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upper gastrointestinal hemorrhage
Upper gastrointestinal (GI) hemorrhage refers to bleeding proximal to the jejunum (or ligament of Treitz). Mortality may be as high as 10%.
Etiology:
- peptic ulcer* (34%)
- duodenal ulcer
- gastric ulcer
- erosive gastritis (13%), NSAID use, H pylori infection
- stress ulceration
- anticoagulation [3]
- esophageal varices*, gastric varices* (33%)
- due to portal hypertension, cirrhosis [3]
- erosive esophagitis (8%)
- Mallory-Weiss tear (6%)
- hematemesis after heavy alcohol use, hematemesis after weightlifting, bulemia [3]
- angiodysplasia (gastric & duodenal) (<6%)
- pyloric channel ulcer (2%)
- gastric antral vascular ectasia
- neoplasm (5%)
- gastric neoplasm*
- esophageal neoplasm*
- gastrointestinal stromal tumor*
- metastatic tumor to the duodenum
- gastric polyps
- erosive duodenitis (2%)
- Dieulafoy's lesion* (1%)
- Cameron erosion
- anastomotic ulcer
- aortoenteric fistula* (patients with aortic graft surgery)
- hematobilia*
- Menetrier's disease
- Schonlein-Henoch purpura
- Osler-Weber-Rendu syndrome
- celiac disease
- hemosuccus pancreaticus
- idiopathic (13%)
* causes of severe upper GI bleed [3]
Epidemiology:
- more common than lower GI bleed [3]
Clinical manifestations:
1) hematemesis
2) coffee-ground emesis
3) melena
4) infrequently, bright-red-blood per rectum [3]
Laboratory:
1) (see gastrointestinal hemorrhage)
2) serum creatinine, serum urea nitrogen
- BUN/creatinine ratio of > 30 suggests upper GI bleed
3) H. pylori serology or other H. pylori testing if biopsy negative for H pylori
Special laboratory:
1) Glasgow-Batchford score (range 0-23)
- when score = 0, 100% negative predictive value for severe GI bleed & need for hospitalization [3]
2) upper GI endoscopy, esophagogastroduodenoscopy (EGD)
a) after hemodynamic stabilization [3]
b) within 24 hours [5]
c) within 12 hours if esophageal varices suspected [3]
d) routine 2nd look not recommended [3,5]
e) endoscopic coagulation or injection for
- actively bleeding ulcers
- visble vessels
- sentinal clots
f) endoscopic ligation or sclerosis of esophageal varices
g) mechanical (clips) vs thermal hemostasis with similar outcomes [6]
h) biopsy for Helicobacter pylori
3) capsule endoscopy
- repeat esophagogastroduodenoscopy with biopsies & colonoscopy or push enteroscopy indicated prior capsule endoscopy if initial studies were of low quality [3]
Radiology:
- CT angiography for hemodynamically unstable patients with small bowel bleeding [3]
- technetium labeled nuclear scan (scintigraphy) provides the best sensitivity for actively bleeding lesion not detected by upper or lower GI endoscopy or capsule endoscopy [3]
- arteriography
a) failure of EGD to visualize source of bleeding
b) bleeding of > 0.5 mL/min at the time of study
c) arterial angiotherapy
1] vasopressin 0.15-2.0 units/min in selectively catheterized bleeding artery
2] arterial embolization
- selective arterial catheterization
- absorbable gelatin powder (Gelfoam)
- upper GI with barium has no role in initial evaluation of active upper GI bleed
Complications:
- higher mortality than lower GI bleed
- mortality (up to 14%)
- tachycardia (> 100/min), hypotension (systolic BP < 100 mm Hg), age > 60 years, comorbidities associated with increased risk for rebleeding & increased mortality [3]
Management:
1) general recommendations: [8]
a) 2 large caliber IV catheters
b) IV crystalloids: target heart rate < 100/min, systolic BP > 100 mm Hg
c) transfuse patients with hemoglobin <7 g/dL in the absence of shock or symptomatic anemia [9,10,17]; < 8 g/dL [23];
- target 7-9 g/dL [3]
d) perform endoscopy early (within 24 hours) for most patients
