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Gastrointestinal Bleeding

  • Pamela Choi
  • Josh Sommovilla
  • Brad Warner
Living reference work entry
  • 3 Downloads

Abstract

)Gastrointestinal bleeding is a commonly encountered problem in pediatric practice. While many causes of gastrointestinal bleeding exist, age and presenting symptoms aid in narrowing the differential diagnosis and in selecting initial diagnostic studies. Management strategies vary depending upon the diagnosis and source of bleeding and may include medical, radiographic, endoscopic, or surgical interventions.

Keywords

Gastrointestinal bleeding Endoscopy Upper gastrointestinal bleeding Lower gastrointestinal bleeding Colonoscopy 

Introduction

Children who present with gastrointestinal (GI) bleeding must first be assessed for hemodynamic stability. Bleeding may be sudden and life-threatening or subtle without visible evidence of blood loss but presenting with non-specific symptoms of fatigue or pallor. The majority of cases are benign and self-limiting, but patients who show signs of hemodynamic instability require immediate resuscitation with subsequent investigation as to the cause of bleeding. The diagnostic approach for gastrointestinal bleeding in children includes definition of etiology, localization of the bleeding site, and determination of the severity of the bleeding; timely and accurate diagnosis is necessary to reduce morbidity and mortality (Romano et al. 2017).

A differential diagnosis can initially be based upon patient presentation and age (Table 1). The gastrointestinal bleed is generally defined anatomically, by location of suspected blood loss relative to the ligament of Treitz. A careful history and physical examination is essential in identifying the likely source of bleeding and guiding the use of appropriate diagnostic tools (Table 2).
Table 1

Differential diagnosis of gastrointestinal bleeding based on age and location

Age

Upper gastrointestinal bleed

Lower gastrointestinal bleed

Newborn (<1 month)

Maternal or swallowed blood

Maternal or swallowed blood

Allergic enterocolitis

Allergic enterocolitis

Esophagitis

Necrotizing enterocolitis

Gastritis

Anal fissure

Gastroduodenal ulcers

Malrotation with midgut volvulus

Mallory-Weiss tear

Hirschsprung disease

Congenital malformation

Intestinal duplication

Intestinal duplication

Coagulopathy

Coagulopathy

Liver disease

Liver disease

Infancy (1 m–2 years)

Esophagitis

Allergic enterocolitis

Gastritis

Anal fissure

Gastroduodenal ulcers

Intussusception

Varices

Meckel’s diverticulum

Mallory-Weiss tears

AVM

Hemangiomas

Infectious colitis

Dieulafoy’s lesion

Intestinal duplication

Allergic enterocolitis

Henoch-Schonlein Purpura

Preschool (2–5 years)

Esophagitis

Anal fissure

Gastritis

Infectious colitis

Gastroduodenal ulcers

Juvenile polyps

Varices

Intussusception

Mallory-Weiss tears

Meckel’s diverticulum

Dieulafoy’s lesion

Angiodysplasia

Intestinal duplication

Henoch-Schonlein Purpura

School age (5–12 years)

Esophagitis

Anal fissure

Gastritis

Infectious colitis

Gastroduodenal ulcers

Juvenile polyps

Varices

Angiodysplasia

Mallory-Weiss tears

Henoch-Schonlein Purpura

Dieulafoy’s lesion

Adolescent (12–18 years)

Esophagitis

Anal fissure

Gastritis

Infectious colitis

Gastroduodenal ulcers

Juvenile polyps

Varices

Angiodysplasia

Mallory-Weiss tears

Inflammatory bowel disease

Dieulafoy’s lesion

Table 2

Diagnostic tools used for gastrointestinal bleeding

Upper gastrointestinal bleeding

 

Esophagitis, gastritis, gastroduodenal ulcers

EGD

Mallory-Weiss tears

EGD

Esophageal or gastric varices

EGD

Lower gastrointestinal bleeding

 

Anorectal fissure

Physical exam

Allergic colitis

History

Necrotizing enterocolitis

Physical exam, KUB

Malrotation with midgut volvulus

Upper GI series

Meckel’s diverticulum

Meckel’s scan

Hirschsprung disease

Lower GI series, suction rectal biopsy

Intussusception

Ultrasound, contrast enema

Infectious diarrhea

History, stool culture

Inflammatory bowel disease

Colonoscopy

Polyp

Colonoscopy

Obscure source of gastrointestinal bleeding

Tagged RBC scan, angiography, capsule enteroscopy, balloon enteroscopy

Resuscitation

Most patients with gastrointestinal bleeding are hemodynamically stable. All children, however, should first be assessed for the status of airway, breathing, and circulation. Stabilization should take precedence over diagnosis.

