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D.Oxygen is administered by nasal cannula. Urine
output should be monitored.
E.Serial hematocrits should be checked and main
tained greater than 30%. Coagulopathy should be
assessed and corrected with fresh frozen plasma,
vitamin K, cryoprecipitate, and platelets.
F.Definitive diagnosis requires upper endoscopy, at
which time electrocoagulation, banding, and/or local
injection of vasoconstrictors at bleeding sites may be
completed. Surgical consultation should be requested
in unstable patients or patients who require more than
6 units of pRBCs.
Clinical Indicators of Gastrointestinal Bleeding
and Probable Source
Probability of Probability of
Upper Gastro- Lower Gastro-
Clinical Indica- intestinal intestinal
tor source Source
Hematemesis Almost certain Rare
Melena Probable Possible
Hematochezia Possible Probable
Blood-streaked Rare Almost certain
stool
Occult blood in Possible Possible
stool
VI.Peptic Ulcer Disease
A.Peptic ulcer disease is the commonest cause of
upper gastrointestinal bleeding, responsible for 27
40% of all upper gastrointestinal bleeding episodes.
Duodenal ulcer is more frequent than gastric ulcer.
Three fourths of all peptic ulcer hemorrhages subside
spontaneously.
B.Upper gastrointestinal endoscopy is the most
effective diagnostic technique for peptic ulcer disease.
Endoscopic therapy is the method of choice for
controlling active ulcer hemorrhage.
C.Proton-pump inhibitor administration is effective
in decreasing rebleeding rates with bleeding ulcers.
Therapy consists of intravenous pantoprazole.
1.Pantoprazole (Protonix) dosage is 80 mg IV,
followed by continuous infusion with 8 mg/hr, then
40 mg PO bid when active bleeding has subsided.
2.Twice daily dosing of oral proton pump inhibitors
may be a reasonable alternative when intravenous
formulations are not available. Oral omeprazole
(Prilosec) for duodenal ulcer: 20 mg qd for 4-8
weeks. Gastric ulcers: 20 mg bid. Lansoprazole
(Prevacid), 15 mg qd. Esomeprazole (Nexium) 20
40 mg qd.
D.Indications for surgical operation include (1)
severe hemorrhage unresponsive to initial
resuscitative measures; (2) failure of endoscopic or
other nonsurgical therapies; and (3) perforation,
obstruction, or suspicion of malignancy.
E.Duodenal ulcer hemorrhage. Suture ligation of the
ulcer-associated bleeding artery combined with a
vagotomy is indicated for duodenal ulcer hemorrhage
that does not respond to medical therapy. Truncal
vagotomy and pyloroplasty is widely used because it
is rapidly and easily accomplished.
F.Gastric ulcer hemorrhage is most often managed
by truncal vagotomy and pyloroplasty with wedge
excision of ulcer.
G.Transcatheter angiographic embolization of the
bleeding artery responsible for ulcer hemorrhage is
recommended in patients who fail endoscopic at
tempts at control and who are poor surgical candi
dates.
VII.Hemorrhagic Gastritis
A.The diffuse mucosal inflammation of gastritis rarely
manifest as severe or life-threatening hemorrhage.
Hemorrhagic gastritis accounts for 4% of upper
gastrointestinal hemorrhage. The bleeding is usually
mild and self-limited. When coagulopathy accompa
nies cirrhosis and portal hypertension, however,
gastric mucosal bleeding can be brisk and refractory.
B.Endoscopic therapy can be effective for multiple
punctate bleeding sites, but when diffuse mucosal
hemorrhage is present, selective intra-arterial infusion
of vasopressin may control bleeding. For the rare case
in which surgical intervention is required, total
gastrectomy is the most effective procedure.
VIII.Mallory-Weiss syndrome
A.This disorder is defined as a mucosal tear at the
gastroesophageal junction following forceful retching
and vomiting.
B.Treatment is supportive, and the majority of patients
stop bleeding spontaneously. Endoscopic coagulation
or operative suturing may rarely be necessary.
Esophageal Varices
Esophageal varices eventually develop in most patients
with cirrhosis, but variceal bleeding occurs in only one
third of them. The initiating event in the development of
portal hypertension is increased resistance to portal
outflow.
