CHAPTER 122

Gastrointestinal Bleeding

George Gershman, MD

Bleeding from the gastrointestinal (GI) tract in infants and children is always stressful and frightening for patients and their parents. Diagnosis and management can also be challenging for a physician, especially if bleeding is severe, although fortunately, encountering life-threatening GI bleeding in pediatric practice is rare. When it does occur, acute GI bleeding in children is a true medical emergency, associated with significant morbidity and mortality, even in high-income countries. A recent retrospective analysis of acute GI bleeding in patients admitted to 47 pediatric tertiary centers in the United States (data extracted from Pediatric Health Information System Database) revealed a mortality of almost 0.4% and 3% in children with the primary and secondary diagnosis of acute GI bleeding, respectively. Therefore, a pediatrician or emergency department (ED) physician should be prepared to initiate effective resuscitation and a diagnostic workup focusing on common age-specific causes of GI bleeding. The primary goal of this approach is a reduction of morbidity associated with significant hemorrhage.

Epidemiology

Upper GI bleeding is uncommon in infants and children, although the exact incidence is unknown. Clinical experience suggests that the incidence in children is significantly less than in adults. This assertion is supported indirectly by epidemiological data from the United Kingdom and United States, which indicate that the incidence of upper GI bleeding in adults younger than 29 years is approximately 18 to 23 per 100,000 adults per year, which is almost 4 to 5 times lower than among older age groups. The risk of upper GI bleeding is relatively high (between 6% and 25%) in pediatric patients admitted to pediatric intensive care units. Clinically significant upper GI bleeding, defined as a drop in hemoglobin level of 2.0 g/dL; indication for blood transfusion; emergent endoscopy; or surgery has been documented in 4% of children presenting to an ED with hematemesis.

Low GI bleeding is quite common in pediatric practice. However, the epidemiology of this problem is not well established. In 1 study, rectal bleeding was the presenting symptom in 0.3% of all visits to a tertiary ED during a 10-month period.

Clinical Presentation

Bleeding into the GI tract can present as hematemesis, melena, occult bleeding, or hematochezia.

Hematemesis is vomiting of bright-red “fresh” blood or coffeeground (dark-brown) “old” blood exposed to hydrochloric acid. Usually, hematemesis reflects acute bleeding from the esophagus, stomach, or proximal duodenum. Swallowed maternal blood in neonates and epistaxis in older children should be ruled out to avoid unnecessary invasive procedures.

Melena is characterized as liquid, coal-black, shiny, sticky, tarry, foul-smelling stool. It suggests bleeding from the upper GI tract. Occasionally, bleeding from the ileum can be associated with melena. However, in this case, the stool is black but not tarry. Melena suggests a minimum loss of 50 to 100 mL of blood in adults (1%–2% of total blood volume) or 2% of the total blood volume in children. Stool may remain black or tarry for a few days after massive hemorrhage, even though active bleeding has ceased.

Occult bleeding is defined as the presence of a non-visible quantity of blood in stool. It usually occurs as chronic, recurrent losses of small amounts of blood, which can lead to severe microcytic anemia. The most commonly used technique for detection of blood in stool is a fecal occult blood test. This test is based on the chemical reaction of a dye (guaiac) with peroxidase-containing substances and hydrogen peroxide. It is not specific for the presence of blood (hemoglobin) in stool. False-positive results could be secondary to peroxidase activity in food products such as cantaloupes, radishes, bean sprouts, cauliflower, broccoli, grapes, and red meat or iron preparations. False-negative results are associated with prolonged colonic transient time and bacterial degradation of hemoglobin to porphyrin, which does not have peroxidase activity.

Currently, a fecal immunochemical test is available for detection of blood in stool based on labeling of human hemoglobin by specific antibodies. The test does not require a special diet. It is more specific for the detection of bleeding from the colon due to enzymatic digestion of the hemoglobin from the upper GI tract.

Hematochezia is the passage of bright-red or maroon-colored blood from the rectum. This may be pure blood, bloody diarrhea, or blood mixed with stool. Typically, it is a sign of lower GI bleeding from the distal colon or, less frequently, from the right colon or distal ileum. Rarely, hematochezia may occur in children with massive bleeding from the duodenum.

Pathophysiology

Compensatory responses to acute bleeding restore depleted intravascular volume, maintain a normal cardiac output and adequate oxygenation of vital organs (ie, brain, heart, lungs, adrenal gland), and mobilize internal energy stores.

Two parameters determine the degree of compensation: volume of blood loss and velocity of bleeding.

Mild Blood Loss (<15% of Circulatory Volume) or Class 1 Bleeding

Relatively slow blood loss of less than 15% of the total blood volume triggers redistribution of depot blood from the venous system to the systemic circulation and a shift of extracellular fluids into the vascular space. Adequate cardiac output without changes in heart rate and blood pressure is maintained, and there are no hemodynamic abnormalities. However, a rapid blood loss (even <10% of blood volume) may compromise cardiac output and trigger tachycardia and other compensatory mechanisms to restore normal blood circulation.

Moderate Blood Loss (Between 15% and 30% of Circulating Volume) or Class 2 Bleeding

Blood loss of more than 15% of the total blood volume leads to tachycardia, an increased systemic vascular resistance caused by activation of the sympathetic nervous system and hypothalamic-pituitary-adrenomedullary axis. In children, cardiac output depends on heart rate rather than stroke volume due to a smaller ventricular mass. With hemorrhage, tachycardia is the principal mechanism for maintenance of an adequate cardiac output in pediatric patients; however, prolonged tachycardia increases myocardial oxygen demand and decreases diastolic-dependent coronary perfusion. This eventually leads to cardiovascular decompensation if fluid resuscitation is delayed or insufficient.

Normal blood pressure and adequate perfusion of vital organs in children with moderate bleeding is maintained by increased systemic vascular resistance and redistribution of blood from skin, muscle, splanchnic organs, and kidney to the brain, heart, lungs, and adrenal gland due to local production of adenosine, nitric oxide, and prostaglandins. Therefore, blood pressure is a poor indicator of cardiovascular homeostasis in children with moderate GI bleeding. In contrast, persistent tachycardia is the red flag of pending cardiovascular collapse.

Severe Blood Loss (>30% of Circulating Volume) or Class 3 Bleeding

Failure of compensatory mechanisms and decreased cardiac output lead to hypotension and tissue hypoxia. Compensatory tachypnea contributes to respiratory alkalosis in the initial phase of severe bleeding. Tissue hypoxia compromises mitochondria functional capacity to generate energy as adenosine triphosphate. This leads to metabolic acidosis due to excessive production of lactic acid and cellular death.

Hypoperfusion of the kidney causes acute spasm of the preglomerular arterioles and acute tubular necrosis and renal failure. Hypoxia and excessive cytokine production can induce liver failure—sudden onset of jaundice due to hepatocellular necrosis, elevation of transaminases, coagulopathy, hypoglycemia, and encephalopathy. Myocardial ischemia is a common consequence of severe bleeding. Sepsis, thrombotic microangiopathy, and a systemic inflammatory response syndrome may occur in the late stages of uncontrolled or inadequately treated severe hemorrhage.

Evaluation

The initial assessment of the child with suspected GI bleeding should be focused on signs of hemodynamic instability and clues for the etiology of bleeding. Four major questions must be answered promptly: Is the patient stable? Is the bleeding real? What is the source of the bleeding? What is the best treatment option?

The first and most important step in the initial assessment of the child with suspected GI bleeding is recognition of hemodynamic instability (Box 122.1).

A prompt assessment of estimated blood loss and the degree of hemodynamic instability should be done using objective criteria, such as mental status, skin color, capillary refill, pulse, blood pressure, and orthostatic maneuvers (Table 122.1). Special attention should be focused on tachycardia and narrowed pulse pressure, which are the earliest signs of impending shock. Hypotension usually occurs in the late phase of shock in children and is an ominous finding. The value of the initial hematocrit may not accurately reflect the severity of blood loss. First, the hematocrit does not fall immediately with hemorrhage due to proportionate reductions of plasma and red cell volumes. Second, the hematocrit begins to fall due to compensatory restoration of the intravascular volume by the shift of extravascular fluids into the vascular bed. This process begins shortly after the onset of bleeding; however, it is not complete for 24 to 72 hours. At this point, plasma volume is larger than normal, and the hematocrit reaches its true nadir, assuming that bleeding has stopped.

Differential Diagnosis

The 3 essential components of the diagnosis of GI bleeding are confirmation that bleeding is real, allocation of the bleeding area to the upper versus lower GI tract, and detection of the specific cause of bleeding.

Abbreviations: –, absent; +, present, mild; ++ present, moderate.

Red staining of emesis or stool can be induced by cranberries, cranberry juice, cherries, strawberries, beets, tomatoes, candies, amoxicillin, phenytoin, red-colored rehydrating drinks (eg, Gatorade, Poweraid), and rifampin. Bismuth preparations, activated charcoal, iron, spinach, blueberries, and licorice can simulate bleeding by staining emesis and coloring stool black. An appropriate history, a normal physical examination, and guaiac-negative stool are sufficient to rule out a true bleeding episode.

It is important to remember that hematemesis or melena can be secondary to epistaxis. History of recent tonsillectomy and adenoidectomy, nasal allergies, dry environment, or nose-picking habits increases the probability of epistaxis. Thorough examination of the nose and oropharynx can help to establish the correct diagnosis.

Detailed history and physical examination help narrow the diagnostic workup. For example, treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) is a risk factor for acute gastric ulcers and bleeding from the stomach. Jaundice, hepatomegaly, spider hemangiomas, prominent vessels of the abdominal wall, or ascites are the signs of chronic liver disease and are suggestive of portal hypertension. However, GI bleeding in a febrile child with hemodynamic instability and jaundice could be secondary to sepsis-related coagulopathy or acute liver failure.

Careful assessment of the perineum can reveal anal fissures, fistulas, or perianal inflammation.

If the source of bleeding is not obvious, the placement of a nasogastric tube is very useful. A tube with the largest bore tolerable should be placed for adequate gastric lavage. A 10F to 12F sump tube is a reasonable choice for small children; a 14F to 16F tube is reasonable for older patients. Room temperature saline is the optimal fluid for irrigation. Iced saline lavage is no longer recommended because it compromises platelet function at the bleeding site and may induce hypothermia (especially in infants) with subsequent clinically significant arrhythmia. A bloody or coffee-ground aspirate indicates upper GI bleeding, if epistaxis was ruled out. The absence of blood in the stomach does not exclude upper GI bleeding because the source of hemorrhage can be in the duodenum. The presence of coffee-ground fluid in gastric aspirate, which promptly clears by gastric lavage, suggests that bleeding has stopped. Failure to obtain clear return on gastric lavage indicates ongoing bleeding.

Results of blood tests give some clues to the nature of bleeding. Low hemoglobin and hematocrit with normal mean corpuscular volume (MCV) are typical for acute blood loss. Elevated levels of blood urea nitrogen is suggestive of volume depletion and absorption of the blood proteins in the small intestine, which supports the diagnosis of upper GI bleeding. Very low hemoglobin, hematocrit, and MCV levels in a hemodynamically stable patient are consistent with chronic GI blood loss.

Knowledge of common causes of GI bleeding in an age-specific group of children helps with diagnostic strategy (Table 122.2).

In general, endoscopy is the method of choice for the diagnosis of the specific causes of acute and chronic GI bleeding related to mucosal and submucosal lesions of the GI tract. The choice of the particular type of endoscopic procedure is related to suspected pathology. Upper and lower GI endoscopy and enteroscopy are routine methods for diagnosis of diseases such as acute or peptic ulcers, esophagitis, gastritis, esophageal varices, vascular malformations, ulcerative colitis, Crohn disease, polyps, and other causes of GI bleeding. Capsule endoscopy is the minimally invasive method of endoscopic investigation of the entire small intestine. It is used for diagnosis of GI bleeding of obscure origin, usually after negative results of conventional endoscopic procedures.

Abbreviation: GI, gastrointestinal.

Plain radiography and abdominal ultrasonography are useful for diagnosis of structural abnormalities such as intussusception, necrotizing enterocolitis, and malrotation.

Technetium Tc 99m pertechnetate scanning is indicated in children with suspected Meckel diverticulum. It is 85% sensitive and 95% specific.

The calculated rate of blood loss serves to guide the method to diagnose the source of hemorrhage. Angiography (rate ≥0.5 mL/minute), computed tomography angiography (0.35 mL/minute), and technetiumlabeled red blood cell scanning (0.2 mL/minute) are alternatives to endoscopy for diagnosis of source of active GI bleeding.

These modalities should be considered when vascular anomalies or hemobilia are suspected.

Age-Associated Causes of GI Bleeding

Neonates

In healthy breastfed neonates and infants, hematemesis could be caused by swallowed maternal blood. In such cases, careful examination of maternal breast and areola can lead to correct diagnosis. In addition, the Apt test can be useful, especially in the first 3 to 4 weeks after birth, while concentration of fetal hemoglobin is still high. The test is based on the chemical reaction of adult hemoglobin with sodium hydroxide, which leads to a color change from bright red to yellow or crusty brown. Fetal hemoglobin is resistant to hydroxylation, and blood from the neonate remains bright red.

Acute gastric or duodenal ulcers should be suspected in neonates who are sick and preterm or who are septic or asphyxiated and full term, or in patients with intracerebral bleeding, increased intracranial pressure, congenital heart disease, respiratory failure, or hypoglycemia. The typical scenario includes sudden onset of hematemesis or melena and signs of hemodynamic instability. Occasionally, severe upper GI bleeding can occur in healthy full-term neonates within the first few days after birth.

Gastrointestinal bleeding is a common manifestation of necrotizing enterocolitis. The warning signs of necrotizing enterocolitis are abdominal distention, feeding intolerance with increased gastric residuals, mild diarrhea, hematochezia, or stool that tests positive for occult blood.

Plain radiographs can be diagnostic if they show pneumatosis intestinalis or gas in the portal vein.

Rare causes of GI bleeding in the first month after birth include Hirschsprung enterocolitis, midgut volvulus, duplication cyst, vascular malformation, and hemorrhagic disease of the newborn, particularly in breastfed neonates who did not receive vitamin K.

Infants Up to First 6 Months of Age

One of the leading causes of GI bleeding in infants younger than 6 months is cow’s milk or soy protein allergy. The spectrum of symptoms includes recurrent vomiting, hematemesis, failure to thrive, and diarrhea with guaiac-positive stools or hematochezia.

Exclusively breastfeeding infants may develop similar symptoms on rare occasions. Elimination of cow’s milk, eggs, peanuts, fish, and tree nuts from maternal diet may lead to resolution of allergic symptoms in the breastfeeding infant. For infants with persistent symptoms or whose mothers are unable to restrict their diet according to current recommendations and for formula-fed infants with cow’s milk protein allergy, hypoallergenic (extensively hydrolyzed and free amino acid–based) formulas can be used to relieve the symptoms. Most infants with GI manifestations of cow’s milk protein allergy will improve within the first 2 weeks of treatment.

An anal fissure is another common cause of bleeding in infants. The diagnosis is made by careful examination of the anus.

Intermittent rectal bleeding with streaks of frank blood mixed with normal-appearing stool can be secondary to intestinal lymphoid hyperplasia of the colon or terminal ileum. During endoscopy, multiple hemispheric smooth nodules of less than 4 mm can be found in clusters or diffusely throughout the GI tract. It is considered an excessive reaction of the GI tract lymphatic tissue (lymphoid follicles and Peyer patches) to food-related or other antigens. Spontaneous regression of lymphoid follicles is quite common. In addition to parental reassurance, an elimination diet for breastfeeding mothers is a reasonable initial treatment. Feeding with extensively hydrolyzed protein formula is the next therapeutic step. Corticosteroid therapy is restricted to infants with a severe form of this disease—recurrent abdominal pain, significant anemia, persistent rectal bleeding, diarrhea, and failure to thrive. In such cases, immunodeficiency has to be excluded.

Esophagitis should be suspected as a cause of bleeding in infants with a history of recurrent emesis and interrupted feeding patterns associated with crying, irritability, or arching. Patients with repaired esophageal atresia with or without tracheoesophageal fistula are at increased risk of severe reflux disease and esophagitis. Bleeding induced by esophagitis is usually recurrent and not intensive. The patients may have hematemesis with streaks of blood or guaiac-positive stool.

Infants or older children can develop minor bleeding due to prolapse of gastric mucosa into the esophagus through the gastroesophageal junction (prolapse gastropathy). This condition is manifested by recurrent emesis with food and appearance of flecks of denatured blood at the end of vomiting. The presence of large amounts of frank blood or clots at the end of recurrent emesis is suggestive of a more serious problem, such as Mallory-Weiss tear.

Infants and Children Younger Than 7 Years

Several diseases have a higher prevalence in this age group compared with other children.

The signs and symptoms of portal hypertension are a large-volume hematemesis, history of omphalitis secondary to catheterization of the umbilical vein, presence of splenomegaly or hepatosplenomegaly, and other stigmata of chronic liver disease, such as jaundice, spider angiomas, caput medusa, and ascites. Esophageal varices are the most common site of bleeding in children with intrahepaticsinusoidal and extrahepatic-presinusoidal forms of portal hypertension. Two-thirds of children with portal hypertension will bleed before 5 years of age. The diagnosis is based on the presence of esophageal or gastric varices or hypertensive gastropathy during an upper GI endoscopy.

Intussusception, which is more common in the first 2 postnatal years, is strongly considered in infants and children with sudden onset of severe, cramping abdominal pain intercepted by pain-free episodes and currant jelly stools. A lead point is often present in children older than 2 years. Diagnosis is confirmed by ultrasonography (positive: “concentric circles” or the “target-shaped sign”) or barium enema. Hydrostatic reduction of intussusceptions is successful in more than 90% of children.

Meckel diverticulum is the most common congenital anomaly in children. It is estimated that approximately 2% of infants have a remnant of the omphalomesenteric duct. However, fewer than 5% of children will develop complications, including GI bleeding. The predominant location of Meckel diverticulum is the distal ileum (40–60 cm above the ileocecal valve). Ectopic tissue is present in up to 80% of symptomatic patients. Gastric mucosa is the most common type of ectopia. The cause of bleeding is peptic ulceration at the junction of the ectopic gastric mucosa and normal ileum, the so-called marginal ulcer. Bleeding can be massive, but it may cease spontaneously secondary to contraction of the splanchnic vessels in response to hypovolemia. This phenomenon explains the intermittent nature of bleeding from Meckel diverticulum. Bleeding is usually painless but sometimes coincides with recurrent abdominal pain.

The diagnostic procedure of choice is technetium Tc 99m pertechnetate scanning.

Juvenile polyps may occur in as many as 1% of children, with peak incidence from 2 to 5 years of age. The common clinical presentation is recurrent, painless bleeding with a small amount of blood on formed stool. Diarrhea and tenesmus can occur when the polyp is large and located in the left colon.

Typical juvenile polyps are smooth, rounded, and red. Polyps of less than 1 cm are usually sessile; polyps larger than 1 cm have short or long stalks. Juvenile polyps are composed of normal but cystically dilated crypts embedded in an abundant lamina propria. Colonic mucosa adjacent to the large polyp has a distinguished, so-called chicken skin appearance. Colonoscopy is indicated due to the high incidence (almost 50%) of coexisting of the rectal polyps with polyps in the more proximal portions of the colon.

Endoscopic polypectomy is the treatment of choice. There is a general consensus that a single juvenile polyp is not a premalignant condition. Therefore, removal of a solid juvenile polyp is curative. Surveillance colonoscopy is not indicated unless the child develops a new episode of rectal bleeding or retains 5 or more juvenile polyps.

Hemolytic uremic syndrome (HUS) should always be suspected in infants and toddlers with bloody diarrhea, which is present in three-quarters of children with epidemic HUS. In two-thirds of these children, Escherichia coli O157:H7 can be isolated. Bloody diarrhea in HUS results from hemorrhagic colitis caused by the presence of endothelial damage produced by verotoxin and Shiga toxin and submucosal hemorrhages. Tenesmus is common. Diffuse, severe abdominal pain with peritoneal signs can occur.

The presence of the so-called thumbprinting sign on a contrast enema or a computed tomography scan reflects a submucosal hemorrhage of the colon. Colitis-related symptoms last no longer than a week, followed by signs of hemolytic anemia and oliguria. Known GI complications of HUS are intussusception, pancreatitis, and intestinal obstruction. Small or large bowel perforation may occur during peritoneal dialysis, which may be performed to manage the acute renal failure that can accompany HUS.

Henoch-Schönlein purpura is most common in children younger than 7 years; the median age of appearance is 4 years. It should be suspected in children with sudden onset of severe diffuse abdominal pain, vomiting, and hematochezia following a viral illness during the winter and early spring and about a week after the appearance of purpuric-type skin lesions on the buttocks or lower extremities.

On rare occasions, GI manifestations may precede the skin rash. Severe anemia is uncommon. The small and large bowels have different degrees of hemorrhagic lesions. These may be apparent on a small bowel radiograph series or contrast enema with coarsening of folds and thumbprinting. Abdominal pain and hematochezia are self-limited. Treatment with corticosteroids is controversial, although it may shorten the course of GI symptoms of abdominal pain by 1 or 2 days.

Children 7 Years and Older

The common causes of GI bleeding in this age group are listed in Table 122.2.

Drug-induced gastritis or acute ulcer should be strongly suspected in children treated with NSAIDs or oral steroids. The degree of bleeding ranges from mild to moderate. The typical clinical presentation is the sudden onset of abdominal discomfort followed by hematemesis or melena. Two types of lesions can occur: gastropathy or acute gastric ulcers due to alteration of the mucosal microcirculation, and mucosal cytoprotection related to suppression of local synthesis of prostaglandins. The incidence of NSAID-related GI bleeding is much higher in patients with Helicobacter pylori gastritis. Therefore, eradication of H pylori infection is recommended before long-term therapy with NSAIDs.

Although peptic ulcer disease is relatively rare in pediatric patients, it accounts for at least one-third of the cases of upper GI bleeding in school-age children. Most bleeding ulcers are located in the duodenal bulb. At least 80% of bleeding episodes from duodenal ulcers cease spontaneously. However, if the bleeding is arterial, it may become life-threatening. Urgent endoscopy is necessary as soon as the patient becomes more stable after fluid resuscitation.

Risk factors for recurrent bleeding are large ulcer (>2 cm), location of the ulcer on the posteroinferior wall of the duodenal bulb, blood spurting from the base of the ulcer, a visible vessel, or an adherent clot. In these circumstances, the risk of recurrent bleeding is relatively high even after initially successful endoscopic hemostasis and acid suppression with intravenous (IV) infusion of proton pump inhibitors. The most critical time for rebleeding is the first 3 days following the initial hemostasis.

The risk of recurrent bleeding is minimal in children with a clear base ulcer or a pigmented spot sign, a small flat thrombus in the center of an ulcer. Endoscopic hemostasis is not indicated in these cases. Hemodynamically stable children without the endoscopically identified risk factors can be treated safely on an outpatient basis.

Colitis is the most common cause of rectal bleeding in older children and teenagers. Infectious colitis is by far more common than inflammatory bowel disease. In general, bacterial colitis is an acute, self-limited disorder manifested by sudden onset of fever, tenesmus, and bloody diarrhea lasting from 5 to 7 days.