Signs of circulatory compromise include tachycardia, hypotension, pallor, altered mental status, lethargy, or decreased urine output. An ill-appearing child should have two large bore IVs placed and be given 10–20 mL/kg boluses of crystalloid. Rapid blood loss may need to be replaced with packed red blood cells and appropriate clotting factors, particularly if the patient continues to be tachycardic and hypotensive despite boluses of crystalloid.

General Diagnostic Principles

In hemodynamically unstable patients, initial attention must be directed toward patient resuscitation. While resuscitation is underway, a basic diagnostic work-up and plan can also be initiated concurrently. In cases when the source of bleeding is unclear, placement and irrigation of a nasogastric tube can provide useful information. Return of frank blood or coffee-ground aspirant suggests a source proximal to the ligament of Treitz. Clear returns favor a more distal source, but this maneuver is insufficiently sensitive to rule out an upper GI bleed since pylorospasm may obscure duodenal bleeding. Risk factors obtained in the history, along with consideration of patient age, can help create a differential diagnosis for the most likely causes of GI bleeding. A rectal examination revealing bloody or heme-positive contents can confirm a gastrointestinal source of blood loss.

Endoscopic examination is generally considered the gold-standard diagnostic tool and also provides the ability to intervene at the source of bleeding. If endoscopy does not reveal bleeding, nuclear imaging and/or angiography may be necessary to identify and manage a gastrointestinal bleed.

When traditional endoscopy of the foregut and colon is unsuccessful at identifying a bleeding source, additional techniques are available for assessing the small intestine. Wireless capsule endoscopy allows for visualization of the entire length of the small bowel. Double-balloon enteroscopy utilizes inflation of a balloon at the distal position of the endoscope to allow progressive advancement of the scope throughout the small bowel. Like capsule endoscopy, this allows for visualization of the entire small bowel but also enables interventions including biopsy, polypectomy, and cautery.

Upper Gastrointestinal Bleeding

Upper gastrointestinal (UGI) bleeding is defined as originating from a site proximal to the ligament of Treitz. UGI bleeds can be broadly categorized as mucosal or related to portal hypertension. In developed countries, bleeding related to mucosal pathology is most common, whereas in developing countries, portal hypertension leads to more UGI bleeding (Singhi et al. 2013; Podder 2019).

Swallowed Maternal Blood

In the newborn presenting with apparent hematemesis, the first diagnostic step requires determining whether the content of emesis is a true GI bleed or maternal blood ingested during delivery. The Apt-Downey test relies on the differing reactive properties of adult and fetal hemoglobin. Briefly, a sample of the suspected hematemesis is placed in a tube, and sterile water is added to hemolyze the sample, followed by sodium hydroxide. Maternal adult hemoglobin will cause the solution to turn a yellow-brown color, while fetal hemoglobin remains clear. If the Apt-Downey test reveals true neonatal hematemesis, then the diagnostic and treatment strategy should continue to address the conditions outlined below.

Hemorrhagic Disease of the Newborn

Bleeding secondary to a vitamin K deficiency, commonly called hemorrhagic disease of the newborn, has become increasingly uncommon in developed countries due to routine administration of vitamin K at birth. Hemorrhagic disease of the newborn results from decreased activity of the vitamin K-dependent clotting factors (II, VII, IX, X). The most common presentation of this condition is intracranial hemorrhage, but a recent series has reported that 16% of patients present with gastrointestinal bleeding (Rana et al. 2009). Risk factors for this condition include maternal use of antibiotics and anticonvulsants, exclusive breastfeeding, cystic fibrosis, and other conditions leading to fat malabsorption, sepsis, and liver disease. When a patient presents with bleeding secondary to vitamin K deficiency, treatment depends on the severity of bleeding and consists of vitamin K administration and/or FFP infusion.

For prevention of this condition, the American Academy of Pediatrics recommends a 0.5–1.0 mg intramuscular administration of vitamin K at birth (American Academy of Pediatrics Committee on and Newborn 2003). Prophylaxis with oral doses of vitamin K are being investigated, but require doses of 2–4 mg be given orally at birth, 2–4 weeks, and 4–6 weeks of age. Non-compliance with subsequent doses can place an infant at risk for late-onset vitamin K deficient bleeding. A recent Canadian study has reported the rate of hemorrhagic disease of the newborn to be 0.45 in every 100,000 births under the current prophylactic regimen (McMillan et al. 2004).

Stress Gastritis Ulcers

Gastritis and stress ulcers are not uncommon in neonatal and pediatric intensive care units. A wide spectrum of severity may be encountered, ranging from mild gastritis to acute and severe hemorrhage. The greatest risk factors are head injury, burns, mechanical ventilation, coagulopathy, trauma, and shock. In fact, the rate of clinically significant upper gastrointestinal bleeding in critically ill children occurs at a rate similar to adults, as high as 20% (Kuusela et al. 2000). In neonatal patients, after swallowed blood and coagulopathy are ruled out as causes, potential GI irritants should be discontinued, and acid anti-secretory medication should be initiated with a proton pump inhibitor or histamine-2 receptor (H2) blocker. Since endoscopy in this age group can be technically difficult and biopsies are rarely necessary, this intervention may be reserved for patients who do not respond to initial anti-secretory therapy.

