Approach to upper gastrointestinal bleeding in children

INTRODUCTION — 

Upper gastrointestinal bleeding (UGIB) commonly presents with hematemesis (vomiting of red blood or coffee ground-like material) and/or melena (black, tarry stools). In comparison, hematochezia (bright red or maroon-colored blood or fresh clots per rectum) is usually caused by lower GI bleeding (LGIB). The presenting symptoms, clinical significance, and management of both entities vary widely depending on the cause and rate and quantity of blood loss.

The initial approach to a child with suspected UGIB is discussed in this topic review. The approach to LGIB in children, or to UGIB in adults, is reviewed separately. (See "Lower gastrointestinal bleeding in children: Causes and diagnostic approach" and "Approach to acute upper gastrointestinal bleeding in adults".)

DEFINITIONS

●Upper gastrointestinal bleeding (UGIB) – UGIB is defined as bleeding that arises from a source proximal to the ligament of Treitz (ie, in the esophagus, stomach, or duodenum).

●Lower gastrointestinal bleeding (LGIB) – LGIB arises from a source distal to the ligament of Treitz (ie, in the jejunum, ileum, or colon).

EPIDEMIOLOGY — 

The incidence of UGIB is not well established in children. A population-based study from France estimated that UGIB occurred in 1 to 2 per 10,000 children per year [1]. A separate study from a single center reported that hematemesis accounted for 0.2 percent of all emergency department visits [2]. One-third of the patients were less than one year old, and two-thirds were younger than five years [2]. The vast majority had minor UGIB (or mimics of UGIB, including epistaxis) and 80 percent were discharged home, while only 4 percent had clinically significant UGIB. In the authors' experience, many children with acute gastroenteritis-associated vomiting have minor coffee ground emesis that is not captured in retrospective database studies, which form the basis for most of our understanding of the epidemiology of UGIB. As a result, the true prevalence of UGIB is likely higher than the above estimates and the proportion of children with clinically significant UGIB is probably even lower.

Pediatric data on predictors of clinically significant UGIB are sparse. Among children presenting to the emergency department, those with clinically significant UGIB tend to be older, present with associated melena, have a large (>250 mL) volume of fresh blood in their vomitus, have significant underlying medical problems, appear unwell, and/or are tachycardic [2]. In the intensive care unit population, predictors of clinically significant UGIB include respiratory failure, coagulopathy, and Pediatric Risk of Mortality score ≥10 [3]. In a study of adults, those who presented with hematemesis and/or melena were more likely to have serious pathology at endoscopy (eg, ulcers, varices), require blood transfusions, and/or rebleed compared with those with coffee ground emesis [4]. Eighty-two percent of those with coffee ground emesis (ie, no hematemesis and/or melena) had minor diagnoses or negative endoscopies.

ETIOLOGY — 

The most common causes of UGIB in children vary depending on age and geographic setting. Regional differences and changes over time likely reflect differences in indications for endoscopy and predisposing conditions. Because most children with clinically insignificant UGIB do not undergo endoscopy [2], the cause is often presumed or inferred from the clinical presentation and context. In particular, coffee ground emesis associated with intense frequent vomiting due to acute gastroenteritis is generally assumed to be related to a Mallory-Weiss tear.

Among children who do undergo endoscopy in North America and Europe, the most common causes are gastric and duodenal ulcers, esophagitis, gastritis, and mucosal trauma related to vomiting (Mallory-Weiss tear or prolapse gastropathy [gastric mucosal hemorrhage]) [5-10]. Exposure to nonsteroidal antiinflammatory drugs (NSAIDs) plays a role in approximately one-third of cases [1,11,12]. The contribution of Helicobacter pylori to UGIB varies across populations and age groups, as does the risk associated with NSAID use [12]; H. pylori infection in children is often asymptomatic. (See "Helicobacter pylori: Diagnosis and management in the pediatric patient".)

Esophageal varices are an uncommon cause of UGIB (approximately 5 percent of cases) but are clinically important because the hemorrhage is often severe and potentially life-threatening. Variceal bleeding predominated in some early case series from the Middle East and South Asia but has been less common in more recent reports [13-16]. In resource-limited settings, varices may represent a higher proportion because endoscopy is reserved for more severe UGIB and, possibly, because of different predisposing conditions (eg, extrahepatic portal venous obstruction) [17]. Rare conditions associated with structural abnormalities of blood vessels (eg, hereditary hemorrhagic telangiectasia, Ehlers-Danlos syndrome) and congenital or acquired coagulopathies can produce bleeding at any time of life [18].

Neonates — UGIB is rare in the first month of life but may occur for a variety of reasons (table 1) [7,19,20]. Important considerations include:

●Swallowed maternal blood – The most common cause of hematemesis in a healthy newborn is swallowed maternal blood during vaginal birth or while breastfeeding (due to bleeding from injured nipples or mammary ducts [sometimes called "rusty pipe syndrome"]). This can mimic UGIB but can be distinguished by the Apt-Downey test. (See 'Mimics of UGIB' below.)

●Stress gastritis or ulcers – These are associated with critical illness, but, in rare instances, they may occur spontaneously, even in the first few days of life [21-26].

●Congenital anomalies – Anomalies such as intestinal duplications or vascular anomalies may present with GI hemorrhage [27-33].

●Coagulopathy – Coagulopathy in a neonate usually presents with other bleeding symptoms, such as a large cephalohematoma after vaginal delivery, oozing from the umbilical stump, prolonged bleeding after circumcision or blood sampling, or intracranial hemorrhage in a term infant [34,35]. Occasionally, these coagulopathies come to medical attention because of GI bleeding, although this is rare during the neonatal period.

Several types of coagulopathies can present during the newborn period, including infection, liver failure, and congenital coagulation factor deficiency including von Willebrand disease and hemophilia. In addition, vitamin K-deficient bleeding (also known as hemorrhagic disease of the newborn) should be considered in neonates and older infants who were not given vitamin K prophylaxis at birth. (See "Overview of vitamin K", section on 'Vitamin K-deficient bleeding in newborns and young infants'.)