Diarrhea lasting 4 weeks or longer is usually associated with chronic inflammatory bowel disease. Rare causes of chronic infectious colitis are Yersinia enterocolitica, tuberculosis, Entamoeba histolytica, Strongyloides stercoralis, and opportunistic infections in immunocompromised patients.

Clostridium difficile colitis should be ruled out, especially in children treated with antibiotics or hospitalized patients.

Ulcerative colitis usually presents with insidious onset of diarrhea, nocturnal diarrhea, and subsequent hematochezia. Clinical manifestations of moderate to severe forms of ulcerative colitis include bloody diarrhea, abdominal cramps, urgency to defecate, malaise, anorexia with weight loss, intermittent low-grade fever, and some degree of anemia and hypoalbuminemia.

Crohn disease has a more indolent onset associated with abdominal pain, diarrhea, poor appetite, and weight loss. Diarrhea is not grossly bloody unless there is bleeding from an anal fistula or colitis that is diffuse or left sided.

Differentiation between bacterial colitis and the early stage of chronic inflammatory bowel disease is always a challenge. A high index of suspicion and negative bacterial stool culture results, including Yersinia species and other rare pathogens, are essential parts of early diagnosis. The definitive diagnosis of chronic inflammatory bowel disease is based on the results of upper and lower GI endoscopy, including multiple biopsies.

Management

Resuscitation

It is imperative to initiate resuscitation of the patient who is hemodynamically unstable almost immediately before any diagnostic procedure is considered. Two large-bore peripheral IV catheters or a central catheter should be placed and secured. Blood is typed and crossmatched and sent for baseline laboratory assessment of levels of hemoglobin, hematocrit, MCV, platelets, electrolytes, creatinine, blood urea nitrogen, liver enzymes, and clotting factors. Oxygen supplementation and large boluses of saline target restoration of circulation and tissue oxygenation. The volume of isotonic solution should be sufficient to improve tachycardia and reverse narrow pulse pressure. Blood transfusion is indicated for patients with

•Persistent tachycardia, abnormal pulse pressure, or orthostatic hypotension after replacement of 15% to 20% of blood volume with isotonic solution.

•Estimated blood loss of 30% or more.

•Hemoglobin of 6 g/dL or less.

•Uncontrolled bleeding.

•Hemorrhagic shock.

•Hemoglobin of 7 to 9 g/dL in children with chronic heart and lung diseases and signs of hypoxia.

Packed red blood cells are the product of choice for replacement of blood loss. Matched whole blood is preferred for patients with massive bleeding. Fresh-frozen plasma is indicated for children with suspected or documented clotting factor deficiency, including those with acute or chronic liver disease. Platelet transfusion is indicated in rare cases of severe bleeding with estimated blood loss of more than 50% of the patient’s blood volume or children with active hemorrhage and platelet count less than 50,000 platelets/mm³. Early blood transfusion is reasonable for children with active bleeding and known chronic heart or lung diseases. Monitoring of vital signs is a more accurate means of assessing the effect of blood transfusion than monitoring of hematocrit soon after transfusion. It is reasonable to wait 6 hours before checking a posttransfusion hematocrit.

Octreotide (a synthetic somatostatin analogue) is an effective adjuvant medical therapy of severe bleeding from esophageal or gastric varices. It should be given to the child with active hemorrhage and any evidence of chronic liver disease or previously diagnosed portal hypertension. The initial IV bolus of 1 mcg/kg is followed by continuous infusion of octreotide with the initial rate of infusion as 1 mcg/kg per hour. The dose can be increased every 6 hours up to 5 mcg/kg per hour.

Endoscopic hemostasis is a standard therapy for moderate to severe upper GI bleeding related to peptic ulcer disease, esophageal or gastric varices, and vascular malformation.

Surgery should be reserved for children with severe uncontrolled bleeding from a known source or specific disorders, such as Meckel diverticulum.

Prognosis

The prognosis for infants and children with GI bleeding depends on the condition causing the bleeding. Early, aggressive treatment of the consequences of blood loss is essential to decreasing morbidity and mortality. Generally, prognosis is good, and overall mortality is less than 5%.

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