The risk profile of stress gastritis and ulcers in older pediatric patients is similar to that of neonates and occurs at a similar rate (Reveiz et al. 2010), with Helicobacter pylori (H. pylori) infection as a notable additional risk factor. In these patients, upper endoscopy should be performed when upper GI bleeding is noted. If gastritis or ulcers are identified, biopsies should be taken for definitive diagnosis. Inciting agents should be discontinued, and as with neonates, proton pump inhibitors or H2-blocking agents should also be initiated. Additionally, critically ill pediatric patients with at least one of the above risk factors should receive routine stress ulcer prophylaxis to prevent such lesions (Jenson et al. 2019).

Other Gastritis and Peptic Ulcer Diseases

Gastritis is an inflammatory condition of the stomach that can occur at all ages of the pediatric population and with a wide range of severity. Common provocateurs of gastritis include H. pylori infection, nonsteroidal anti-inflammatory drugs, ingestion of irritants, Crohn’s disease, portal hypertension, trauma, burns, and critical illness.

Even though the incidence of H. pylori is much less common in children than in adults, it must be considered as a possible cause of gastritis, peptic ulcer disease, or chronic anemia in the pediatric population. Duodenal ulcers, in particular, have up to a 90% association with H. pylori infection. A recent study has estimated that the incidence of bleeding secondary to peptic ulcer disease in the USA is approximately 0.5–0.9 per 100,000 individuals in the pediatric population (Brown et al. 2012). Current guidelines support eradication of the organism through triple-drug regimens (Koletzko et al. 2011).

Esophageal Varices

Bleeding secondary to esophageal and gastric varices is a leading cause of morbidity and mortality in children with portal hypertension. Portal hypertension is most commonly secondary to cirrhosis, but may also be caused by extrahepatic portal vein obstruction.

Variceal hemorrhage should be suspected in any child presenting with a history of liver disease or any other signs of cirrhosis or portal hypertension. In the setting of an acute variceal bleed, resuscitation should be aggressive. Transfusion with packed red blood cells, plasma, as well as platelets may be necessary as these bleeding patients often have both coagulopathy and thrombocytopenia.

Pharmacologic therapy can also be given to help control or even stop hemorrhage. Octreotide, a somatostatin analogue, has the widest body of evidence supporting its use in control of variceal bleeding. It has been shown to be efficacious in about 70% of cases of pediatric upper GI bleeds.

Once hemodynamic stability is achieved, endoscopy should be performed as soon as possible. This is required for the initial diagnosis of variceal bleeding and allows for several therapeutic options. The most commonly used endoscopic treatments are band ligation and sclerotherapy. Randomized controlled trials in both adults and children have shown ligation to be superior for several reasons. It is less expensive and more efficacious in eradicating varices with a lower incidence of recurrent bleeding. However, ligation may be technically difficult in smaller toddlers and infants, and in these cases sclerotherapy remains an effective option. Furthermore, there are no randomized clinical trials assessing band ligation versus beta-blockers for primary prophylaxis of esophageal variceal bleeding in children with thoracic liver disease or portal vein thrombosis (Ganna et al. 2019).

If bleeding becomes refractory, rescue measures may be required to relieve portal hypertension. For patients with end-stage liver disease, listing for liver transplantation may be indicated. In other cases, or for listed patients without an available organ, portosystemic shunts may be necessary. There is a growing body of evidence supporting the use of transjugular intrahepatic portosystemic shunting (TIPS) in the pediatric population (Garcia-Pagan et al. 2013). In cases where TIPS is not feasible, surgical shunts can be created but are rarely used.

For non-cirrhotic patients with extrahepatic portal vein obstruction, either from thrombosis or congenital anomaly, management of acute bleeding is similar to the above. These patients, however, have an additional surgical option in the meso-Rex shunt, which uses an autologous vein graft to connect the superior mesenteric vein to an intrahepatic portal branch, thus bypassing the extrahepatic obstruction. This procedure is equally efficacious at relieving the sequelae of portal hypertension as portosystemic shunts, with the added benefit of restoring portal venous circulation (Lautz et al. 2013).

In cases of acute massive hemorrhage where access to definitive management is limited, a balloon tamponade with a Sengstaken-Blakemore tube may provide life-saving temporization. However, this therapy is rarely used and poses a moderate risk of esophageal ischemia and perforation. Transfer to a facility with resources for definitive management should occur immediately, as these devices should be removed within 48 hours.