●Food protein intolerance – Food protein intolerance (sometimes described as an "allergy" and usually involving cow's milk) may present with UGIB, although lower GI bleeding (LGIB) is much more common. Care must be taken to exclude other causes of UGIB, as outlined below, because UGIB or passage of blood per rectum alone is not diagnostic of milk protein intolerance. (See "Food protein-induced allergic proctocolitis of infancy".)

Infants, children, and adolescents — The spectrum of causes of UGIB in children is similar to that of adults, although some risk factors vary with age (table 1) [19,36]. Particular considerations include:

●Mallory-Weiss syndrome – Mallory-Weiss syndrome (or Mallory-Weiss "tear") is characterized by longitudinal mucosal lacerations in the distal esophagus, usually developing after forceful retching. The bleeding is usually small and self-limited but occasionally is severe. (See "Mallory-Weiss syndrome".)

●Esophageal or GI foreign body – A foreign body can cause GI bleeding if it is sharp, caustic, and/or lodged in the esophagus. Clinical clues to this possibility include a history of a choking episode, even if it was transient. Rarely, ingestion of a button battery has led to severe UGIB due to aortoesophageal fistula, which can be fatal [37]. (See "Foreign bodies of the esophagus and gastrointestinal tract in children" and "Button and cylindrical battery ingestion: Clinical features, diagnosis, and initial management".)

●Esophagitis – Esophagitis in this age group usually is caused by gastroesophageal reflux disease, eosinophilic esophagitis, infection (primarily in immunosuppressed patients [herpes simplex virus, cytomegalovirus, Candida]), and, occasionally, by caustic ingestion. Peptic esophagitis also may develop after recurrent vomiting from other causes. (See "Gastroesophageal reflux disease in children and adolescents: Clinical manifestations and diagnosis" and "Caustic esophageal injury in children" and "Clinical manifestations and diagnosis of eosinophilic esophagitis (EoE)".)

●Peptic ulcers and gastritis – Gastritis and ulcers occasionally occur in all age groups, typically in the setting of critical illness or use of NSAIDs. Young children are particularly susceptible to developing UGIB after NSAID use [1]. Binge drinking of alcohol is an important cause of gastritis in adolescents. Gastritis or peptic ulcers also may be related to H. pylori infection or, occasionally, to a viral infection including cytomegalovirus [36]. In these disorders, epigastric discomfort and/or vomiting typically precede the hematemesis, which usually is low grade. (See "Causes of acute abdominal pain in children and adolescents", section on 'Peptic ulcer disease' and "Helicobacter pylori: Diagnosis and management in the pediatric patient" and "Chronic abdominal pain in children and adolescents: Approach to the evaluation".)

●Pill esophagitis – Pill esophagitis is caused by direct injury to the esophageal mucosa from prolonged contact with certain drugs, including tetracyclines (doxycycline and minocycline) that are commonly used for treatment of acne, or by NSAIDs, including aspirin, erythromycin, clindamycin, or bisphosphonates. The condition presents with pain with swallowing (odynophagia) and may progress to hematemesis. Similar symptoms may be caused by infectious esophagitis (due to Candida, cytomegalovirus, or herpes simplex). (See "Pill esophagitis" and "Gastroesophageal reflux disease in children and adolescents: Clinical manifestations and diagnosis", section on 'Dysphagia or odynophagia'.)

●Trauma – Placement or aggressive suctioning of a nasogastric tube can cause UGIB, especially in critically ill children and/or young children. This bleeding is generally minor but occasionally requires endoscopy to exclude other causes. In addition, epistaxis leading to swallowed blood can be mistaken for a UGIB. (See 'Mimics of UGIB' below.)

●Esophageal varices – Variceal bleeding is the most common cause of severe acute UGIB in children. Esophageal varices are caused by portal vein hypertension. Clues to portal hypertension include splenomegaly and/or a history of thrombocytopenia, even in a patient without a history of liver disease. Causes of portal hypertension include:

•Cirrhosis due to chronic liver disease (eg, cystic fibrosis-related liver disease, biliary atresia, intestinal failure-associated liver disease). (See "Cystic fibrosis: Hepatobiliary disease" and "Biliary atresia" and "Intestinal failure-associated liver disease in infants".)

•Portal vein thrombosis is most commonly associated with a history of umbilical vein catheterization or sepsis during the neonatal period. In some patients, the disorder first presents as an acute variceal bleed, which can be severe [38]. (See "Chronic portal vein thrombosis in adults: Clinical features, diagnosis, and management".)

•Hepatic vein obstruction (Budd-Chiari syndrome). (See "Budd-Chiari syndrome: Epidemiology, clinical manifestations, and diagnosis".)

●Arterial bleeding – Rarely, severe acute UGIB is from an artery, either from an overlying peptic ulcer or a Dieulafoy lesion [39,40]. (See "Causes of upper gastrointestinal bleeding in adults", section on 'Vascular lesions'.)

●Immunoglobulin A vasculitis – Immunoglobulin A vasculitis, formerly called Henoch-Schönlein purpura, typically presents with purpura, with variable combinations of arthralgias, abdominal pain, and kidney injury. The vasculitis can involve the upper and/or lower GI tract and often causes low-grade bleeding and, rarely, more significant hemorrhage. (See "IgA vasculitis (Henoch-Schönlein purpura): Clinical manifestations and diagnosis".)

●Other – Unusual causes of UGIB in children have been described in case reports, including other vasculitides, hemangiomas [29,41], aortoesophageal fistulas [37,42], hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome) [43], Kasabach-Merritt syndrome [44], duplication cysts [31,32,45], parasites [46], gastric polyps, annular pancreas [47,48], antral or duodenal web [49,50], systemic mastocytosis [19,36,51], or esophageal perforation [52].

