussusceptum
 A central linear column of contrast media may be visible in the
compressed lumen of the intussusceptum, and a thin rim of contrast may
be seen trapped around the invaginating intestine in the folds of mucosa
within the intussuscipiens (coiled-spring sign)
http://eradiology.bidmc.harvard.edu/LearningLab/gastro/Daftary.pdf
DIFFERENTIAL DIAGNOSIS
 The bloody stools and abdominal cramps that accompany enterocolitis
can usually be differentiated from intussusception
 in enterocolitis the pain is less severe and less regular, there is diarrhea, and
the infant is recognizably ill between pains.
 Bleeding from Meckel diverticulum is usually painless
 Because intussusception can be a complication of this disorder,
ultrasonography may be needed to distinguish the conditions
Treatment
 Reduction of an acute intussusception is an emergency procedure and
performed immediately after diagnosis in preparation for possible
surgery
 patients with prolonged intussusception with signs of shock, peritoneal
irritation, intestinal perforation, or pneumatosis intestinalis, reduction
should not be attempted.
 An ileoileal intussusception is best demonstrated by abdominal
ultrasonography
 An ileoileal intussusception is best demonstrated by abdominal
ultrasonography
Prognosis
 Untreated intussusception in infants is usually fatal; the chances of
recovery are directly related to the duration of intussusception before
reduction.
 Most infants recover if the intussusception is reduced in the 1st 24 hr.
 But the mortality rate rises rapidly after this time, especially after the 2nd
day.
 Spontaneous reduction during preparation for operation is not uncommon.
 The recurrence rate after reduction of intussusceptions is ≈10%
 and after surgical reduction it is 2–5%;
 none has recurred after surgical resection
GI BLEEDING
 Upper G.I bleeding
 Upper GI (UGI) bleeding is any GI bleeding originating proximal to the ligament of Treitz.
 PATHOPHYSIOLOGY
 PEPTIC ULCER DISEASEAwareness that aspirin, nonsteroidal anti-inflammatory drugs
(NSAIDs), and smoking cause bleeding and increased recognition and treatment of H.
pylori infection
 EROSIVE GASTRITIS AND ESOPHAGITIS Erosive gastritis, esophagitis, and duodenitis are
also common causes of GI hemorrhage, Common predisposing factors include alcohol,
salicylates, and NSAIDs.
 ESOPHAGEAL AND GASTRIC VARICES result from portal hypertension, most often a
result of alcoholic liver disease
 MALLORY-WEISS SYNDROME Mallory-Weiss syndrome is bleeding secondary to a
longitudinal mucosal tear at the gastroesophageal junction.
 The classic history is repeated vomiting followed by bright red hematemesis. The
syndrome can be associated with alcoholic binge drinking, diabetic ketoacidosis, or
chemotherapy administration
 Diagnosis
 HISTORY  Ingestion of iron or bismuth can simulate melena.
 Ask about hematemesis, coffee-ground emesis, or Liquid medications with red dye, as well as certain
melena. foods, such as beets, can simulate hematochezia.
 Vomiting and retching, followed by hematemesis,
suggest a Mallory-Weiss tear PHYSICAL EXAMINATION
 Be sure to ask about prior episodes of GI bleeding Visual inspection of the vomitus for a bloody,
and any interventions performed. maroon, or coffeeground appearance is the most
 Salicylates, glucocorticoids, NSAIDs, and reliable way to diagnose UGI bleeding
anticoagulants all place the patient at high risk for Vital signs may reveal obvious hypotension and
GI bleed. tachycardia or more subtle findings such as
 Alcohol abuse is strongly associated with a decreased pulse pressure or tachypnea.
number of causes of bleeding, including peptic Cool, clammy skin is an obvious sign of shock
ulcer disease, erosive gastritis, and esophageal
 Petechiae and purpura suggest an underlying
varices.
coagulopathy.
Lab test
 In patients with significant bleeding, the single most important laboratory test is
to obtain blood for type and cross-match in case transfusion is needed
 UGI hemorrhage will elevate BUN levels through digestionand absorption of
hemoglobin.
 A BUN:creatinine ratio ≥30 suggests a UGI source of bleeding
 INR, partial thromboplastin time, and platelet count, are useful in patients
taking anticoagulants and those with underlying hepatic disease.
 Obtain an ECG in patients with underlying coronary artery disease.
 Routine abdominal and chest radiographs are of limited value and are not
needed in the absence of specific clinical indications.
 Scintigraphy and angiography help localize the source of bleeding to determine
whether medical or surgical management is optimal.
GI BLEEDING
UPPER GI BLEEDING
 Treatment
 Initial management is stabilization. patients with a UGI bleed who are receiving
 Patients in hemorrhagic shock require emergent anticoagulants.
resuscitation, including two large-bore IVs, typed and  International consensus guidelines recommend
cross-matched blood with the consideration of reversal of coagulopathy for UGI bleed patients who
massive transfusion protocols, and in selected cases, have an elevated INR or platelet counts <50,000/μL
early airway management.  PROTON PUMP INHIBITORS for patients with
 BLOOD TRANSFUSIONS nonvariceal bleeding from peptic ulcer disease, When
  If a large amount of blood product is anticipated, proton pump inhibitors are given at high dose, the
use massive transfusion,if less severe : the decision to gastric pH remains neutral. Clot formation from
transfuse can be difficult because hemoglobin platelet aggregation is dependent on a pH >6.0
concentrations do not fall until after hemodilution has  SOMATOSTATIN ANALOGS/OCTREOTIDE
occurred somatostatin that elicits several actions in patients
  Liberally transfusing all bleeding patients using a with UGI bleeding. It inhibits the secretion of gastric
high threshold (hemoglobin <9 grams/dL) can cause Acid, reduces blood flow to the gastroduodenal
harm mucosa, and causes splanchnic vasoconstriction
 COAGULOPATHY   The dose is a 50-microgram bolus followed

