Pediatric Gastrointestinal Bleeding

Age-specific etiologies for GI bleeding are discussed below for the following groups:

• Neonates

• Children aged 1 month to 1 year

• Children aged 1-2 years

• Children older than 2 years

Neonates

Anal fissures are the most common cause of GI bleeding in infants. Typically, bright red blood streaks the stool or causes spots of blood in the diaper. The cause is a tear at the mucocutaneous line, most commonly located dorsally in the midline.

Other common causes of apparent neonatal GI bleeds include bacterial enteritis, milk protein allergies, intussusception, swallowed maternal blood, and lymphonodular hyperplasia. Milk or soy enterocolitis, or allergic colitis, is a cause for vomiting with blood staining after the introduction of these food products into the diet.

Erosions of the esophageal, gastric, and duodenal mucosa are also a frequent cause for true neonatal GI bleeding. Presumably, this damage is caused by the dramatic increase in gastric acid secretion and the laxity of gastric sphincters in infants.

Maternal stress in the third trimester has been proposed to increase maternal gastrin secretion and enhance infantile peptic ulcer formation.

Neonatal peptic ulcer disease has not been associated with mode of feeding or hyperalimentation.

Some drugs are implicated in neonatal GI bleeds. These include NSAIDs, heparin, and tolazoline, which are used for persistent fetal circulation.

Indomethacin, used for patent ductus arteriosus in neonates, may cause GI bleeding through intestinal vasoconstriction and platelet dysfunction.

Maternal medications can cross the placenta and cause problems in the developing fetus and in the neonate on delivery. Aspirin, cephalothin, and phenobarbital are well-known causes of coagulation abnormalities in neonates.

Stress gastritis occurs in up to 20% of patients cared for in neonatal intensive care units (ICUs). Prematurity, neonatal distress, and mechanical ventilation are all associated with stress gastritis.

Stress ulcers in newborns are associated with dexamethasone, which can be used for fetal lung maturation.

Rarer causes of GI bleeding in a neonate include volvulus, coagulopathies, arteriovenous malformations, necrotizing enterocolitis (NEC; especially in preterm infants), Hirschsprung enterocolitis, and Meckel diverticulitis.

Hemorrhagic disease of the newborn is a self-limited bleeding disorder resulting from a deficiency in vitamin K–dependent coagulation factors. levels of clotting factors II, VII, IX, and X decline rapidly after birth, reaching their nadir at 48-72 hours of life. In 0.25%-0.5% of neonates, severe hemorrhage may result.

Upper gastrointestinal bleeding in children aged 1 month to 1 year

Peptic esophagitis caused by gastroesophageal reflux (GER) is a common cause of bleeding in this age group.

Gastritis is primary or secondary in etiology. Primary gastritis is associated with Helicobacter pylori infection and is the most common cause of gastritis in children. Other causes of primary gastritis include steroidal and nonsteroidal anti-inflammatory drug (NSAID) use, Zollinger-Ellison syndrome, and Crohn disease.

Secondary gastritis occurs in association with severe systemic illnesses that result in mucosal ischemia and produce diffuse erosive and hemorrhagic gastric mucosa.

Lower gastrointestinal tract bleeding in children aged 1 month to 1 year

Anal fissures produce bright red blood that streaks the stool or causes spots of blood in the diaper. The cause is a tear at the mucocutaneous line, most commonly located dorsally in the midline. (In older children, as in adults, refractory anal fissures or those located off the midline should raise suspicion for inflammatory bowel disease [IBD], specifically Crohn disease.)

Evidence is emerging that IBD presenting in children less than 2 years of age may have significant differences from IBD presenting in older aged children.[1]

Intussusception is a cause of lower GI bleeding in infants.

Gangrenous bowel is another, less common cause of lower GI bleeding. Causes include malrotation with volvulus, omphalomesenteric remnant with volvulus, internal hernia with strangulation, segmental small-bowel volvulus, and, rarely, sigmoid volvulus.

Milk protein allergy causes a colitis that may be associated with occult or gross lower GI bleeding. It is a common allergy observed in infancy and is caused by an adverse immune reaction to cow's milk.

Upper gastrointestinal tract bleeding in children aged 1-2 years

In children older than 1 year, peptic ulcer disease is a common cause of hematemesis. The etiologies, which include NSAID use, are similar to those mentioned in the above discussion of gastritis.

When an ulcer not associated with H pylori infection is diagnosed, a fasting plasma gastrin level is measured to exclude Zollinger-Ellison syndrome.

Most of the peptic ulcers occurring in children of this age range are secondary to other systemic diseases, such as burns (Curling ulcer), head trauma (Cushing ulcer), malignancy, or sepsis.

Lower gastrointestinal tract bleeding in children aged 1-2 years

Most polyps in persons of this age group are the juvenile type and are located throughout the colon. These are benign hamartomas and usually require no treatment, because they autoamputate. (A juvenile polyp is seen below.)