- stabilize patients hemodynamically with fluids & erythrocytes prior to endoscopy
- endoscopy within 12 hours if esophageal varices suspected [3]
- endoscopy within 6 hours no better thqn later endoscopy [24]
e) do not delay endoscopy to correct coagulopathies or to administer proton-pump inhibitor (PPI) therapy to downsize lesions
f) if endoscopic treatment fails, percutaneous embolization can be considered as an alternative to surgery
g) bolus- & continuous-infusion PPI for high-risk patients for 3 days after successful endoscopy for high-risk peptic ulcer or adherent clots [3]
- proton pump inhibitor of no benefit for acute peptic ulcer bleeding or other cause of acute upper GI bleed before [11] or after endoscopy [12]
- H2 receptor blockers are not beneficial
h) hospitalize high-risk patients at least 72 hours
- Glasgow-Blatchford score <= 1 predicts low-risk patients [18]
i) discharge low-risk patients soon after endoscopy
- see peptic ulcer to "low risk" criteria
- no benefit of observing for 24 hours in hospital [3]
j) prescribe daily proton pump inhibitor at discharge
k) in patients with peptic ulcers, test for, treat, & eradicate Helicobacter pylori [5,8]
l) nonspecific NSAIDs plus a proton pump inhibitor or a COX2 inhibitor alone associated with bleeding risk; COX-2 inhibitor plus a PPI recommended if NSAID required
m) restart low-dose aspirin for cardiovascular prophylaxis as soon as benefit outweighs bleeding risk
- restarting low-dose aspirin 3-5 days after upper GI bleed reduces 30-day mortality 10-fold in patients with cardiovascular disease, while increasing rebleeding rates only 2-fold [3]
- clopidogrel confers higher risk aspirin plus a proton pump inhibitor [8]
n) restart anticoagulation after resolution of bleeding [3]
m) use prognostic scales to assess risk for rebleeding & death
2) general measures (see gastrointestinal hemorrhage)
a) do not insert nasogastric tube for aspiration to confirm diagnosis [3]
b) also see algorithm for management of GI bleed
3) Minnesota Esophagogastric Tamponade Tube for acute bleeding refractory to other measures (see esophageal varices)
4) esophagogastroduodenoscopy (EGD) see above
a) stabilize patients hemodynamically with fluids & erythrocytes prior to endoscopy
b) IV bolus of proton pump inhibitor before endoscopy, followed by infusion after EGD [2, 5]
c) octreotide 50 ug IV bolus, then 25-50 ug/hour IV drip (superior to vasopressin)
- for use in conjunction with EGD
- octreotide alone does not improve outcome of non- esophageal varices upper GI bleed [3]
d) H2-receptor antagonists are NOT effective in stopping active UGI bleed
5) therapy for specific lesions
a) peptic ulcer:
- continue proton pump inhibitor only if peptic ulcer is the source of bleeding [3]
b) esophageal varices
c) Mallory-Weiss tear
d) aortoenteric fistula
e) angiodysplasia
6) empiric prophylactic therapy with broad-spectrum antibiotics is indicated in patients with cirrhosis [3]
7) prognosis
- patients taking NSAIDs at the time of hemorrhage
- switching to COX-2 inhibitor or adding omeprazole to NSAID results in similar rebleed rate = 5% [4]
8) prophylaxis
- proton pump inhibitor reduces risk of GI bleed associated with anti-platelet agent [7]
Related
aortoenteric fistula; aortoduodenal fistula
comorbid conditions that increase mortality of upper GI bleed
esophageal varices
melena
Minnesota esophagogastric tamponade tube
octreotide (Sandostatin)
peptic ulcer disease (PUD)
stress ulceration
upper gastrointestinal (GI) endoscopy; esophagogastroduodenoscopy (EGD)
Specific
Dieulafoy's lesion
Esophageal Hemorrhage
hematemesis
hemosuccus pancreaticus
Mallory-Weiss tear
small intestinal hemorrhage
General
gastrointestinal hemorrhage
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