  An INR ≥1.5 is a significant predictor of mortality in  by a continuous infusion of 25 to 50 micrograms/h

Lower GI bleeding
 Lower GI (LGI) bleeding is the loss of blood from the GI tract distal to the
ligament of Treitz.
 LGI bleeding is a common problem in emergency medicine and should be
considered potentially life threatening until proven otherwise.
 Among patients with an established LGI source of bleeding (i.e.,
bleeding past the ligament of Treitz), the most common cause is
diverticular disease, followed by colitis, adenomatous polyps, and
malignancies
 DIAGNOSIS
 Factors associated with a high morbidity rate are
 hemodynamic instability, repeated hematochezia, gross blood on initial rectal examination, initial
hematocrit <35%, syncope, nontender abdomen (predictive of severe bleeding), aspirin or
nonsteroidal anti-inflammatory drug use (predictive of diverticular hemorrhage), and more than
two comorbid condition

 History
 Physical examination  The abdominal examination may disclose tenderness, masses, ascites, or
organomegaly, In patients with LGI bleeding, a lack of abdominal tenderness suggests bleeding
from disorders involving the vasculature, such as diverticulosis or angiodysplasia.
 Inflammatory bowel disorders with LGI bleeding are associated with abdominal tenderness on
examination.
 LAB TEST  The most important laboratory tests are the CBC, coagulation studies,
 and typed and cross-matched blood. Bleeding from a source higher in the GI tract may elevate
blood urea nitrogen levels through digestion and absorption of hemoglobin.
dIAGNOSIS
 IMAGING  Routine abdominal radiographs are of limited value without
specific
 indications such as perforation, obstruction, or foreign bodies, The initial
diagnostic procedure of choice—angiography, scintigraphy, or endoscopy
 TREATMENT
1. Resuscitate unstable or actively bleeding patients.
2. Administer oxygen and institute cardiac monitoring.
3. Place two large-bore IV lines and replace volume with crystalloids.
 4. initiation of blood transfusion are continued active bleeding and failure to
improve perfusion and vital signs after the infusion of 2 L of crystalloid.
 5. Consider the placement of a nasogastric tube if LGI bleeding is significant.
Diagnostic and management strategies for gastrointestinal
bleeding
UPPER GI BLEEDING