Meckel diverticulum (see the images below) is often summarized by clinicians by "The Rule of Twos": it occurs in 2% of the population, it usually presents prior to 2 years of age, it usually is located within 2 feet of the ileocecal valve, is 2 inches in length, and has 2 types of heterotrophic mucosa. The etiology of GI bleeding due to Meckel diverticulum is ileal ulceration caused by acid secretion from the ectopic gastric mucosa. Erosion into small arterioles leads to painless, brisk rectal bleeding. The site of ulceration is generally at the base of the diverticulum where the ectopic mucosa and the normal ileum join. More rarely, the ulcer appears distally in the ileum.

Upper gastrointestinal tract bleeding in children older than age 2 years

Esophageal varices result can from portal hypertension, regardless of the age group. The increased resistance to blood flow through the portal system is due to prehepatic, intrahepatic, and suprahepatic obstruction, but the most common causes of portal hypertension in children include portal vein thrombosis (prehepatic) and biliary atresia (intrahepatic).

The most common causes of upper GI bleeding in children older than 12 years are duodenal ulcers, esophagitis, gastritis, and Mallory-Weiss tears.

Lower gastrointestinal tract bleeding in children older than age 2 years

A common cause of lower GI bleeding in children older than 2 years is juvenile polyps; this remains true until the patients are teenagers.

Inflammatory bowel disease (IBD) also becomes a common cause of GI bleeding in this age group. Approximately 10% of all cases of IBD have a pediatric onset.[2] Bleeding is less common in individuals with Crohn disease than in persons with ulcerative colitis, but both may have bloody diarrhea as part of the clinical scenario. These children generally have the diagnosis of IBD well established before acute or chronic bleeding necessitates intervention.

Infectious diarrhea is suspected when lower GI bleeding occurs in association with profuse diarrhea. Recent antibiotic use raises suspicion for antibiotic-associated colitis and Clostridium difficile colitis. Two common pathogens producing infectious diarrhea are Escherichia coli and species of Shigella.

Vascular lesions include a wide variety of malformations, including hemangiomas, arteriovenous malformations, and vasculitis.

Summary

The causes of upper and lower gastrointestinal bleeding, according to age group, are summarized in the table below.

Table. Common Sources of Gastrointestinal Bleeding in Pediatrics (Open Table in a new window)

 

Severe GI bleeds are rare in the general pediatric population and are therefore not well documented.

In the pediatric ICU population, 6-20% of the general pediatric population has upper GI bleeds. The incidence of lower GI bleeding has not been well established.

In one report, rectal bleeding alone accounted for 0.3% of the chief complaints in more than 40,000 patients presenting to a major urban emergency department.

An investigation into the epidemiology of GI bleeding in hospitalized children in the United States reported that there were 23,383 pediatric discharges with a diagnosis of GI bleeding accounting for 0.5% of all discharges. Children with a GI bleeding were more likely to be male (54.5% vs. 45.8%), and older (children ≥11 years; 50.8% vs. 38.7%). Children 11-15 years of age had the highest incidence of GI bleeding (84.2 per 10,000 discharges) and children less than 1 year of age the lowest (24.4 per 10,000 discharges). The highest incidence of GI bleeding was attributable to cases coded as blood in stool (17.6 per 10,000 discharges) followed by hematemesis (11.2 per 10,000 discharges). The highest mortality rates associated with GI bleeding were observed in cases with intestinal perforation (8.7%) and esophageal perforation (8.4%).[3]

Since most patients with GI bleeding are not hospitalized, emergency department (ED) visits may provide more insight into epidemiology of GI bleeding. A recent report used ICD-9-CM codes for GI Bleeding to extract data from a large United States database. Between 2006-2011, a total of 437,283 ED visits were coded for GI Bleeding. The greatest number of visits occurred in patients 15-19 years of age (39.2%); the second greatest number of visits occurred in children less than five years of age (38.2%).[4]

A complete history can often identify a presumptive GI bleeding source and direct an efficient workup. For example, NEC in most neonates is diagnosed based on history and clinical presentation.

Ask age- and etiology-specific questions. Ask about acuteness or chronicity of bleeding, color and quantity of the blood in stools or emesis, antecedent symptoms, history of straining, abdominal pain, and trauma.

Melena, rather than bright red blood per rectum, is usually a sign of bleeding that comes from a source proximal to the ligament of Treitz. However, massive upper GI bleeding can produce bright red blood per rectum if GI transit time is rapid.

Blood mixed in stool or dark red blood implies a proximal source with some degree of digestion of the blood.

Intestinal malrotation is suspected with the sudden onset of melena in combination with bilious emesis in a previously healthy, nondistended baby.

For complaints of bloody stool, make sure to elicit a history of foods consumed or drugs used that may give a stool bloody appearance. This list includes certain antibiotics, iron supplements, red licorice, chocolate, Kool-Aid, flavored gelatin, or bismuth-containing products (eg, Pepto-Bismol).

A history of vomiting, diarrhea, fever, ill contacts, or travel suggests an infectious etiology.