Causes of Portal Hypertension
Presinusoidal
Extrahepatic causes
Portal vein thrombosis
Extrinsic compression of the portal vein
Cavernous transformation of the portal vein
Intrahepatic causes
Sarcoidosis
Primary biliary cirrhosis
Hepatoportal sclerosis
Schistosomiasis
Sinusoidal: Cirrhosis, alcoholic hepatitis
Postsinusoidal
Budd-Chiari syndrome (hepatic vein thrombosis)
Veno-occlusive disease
Severe congestive heart failure
Restrictive heart disease
I.Pathophysiology
A.Varices develop annually in 5% to 15% of patients
with cirrhosis, and varices enlarge by 4% to 10% each
year. Each episode of variceal hemorrhage carries a
20% to 30% risk of death.
B.After an acute variceal hemorrhage, bleeding re
solves spontaneously in 50% of patients. Bleeding is
least likely to stop in patients with large varices and a
Child-Pugh class C cirrhotic liver.
II.Management of variceal hemorrhage
A.Primary prophylaxis
1.All patients with cirrhosis should undergo endos
copy to screen for varices every 2 to 3 years.
2.Propranolol (Inderal) and nadolol (Corgard)
reduce portal pressure through beta blockade.
2
Beta-blockade reduces the risk of bleeding by 45%
and bleeding-related death by 50%. The
beta-blocker dose is adjusted to decrease the
resting heart rate by 25% from its baseline, but not
to less than 55 to 60 beats/min.
3.Propranolol (Inderal) is given at 10 to 480 mg
daily, in divided doses, or nadolol (Corgard) 40 to
320 mg daily in a single dose.
B.Treatment of acute hemorrhage
1.Variceal bleeding should be considered in any
patient who presents with significant upper gastroin
testinal bleeding. Signs of cirrhosis may include
spider angiomas, palmar erythema, leukonychia,
clubbing, parotid enlargement, and Dupuytren's
contracture. Jaundice, lower extremity edema and
ascites are indicative of decompensated liver
disease.
2.The severity of the bleeding episode can be
assessed on the basis of orthostatic changes (eg,
resting tachycardia, postural hypotension), which
indicates one-third or more of blood volume loss.
3.Blood should be replaced as soon as possible.
While blood for transfusion is being made available,
intravascular volume should be replenished with
normal saline solution. Once euvolemia is estab
lished, the intravenous infusion should be changed
to solutions with a lower sodium content (5% dex
trose with 1/2 or 1/4 normal saline). Blood should be
transfused to maintain a hematocrit of at least 30%.
Serial hematocrit estimations should be obtained
during continued bleeding.
4.Fresh frozen plasma is administered to patients
who have been given massive transfusions. Each 3
units of PRBC should be accompanied by CaCL2 1
gm IV over 30 min. Clotting factors should be
assessed. Platelet transfusions are reserved for
counts below 50,000/mL in an actively bleeding
patient.
5.If the patient's sensorium is altered because of
hepatic encephalopathy, the risk of aspiration
mandates endotracheal intubation. Placement of a
large-caliber nasogastric tube (22 F or 24 F) permits
tap water lavage for removal of blood and clots in
preparation for endoscopy.
6.Octreotide acetate (Sandostatin) is a synthetic,
analogue of somatostatin, which causes splanchnic
vasoconstriction. Octreotide is the drug of choice in
the pharmacologic management of acute variceal
bleeding. Octreotide infusion should be started with
a loading dose of 50 micrograms, followed by an
infusion of 50 micrograms/hr. Treatment is contin
ued until hemorrhage subsides. Definitive endo
scopic therapy is performed shortly after hemostasis
is achieved.
7.Endoscopic therapy
a.A sclerosant (eg, morrhuate [Scleromate]) is
injected into each varix. Complications include
bleeding ulcers, dysphagia due to strictures, and
pleural effusions.
b.Endoscopic variceal ligation with elastic bands
is an alternative to sclerotherapy because of
fewer complications and similar efficacy.
c.If bleeding persists (or recurs within 48 hours of
the initial episode) despite pharmacologic therapy
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