UPPER GI BLEED: HISTORY, PE, PATHOPHYSIOLOGY, DIAGNOSTICS AND

TREATMENT

History:

Physical examination:
Measurement of the heart rate and blood pressure best way to initially assess a
patient with GIB.
Clinically significant bleeding leads to postural changes in heart rate or blood
pressure, tachycardia, and, finally, recumbent hypotension.
Hemoglobin does not fall immediately with acute GIB, due to proportionate
reductions in plasma and red cell volumes. It may be normal or only minimally
decreased at the initial presentation of a severe bleeding episode.
As extravascular fluid enters the vascular space to restore volume, the hemoglobin
falls, but this process may take up to 72 hours.
Transfusion is recommended when the hemoglobin drops below 7 g/dL,
decreasing rebleeding and death in acute UGIB compared with a transfusion
threshold of 9 g/dL.
Patients with slow, chronic GIB may have very low hemoglobin values despite
normal blood pressure and heart rate.
With the development of iron-deficiency anemia, the mean corpuscular volume
will be low and red blood cell distribution width will increase.
Baseline characteristics predictive of rebleeding and death include:
o hemodynamic compromise (tachycardia or hypotension),
o increasing age
o comorbidities.

PPI infusion may be considered at presentation: it decreases high-risk ulcer

stigmata (e.g., active bleeding) and need for endoscopic therapy but does not
improve clinical outcomes such as further bleeding, surgery, or death.
Cirrhotic patients presenting with UGIB should be placed on antibiotics (e.g.,
quinolone, ceftriaxone) and started on a vasoactive medication (octreotide,
terlipressin, soma- tostatin, vapreotide) upon presentation, even before endoscopy.
Antibiotics decrease bacterial infections, rebleeding, and mortality in this
population, and vasoactive medications appear to improve control of bleeding in
the first 12 h after presentation.

Diagnostics:
Upper endoscopy should be performed within 24 h in most patients with UGIB.
Patients at higher risk (e.g., hemodynamic instability, cirrhosis) may benefit from
more urgent endoscopy within 12 h.
Early endoscopy is also beneficial in low-risk patients for management decisions.
 Patients with major bleeding and high- risk endoscopic findings (e.g., varices,
ulcers with active bleeding or a visible vessel) benefit from endoscopic
hemostatic therapy, whereas patients with low-risk lesions (e.g., clean-based
ulcers, nonbleeding Mallory-Weiss tears, erosive or hemorrhagic gastropa- thy)
who have stable vital signs and hemoglobin and no other medi- cal problems can
be discharged home.

DIFFERENTIATION OF UGIB FROM LGIB

Hematemesis indicates an upper GI source of bleeding (above the ligament of

Treitz).
Melena indicates blood has been present in the GI tract for at least 14 h, and as
long as 35 days.
The more proximal the bleeding site, the more likely melena will occur.
Hematochezia usually represents a lower GI source of bleeding, although an
upper GI lesion may bleed so briskly that blood transits the bowel before melena
develops.
When hematochezia is the presenting symptom of UGIB, it is associated with
hemodynamic instability and dropping hemoglobin.
Bleeding lesions of the small bowel may present as melena or hematochezia.
Other clues to UGIB include hyperactive bowel sounds and an elevated blood
urea nitrogen (due to volume depletion and blood proteins absorbed in the small
intestine).
A nonbloody nasogastric aspirate may be seen in up to ~18% of patients with
UGIB, usually from a duodenal source.

SOURCES OF GASTROINTESTINAL BLEEDING

Peptic ulcers are the most common cause of UGIB, accounting for 50% of
cases.
Mallory-Weiss tears account for ~510% of cases.
The proportion of patients bleeding from varices varies widely from ~540%,
depending on the population.
Hemorrhagic or erosive gastropathy (e.g., due to nonsteroidal anti-inflammatory
drugs [NSAIDs] or alcohol) and erosive esophagitis often cause mild UGIB, but
major bleeding is rare.

PEPTIC ULCERS

Definition:
One-third of patients with active bleeding or a nonbleeding visible vessel have
further bleeding that requires urgent surgery if they are treated conservatively.
These patients benefit from endoscopic therapy with bipolar electrocoagulation,
heater probe, injection therapy (e.g., absolute alcohol, 1:10,000 epinephrine),
and/or clips with reductions in bleeding, hospital stay, mortality, and costs.
In contrast, patients with clean-based ulcers have rates of recurrent bleeding
approaching zero.
Patients without clean-based ulcers usually remain in the hospital for 3 days
because most episodes of recurrent bleeding occur within 3 days.
Approximately one- third of patients with bleeding ulcers will rebleed within the
next 12 years if no preventive strategies are employed.
Prevention of recurrent bleeding focuses on the three main factors in ulcer
pathogenesis:
o Helicobacter pylori
o NSAIDs
 o Acid
Eradication of H. pylori in patients with bleeding ulcers decreases rates of
rebleeding to <5%.
If a bleeding ulcer develops in a patient taking NSAIDs, the NSAIDs should be
discontinued. If NSAIDs must be given, a cyclooxygenase 2 (COX-2) selective
inhibitor (coxib) plus a PPI should be used.
Patients with established cardiovascular disease who develop bleeding ulcers
while taking low-dose aspirin should restart aspirin as soon as possible after their
bleeding episode (17 days).
Treatment:

MALLORY-WEISS TEARS

Definition:
The classic history is vomiting, retching, or coughing preceding hematemesis,
especially in an alcoholic patient.
Bleeding from these tears, which are usually on the gastric side of the
gastroesophageal junction, stops spontaneously in 8090% of patients and recurs
in only 010%.
Endoscopic therapy is indicated for actively bleeding Mallory-Weiss tears.
Angiographic therapy with embolization and operative therapy with oversewing
of the tear are rarely required.
Treatment:

ESOPHAGEAL VARICES

Definition:
Patients with variceal hemorrhage have poorer outcomes than patients with other
sources of UGIB.
Urgent endoscopy within 12 h is recommended in cirrhotics with UGIB, and if
esophageal varices are present, endoscopic ligation is performed and an IV
vasoactive medication (e.g., octreotide 50 g bolus and 50 g/h infusion) is given
for 25 days.
Combination endoscopic and medical therapy appears to be superior to either
therapy alone in decreasing rebleeding. In patients with advanced liver disease
(e.g., Child-Pugh class C with score 1013), a transjugular intrahepatic
portosystemic shunt (TIPS) should be strongly considered within the first 12
days of hospitalization because randomized trials show significant decreases in
rebleeding and mortality compared with standard endoscopic and medical
therapy.
Over the long term, treatment with nonselective beta blockers plus endoscopic
ligation is recommended because the combination of endoscopic and medical
therapy is more effective than either alone in reduction of recurrent esophageal
variceal bleeding.
In patients who have persistent or recurrent bleeding despite endoscopic and
 medical therapy, TIPS is recommended.
Decompressive surgery (e.g., distal splenorenal shunt) may be considered instead
of TIPS in patients with well-compensated cirrhosis.
Portal hypertension is also responsible for bleeding from gastric varices, varices
in the small and large intestine, and portal hypertensive gastropathy and
enterocolopathy.
Bleeding gastric varices due to cirrhosis are treated with endoscopic injection of
tissue adhesive (e.g., n-butyl cyanoacrylate), if available; if not, TIPS is
performed.
Treatment:

HEMORRHAGIC AND EROSIVE GASTROPATHY

Hemorrhagic and erosive gastropathy, often labeled gastritis, refers to

endoscopically visualized subepithelial hemorrhages and erosions.
These are mucosal lesions and do not cause major bleeding due to the absence of
arteries and veins in the mucosa.
Erosions develop in various clinical settings, the most important of which are
NSAID use, alcohol intake, and stress.
Half of patients who chronically ingest NSAIDs have erosions, whereas up to
20% of actively drinking alcoholic patients with symptoms of UGIB have
evidence of subepithelial hemorrhages or erosions.
Stress-related gastric mucosal injury occurs only in extremely sick patients, such
as those who have experienced serious trauma, major surgery, burns covering
more than one-third of the body surface area.
Severe bleeding should not develop unless ulceration occurs. The mortality rate in
these patients is quite high because of their serious underlying illnesses.
Treatment:

OTHER CAUSES

Other less frequent causes of UGIB include erosive duodenitis, neoplasms,

aortoenteric fistulas, vascular lesions (includ- ing hereditary hemorrhagic
telangiectasias [Osler-Weber-Rendu] and gastric antral vascular ectasia
[watermelon stomach]), Dieulafoys lesion (in which an aberrant vessel in the
mucosa bleeds from a pin- point mucosal defect), prolapse gastropathy (prolapse
of proximal stomach into esophagus with retching, especially in alcoholics), and
hemobilia or hemosuccus pancreaticus (bleeding from the bile duct or pancreatic
duct).

Small-Intestinal Sources of Bleeding

Small-intestinal sources of bleeding (bleeding from sites beyond the reach of the
standard upper endoscope) are often difficult to diagnose and are responsible for
the majority of cases of obscure GIB.
 Fortunately, small-intestinal bleeding is uncommon.
The most common causes in adults are vascular ectasias, tumors (e.g., GI stromal
tumor, carcinoid, adenocarcinoma, lymphoma, metastases), and NSAID-induced
erosions and ulcers.
Other less common causes in adults include Crohns disease, infec- tion,
ischemia, vasculitis, small-bowel varices, diverticula, Meckels diverticulum,
duplication cysts, and intussusception.
Meckels diverticulum is the most common cause of significant LGIB in children,
decreasing in frequency as a cause of bleeding with age.
Vascular ectasias should be treated with endoscopic therapy if possible.
Treatment: