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Module 13 • GI/Endocrine
Hepatic Failure, GI & Endocrine Emergencies
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Hepatic Failure, GI & Endocrine Emergencies
Stephanie N. Bass ~3 min read Module 13 of 20
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Hepatic Failure/GI/Endocrine Emergencies

5

Mortality at 28 days after hospital admission for non-variceal hemorrhage is about 13%, whereas

mortality after variceal hemorrhage is about 20%. Mortality rates after both UGIB classifications seem

to be decreasing with advances in care.

B.Etiologies
1

Nonvariceal hemorrhage

Gastric and/or duodenal ulcer

Most common cause of severe cases of UGIB, accounting for 47% of all UGIB episodes

ii.

Bleeding is more common in the setting of anticoagulant use and is typically self-limited.

iii.

Most commonly caused by an H. pylori infection, but may also be secondary to NSAIDs,

hyperacidity (e.g., in Zollinger-Ellison syndrome), or stress-related mucosal disease (stress-

related mucosal damage is discussed in detail in the Supportive and Preventive Medicine

chapter)

Esophagitis

Noted in around 13% of patients with UGIB

ii.

Risk factors include history of gastroesophageal reflux disease, medication use (e.g., NSAIDs,

oral bisphosphonates, tetracycline), and infection (e.g., Candida, herpes simplex virus).

iii.

Commonly presents with hematemesis and less commonly associated with melena

iv.

Lower rebleeding and mortality rate than other sources of UGIB

Gastroduodenal erosions (erosive gastritis/duodenitis): Defects of the gastric/duodenal mucosal

layer that lead to inflammation without ulcer formation

Causes are similar to those for gastric/duodenal ulcers. Additional risk factors include excessive

alcohol consumption, radiation injury, bariatric surgery, and chronic bile reflux.

ii.

Bleeding is more common in the setting of anticoagulant use and is typically self-limited.

iii.

May progress to ulcer formation

d.Mallory-Weiss tear: A longitudinal mucosal laceration in the distal esophagus and proximal

stomach (an intramural dissection)

A sudden increase in intra-abdominal pressure leads to forceful distention of the

gastroesophageal junction and a resultant mucosal tear.

ii.

Typically caused by forceful vomiting

Less common causes: Vascular malformation, malignant formations, aortoenteric fistulas, gastric

antral vascular ectasia, and prolapse gastropathy

2Variceal hemorrhage

Relatively few severe cases of UGIB are secondary to variceal hemorrhage (< 5%), but the incidence

is higher in patients with cirrhosis.

Mortality rate is around 20% at 6 weeks.

Portal hypertension caused by the obstruction of venous blood flow through the cirrhotic liver leads

to increased pressure in the portal vein and causes the redirection of blood flow to other areas of

the body.

d.Varices may be present in any portion of the GI tract, but they are most common in the esophagus

and stomach.

Gastroesophageal varices are present in about 50% of patients with cirrhosis. About 12% of patients

with varices will develop variceal hemorrhage within 1 year of diagnosis, and the recurrence rate

for variceal hemorrhage within 1 year is about 60%.

C.Initial Assessment and Risk Stratification
1

Most patients (50%) present with both melena and hematemesis; 30% have hematemesis (either red

blood or β€œcoffee-ground” emesis) alone, and 20% have melena alone.

2Hematochezia (bright red blood per rectum) may also be present (in about 5% of patients), which may

represent a swift UGIB (about 1 L of blood is needed in the stomach to cause hematochezia, whereas

only 50–100 mL is needed to cause melena).

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