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Gastrointestinal (GI) bleeding can be occult (not readily visible)
or overt. This chapter will focus on overt GI bleeding that is acute
or subacute. Separate chapters (e.g., Chapters 13 and 16) will cover
aspects of chronic or occult GI blood loss in more detail. The source
of visible blood in stool or vomit may be from the upper GI (UGI)
tract, lower GI (LGI) tract, extraintestinal (e.g., swallowed blood
from a nosebleed), or an exogenous substance (e.g., red-colored
foods). Regardless of the source, obvious blood from the GI tract
tends to be a very distressing problem for patients and their families
that quickly bring them to medical attention. GI bleeding can be
serious and life threatening. Thankfully, serious GI bleeding is
uncommon in the pediatric age group and the problem often resolves
without specific intervention. The key to approaching a patient
with GI bleeding is a rapid assessment of the severity of bleeding
and hemodynamic status of the child. Given the nature of the content,
this chapter will focus on differential diagnosis, diagnostic approach,
and treatment based on clinical presentation: hematemesis or coffee
ground emesis, hematochezia, and melena.
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UGI bleeding is defined as a source
proximal to the ligament of Treitz (where the duodenum meets the jejunum). LGI bleeding is from a source distal
to the ligament of Treitz (see Figure 6–1).
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Hematemesis refers to vomiting bright
red blood, usually indicating fairly brisk bleeding. Coffee ground emesis usually occurs
with slower bleeding and coagulation of blood after exposure to
gastric acid. Melena refers to stools
that are jet black and tarry, and often have a distinctive foul
odor. Melena occurs when intestinal bacteria have time to oxidize
heme to hematin, usually indicating a relatively slow bleed proximal
to the cecum. Hematochezia refers to
bright red or maroon blood in stools, usually from a colonic bleed
but can occur with high-volume UGI bleeding with rapid transit time.
Bleeding, if severe, can also become symptomatic (dizziness, syncope,
pallor, tachycardia, and hypotension) before the passage of a bloody stool.
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The pathogenesis of true GI bleeding varies greatly by etiology.
A few broad categories of pathology underlie most causes of bleeding.
Vascular anomalies (e.g., arteriovenous malformations or hemangiomas),
collateral vessel formation (e.g., esophageal varices), or erosion
of the intestinal mucosa (e.g., inflammation, ulceration, sloughing,
and perforation) bring blood vessels in close proximity to the intestinal
lumen and may make them prone to rupture. Acute or chronic vascular congestion,
thrombosis, and/or ischemia may also lead to bleeding.
Any illness (most often viral gastroenteritis) that causes persistent
retching and vomiting can cause bleeding from mucosal tears in the
lower esophagus and upper stomach (Mallory–Weiss tears)
and/or broken capillaries in the gastric mucosa (emetogenic
gastropathy).