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Upper
GI Bleeding
The upper
GI tract is considered any location proximal to the
ligament of Treitz (distal duodenum).
The common manifestations are hematemesis or
melena, while only very
brisk UGI bleeding can present with hemodynamic changes (symptoms of
dizziness,
dyspnea or shock) and/or hematochezia.
The age of the pediatric patient is helpful when
determining the
differential diagnosis.
Etiology
The most
common general causes for UGI bleeding
in Western children are traumatic (Mallory-Weiss tear), ulcers of the
stomach
and duodenum, esophagitis, and gastritis, while variceal bleeding is
less
common. Coagulopathies (acquired
or congenital), molecular abnormalities of blood vessel wall structure
(e.g.
Ehlers-Danlos), and macroscopic vessel malformation (AVMs) also
predispose to
bleeding. This framework is
helpful to keep in mind when considering your differential diagnosis.
Most
Common Etiologies by Age:
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Neonate
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Maternal blood
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Gastritis
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Stress, Sepsis, Cow milk
intolerance, Trauma from NG tube
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NEC
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Coagulopathies
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1 month - 1 year
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Substantial Hemorrhage
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Peptic ulcer, Curling
ulcer, Duplication cyst, Foreign body
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Mild hemorrhage
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Reflux esophagitis,
Gastritis
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Stress
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Medication
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ASA, NSAIDs
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Caustic ingestion
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3-5 years
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Peptic ulceration
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Gastritis
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ASA, NSAIDs
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Varices
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Epistaxis
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Mallor-Weiss tear
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5+ years
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Varices
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Peptic ulcer
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Coagulopathies
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ITP, chemotherapy
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Specific
Etiologies in the Newborn:
- Quite
often, the cause of bleeding is not identified and the bleeding ceases
in less than 24 hours.
- Major bleeding may be
the result of hemorrhagic gastritis or stress ulcers caused by a
perinatal insult of hypoxia, sepsis, or lesions of CNS.
- Hemorrhagic disease of
the newborn secondary to vitamin K deficiency.
1.
Consider
if newborn was
not administered vitamin K at birth
4.
Other
coagulopathy,
either hereditary of secondary to liver failure (loss of coagulation
factor
production) or infection (e.g. DIC)
5.
Swallowed
water and
maternal blood can appear as upper GI bleeding. To differentiate
mother's from
baby's blood, perform an alum-precipitated toxoid test (Apt test) -
fetal blood
remains pink, while maternal blood turns yellow brown.
6.
Intolerance
to cows'
milk and soy protein can lead to hematemesis and/or rectal bleeding.
These
patients usually also have elevated WBC with neutrophilia.
7.
Congenital
vascular
anomalies
8.
Extraheptic
portal vein
obstruction leading to varices of the stomach or esophagus occurs as a
result
of omphalitis, secondary to catheterization of the umbilical vein, or
secondary
to a spontaneous inflammatory process of the umbilical blood vessels.
Specific
Etiologies in Infants and Children:
1.
Mallory-Weiss
tear is a
laceration of the posterior wall of the GE junction. The tear follows
forceful
emesis or repeated retching. These have been reported in children as
young as
16 weeks of age. These usually spontaneously resolve.
1.
Likely
with hx of
vomiting followed by hematemesis
- Erosion
of the gastric mucosa may occur acutely after any trauma, burn, shock
or sepsis. This is usually superficial and occurs mainly in the fundus
of the stomach.
- Deeper erosions may
involve the esophagus, stomach, or duodenum, and develop more commonly
after intracranial surgery and head injuries.
- Peptic ulcer disease
can present with abdominal pain with nighttime awakening. In idiopathic
peptic ulcer disease nearly 70% will have family history of ulcer
disease. Gastric ulcers commonly cause hematemesis, and duodenal ulcers
commonly cause melena.
- NSAID-induced gastritis
or ulcers
- Esophagitis from reflux
causing hematemesis is uncommon.
- Bleeding from caustic
agents is usually not massive. Iron ingestions can be associated with
vomiting of blood.
- Foreign body ingestion
is a rare cause of bleeding.
- Polyps, hemangiomas,
and arteriovenous malformations of the esophagus and stomach are very
rare, and even if present, hematemesis is usually not the typical
presentation.
- Adenocarcinoma of the
gastroephageal junction or gastric mucosa is extremely rare in patients
less than 18 years of age, and usually does not present with
hematemesis.
- Intrahepatic
obstruction leading to varices of the stomach and esophagus is
secondary to cirrhosis developing from congenital hepatitis, hepatic
fibrosis, and cystic fibrosis.
- Other uncommon
etiologies: Dieulafoy lesion, aortoesophageal fistula, hereditary
hemorrhagic telangiectasia (Osler-Weber-Rendu), vasculitis, systemic
mastocytosis
History:
The
history can play an important role in determining the
source. Were there preceding
complaints/signs of dyspepsia, dysphagia, abdominal pain, weight loss? What drugs have the patient taken
recently that may contribute to gastritis or coagulopathy?
Personal or family hx of easy bruising
or bleeding? Jaundice or change in
stool color may signify underlying liver dysfunction.
A preceding choking bout may signify foreign body
ingestion. Frequent epistaxis may
indicate a nasopharyngeal source.
Diagnosis:
- Is
bleeding truly present? Red foods/liquids
in the diet can resemble hematemesis. Perform
Gastroccult/Hemoccult test if unclear.
- Consider
naso/oropharyngeal or respiratory sources of bleeding. A careful exam
of the nares and oral pharynx should be done.
- The presence of "coffee
ground emesis” represents blood altered by gastric contents and usually
means that there has been slow bleeding from the region between the
esophagus and the duodenum.
- Perform NG tube
aspirate if significant blood loss estimated (more than teaspoon). In addition to decreasing aspiration risk,
this will aid in visualization via endoscope.
- Other characteristics
of upper GI bleeding are elevated BUN and hyperactive bowel sounds,
although these findings are not sensitive.
- Endoscopy is the
preferred diagnostic modality, and 90% of cases can be diagnosed if
endoscopy performed within the first 24 hours. The most common causes
have been identified as gastritis, esophagitis, duodenal ulcers, and
esophageal varices.
- Abdominal US can assess
portal HTN.
- Angiography can be
performed if endoscopy unsuccessful.
Assessment
of the
patient:
1.
Hemodynamic
stability is
assessed by vital signs, which reflect the
degree of blood loss.
1.
Age-adjusted
increased
heart rate is always the first compensatory mechanism, while increased
capillary refill, orthostatic hypotension, weakness/dizziness, and
syncope are
also signs
2.
Consider
NG lavage if
bleeding is significant (>1 teaspoon)
3.
Labs:
CBC, coags,
BUN/Cr, LFTs
4.
Resuscitate
if
hemodynamically unstable (see below)
Resuscitation:
- Typing
and cross matching of blood should be done to be prepared if necessary.
- Fluid depletion should
be corrected with isotonic fluid (Lactated Ringers), as fast as
necessary to reverse orthostatic hypotension.
1.
If IV
access difficult
to establish, consider intraosseous
3.
Continuous
monitoring of
vital signs. Hct is not a good measure of blood volume during acute
hemorrhage.
4.
If the
bleeding is
assessed to be severe, then the following should be considered:
oxygenation,
foley catheterization of the bladder, central venous line, transfusion
of whole
blood or PRBC, use of pharmacologic agents, intubation and ventilator
support.
Reference:
- Ament ME.
Diagnosis and management of upper gastrointestinal tract bleeding in
the pediatric patient. Peds Review 1990; 12(4): 107-116.
- Case Records of the
Massachusettes General Hospital. A five month old girl with coffee-ground emesis. NEJM Vol. 341
No.21. Nov.18, 1999.
- Squires RH. Gastrointestinal Bleeding. Pediatrics in Review.
1999; 20:95-101.
- Boyle J. GI Bleeding in Infants and
Children Pediatrics in Review. February 2008
- Rodgers BM. Upper
gastrointestinal hemorrhage. Pediatrics in Review. 1999;20(5):171.
- Fox VL.
Gastrointestinal bleeding in infancy and childhood. Gastroenterol Clin
North Am. 2000;29(1):3
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