Mimics of UGIB — The differential diagnosis of UGIB includes vomited blood originating from structures or organs other than the GI tract and ingested blood or blood-like substances:

●Swallowed maternal blood – Neonates and infants may swallow maternal blood during delivery or while nursing, and this can mimic UGIB [53]. One method to distinguish maternal from neonatal blood is the Apt-Downey test. This test differentiates the origin of the hemoglobin (Hgb) based on the conversion of oxyhemoglobin to hematin when mixed with alkali. Because fetal Hgb is resistant to denaturation in an alkaline solution, it remains red or pink, while adult Hgb discolors to a brownish yellow. The Apt-Downey test is valid for only the first few months of life because the percentage of fetal Hgb decreases sharply during this period. (See "Lower gastrointestinal bleeding in children: Causes and diagnostic approach", section on 'Swallowed maternal blood'.)

●Epistaxis – Swallowed blood from the child's nasopharynx or respiratory tract can cause hematemesis or melena and can be difficult to distinguish from UGIB [54]. To evaluate this possibility, routinely inquire about recent epistaxis and inspect the nares for evidence of venous injury in the anterior medial septums and other abnormalities, including a foreign body. (See "Evaluation of epistaxis in children".)

●Substances that resemble blood – Red food colorings and dyes (eg, red-colored drinks, candies, or liquid medications including some formulations of acetaminophen or ibuprofen) and some foods (eg, tomato peel, beets) in vomitus may be confused with blood. While this can frequently be suspected from this history, bedside tests for occult blood also can be helpful. These tests rely on color changes to detect the presence of Hgb. However, some of the commercial tests (such as Hemoccult) may produce false-negative results in the presence of acid. It is preferable to use a kit designed specifically for detection of blood in gastric secretions (eg, Gastroccult); this kit incorporates additional alkali to neutralize the gastric acid present in emesis [55].

Other substances can cause the stool to appear red (similar to fresh blood) or black (similar to melena), as outlined in the table (table 2). If needed, hemoccult testing can often (but not always) distinguish blood from a mimic. However, point-of-care hemoccult tests can be inaccurate.

●Lower respiratory tract bleeding – Children with acute or chronic pulmonary disease can very rarely have lower respiratory tract bleeding with hemoptysis that mimics UGIB.

●Medical child abuse – Rare cases of factitious UGIB have been reported, in which blood or blood-like substance was surreptitiously administered to a child by a caregiver [56]. The patient or siblings may have a history of frequent recurrent illnesses without a clear etiology. (See "Medical child abuse (Munchausen syndrome by proxy)".)

CLINICAL PRESENTATION — 

Acute clinically significant UGIB typically presents with hematemesis and/or melena. Isolated coffee ground emesis generally indicates a slower rate of bleeding and is often clinically insignificant.

●Hematemesis – Bright red blood usually indicates brisk or very fresh bleeding. In one study of children who underwent endoscopy for UGIB, 73 percent presented with hematemesis [5].

The presence of coffee ground-like material in emesis is a very common complaint in the emergency department setting, often in the context of frequent vomiting in children with acute gastroenteritis (see "Mallory-Weiss syndrome"). The coffee ground appearance generally indicates a slower rate of bleeding. In the absence of signs of hemodynamic instability, such children do not require further investigations and can be treated symptomatically. The coffee ground appearance is caused by the effect of gastric acid on blood.

●Melena – Melena (dark red or black and sticky stools) usually indicates UGIB. In one study of children who underwent endoscopy for UGIB, 20 percent presented with melena [5]. However, melena occasionally can be seen with bleeding from a source in the proximal lower GI tract (eg, the proximal jejunum or, occasionally, ileum [eg, some cases of Meckel diverticulum [57]]).

●Hematochezia – Hematochezia (bright red blood in stool) usually indicates a lower GI source (eg, colitis, proctitis, superficial anal bleeding, ileum [Meckel diverticulum [57]]). However, it is occasionally seen with clinically significant UGIB, especially in neonates and infants (compared with older children or adults) because of their short intestinal transit time [2]. (See "Lower gastrointestinal bleeding in children: Causes and diagnostic approach", section on 'Diagnostic approach'.)

●Occult blood in stool – Occult blood in stool (without melena or hematochezia) can be a consequence of either UGIB or lower GI bleeding (LGIB). It tends to indicate a slower rate and/or lower volume of bleeding, which may not be clinically significant.

●Hypovolemic shock – This has been reported as the presenting symptom in approximately 3 percent of children [1].

INITIAL ASSESSMENT

Rapid assessment — The initial evaluation of the patient with UGIB should include (algorithm 1):

●Hemodynamic assessment – Vital signs, including the heart rate, blood pressure, presence of orthostatic changes, and capillary refill, are used to assess and monitor the hemodynamic state of the patient. Supportive signs of hypovolemia include pallor, mottling, and cool skin. (See "Assessment of systemic perfusion in children".)

●Focused history – The initial rapid history should include risk factors for severe UGIB, including known liver disease, bleeding disorders in the child or family, and/or current use of nonsteroidal antiinflammatory drugs (NSAIDS) or ethanol.

●Focused physical examination – Key assessments are inspection of the nares and oropharynx for evidence of epistaxis (which can mimic UGIB), abdominal examination to elicit evidence of tenderness, signs of an acute abdomen, or features of liver disease (hepato- or splenomegaly suggestive of portal hypertension and risk of esophageal varices). If a gastrostomy tube is present, aspiration should be performed to assess for the presence of blood. Bruising or petechiae could suggest a coagulopathy or thrombocytopenia.

●Blood tests – In general, routine laboratory testing is of limited utility and the need should be guided by results of the history and examination. If there are concerns for clinically significant UGIB based on symptoms or risk factors (eg, melena, hematochezia, unwell appearance, moderate to large volume of fresh blood in the vomitus), a complete blood count including platelets, prothrombin time/partial thromboplastin time, international normalized ratio, and blood type and screen should be obtained urgently. Note that the initial hematocrit may be normal in children with acute bleeds because it takes time for extravascular fluid to accumulate, which is required to lower the hematocrit. If the initial hemoglobin (Hgb) or hematocrit is abnormal, or if bleeding continues, repeat the measurement every two to six hours or as clinically indicated. (See 'Laboratory evaluation' below.)

●Nasogastric tube – A nasogastric tube is generally not needed for the diagnosis or management of UGIB (except possibly to obtain a sample for the Apt-Downey test in a neonate to identify swallowed maternal blood). (See 'Nasogastric tube (generally not needed)' below.)

Bleeding severity

●Features of severe bleeding – Clinical features that suggest a clinically significant acute UGIB are (table 3) [2,58]:

•Hemodynamic instability (tachycardia or prolonged capillary refill time, with or without hypotension) or generally unwell appearance

•Melena or large hematochezia

•Large-volume hematemesis or nasogastric aspirates (if performed), although the amount of blood can be very difficult to estimate due to dilution

•Known or suspected esophageal varices (eg, known liver disease or splenomegaly) or previous intestinal surgery

•Significant anemia (ie, Hgb >20 percent below lower limit for age, decrease of >20 percent from a recent value, or need for transfusion [58,59])

●Acute severe UGIB – Children with any of the above signs should be resuscitated in an acute care setting (emergency department or intensive care unit) in consultation with a gastroenterologist. The priority is to achieve hemodynamic stability, then to identify the source of the bleeding, usually with upper endoscopy within 24 to 48 hours of presentation. (See 'Stabilization' below and 'Patients with severe or persistent UGIB' below.)

●Nonsevere UGIB – Children without the above signs are less likely to have severe UGIB. Most children can be evaluated in an outpatient setting, with the need for further testing, treatment, and hospitalization determined based on the likely etiology. (See 'Further assessment' below and 'Patients with nonsevere UGIB' below.)

FURTHER ASSESSMENT

History — The clinical history should include information concerning the time course of the bleeding episode, estimated blood loss, and any associated symptoms (table 4). The presence of hematemesis, coffee ground appearance, melena, or hematochezia should be documented; these characteristics provide clues about the source, rate, and volume of bleeding (see 'Clinical presentation' above). Particular attention should be given to GI symptoms including vomiting, heartburn, abdominal pain, dysphagia, and weight loss. In infants, these features may be reflected in poor feeding and irritability.

The history should also include information about the following symptoms or signs, which may provide clues to an underlying disorder:

●Signs and symptoms:

•Vomiting or retching – A history of forceful and frequent vomiting that preceded the UGIB suggests possible Mallory-Weiss syndrome.

•Diarrhea – Points to acute infectious gastroenteritis as a possible etiology for vomiting.

•Jaundice or change in stool color – Possible underlying liver disease.

•Epistaxis – Possible nasopharyngeal (rather than GI) source of bleeding. (See 'Mimics of UGIB' above.)

•Easy bruising or bleeding – Possible thrombocytopenia, platelet dysfunction, or coagulation disorder (including related to liver disease or disseminated intravascular coagulation due to sepsis). In neonates, it is crucial to confirm that the routine neonatal dose of vitamin K was administered. (See "Overview of the routine management of the healthy newborn infant", section on 'Vitamin K'.)

●Maternal cracked nipples – Relevant in breastfeeding infants. If present, the infant's hematemesis may be due to swallowed maternal blood rather than a GI source.

●Foreign body ingestion – For young children (eg, <5 years), inquire about possible foreign body ingestion (eg, button battery), including access to small objects, putting objects in mouth, and/or a choking episode.

●Medical and family history – A history of hepatobiliary disease, including cirrhosis, cystic fibrosis, biliary atresia, portal vein thrombosis, or Budd-Chiari syndrome raises the possibility of variceal bleeding. A personal or family history of H. pylori infection, liver or kidney disease, or coagulation disorder may provide clues to a specific disorder. (See "Helicobacter pylori: Diagnosis and management in the pediatric patient" and "Chronic kidney disease in children: Complications" and "Approach to the child with bleeding symptoms".)

Patients with congenital heart disease associated with right heart failure are at risk for developing GI angiodysplasia and/or liver disease, leading to esophageal varices. (See "Angiodysplasia of the gastrointestinal tract" and "Management of complications in patients with Fontan circulation", section on 'Liver disease'.)

●Medications – A drug history is important to assess potential contributions from medications, including:

•Nonsteroidal antiinflammatory drugs (NSAIDs) and corticosteroids, which may induce ulceration. Even short-term use of NSAIDs, especially at high doses, can cause gastric ulcers [60]. Clinicians should also ask about the use of over-the-counter "cold and flu" medications since some of these products contain NSAIDs (eg, ibuprofen, aspirin) or acetaminophen. If the patient and family are not aware of these ingredients, they may administer these drugs separately, which can lead to excessive doses and NSAID-related UGIB or acetaminophen-related hepatotoxicity. (See "Peptic ulcer disease: Epidemiology, etiology, and pathogenesis", section on 'NSAIDs, including aspirin'.)

•Tetracyclines, which are commonly used to treat acne, may cause pill esophagitis. (See "Pill esophagitis".)

•Antiplatelet medications (eg, aspirin and other NSAIDs) and anticoagulants (eg, warfarin, enoxaparin, direct oral anticoagulants) can exacerbate bleeding from another cause. Certain herbal medicines can also contribute to abnormal bleeding (eg, ginger, feverfew, ginkgo biloba). (See "Approach to the child with bleeding symptoms", section on 'Medications'.)

In addition, it is important to know if the patient is taking medication or has a cardiac condition that impairs the physiologic response to anemia (eg, if the patient is taking a beta blocker or has a pacemaker) because these may mask tachycardia associated with life-threatening blood loss.

●Other – Alcohol ingestion (in particular, binge drinking) increases acid secretion and can cause dyspepsia and gastritis, which is generally associated with nonsevere or chronic UGIB. Alcohol and tobacco use also can contribute to the risk of peptic ulcer disease in the presence of other major risk factors such as NSAID use or H. pylori infection. (See "Peptic ulcer disease: Epidemiology, etiology, and pathogenesis".)