Bloody diarrhea and signs of obstruction suggest volvulus, intussusception, or necrotizing enterocolitis, particularly in premature infants. Acute bloody diarrhea should be considered a medical emergency.[5]

Recurrent or forceful vomiting is associated with Mallory-Weiss tears.

Familial history or NSAID use may suggest ulcer disease.

Ingested substances, such as NSAIDs, tetracyclines, steroids, caustics, and foreign bodies, can irritate the gastric mucosa enough to cause blood to be mixed with the vomitus.[6]

Ask questions that may reveal underlying, but as yet undiagnosed, organ dysfunction.

Recent jaundice, easy bruising, and changes in stool color may signal liver disease.

Other evidence of coagulation abnormalities elicited from the history may also point to disorders of the kidney or reticuloendothelial system.

The rest of this section provides an age-specific discussion of patient history.

Neonates

Milk or soy enterocolitis, or allergic colitis, is a cause for vomiting with blood staining after the introduction of these food products into the diet.

Some drugs are implicated in neonatal GI bleeds. These include NSAIDs, heparin, and tolazoline, which are used for persistent fetal circulation.

Indomethacin, which is used for patent ductus arteriosus in neonates, may cause GI bleeding through intestinal vasoconstriction and platelet dysfunction.

Maternal medications can cross the placenta and cause problems in the developing fetus and neonate on delivery. Aspirin, cephalothin, and phenobarbital are well-known causes of coagulation abnormalities in neonates.

Prematurity, neonatal distress, and mechanical ventilation are all associated with stress gastritis.

Lower gastrointestinal tract bleeding in children aged 1 month to 1 year

Episodic abdominal pain that is cramping in nature, vomiting, and currant jelly stools are findings in children with intussusception.

In milk protein allergy, the child displays, in addition to bleeding, such symptoms as fussiness and increased frequency of bowel movements; frank diarrhea is atypical.

Upper gastrointestinal tract bleeding in children aged 1-2 years

NSAID use is one of the factors in the development of peptic ulcer disease in children older than 1 year. However, most of the ulcers occurring in children aged 1-2 years are secondary to systemic diseases, such as burns (Curling ulcer), head trauma (Cushing ulcer), malignancy, or sepsis.

Lower gastrointestinal tract bleeding in children aged 1-2 years

Children with polyps are found to have painless bleeding per rectum, which often streaks the stool with fresh blood.

Lower gastrointestinal tract bleeding in children older than age 2 years

Bleeding is less common in individuals with Crohn disease than in those with ulcerative colitis, but persons with either disease may have bloody diarrhea as part of the clinical scenario. These children generally have the diagnosis of IBD well established before acute or chronic bleeding necessitates intervention.

Infectious diarrhea is suspected when lower GI bleeding occurs in association with profuse diarrhea. Recent antibiotic use raises suspicion for antibiotic-associated colitis and Clostridium difficile colitis.

Look for signs of shock, and document findings such as heart rate, blood pressure, capillary refill, and orthostatic changes.[7]

During examination of the head, ears, eyes, nose, and throat, look for causes such as epistaxis, nasal polyps, and oropharyngeal erosions from caustics and other ingestions.

Examine abdominal surgical scars and elicit the reason for the surgery.

Specifically include bowel-sound frequency in the abdominal examination. Hyperactive bowel sounds are more common in upper GI bleeding.

Abdominal tenderness, with or without a mass, raises the suspicion of intussusception or ischemia.

Hepatomegaly, splenomegaly, jaundice, or caput medusa suggests liver disease and subsequent portal hypertension.

Inspection of the perianal area may reveal fissures, fistulas, skin breakdown, or evidence of trauma. Gentle digital rectal examination may reveal polyps, masses, or occult blood.

Looking for evidence of child abuse, such as perianal tearing, tags, or irregularities in anal tone and contour, is also important.

Examination of the skin may reveal evidence of systemic disorders, such as IBD, Henoch-Schönlein purpura, and Peutz-Jeghers polyposis.

Anoscopy can be performed (if required in an infant) by gently placing a lubricated red-top or purple-top test tube into the anus to enable visualization of the inner anal anatomy.

Lower gastrointestinal tract bleeding in children aged 1 month to 1 year

Diagnosis of anal fissures is made by anal examination, sometimes performed with a nasal speculum. Further tests are unnecessary. (In older children, as in adults, refractory anal fissures or those located off the midline should raise suspicion for IBD, specifically Crohn disease.)

Symptoms of intussusception include a palpable, sausage-shaped mass.

Children with a gangrenous bowel present with evidence of bowel obstruction, abdominal distension, dehydration, and peritonitis.

For upper GI bleeding, a nasogastric tube can be placed to confirm the presence of fresh blood and to evaluate the degree of active bleeding. If fresh or active bleeding is confirmed, esophagogastroduodenoscopy (EGD) can determine the source of upper GI bleeding in 90% of children when performed in the first 24 hours. Alternatively, colonoscopy identifies the cause of bleeding in 80% of children with lower GI bleeding.

A cohort study by Bose et al included 56 hospitalized infants with GI bleeding who underwent EGD and/or colonoscopy/flexible sigmoidoscopy. Seven of the endoscopies detected sources of bleeding (eg, gastric ulcers, duodenal ulcer, gastric angiodysplasia, esophageal varices, and an anastomotic ulcer); however, three patients in the study presented with a GI perforation soon after the procedure.[8]

In general, trace or small amounts of blood that are a one- or first-time occurrence are not of emergent concern. Children rarely require an extensive laboratory workup or invasive procedures, and parents can be advised to observe the child at home to see if these situations arise again.

Patients with substantial upper or lower GI bleeding, as determined from their history or examination, should receive a complete blood count (CBC), coagulation studies, and a chemistry panel. The CBC reveals anemia and thrombocytopenia.

A normal hematocrit may provide false reassurance regarding some children with hypovolemia and hemoconcentration.

Leukocytosis with increased bands may indicate an infectious etiology or complication responsible for the bleeding.

Elevated, abnormal prothrombin time indicates coagulopathy (ie, disseminated intravascular coagulation) or profound impairment of liver synthetic function.

A prolonged activated partial thromboplastin time indicates a hemophiliac patient or coagulopathy.

A chemistry panel may reveal a high blood urea nitrogen (BUN) level, suggesting an upper GI source that has had time to allow the body to reabsorb blood leading to a higher BUN level compared with a lower GI source.

For children who have tenderness in the right upper quadrant or a history suggestive of liver disease, aspartate aminotransferase and alanine aminotransferase enzyme levels may indicate hepatitis and increased risk of portal hypertension.

The history should also be used as a guide with regard to when fecal leukocytes, parasites, or cultures should be ordered, if an infectious etiology is suspected.

In cases of episodic or obscure bleeding, nuclear medicine radionucleotide studies, arteriography, and wireless video capsule endoscopy are used to assist in identifying the site of blood loss.

Radionuclear imaging with technetium-labeled red blood cells can be used to detect bleeding at a rate as low as 0.1 mL per minute. This technique is somewhat imprecise; however, it may direct localization for either selective angiography, suggest a need for video capsule endoscopy, or provide some direction for laparotomy search and resection, a notoriously difficult process for the control of GI bleeding.

Arteriography can be used to detect bleeding at a rate of 0.5 mL per minute and offers the advantage of providing treatment and diagnosis. The treatment consists of embolization and intra-arterial administration of vasoconstrictors.

When arteriography and nuclear scanning fail to diagnose or localize the cause of bleeding, further options remain, including repeat endoscopy and push enteroscopy (often also referred to as double balloon endoscopy or enteroscopy).[9]

In many cases, wireless video capsule endoscopy reveals the cause noninvasively, but its main disadvantage is the inability to collect tissue samples for biopsy examination.[10]

If all else fails, diagnostic laparoscopy and intraoperative endoscopy can be performed as means of last resort.

An age-specific discussion of diagnostic workups for GI bleeding follows.

Go to Imaging of Upper Gastrointestinal Bleeding and Imaging of Esophageal Varices for complete information on these topics.

Neonates

In most neonates with stress gastritis, the diagnosis is presumptive. If necessary, definitive diagnosis is made with upper endoscopy, demonstrating erythema, diffuse bleeding, erosions, or ulcerations of the gastric mucosa.

Upper gastrointestinal bleeding in children aged 1 month to 1 year

Diagnostic workup for GER often begins with a barium swallow. Other diagnostic modalities include pH probes, esophagoscopy, esophageal manometry, and nuclear medicine studies.

Gastritis is primary or secondary in etiology. Primary gastritis is associated with Helicobacter pylori infection and is the most common cause of gastritis in children. H pylori is detected using serum immunoglobulin G (IgG) levels, rapid urease testing (CLOtest), or mucosal biopsy.

Lower gastrointestinal tract bleeding in children aged 1 month to 1 year

In cases of intussusception, ultrasonography may be used as the initial diagnostic study to avoid a more invasive barium or pneumatic enema. The ultrasonographic finding of a "target" sign or a "pseudokidney" sign is highly suggestive for intussusception. Because ultrasonographic studies are only diagnostic, many clinicians choose to proceed directly to barium, saline, or pneumatic enema, which are both diagnostic and potentially therapeutic.

In patients with gangrenous bowel, upper and lower contrast studies aid in diagnosis.

Upper gastrointestinal tract bleeding in children aged 1-2 years

When a peptic ulcer that is not associated with H pylori infection is diagnosed, a fasting plasma gastrin level is measured to exclude Zollinger-Ellison syndrome.

Significant upper GI bleeding in patients with ulcer is evaluated and treated with immediate endoscopy. Biopsy samples are taken, if warranted.

Lower gastrointestinal tract bleeding in children aged 1-2 years

Most polyps in persons of this age group are the juvenile type and are located throughout the colon. These are benign hamartomas and usually require no treatment, because they autoamputate. In cases of polyps, colonoscopy is the diagnostic evaluation of choice, because it allows examination of the entire colon and the potential excision of bleeding polyps when they are identified. Colonoscopy is helpful in diagnosing other polyposis syndromes, such as familial polyposis syndromes and adenomatous polyps.

