Gastrointestinal Bleeding and Management




There is a broad clinical spectrum of gastrointestinal bleeding in children, ranging from subtle laboratory findings to dramatic clinical presentations. This review provides a framework for the evaluation and management of gastrointestinal hemorrhage for pediatricians. It outlines strategies for obtaining a tailored patient history and conducting a thorough physical examination that can shed light on the location, severity, and likely etiology of bleeding. It appraises blood tests, radiologic tools, and endoscopic modalities frequently used to identify and control a source of bleeding.


Key points








  • There is a broad clinical spectrum of gastrointestinal hemorrhage.



  • Obtaining an accurate history and conducting a thorough physical examination can provide important clues about the location, severity, and likely etiology of gastrointestinal bleeding.



  • There are blood tests, radiologic tools, and endoscopic methods to identify a bleeding source.



  • Early consultation with a gastroenterologist is recommended, as endoscopy is often required for evaluation and may be needed to control hemorrhage.






Introduction


The presentation of gastrointestinal bleeding in children can vary from subtle findings of pallor and iron-deficiency anemia to obvious episodes of vomiting frank blood. Children present with this chief complaint in a variety of clinical settings, but there is a paucity of literature capturing the epidemiology of pediatric gastrointestinal hemorrhage. Gastrointestinal bleeding can manifest in several ways. Hematemesis is the expulsion of bright red or “coffee-ground” colored material from the mouth. This usually indicates bleeding proximal to the Ligament of Treitz, as fresh red blood exposed to an acidic environment turns brown. Melena typically correlates with an esophageal, gastric, or proximal small intestinal bleeding source and leads to passage of black, tarry stool per rectum. This appearance can be attributed to oxidization by intestinal bacteria that convert hemoglobin to hematin. In contrast, hematochezia is bright red or maroon-colored material that passes from the rectum. Although hematochezia most often occurs with lower small intestinal or colonic bleeding sources, a brisk upper gastrointestinal bleed may present as bright red blood per rectum, with blood in the intestinal lumen acting as a cathartic agent and accelerating transit. Obscure gastrointestinal bleeding is blood loss that is not identified by upper endoscopy, colonoscopy, and radiologic evaluation of the small intestine. It can be further classified into obscure overt and obscure occult bleeding, based on extent of clinically obvious bleeding. There are many exhaustive reviews of etiologies of pediatric gastrointestinal bleeding. Our goal is to provide a framework for evaluation of patients with gastrointestinal bleeding and to review management principles.




Introduction


The presentation of gastrointestinal bleeding in children can vary from subtle findings of pallor and iron-deficiency anemia to obvious episodes of vomiting frank blood. Children present with this chief complaint in a variety of clinical settings, but there is a paucity of literature capturing the epidemiology of pediatric gastrointestinal hemorrhage. Gastrointestinal bleeding can manifest in several ways. Hematemesis is the expulsion of bright red or “coffee-ground” colored material from the mouth. This usually indicates bleeding proximal to the Ligament of Treitz, as fresh red blood exposed to an acidic environment turns brown. Melena typically correlates with an esophageal, gastric, or proximal small intestinal bleeding source and leads to passage of black, tarry stool per rectum. This appearance can be attributed to oxidization by intestinal bacteria that convert hemoglobin to hematin. In contrast, hematochezia is bright red or maroon-colored material that passes from the rectum. Although hematochezia most often occurs with lower small intestinal or colonic bleeding sources, a brisk upper gastrointestinal bleed may present as bright red blood per rectum, with blood in the intestinal lumen acting as a cathartic agent and accelerating transit. Obscure gastrointestinal bleeding is blood loss that is not identified by upper endoscopy, colonoscopy, and radiologic evaluation of the small intestine. It can be further classified into obscure overt and obscure occult bleeding, based on extent of clinically obvious bleeding. There are many exhaustive reviews of etiologies of pediatric gastrointestinal bleeding. Our goal is to provide a framework for evaluation of patients with gastrointestinal bleeding and to review management principles.