Physical examination — The rapid assessment of hemodynamic status is described above. The remainder of the physical examination should include the following elements, which suggest possible sources for the bleeding (table 5):

●Skin and mucus membranes

•Pallor, mottling, or cool skin – Suggests hypovolemia and/or anemia due to substantial blood loss. In children with dark skin pigmentation, pallor is best appreciated in the palpebral conjunctivae, buccal mucosa, palmar creases, and nailbeds.

•Peripheral pulses or capillary refill – Absent or weak pulses or delayed capillary refill could also indicate hypovolemia and/or anemia.

•Bruising, petechiae, or mucosal bleeding – Depending on the presentation and pattern, these findings may suggest a bleeding disorder (eg, coagulopathy, thrombocytopenia). (See "Approach to the child with bleeding symptoms".)

•Vascular malformations – The presence of cutaneous hemangiomas (especially five or more) suggests the possibility of GI hemangiomatosis. However, up to 50 percent of infants with visceral hemangiomas do not have cutaneous hemangiomas [41]. Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome) is characterized by mucocutaneous telangiectasia (picture 1) and commonly presents with recurrent epistaxis and/or GI bleeding. (See "Infantile hemangiomas: Epidemiology, pathogenesis, clinical features, and complications" and "Clinical manifestations and diagnosis of hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)".)

●Nasopharynx – Inspection of the nasopharynx for evidence of disrupted mucosa or inflamed tonsils, as well as inspection of the anterior nares and hypopharynx for evidence of epistaxis. If present, these findings suggest the possibility of a nasopharyngeal bleed with swallowed blood, rather than UGIB. (See 'Mimics of UGIB' above and "Evaluation of epistaxis in children".)

●Abdomen – Abdominal examination for evidence of tenderness; signs of an acute abdomen; or features suggestive of liver disease and portal hypertension, such as hepato- or splenomegaly, ascites, or prominent cutaneous abdominal and hemorrhoidal vessels and a protruding abdomen. Portal hypertension often leads to esophageal varices, which may hemorrhage.

Laboratory evaluation — The laboratory assessment depends on the clinical scenario and magnitude of the blood loss:

●All patients – For patients with coffee ground vomitus or a small amount (eg, flecks) of blood in the vomitus and a likely explanation (eg, assessment consistent with gastritis or Mallory-Weiss syndrome), laboratory testing is not routinely indicated.

For patients with risk factors or historical or clinical features concerning for a significant UGIB, perform a complete blood count including platelet count, coagulation studies (partial thromboplastin time and international normalized ratio), blood urea nitrogen (BUN), and serum creatinine. If the initial hemoglobin (Hgb) or hematocrit is abnormal, or if bleeding continues, repeat the measurement every two to six hours as clinically indicated.

An elevated BUN-to-creatinine ratio (>30) strongly suggests a UGIB (98 to 100 percent specific) because blood in the proximal GI tract has relatively more time to be absorbed, leading to an increase in the BUN [61,62]. However, a lower ratio does not rule out UGIB (<70 percent sensitivity).

Alanine aminotransferase, aspartate aminotransferase, bilirubin, and albumin levels can help evaluate liver function and assess for evidence of hepatocellular injury.

●Severe acute UGIB or known varices – Include a specimen to type and crossmatch blood in case transfusion is required.

●Epigastric pain – For those with marked epigastric abdominal pain, include a lipase to evaluate for pancreatitis, which can be associated with gastritis, duodenitis, and peptic ulcer disease.

Helicobacter pylori testing — This should be considered in children with peptic ulcer disease symptoms such as epigastric abdominal pain or tenderness, dysphagia, or odynophagia along with UGIB. The approach to testing is discussed separately. (See "Helicobacter pylori: Diagnosis and management in the pediatric patient".)

Imaging — Imaging tests can be helpful in specific clinical settings:

●Conventional (plain) radiographs are helpful to evaluate for bowel obstruction or perforation (eg, as complications of peptic ulcer disease) in patients with significant abdominal pain, distension, or tenderness. They are also appropriate if foreign body ingestion is suspected from the clinical history, as an initial step. However, many foreign bodies are radiolucent, so a normal plain radiograph may not exclude foreign body ingestion. (See "Emergency evaluation of the child with acute abdominal pain", section on 'Imaging' and "Foreign bodies of the esophagus and gastrointestinal tract in children", section on 'Imaging'.)

●Abdominal ultrasound can be used to evaluate for the presence of hepato- or splenomegaly and portal hypertension and should be performed in patients with severe acute UGIB suggestive of variceal bleeding, known or suspected liver disease, or signs of portal hypertension on examination (eg, splenomegaly, prominent abdominal wall vessels).

●A UGI contrast study can identity the presence of intestinal malrotation with intermittent volvulus. If this test is planned, water-soluble contrast should be used. Barium contrast should not be used in the setting of UGIB, because the contrast will interfere with subsequent endoscopy, angiography, or surgery.

Endoscopy — Endoscopy is often required in patients with UGIB for both diagnostic and therapeutic purposes, as discussed below. Endoscopy is usually indicated within 24 to 48 hours for those with severe or ongoing UGIB. (See 'Endoscopy' below.)

Other diagnostic tests — Rarely, angiography or radionuclide imaging may be needed to identify a source of bleeding:

●Angiography may be useful in patients with rapid bleeding in whom endoscopy is unsuccessful in finding a source. For diagnostic purposes, magnetic resonance angiography or computed tomographic angiography may be used [63,64]; the preferred method may be specific to a particular institution. For therapeutic purposes, conventional contrast angiography with embolization may be useful in treating some patients with vascular anomalies, hemobilia, or some ulcers that are not amenable to other types of treatment [65]. (See "Angiographic control of nonvariceal gastrointestinal bleeding in adults".)