In patients with Meckel diverticulum, technetium-99m (99m Tc) pertechnetate scanning is used to identify this congenital anomaly, with 90% accuracy. This isotope has a high affinity for parietal cells of gastric mucosa and allows identification of normal and ectopic gastric mucosa. The use of H2 blockers and proton pump inhibitors (PPIs), pentagastrin, and glucagon may enhance the accuracy of this test, since H2 blockers inhibit excretion of the isotope, pentagastrin enhances gastric mucosal uptake, and glucagon inhibits peristalsis.

Upper gastrointestinal tract bleeding in children older than age 2 years

After the initial stabilization of patients with upper GI bleeding, upper endoscopy is the preferred diagnostic and therapeutic tool. The esophagus and stomach are assessed for the presence of varices and in order to exclude gastritis or ulcer disease as the source of bleeding. Gastric varices are most commonly found in the fundus.

Lower gastrointestinal tract bleeding in children older than age 2 years

Vascular lesions include a wide variety of malformations, including hemangiomas, arteriovenous malformations, and vasculitis. If these lesions are located in the colon, colonoscopy may be diagnostic and therapeutic. However, brisk bleeding may obscure the visual field, making localization the bleeding impossible. Arteriography assists in localizing the source and embolizing the feeding vessel.

In all children, the presence of blood can be confirmed by the use of peroxide-based tests, such as the Hemoccult or Hematest for lower GI bleeding and Gastroccult for upper GI bleeding.

Certain ingestions, such as red meat, iron, and peroxidase-containing vegetables (eg, turnips, horseradish, broccoli, cauliflower, and cantaloupe), can give false-positive results.

Patients with suspected obstruction should undergo plain abdominal radiography. Abdominal radiography may also be helpful in neonates in whom NEC is a possibility; the images may show free air, pneumatosis intestinalis (bubbles in the bowel wall), or portal air.

Imaging for nonemergency pediatric GI bleeding may begin with barium contrast studies (barium swallows, upper GI series, small bowel follow-throughs, or barium enemas) to point to foreign bodies, esophagitis, IBD, or polyps. For neonates with malrotation with midgut volvulus, oral contrast may reveal a "corkscrew" of small bowel or a "bird's beak".

When intestinal malrotation is suspected, an immediate upper GI contrast study should be performed to confirm the diagnosis of malrotation with midgut volvulus. Free air in the perineum suggests bowel perforation.

For suspected intussusception, color Doppler ultrasonography can be used. Its sensitivity is 98-100%, and its specificity is 89-100%; these rates are operator-dependent.

Enema studies can successfully reduce intussusception in most patients.

Barium enema studies have traditionally been used with success rates of 50-90%. Rates improve when symptoms are present for less than 24 hours. Barium study is contraindicated if perforation is suspected.

Air and water-soluble contrast enemas have also been used with similar success rates. Air enemas require less radiographic exposure but have slightly higher perforation rates, while enemas with a water-soluble (or saline) contrast agent require experienced sonographers.

If an enema successfully reduces intussusception, in-hospital observation is warranted because reoccurrence is not uncommon.

A Meckel scan uses99m Tc pertechnetate to highlight the ectopic gastric mucosa.

Arteriography is used to localize lesions when endoscopy has failed or when the patient cannot cooperate. The modality can be helpful for bleeding that is distal to the ligament of Treitz.

Children whose history and physical findings suggest significant bleeding from an upper GI source receive a nasogastric tube for diagnostic purposes.

Return of coffee-ground-like material or Gastroccult-positive material confirms an upper GI bleed.

Still, the false-negative rate is 16% if duodenopyloric regurgitation is absent. Therefore, a clear nasogastric aspirate alone cannot be used to rule out of a GI bleed.

Patients with severe upper GI bleeding should receive endoscopy within the first 12 hours of the hemorrhagic episode if they are sufficiently stable, because early endoscopy improves the diagnostic index.

The site of upper GI bleeding can be identified in 90% of cases when endoscopy is performed within 24 hours. This modality is also beneficial in predicting the likelihood of continued bleeding.[11]

The Forress classification divides endoscopic findings into the following 3 categories:

• I - Active hemorrhage (Ia = bright-red bleeding, Ib = slow bleeding)

• II - Recent hemorrhage (IIa = nonbleeding visible vessel, IIb = adherent clot on base of lesion, IIc = flat pigmented spot)

• III - No evidence of bleeding.

The incidence of rebleeding decreases dramatically, because less evidence of ulceration or bleeding is seen.

Push enteroscopy in some studies has been shown to have a higher diagnostic yield than standard esophagogastroduodenoscopy (EGD). Essentially, this modality uses a long endoscope that is placed through the mouth into the jejunum and can reach about 160 cm beyond the ligament of Treitz.

In one study, push enteroscopy identified a large number of mucosal lesions that could not be identified by a standard endoscope.[12]

Double-balloon enteroscopy is another technology that has shown high therapeutic and diagnostic yield. This modality employs a high-resolution video endoscope with latex balloons attached at the tip, with an overtube that can be inflated and deflated. It can be inserted either orally or anally.

