The upper GI tract is considered any location proximal to the Ligament of Treitz (distal duodenum). The common manifestations are hematemesis or melena, while 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.
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. 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:
a. Maternal blood
i. Stress, Sepsis, Protein Intolerance, Trauma (i.e. NG tube)
One Month - One Year
a. Substantial Hemorrhage
i. Peptic ulcer, Curling ulcer, Duplication cyst, Foreign body
b. Mild Hemorrhage
i. Reflux esophagitis, Gastritis
i. ASA, NSAIDs
d. Caustic Ingestion
Three Years - Five Years
a. Peptic Ulceration
i. ASA, NSAIDs
e. Mallory-Weiss tear
a. Peptic Ulceration
i. ITP, chemotherapy
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. Consider if the newborn was not administered vitamin K at birth.
- Other coagulopathy, either hereditary of secondary to liver failure (loss of coagulation factor production) or infection (e.g. DIC)
- 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.
- Intolerance to cows' milk and soy protein can lead to hematemesis and/or rectal bleeding. These patients usually also have elevated WBC with neutrophilia.
- Congenital vascular anomalies
- 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:
- Likely with hx of vomiting followed by hematemesis
- 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.
- 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
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.
- 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
- Hemodynamic stability is assessed by vital signs, which reflect the degree of blood loss.
- Age-adjusted increased heart rate is always the first compensatory mechanism, while increased capillary refill, orthostatic hypotension, weakness/dizziness, and syncope are also signs
- Consider NG lavage if bleeding is significant (>1 teaspoon)
- Labs: CBC, coags, BUN/Cr, LFTs
- Resuscitate if hemodynamically unstable (see below)
- 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.
- If IV access difficult to establish, consider intraosseous
- Continuous monitoring of vital signs. Hct is not a good measure of blood volume during acute hemorrhage.
- 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.
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