●Radionuclide imaging (a tagged red blood cell [RBC] scan) also can be used to detect an obscure bleeding source for patients with very brisk bleeding. However, this is only helpful for suspected lower GI bleeding (LGIB) that cannot be localized by other means. It is not helpful to evaluate for UGIB, because endoscopy is far more sensitive for evaluating bleeding in the UGI tract. (See "Evaluation of suspected small bowel bleeding (formerly obscure gastrointestinal bleeding)".)

MANAGEMENT — 

Management of UGIB depends on the severity and clinical course, as summarized in the algorithm (algorithm 1).

Stabilization — Patients with hemodynamic instability (tachycardia, poor perfusion, hypotension) require emergency resuscitation and close observation in an intensive care unit. Such patients should be stabilized prior to endoscopy. Both a gastroenterologist and a surgeon should be notified promptly of all patients with severe acute UGIB.

●Airway and breathing – Respiratory support should be provided to patients with respiratory distress or an inability to maintain their airway. (See "Acute respiratory distress in children: Emergency evaluation and initial stabilization" and "Technique of emergency endotracheal intubation in children".)

●Circulation – Patients with hemodynamic instability (tachycardia, poor perfusion, hypotension) require emergency resuscitation.

•Resuscitation requires intravenous (IV) access, which can be difficult in severely volume-depleted patients (algorithm 2). Intraosseous or central venous access may be required in this setting. (See "Emergency and elective venous access in children", section on 'Emergency venous access' and "Intraosseous infusion".)

•Fluid resuscitation begins with a balanced crystalloid IV fluid (eg, Lactated Ringer, PlasmaLyte) or with 0.9% saline. (See "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management", section on 'Fluid resuscitation'.)

•Red blood cell (RBC) transfusion may be necessary in patients with significant blood loss, as discussed below (see 'Transfusion' below). Coagulation abnormalities should be managed aggressively with IV vitamin K (given empirically for patients with liver disease), fresh frozen plasma, and platelets as needed.

Patients with nonsevere UGIB — Most patients presenting to an emergency department with UGIB have nonsevere bleeding with a likely explanation (eg, Mallory-Weiss syndrome, gastritis). For these patients, supportive care with observation generally is sufficient and many patients (eg, those with coffee ground emesis, those who vomited a small amount [eg, flecks] of blood and are otherwise well) can be discharged home following initial evaluation. Patients suspected of having nonspecific mucosal lesions (eg, esophagitis, gastritis, duodenitis) may benefit from neutralization of gastric acidity through administration of antacids or oral proton pump inhibitors (PPIs) to reduce the risk of rebleeding. Those with ongoing vomiting due to acute viral gastroenteritis may benefit from ondansetron. (See "Acute viral gastroenteritis in children in resource-abundant countries: Management and prevention", section on 'Antiemetic agents'.)

Patients with severe or persistent UGIB — Clinical features suggesting a severe acute UGIB are summarized in the table (table 3) (see 'Bleeding severity' above). For these patients, the first priority is to achieve hemodynamic stability. (See 'Stabilization' above.)

After stabilization, management typically includes one or more of the following interventions:

Nasogastric tube (generally not needed) — Placement of a nasogastric tube is not routinely necessary in most patients with UGIB. Considerations include:

●Diagnostic – Placement of a nasogastric tube and gastric lavage is no longer routinely recommended for diagnostic purposes or for monitoring the rate of bleeding, primarily based on studies in adults showing that routine lavage does not improve outcomes [66-68]. However, practice varies and some clinicians place a nasogastric tube when they are concerned that the hemorrhage may be severe and ongoing, to help estimate the quantity and pace of bleeding. In addition, a nasogastric tube may be needed to obtain a sample for the Apt-Downey test in a neonate to identify swallowed maternal blood. (See "Lower gastrointestinal bleeding in children: Causes and diagnostic approach", section on 'Swallowed maternal blood'.)

●Therapeutic – Lavage should not be used for therapeutic purposes, because it does not slow bleeding. In particular, the historical practice of using cold (eg, ice water) fluids is not recommended, because it is ineffective [69] and may induce iatrogenic hypothermia, particularly in infants and small children. Moreover, frequent lavage can lead to electrolyte imbalances.

●Endoscopy preparation – To remove particulate matter from the stomach to facilitate endoscopy, the use of a prokinetic medication (eg, erythromycin) is generally preferred rather than lavage, based on adult guidelines and supported by clinical practice in children [68,70].

If the decision is made to perform lavage, room-temperature water or normal saline should be used and electrolytes should be monitored.

Medications — Acid suppression usually is appropriate for children with clinically significant UGIB to treat or prevent any peptic component of the underlying disorder. Vasoactive agents may be helpful for selected cases of vascular bleeding (eg, from esophageal varices). The most commonly used drugs and doses are summarized in the table (table 6).

Acid suppression — We suggest acid suppression for children with clinically significant UGIB. For hemodynamically unstable children or those with large-volume bleeding or frequent vomiting, we suggest an IV preparation of a PPI (esomeprazole or pantoprazole). For hemodynamically stable children with nonsevere bleeding, we suggest oral administration of a PPI, such as esomeprazole, omeprazole or pantoprazole.

This suggestion for acid suppression is primarily based on studies in adults that examined the effect of acid suppression given before or after endoscopy (with or without therapeutic intervention). In the setting of active UGIB due to peptic ulcers, high-dose antisecretory therapy with an IV infusion of PPI significantly reduced the rate of rebleeding compared with standard treatment in patients with bleeding ulcers. Oral and IV PPI therapy also decrease the hospital stay, rebleeding rate, and need for blood transfusion in adult patients with high-risk ulcers treated with endoscopic therapy. (See "Overview of the treatment of bleeding peptic ulcers", section on 'Acid suppression'.)

Octreotide — Octreotide is a somatostatin analog that can be used to help control variceal bleeding in select patients, eg, before endoscopy or when endoscopy is unsuccessful, contraindicated, or unavailable [71-73]. It reduces bleeding by decreasing lymphatic, splanchnic, hepatic, and portal blood flow and by modulating the motility of the stomach and small bowel [74]. Although octreotide and somatostatin have similar effects, octreotide is generally preferred in clinical practice because it has higher resistance to degradation and a longer half-life (one to two hours) compared with somatostatin (two to three minutes).