Wireless capsule endoscopy is under investigation for children, although it can be used only diagnostically, not therapeutically.

For lower GI bleeds, colonoscopy can reveal the source of bleeding more effectively than barium enema can, and it has 80% sensitivity.

Colonoscopy should be performed only when the patient is stable and when blood and feces will not conceal proper visualization.

Sigmoidoscopy alone has also been used in children who have had symptoms of chronic lower GI bleeding for 1 year or longer. The study reveals the most common etiologies, such as juvenile colorectal polyps and nonspecific proctitis.

Provide hydration and volume support in patients with gastrointestinal (GI) bleeding. Transfusion may be required.

If an acute bleed is suspected and there is hemodynamic instability, access with 2 large-bore intravenous (IV) catheters must be obtained.

Patients with severe GI bleeds should be admitted to the pediatric ICU.

For variceal bleeds, GI consultants may endoscopically control active hemorrhage with sclerotherapy, an elastic ligature (for esophageal varices or for hemorrhoids), or (in rare cases) a transjugular intrahepatic portosystemic shunt (TIPS).

Failure to control bleeding may require the placement of a Sengstaken-Blakemore balloon for temporary tamponade if endoscopic treatment fails or is not possible at the time due to the massive bleeding.

Significant GI bleeding that cannot be controlled (eg, due to duodenal ulcers or varices in the proximal GI tract, vascular malformations, nonreducible points of intussusception) by using the previously mentioned techniques may require surgical intervention, such as laparoscopy.

Patients with first-time occurrences of nonsignificant amounts of bleeding who are discharged should be followed by their primary care pediatrician for further episodes. Again, most of these cases are benign and self-limiting.

Children who present with upper or lower GI hemorrhage to hospitals without a pediatric ICU should be transferred to such a facility when sufficiently stable.

Age-specific treatment and management strategies are discussed below.

Go to Upper Gastrointestinal Bleeding for complete information on this topic.

Upper gastrointestinal tract bleeding in neonates

Treatment for stress gastritis in neonates is supportive and includes adequate resuscitation to reduce the underlying hypoxemia, nasogastric suction, and IV H2 blockers or PPIs. Studies have advocated identifying high-risk neonates and treating them prophylactically with acid-reducing agents. Extremely rarely, continued or massive hematemesis despite medical therapy leads to operative interventions, such as gastric resection, vagotomy and pyloroplasty, or antrectomy and vagotomy.

Hemorrhagic disease of the newborn is a bleeding disorder resulting from a deficiency in vitamin K–dependent coagulation factors. Although it is normally self-limited, in 0.25%-0.5% of neonates, severe hemorrhage may result.

Prophylactic vitamin K administration in the newborn period virtually eliminates hemorrhagic disease. If the disorder occurs, IV administration of 1 mg of vitamin K generally stops the hemorrhage within 2 hours. If the clinical condition warrants, fresh frozen plasma and packed red blood cells are administered in addition to the vitamin K.

Lower gastrointestinal tract bleeding in neonates

For neonates with NEC, the standard treatment is aggressive medical resuscitation with bowel rest, antibiotics, total parenteral nutritional, and nasogastric decompression.

Nonoperative management of NEC yields a 70-80% recovery rate, but urgent laparotomy or drain placement is required in neonates in whom conservative therapy is unsuccessful owing to progressive sepsis, bowel perforation, or persistent bleeding. Recurrent bleeding in a baby who has recovered from NEC may indicate a second occurrence of the disease or an enterocolitis stricture.

Upper gastrointestinal tract bleeding in children aged 1 month to 1 year

Peptic esophagitis caused by GER is the most common cause of bleeding in this age group. Treatment begins with acid-reducing agents, thickened feeds, upright positioning, and prokinetic agents.

Antireflux procedures are rarely performed to control bleeding but may be necessary to treat complications of GER (eg, apnea, esophageal stricture, lung disease) that are refractory to medical therapy.

Gastritis is primary or secondary in etiology. Primary gastritis is associated with Helicobacter pylori infection and is the most common cause of gastritis in children. Treatment is a combination of H2 blockage, antibiotic therapy, and bismuth.

Secondary gastritis occurs in association with severe systemic illnesses that result in mucosal ischemia and produce diffuse erosive and hemorrhagic gastric mucosa. Correction of the underlying metabolic derangements and acid reduction are successful treatment measures in most patients.

Lower gastrointestinal tract bleeding in children aged 1 month to 1 year

Treatment for anal fissures consists of the administration of stool softeners and the use of rectal dilation.

In patients with intussusception, barium, saline, and pneumatic enema, while diagnostic, are potentially therapeutic as well. Successful reduction in intussusception is achieved in up to 90% of cases. Unsuccessful enema necessitates laparotomy and manual reduction or resection of the intussusception.

In cases of gangrenous bowel, laparotomy is usually necessary for definitive treatment.