Discussion


Historical Report


A careful history may shed light on the source of bleeding and rate of blood loss. It is important to inquire about the color, quantity, and location of bleeding. The temporal association of the bleeding episode to other signs and symptoms, including abdominal pain, vomiting, and fevers should be characterized. Eliciting this history in an emergency scenario with distraught patients or unwitnessed events can be challenging. For instance, hemoptysis can be mistaken for hematemesis. However, unveiling key historical details may provide critical clues to localize the bleeding source. A history of recent tonsillectomy, dental procedure, epistaxis, or nasogastric tube placement may indicate nasopharyngeal or oropharyngeal bleeding. An underlying anxiety disorder may be accompanied by chronic cheek chewing (morsicatio buccarum) with bleeding from the mouth or vomiting swallowed blood. Ingestion of a button battery or sharp foreign body may cause mucosal tears, ulcerations, or even life-threatening aortoenteric fistulae. Discovery of prior intestinal operation could heighten concern for a bleeding ulcer from a surgical anastomosis ( Fig. 1 ). A thorough medication history may reveal use of aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs) that could increase bleeding risk. Many substances can give the false appearance of red blood (beets, food coloring, gelatin, candy ) or black, tarry stool (iron supplements, bismuth). Cefdinir, a third-generation cephalosporin, has been reported to cause maroon or red discoloration to stool in pediatric patients due to formation of a precipitate with iron-containing supplements. Additional historical clues and corresponding etiologic sources in children and adolescents are summarized in Table 1 .




Fig. 1


Ulcer at jejunocolonic anastomosis in young girl with a history of jejunal atresia and multiple bowel resections as a neonate.


Table 1

Using historical clues to identify sources of bleeding








































Site of Suspected Bleed Historical Clues and Physical Examination Findings ( Potential Etiology in Italics )
No gastrointestinal bleeding source


  • Consumption of beets, food coloring, licorice, other candy ( substances that can give appearance of hematemesis or melanotic stools )



  • Use of cefdinir, iron, bismuth ( medications that can discolor stool )



  • Menstruation, hematuria, hemoptysis ( extra-intestinal bleeding sources )



  • Recent consumption of horseradish, turnip, tomatoes, red cherries, meat ( false-positive guaiac test )



  • Recent tonsillectomy, adenoidectomy, dental procedure, epistaxis, habitual chewing of buccal mucosa ( oropharyngeal or nasopharyngeal bleeding source )



  • Breastfeeding infant’s mother with cracked nipples ( swallowed blood )



  • Unexplained bleeding, discordant clinical picture and workup ( Munchausen syndrome by proxy )

Esophageal mucosal injury


  • Odynophagia after ingestion of doxycycline, alendronate, iron, potassium chloride ( medication-induced esophageal erosions or ulcers )



  • Symptoms of gastroesophageal reflux ( erosive esophagitis due to gastroesophageal reflux disease )



  • Esophageal foreign body or nasogastric tube trauma ( mucosal erosion, ulceration, bleeding )



  • Vomiting, retching, bulimia, or alcohol intoxication ( Mallory-Weiss tear )



  • Retrosternal chest pain, odynophagia, dysphagia, especially in immunocompromised patient ( herpes esophagitis or other infectious esophagitis )

Esophageal/gastric variceal disease or portal gastropathy


  • Ascites, jaundice, splenomegaly, palmar erythema, prominent abdominal vessels, skin excoriations due to pruritus ( portal hypertension or chronic liver disease )

Gastric or duodenal mucosal injury


  • Epigastric abdominal pain, Helicobacter pylori , nonsteroidal anti-inflammatory drug use, critically ill patient, burns, sepsis, mechanical ventilation ( stress gastritis and peptic ulcer disease )

Iatrogenic causes


  • Prior intestinal operation ( anastomotic ulcer )



  • Surgical diversion of fecal stream ( diversion colitis )



  • History of recent endoscopy ( duodenal hematoma, mucosal tear from stricture dilation, post-sphincterotomy or post-polypectomy bleeding )



  • Recent liver biopsy, endoscopic retrograde cholangiopancreatography, or percutaneous cholangiogram ( hemobilia )