Octreotide is most commonly administered as an initial bolus of 1 to 2 micrograms/kg body weight (maximum 50 micrograms) over 30 minutes, followed by 1 to 2 micrograms/kg/hour as a continuous IV infusion [73]. The infusion rate should be titrated to the response. Adverse effects include bradycardia and hyperglycemia. If bleeding stops, octreotide doses are typically tapered gradually over approximately 24 hours. Discovering and treating the cause of the GI bleed should remain the priority.

The use of octreotide for the management of severe acute UGIB in children is based primarily on evidence of efficacy in adults when used in association with endoscopic procedures for the treatment of esophageal variceal bleeding in cirrhotic patients [75]. Importantly, octreotide administration reduces the risk of rebleeding in adult patients with variceal hemorrhage [76,77]. In addition, these medications may reduce the risk of bleeding due to nonvariceal causes [78]. Evidence in children is sparse, but small case series describe use of octreotide to control severe UGIB including acute variceal bleeding [71-73,79-81]. (See "Methods to achieve hemostasis in patients with acute variceal hemorrhage", section on 'Pharmacologic therapy'.)

Transfusion — RBC transfusion is appropriate for children with significant blood loss due to severe acute UGIB. This includes:

●Patients with hemodynamic instability that persists despite IV fluid resuscitation – In these patients, RBC transfusion is appropriate regardless of the hemoglobin (Hgb) level. In patients requiring large-volume blood replacement, use of a massive transfusion protocol including whole blood may be beneficial [82]. (See "Red blood cell transfusion in infants and children: Selection of blood products", section on 'Whole blood'.)

●Hemodynamically stable patients with Hgb <8 g/dL – We suggest using a Hgb threshold of 8 g/dL to trigger RBC transfusion in most hemodynamically stable patients with severe acute UGIB. This value is slightly higher than the restrictive transfusion threshold (Hgb 7 g/dL) used for most pediatric patients with other types of critical illness [83]. The rationale for transfusing at a higher Hgb value in patients with acute UGIB is that these patients may have ongoing or recurrent bleeding and are likely to have a subsequent drop in Hgb. Moreover, dehydration due to vomiting or diarrhea may artificially raise Hgb.

Additional details regarding RBC transfusion in children are provided separately. (See "Red blood cell transfusion in infants and children: Indications" and "Red blood cell transfusion in infants and children: Administration and complications" and "Approach to the patient who declines blood transfusion".)

Correction of coagulopathy — If there is evidence of coagulopathy or thrombocytopenia, management should be based on the likely cause and severity of the abnormality:

●For patients with known or suspected liver disease, empiric administration of vitamin K (single dose of 1 mg for infants or 5 mg for adolescents) should be administered. Improvement in the coagulopathy suggests that it was caused by vitamin K deficiency. Lack of improvement suggests that it was caused by liver failure. (See "Acute liver failure in children: Management, complications, and outcomes", section on 'Coagulopathy'.)

●Patients receiving anticoagulant therapy who experience severe UGIB may require reversal of the anticoagulant. Guidance for reversal of different anticoagulant classes is provided separately. (See "Heparin and LMW heparin: Dosing and adverse effects", section on 'Reversal' and "Management of warfarin-associated bleeding or supratherapeutic INR" and "Management of bleeding in patients receiving direct oral anticoagulants".)

●Patients with underlying bleeding disorders (eg, hemophilia, von Willebrand disease) may require factor replacement, as discussed separately. (See "Acute treatment of bleeding and surgery in hemophilia A and B" and "von Willebrand disease (VWD): Treatment of major bleeding and major surgery".)

●For patients with thrombocytopenia, transfusion of platelets (targeting a platelet count >50,000/microL) is generally warranted if there is severe ongoing bleeding. (See "Platelet transfusion: Indications, ordering, and associated risks", section on 'Actively bleeding patient' and "Approach to the child with unexplained thrombocytopenia", section on 'Diagnostic evaluation' and "Approach to the child with bleeding symptoms", section on 'Diagnostic approach'.)

Endoscopy — Endoscopy should be performed within 24 to 48 hours for infants and children presenting with acute severe UGIB, [84]. Earlier endoscopy with hemostatic interventions may be needed if bleeding cannot be controlled (eg, for active variceal bleeding). Hemodynamically unstable patients should be stabilized prior to endoscopy, including transfusion and correction of coagulopathy if present. Endoscopy is also appropriate for children with low-grade bleeding that is unexplained and persistent or recurrent [19].

Upper endoscopy permits identification of the bleeding source, allows for risk stratification regarding the likelihood of continued bleeding, and permits therapeutic intervention. Multiple reports have attested to the safety of upper endoscopy in children [85-89]. The techniques involved in performing an endoscopy and therapeutic intervention are similar for children and adults and include thermal coagulation or clips for bleeding ulcers, ligation (banding) or sclerotherapy for variceal bleeding, and, in some cases, topical hemostatic agents [90]. (See "Overview of the treatment of bleeding peptic ulcers" and "Methods to achieve hemostasis in patients with acute variceal hemorrhage".)

However, there are several considerations pertinent to children:

●Children often require deep sedation or general anesthesia for upper endoscopy. For patients with active or severe bleeding, or if endoscopic therapy is anticipated, general anesthesia with endotracheal intubation is appropriate. This approach optimizes the examination and minimizes the risk of aspiration of the blood. Moreover, in some series, use of general anesthesia, administered by a dedicated anesthesiologist, was associated with a lower rate of complications compared with use of deep sedation [91,92]. Children undergoing endoscopy for a GI bleed should be carefully monitored during the procedure; sedation in these cases should be guided by a clinician experienced in anesthesiology or intensive care.

●Smaller-caliber endoscopes limit the size of catheters that can be passed through the working channel.

●For bleeding from esophageal varices, band ligation is often possible. However, the use of this technique in small children is limited by the small diameter of the esophagus [93-96]. In small children, an overtube generally should be avoided [19]. (See "Endoscopic variceal ligation".)

Surgery or contrast angiography with embolization is reserved for the uncommon patients in whom endoscopy fails to control bleeding or in whom an anatomic abnormality exists that requires surgery, as well as if the patient cannot be fully stabilized despite resuscitative measures.

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Gastrointestinal bleeding in children" and "Society guideline links: Acquired bleeding disorders" and "Society guideline links: Rare inherited bleeding disorders" and "Society guideline links: Peptic ulcer disease".)

INFORMATION FOR PATIENTS — 

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient education" and the keyword(s) of interest.)

●Basics topics (see "Patient education: GI bleed (The Basics)" and "Patient education: GI bleed – Discharge instructions (The Basics)" and "Patient education: Upper endoscopy (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Clinical presentation – Upper gastrointestinal bleeding (UGIB) can present with hematemesis (vomiting of blood or coffee ground-like material) and/or melena (black, tarry stools). The appearance of the stool is not a reliable indicator of the source of the bleeding. Although melena suggests UGIB, it may also occur in patients with proximal lower GI bleeding (LGIB). Conversely, patients with brisk UGIB and rapid intestinal transit time occasionally present with hematochezia, particularly if they are infants or toddlers. (See 'Clinical presentation' above.)

●Causes – The most common causes of UGIB in children vary depending on age and geographic setting. In North America and European countries, the most common causes are Mallory-Weiss tears, gastric and duodenal ulcers (often related to nonsteroidal antiinflammatory drugs [NSAIDs]), esophagitis, gastritis, and varices (table 1). Very rapid UGIB is characteristic of variceal hemorrhage and may be the presenting symptom of portal hypertension. (See 'Etiology' above.)

●Clinical assessment – Initial assessment and stabilization of the patient with UGIB is summarized in the algorithm (algorithm 1).

•Rapid assessment – The initial evaluation of the patient with UGIB involves an assessment of hemodynamic stability and severity of bleeding. (See 'Rapid assessment' above.)

Features of severe acute UGIB are outlined in the table (table 3). (See 'Bleeding severity' above.)

•History and physical examination – The pattern of vomiting, associated symptoms, and underlying diseases help to identify the likely cause of the bleeding, as summarized in the table (table 4). On the physical examination, important clues include bruises, petechiae, or mucosal bleeding (suggesting a bleeding disorder or trauma), as well as splenomegaly (suggesting portal hypertension) (table 5). Key considerations include:

-History of recent NSAID use, which is an important risk factor for gastritis and peptic ulcer disease.

-History of frequent nonbloody emesis, retching, or forceful coughing prior to the onset of UGIB, which suggests a Mallory-Weiss tear.

-History of epistaxis and/or signs of blood in the nose and oropharynx suggest a nasopharyngeal bleeding source. Swallowed blood from the nasopharynx may present with hematemesis or melena and may be difficult to distinguish from UGIB. (See 'Mimics of UGIB' above and 'Physical examination' above.)

●Management – Management of UGIB depends on the severity and clinical course (algorithm 1).

•Nonsevere UGIB – Most patients presenting to an emergency department with UGIB have nonsevere bleeding with a likely explanation (eg, Mallory-Weiss syndrome, gastritis). For these patients, supportive care with observation generally is sufficient, usually with acid suppression. Those with ongoing vomiting due to acute viral gastroenteritis may benefit from ondansetron. Their disposition depends on the identified source and clinical course during the evaluation. (See 'Patients with nonsevere UGIB' above.)

•Acute severe UGIB – Children with severe UGIB should be resuscitated in an acute care setting (emergency department or intensive care unit) in consultation with a gastroenterologist. The first priority is to achieve hemodynamic stability, then to identify and treat the source of the bleeding. (See 'Patients with severe or persistent UGIB' above.)

-Initial stabilization – Patients with severe UGIB should be stabilized and closely monitored in an intensive care unit prior to endoscopy. Patients with hemodynamic instability (tachycardia, poor perfusion, hypotension) require fluid resuscitation; red blood cell (RBC) transfusion may be necessary in patients with significant blood loss. Coagulopathy, if present, should be corrected prior to endoscopy. (See 'Stabilization' above and 'Transfusion' above and 'Correction of coagulopathy' above.)

-Acid suppression – For all patients with clinically significant UGIB, we suggest treatment with a proton pump inhibitor (PPI; eg, esomeprazole, pantoprazole) (Grade 2C). In patients with severe acute UGIB, the PPI is given intravenously (IV) and is started during the initial management prior to endoscopy. Dosing guidance is provided in the table (table 6). Subsequent dosing depends on the endoscopic findings. (See 'Acid suppression' above.)

-Preendoscopic management – Placement of a nasogastric tube is not necessary in most patients with UGIB. For patients with acute severe UGIB, either erythromycin administration or nasogastric tube lavage is performed shortly before endoscopy to remove fresh blood or particulate matter from the stomach to facilitate endoscopy. (See 'Nasogastric tube (generally not needed)' above.)

-Endoscopy – Upper endoscopy should be performed in patients with acute severe UGIB or lower-grade persistent or recurrent hemorrhage. Endoscopy usually permits identification of the bleeding source, allows for risk stratification regarding the likelihood of continued bleeding, and may permit therapeutic intervention (eg, for bleeding ulcers or variceal bleeding). (See 'Endoscopy' above.)

•Treatment of the underlying cause – If a source of bleeding is identified on endoscopy, treatment should be targeted at the specific cause, as discussed in separate topic reviews:

-Mallory-Weiss syndrome (see "Mallory-Weiss syndrome", section on 'Post-endoscopic management')

-Gastric and duodenal ulcers (see "Overview of the treatment of bleeding peptic ulcers")

-Esophagitis and gastritis (see "Gastroesophageal reflux disease in children and adolescents: Management", section on 'Esophagitis')

-Varices (see "Methods to achieve hemostasis in patients with acute variceal hemorrhage")