The symptoms of milk protein allergy generally resolve in 48 hours to 2 weeks after withdrawal of the offending milk product.

Upper gastrointestinal tract bleeding in children aged 1-2 years

Significant upper GI bleeding caused by peptic ulcers is evaluated and treated with immediate endoscopy. Cautery, epinephrine therapy, fibrin sealants, and Endoclips are treatment options for ulcers, and biopsy samples are taken, if warranted.

Therapy for peptic ulcer disease in children mimics that in adults and centers around acid reduction and control of the underlying condition. Obstruction and/or persistent bleeding are indications for surgery.

Lower gastrointestinal tract bleeding in children aged 1-2 years

Most polyps in persons of this age group are the juvenile type and are located throughout the colon. These are benign hamartomas and usually require no treatment, because they autoamputate. Colonoscopy, the diagnostic evaluation of choice, can be used to excise bleeding polyps when they are identified.

In Meckel diverticulum, bleeding may be brisk, and transfusion is often required. However, the bleeding is usually self-limited and resolves spontaneously with episodic recurrences.

The treatment of ulceration in Meckel diverticulum is surgical resection after preoperative fluid resuscitation and adequate transfusion. A right lower quadrant incision is used, and the diverticulum is mobilized. (A bleeding, ulcerated Meckel diverticulum is seen below.)

Careful visual inspection and palpation locate the ectopic gastric mucosa and ulceration. If the ulcer is confined to the diverticulum, diverticulectomy alone is performed and closed in a transverse fashion with sutures or a stapling device.

If the diverticulum is broad based or the ulcer cannot be included in the diverticulum specimen, segmental bowel resection is necessary, with an end-to-end anastomosis. An appendectomy is often performed with the resection.

Upper gastrointestinal tract bleeding in children older than 2 years

Esophageal varices result from portal hypertension, regardless of the age group. Once the diagnosis of gastric or esophageal varices has been confirmed, treatment is initiated. Most bleeding episodes stop spontaneously and respond to blood products and careful monitoring.

Pharmacologic therapy, administered as necessary, is directed at reducing portal venous blood flow. Vasopressin, octreotide, and beta blockers have been used systemically to control bleeding varices.

Balloon tamponade with a Sengstaken-Blakemore or Minnesota tube has yielded up to an 80% success rate in controlling bleeding varices, but rebleeding and serious complications, such as pressure necrosis or misplacement, make this technique less useful.

Endoscopic sclerotherapy with injection of sodium morrhuate controls bleeding with a success rate of 90%-95%. Generally, endoscopic sclerotherapy is repeated at 2- to 4-week intervals after the acute bleed to prevent recurrence.

Variceal banding offers results at least comparable to sclerotherapy but is more difficult to perform in children because of the smaller size of the esophagus.

In the approximately 20% of cases in which conservative management fails (defined by multiple transfusion requirements or an inability to maintain hemodynamic stability) with combined pharmacotherapy and endoscopic treatments, shunt and non-shunt surgeries are the definitive treatment.

For intrahepatic portal hypertension, TIPS provides temporary decompression of the intrahepatic portal vein into the hepatic veins. Surgical portosystemic or portoportal shunts are reserved for refractory cases and/or when liver transplantation is not an option.

Nonshunt operations include esophageal transaction and devascularization of the gastroesophageal varices (Sugiura procedure), but neither is commonly performed.

A study reviewed the diagnosis and management of upper gastrointestinal bleeding in children. The study determined that after the diagnosis is established, the physician should start a proton pump inhibitor or histamine 2 receptor antagonist in children with upper gastrointestinal bleeding. The study added that consideration should also be given to the initiation of vasoactive drugs in all children in whom variceal bleeding is suspected.[13]

Lower gastrointestinal tract bleeding in children older than 2 years

In patients with IBD, the occurrence of acute or persistent bleeding with resultant anemia, despite the use of maximal medical therapy, is considered to be an indication for surgery. Therapy for ulcerative colitis is a total proctocolectomy with an ileal pouch–anal pull-through. The goal of surgical treatment in Crohn disease is resection of all grossly diseased bowels with primary anastomosis, provided previous surgery (or the current resection) has not created a short-bowel situation.

Infectious diarrhea is suspected when lower GI bleeding occurs in association with profuse diarrhea. Recent antibiotic use raises suspicion for antibiotic-associated colitis and Clostridium difficile colitis. The former should be self-limited and should resolve after cessation of antibiotics, while Clostridium difficile colitis requires therapy with oral metronidazole or vancomycin. Escherichia coli and Shigella species are the two most common pathogens in infectious diarrhea. Treatment is supportive with antibiotic therapy, as indicated.

Vascular lesions include a wide variety of malformations, including hemangiomas, arteriovenous malformations, and vasculitis. If these lesions are located in the colon, colonoscopy may be diagnostic and therapeutic. However, brisk bleeding may obscure the visual field, making localization of the bleeding impossible. Arteriography assists in localizing the source and embolizing the feeding vessel.