Vascular issue


  • Sudden massive hematemesis, melena, hemodynamic instability ( Dieulafoy lesion )



  • Button battery ingestion, torrential bleeding episode ( aortoenteric fistula )



  • Multifocal cutaneous vascular malformations ( blue rubber bleb nevus syndrome )



  • Limb hypertrophy, hematochezia ( Klippel-Trenaunay syndrome with vascular malformation )



  • Cutaneous hemangiomas and rectal bleeding ( infantile visceral hemangiomas )



  • Epistaxis, multiple telangiectases, positive family history ( Osler-Weber-Rendu or hereditary hemorrhagic telangiectasi a)



  • Abdominal pain, purpuric rash, arthritis, hematuria ( vasculitis-Henoch-Schönlein purpura )



  • Turner syndrome, intermittent melena or hematochezia ( telangiectasia, venous ectasia )



  • Translucent skin, thin face, pinched nose, visible veins on chest, epigastric pain, melena ( type IV [vascular subtype] Ehlers-Danlos syndrome with mucosal fragility, ulcer disease, delicate vessels )



  • Congenital red-brown skin macules with thrombocytopenia and gastrointestinal bleeding ( cutaneovisceral angiomatosis with thrombocytopenia )



  • Other gastrointestinal venous or arteriovenous malformation

Polyps and tumors


  • Painless intermittent rectal bleeding with normal stooling pattern in young child ( juvenile polyp )



  • Phosphate and tensin homologue deleted on chromosome ten hamartoma tumor syndrome or Bannayan-Riley-Ruvalcaba syndrome with macrocephaly, autism spectrum, pigmented macules on penis ( juvenile polyposis syndrome )



  • Pigmented macules on lips or buccal mucosa, intussusception ( Peutz-Jeghers syndrome with associated hamartomatous polyps )



  • Family history of early-onset colorectal cancer ( familial adenomatous polyposis )



  • Gastrointestinal stromal tumor

Infectious and inflammatory conditions


  • Infantile cow milk protein allergy ( allergic proctocolitis )



  • Antibiotic use, recent travel to endemic areas, consumption of undercooked meats, or immunocompromised state ( salmonella, shigella, Yersinia enterocolitica, Campylobacter jejuni, Escherichia coli, Cytomegalovirus, Clostridium difficile, Entamoeba histolytica )



  • Family history of inflammatory bowel disease or other autoimmune diseases, chronic abdominal pain, growth issues, or bloody diarrhea with urgency, frequency, tenesmus, nighttime symptoms, abdominal pain ( ulcerative colitis or Crohn disease )



  • Abdominal distension, vomiting, pain, fever, explosive diarrhea, rectal bleeding in infant with history of delayed meconium passage ( Hirschsprung-associated enterocolitis )

Intestinal ischemia


  • History of drug use ( cocaine-induced intestinal ischemia )



  • Congenital heart disease ( mesenteric ischemia of childhood in hypoplastic left heart syndrome )



  • Prematurity, very low birth weight ( necrotizing enterocolitis )



  • Complicated intussusception ( Meckel diverticulum, intestinal duplication )



  • Bilious emesis ( malrotation with midgut volvulus )



  • Mesenteric vein thrombosis

Mucosal injury in immunosuppressed state


  • History of bone marrow transplantation ( graft-versus-host disease, infectious colitis )



  • Abdominal pain, neutropenia, fever, bloody stool ( neutropenic enterocolitis )



  • Radiation enteritis



  • Chemotherapy exposure ( mycophenolate-induced colitis )

Anorectal bleeding source


  • Bowel movements with bright red blood coating hard stool ( fissure, hemorrhoids )



  • Rectal foreign body, physical or sexual abuse


This table summarizes potential site of gastrointestinal bleeding in children based on historical clues. Potential etiologies to explain the historical clues are noted in italics and parentheses.


Special Considerations in Neonates and Infants


There are unique etiologies of gastrointestinal bleeding in neonates and infants younger than 12 months. Common causes of gastrointestinal bleeding in an otherwise healthy infant are anal fissures and swallowed maternal blood (from delivery or from fissured nipples). To distinguish between fetal and maternal origin of blood, the Apt-Downey test can be applied, which capitalizes on the different denaturing properties of fetal and maternal hemoglobin in the presence of sodium hydroxide. Occult gastrointestinal bleeding, hematochezia, or hematemesis may be presenting signs of cow’s milk protein allergy in an infant. Gastrointestinal bleeding can be a presenting symptom of an underlying coagulopathy. Vitamin K deficiency bleeding should be considered in neonates, particularly those with maternal exposure to antiepileptic medications that affect vitamin K, dysbiosis from antibiotic exposure, cholestasis, short bowel syndrome, or failure to receive perinatal vitamin K prophylaxis (eg, home delivery). Clinically unstable, premature, or very low birth weight infants should be evaluated for necrotizing enterocolitis. Bilious emesis warrants consideration of intestinal malrotation, as midgut volvulus can progress quickly to intestinal ischemia, sepsis, and death. Hematochezia is a late clinical sign in many surgical emergencies, from volvulus to intussusception, and can herald compromise of vascular supply.


Clinical Assessment


The clinician’s physical examination serves to stratify the patient’s illness severity and localize the source of bleeding. It is important to identify a patient who is ill-appearing, in pain, or has an altered sensorium. Assessment of the vital signs is an important early step. Children are known to have increased physiologic reserve compared with elderly patients and may maintain normal vital signs after an acute blood loss. Studies in pediatric trauma patients have demonstrated that hypotension may not be present until up to 25% of the circulating blood volume (80 mL/kg in children) has been compromised. Therefore, heart rate, capillary refill, and pulse pressure may be more sensitive markers of hemodynamic instability than blood pressure soon after an acute blood loss. Careful consideration of the patient’s other comorbidities prevents clinicians from being falsely reassured by normal vital signs. For instance, tachycardia may not be a reliable marker of hemodynamic decompensation in a patient on beta-blocker therapy.


The head and neck examination should screen for scleral icterus, conjunctival pallor, dental trauma, active bleeding in the oral cavity, epistaxis, or abnormal pigmentation of lips or buccal mucosa. The abdominal examination should evaluate for distension, tenderness to palpation, enlarged liver or spleen, and other stigmata of chronic liver disease (eg, ascites, prominent abdominal veins). A rectal examination may reveal perianal skin tags suspicious for Crohn disease, a palpable polyp in the rectal vault, fissures, hemorrhoids, or an anorectal vascular anomaly ( Fig. 2 ). There also may be subtle clues to the chronicity of an illness. In addition to jaundice, bruising, and rashes, skin findings such as telangiectasias, blue nodules, hemangiomas, or pigmented macules (lentigines) could also raise suspicion for multisystem vascular disorders such as hereditary hemorrhagic telangiectasia, blue rubber bleb nevus syndrome, and cutaneovisceral angiomatosis with thrombocytopenia, or polyposis disorders, such as Peutz-Jeghers syndrome and juvenile polyposis syndrome ( Fig. 3 ).




Fig. 2


Polypoid solitary rectal ulcer/mucosal prolapse lesion in distal rectum ( A ). Anal hemorrhoidal engorgement associated with rectal venous malformation ( B ).



Fig. 3


Oral lentigines or pigmented macules in patient with Peutz-Jeghers syndrome ( A ). Multiple reddish-brown vascular skin lesions in child with cutaneovisceral angiomatosis with thrombocytopenia ( B ). Nodular blue cutaneous venous malformations in a boy with blue rubber bleb nevus syndrome ( C ). Regional face and scalp hemangioma in a female infant with PHACES syndrome (Posterior fossa malformations, Hemangiomas, Arterial anomalies, Cardiac defects and coarctation of the aorta, Eye abnormalities, and Sternal abnormalities or ventral developmental defects) ( D ). Pigmented macules on glans of penis in boy with phosphate and tensin homologue deleted on chromosome ten hamartoma tumor syndrome and juvenile polyposis ( E ).

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Oct 2, 2017 | Posted by in PEDIATRICS | Comments Off on Gastrointestinal Bleeding and Management

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