Good day Doctors, This is PGI Rivera and to
The most important cause of
continue. Gastrointestinal bleeding may be
categorized by the source or the site of the
bleeding.
Generally, this may be classified into 3 namely
upper gastrointestinal sources, small intestinal
sources, and colonic sources.
Upper gastrointestinal causes include Peptic ulcers,
the most common cause of UGIB which account for
~50% of UGIB hospitalizations (this will be
discussed further later), // Mallory Weiss Tears
accounting for ~2-10% of UGIB hospitalizations
presenting with classic history of 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 ~80-90% of patients and recurs
only in 0-10%. // On the other hand, the proportion
of UGIB hospitalizations due to varices varies
widely from ~2-40%, depending on the population.
Patients with variceal hemorrhage often have
poorer outcomes than patients with other sources
of UGIB. Approximately 5–15% of cirrhotics per
year develop varices, and it is estimated that the
majority of patients with cirrhosis will develop
varices over their lifetimes. Furthermore, it is
anticipated that roughly one-third of patients with
varices will develop bleeding. Several factors
predict the risk of bleeding, including the severity
of cirrhosis (Child-Pugh class, Model for End-Stage
Liver Disease [MELD] score); the height of wedged-
hepatic vein pressure; the size of the varix; the
location of the varix; and certain endoscopic
stigmata, including red wale signs, hematocystic
spots, diffuse erythema, bluish color, cherry red
spots, or white-nipple spots. Patients with tense
ascites are also at increased risk for bleeding from
varices. // Lastly, erosions are endoscopically
visualized breaks that are confined to the mucosa
and do not cause major bleeding because arteries
and veins are not present in the mucosa. Erosions
in the esophagus, stomach, or duodenum
commonly cause mild UGIB, with erosive gastritis
and duodenitis accounting for ~10-15% and erosive
esophagitis (primarily due to gastroesophageal
reflux disease) accounting for ~1-10% of UGIB
hospitalizations.
gastric and duodenal erosions is NSAID use: where
~50% of patients who chronically ingest NSAIDs
may have gastric erosions. Other potential causes
include alcohol intake, H. pylori infection, and
stress related mucosal injury. // Less common
causes of UGIB include neoplasms, vascular
ectasias (including hereditary hemorrhagic
telangiectasias or Osler Weber Rendu and gastric
antral vascular ectasia, Dieulafoy’s lesion in which
an aberrant vessel in the mucosa bleeds from a
pinpoint mucosal defect, prolapse gastropathy
(prolapse of proximal stomach into esophagus with
retching, especially in alcoholics, aortoenteric
fistulas, and hemobilia or hemosuccus pancreatus
or bleeding from the bile duct or pancreatic duct.
Focusing on the most common cause of UGIB,
Peptic ulcers account for ~50% of UGIB
hospitalizations. A peptic ulcer is defined as
disruption of the mucosal integrity of the stomach
and/or duodenum leading to a local defect or
excavation due to active inflammation. Although
burning epigastric pain exacerbated by fasting and
improved with meals is a symptom complex
associated with peptic ulcer disease, it is now clear
that >90% patients with this symptom complex
(dyspepsia) do not have ulcers and that the
majority of patients with peptic ulcers may be
asymptomatic. Ulcers occur within the stomach
and/or duodenum and are often chronic in nature.
Patients without a source of GIB identified on
upper endoscopy and colonoscopy were previously
labeled as having obscure GIB but with the advent
of improved diagnostic modalities, ~75% of GIB
previously labeled as obscure is now estimated to
originate in the small intestine beyond the extent
of a standard upper endoscopic exam. Small
intestinal GIB may account for ~5% of GIB cases.
The most common causes in adults include vascular
ectasias, neoplasm like gastrointestinal stromal
tumor, carcinoid, adenocarcinoma, lymphoma,
metastases, and NSAID induced erosions and
ulcers. Other less common causes of small
intestinal GIB include Crohn’s disease, infection,
ischemia, vasculitis, small bowel varices,
diverticular, intussusception, Dieulafoy’s lesions,
aortoenteric fistulas, and duplication cysts.
 right colon; chronic or occult bleeding is not
Lastly, for the colonic causes. characteristic. Patients at increased risk for
bleeding tend to be hypertensive, have
Hemorrhoids are probably the most common cause atherosclerosis, and regularly use antithrombotic
of LGIB; anal fissures also cause minor bleeding and therapy and nonsteroidal anti-inflammatory
pain. If these local anal processes, which rarely agents. Additional risk factors include obesity and a
require hospitalization, are excluded, the most history of diabetes mellitus. Most bleeds are self-
common cause of LGIB in adults would be limited and stop spontaneously with bowel rest.
diverticulosis. Other causes include vascular The lifetime risk of rebleeding is 25%
ectasias (especially in the proximal colon of
patients >70 years), neoplasms (primarily
adenocarcinoma), colitis (ischemic, infectious,
Crohn’s or ulcerative colitis, NSAID induced colitis
or ulcers), postpolypectomy bleeding, and radiation
proctopathy. Rarer causes include solitary rectal
ulcer syndrome, varices (most commonly rectal),
lymphoid nodular hyperplasia, vasculitis, trauma,
and aortocolic fistulas.

Focusing on the most common ones we have

Hemorrhoids: Hemorrhoidal cushions are a normal

part of the anal canal. The vascular structures
contained within aid in continence by preventing
damage to the sphincter muscle. Engorgement and
straining lead to prolapse of this tissue into the
anal canal. Over time, the anatomic support system
of the hemorrhoidal complex weakens, exposing
this tissue to the outside of the anal canal where it
is susceptible to injury. Patients with hemorrhoidal
disease commonly present in the clinics for two
reasons: bleeding and protrusion. Pain is less
common than with fissures and if present, is
described as dull ache from engorgement of the
hemorrhoidal tissue. Severe pain may indicate a
thrombosed hemorrhoid. Hemorrhoidal bleeding is
described as painless bright red blood seen either
in the toilet or upon wiping. Occasional patients
can present with significant bleeding, which may be
a cause of anemia; however, the presence of a
colonic neoplasm must be ruled out in anemic
patients.

Hemorrhage from a colonic diverticulum is the

most common cause of hematochezia in patients
>60 years, yet only 20% of patients with
diverticulosis will have gastrointestinal bleeding.
Diverticular bleeding is abrupt in onset, usually
painless, sometimes massive, and often from the