Surgery is necessary when bleeding cannot be controlled using these techniques. Localization of hemorrhage in the small bowel is a challenge to surgeons and may require intraoperative endoscopy to find the lesion.

Further inpatient or outpatient care

Critically ill pediatric patients may benefit from receiving prophylactic treatment to prevent upper gastrointestinal bleeding. However, evidence to guide clinical practice remains limited.[14]

Direct consultation toward the discipline appropriate to the diagnosis (eg, a radiologist for a barium enema study in intussusception, a pediatric ICU specialist and a pediatric surgeon for NEC, a gastroenterologist for presumed ulcer disease).

The European Society of Gastrointestinal Endoscopy (ESGE) and the European Society for Paediatric Gastroenterology Hepatology and Nutrition (ESPGHAN) put together guidelines on pediatric gastrointestinal endoscopy. The guidelines include the following strong recommendations for upper and lower pediatric GI bleeding and endoscopic hemostasis technique[15, 16] :

• In cases of upper gastrointestinal bleeding with known esophageal varices, after standard medical intervention, esophagogastroduodenoscopy (EGD) be performed < 12 h.

• Use band ligation (preferred) or sclerotherapy for hemostasis of pediatric esophageal variceal bleeding.

Histamine-2 blockers or proton-pump inhibitors (PPI) are used to inhibit gastric acid production in peptic ulcer disease, gastroesophageal reflux disease (GERD), and duodenal ulcer disease. Alkaline suspensions are used to directly neutralize gastric acid secretions. Bleeding from esophageal varices may be prevented with vasoconstrictors, such as octreotide. Those with the etiology of infectious diarrhea should not be given antimotility agents, though some may benefit from antibiotics.

Somatostatin is not currently available in the United States for pediatric use. It is a hormone produced by the body that inhibits adenylate cyclase and therefore the production of cyclic AMP. Although it decreases pituitary secretion of growth hormone and thyrotropin, it also has physiologic effects of inhibiting secretion of serotonin, gastrin, vasoactive intestinal peptide (VIP), and many other hormones (eg, insulin, glucagon). It decreases intestinal motility and gastric emptying, but it is not recommended for use. Octreotide, a somatostatin analog, has been more widely adopted for the indication of variceal bleeding as secondary prophylaxis and, in some, primary prophylaxis.

Class Summary

H2 blockers are reversible competitive blockers of histamine at H2 receptors, particularly those in the gastric parietal cells (where they inhibit acid secretion). The H2 antagonists are highly selective, they do not affect the H1 receptors, and they are not anticholinergic agents.

Some gastroenterologists recommend PPIs as being more effective than H2 blockers in promoting lesion cicatrization for hemorrhagic esophagitis and gastroesophageal reflux. Studies with omeprazole (Prilosec) and pantoprazole (Protonix) in intravenous (IV) forms have been encouraging, but they are not yet approved by the US Food and Drug Administration (FDA) for use in children.

Ranitidine (Zantac)

This agent inhibits histamine stimulation of H2 receptors in gastric parietal cells, which reduces gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Famotidine (Pepcid)

Famotidine competitively inhibits histamine at the H2 receptors in gastric parietal cells, reducing gastric acid secretion, gastric volume, and hydrogen concentrations.

Nizatidine (Axid, Axid AR)

This agent competitively inhibits histamine at the H2 receptor of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.

Cimetidine (Tagamet HB 200)

This agent inhibits histamine at H2 receptors of gastric parietal cells, which results in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.

Class Summary

These agents are used to neutralize gastric acidity.

Aluminum and magnesium hydroxide (Maalox, Alamag, Mag-AL, Mag-Al Ultimate)

This is a drug combination that neutralizes gastric acidity and increases the pH of the stomach and duodenal bulb. Aluminum ions inhibit smooth muscle contraction and gastric emptying. Magnesium-aluminum antacid mixtures are used to avoid changes in bowel function.

Class Summary

Pharmacologic treatment to reduce portal pressure is important for the treatment of bleeding from esophageal varices. Propranolol has been studied for primary and secondary prophylaxis of esophageal varices; although it is helpful for adults, studies in children are limited. Therefore, these drugs are not currently considered the standard of care for this population.

In addition, vasopressin had been used as a splanchnic vasoconstrictor, but its many adverse effects (eg, bowel-wall or cutaneous ischemia, hypertension, abdominal pain) have made it less desirable than other options are, even when tempered with the vasodilatory effects of nitroglycerin. As a result, octreotide has emerged as the recommended treatment, especially in conjunction with sclerotherapy for patients with variceal bleeding, because it blunts sudden increases in pressure due to postprandial hyperemia.

Octreotide (Sandostatin, Sandostatin LAR)

A synthetic polypeptide, octreotide acts as natural somatostatin but is more resistant to enzymatic degradation and has a longer half-life in circulation than somatostatin. These factors make octreotide easier to use clinically.

Vasopressin (Pitressin)

At high doses, vasopressin can cause vasoconstriction, with many other effects (eg, promoting water resorption, increasing peristaltic activity). It is effective in reducing portal pressure.