Lower Gastrointestinal Bleeding

Any bleeding that originates from the intestine distal to the ligament of Treitz is defined as lower gastrointestinal bleeding. The causes of lower gastrointestinal bleeding vary with patient age. Patients usually present with bloody diarrhea, hematochezia, blood seen on toilet paper, or blood mixed with stool. As with upper gastrointestinal bleeding, the diagnostic work-up depends on the patient’s age and presentation. The diagnostic modalities for identifying causes of lower gastrointestinal bleeding in children include endoscopy and colonoscopy, cross-sectional and nuclear medicine imaging, video capsule endoscopy, or enteroscopy (Sahn and Bitton 2016).

Anal Fissures

Anal fissures are the most common source of rectal bleeding in infants less than 2 years of age. They are the result of a superficial tear of the squamous lining of the anal canal caused by the passage of a large, hard stool. Fissures may be found in all age groups and present as pain with defecation and bright red streaks outside of stool. The diagnosis may be made by physical exam. Most fissures are posterior below the dentate line. Treatment includes stool softeners and sitz baths. Recurrent fissures should be evaluated for inflammatory bowel disease.

Allergic Colitis

Food allergy colitis may present in newborns or infants younger than 3 months with gross or occult blood with stools. Cow’s milk and soy protein are the most common causative agents. The diagnosis may be made by eliminating the suspected agent and observing resolution of symptoms.

Necrotizing Enterocolitis

One of the most worrisome causes of gastrointestinal bleeding, necrotizing enterocolitis, is a disease of premature neonates caused by the loss of the intestinal mucosal barrier and bacterial translocation. Neonates generally have symptoms of vomiting, abdominal distention, tenderness, lethargy, and abdominal wall erythema. Gross blood in the stool may or may not be seen as there is a wide range of reported incidence of 25–63% (Kanto et al. 1994; Chandler and Hebra 2000). Laboratory findings include thrombocytopenia, neutropenia, and metabolic acidosis.

A two view abdominal x-ray may reveal dilated loops, pneumatosis intestinalis, or portal venous gas. However, 40% of infants with confirmed perforation at operation will have no signs of free air on preoperative imaging (Frey et al. 1987).

Initial treatment consists of ceasing enteral feeds with gastric decompression and broad spectrum antibiotics with frequent abdominal radiographs. Signs of perforation or clinical deterioration are indications for surgical intervention.

Malrotation with Midgut Volvulus

Midgut volvulus secondary to malrotation is the most common in neonates, and 90% of infants are symptomatic before 1 year of age (Ford et al. 1992). Bowel that fails to undergo normal rotation and fixation is at a high risk for volvulus as the duodenum and cecum are fixed in close proximity to each other around the root of the mesentery. Twisting around this narrow mesenteric pedicle leads to vascular compromise of the majority of the small intestine.

The symptoms of midgut volvulus include bilious emesis, abdominal distention, and sometimes melena from ischemic mucosal injury. Patients with concern for malrotation require an urgent upper gastrointestinal series; however, decompensation or peritoneal signs warrant emergent laparotomy even without radiologic confirmation.

The surgical approach for volvulus is to first untwist the intestine by rotating the bowel in a counterclockwise motion until the duodenum and cecum are parallel. The malrotation is then managed by a Ladd’s procedure in which mesenteric bands over the duodenum are lysed, the mesentery is broadened to separate the duodenum and cecum, the small bowel is placed on the right side of the abdomen with the colon on the left, and the appendix is removed.

Meckel’s Diverticulum

Healthy infants or preschool children with painless rectal bleeding should be evaluated for Meckel’s diverticulum, a true congenital diverticulum resulting from incomplete obliteration of the omphalomesenteric duct. Bleeding is typically profuse and intermittent, resulting from ulceration of the ileal mucosa on the antimesenteric side by acid secreted by ectopic gastric mucosa within the diverticulum, which occurs in 50% of all cases. Patients may also present with obstruction from intussusception, internal herniation, or volvulus as well as from diverticulitis or perforation.

Meckel’s diverticulum is often defined by the rule of twos: it occurs in 2% of the population, has a 2:1 male/female ratio, is located within 2 ft of the ileocecal valve, is 2 in. in length, can contain two types of ectopic tissue, and is most common before 2 years of age.

Diagnosis may be confirmed with a Tc-99 pertechnetate nuclear scan with a sensitivity of 68–85% (Fig. 1). The sensitivity may be increased with a histamine antagonist, pentagastrin, and glucagon. However with a negative predictive value of 74%, a negative nuclear scan does not necessarily rule out Meckel’s diverticulum if there is high clinical suspicion.
Fig. 1

(a)Tc-99 pertechnetate nuclear scan in pediatric patient presenting with bright red blood per rectum, revealing a focus of tracer uptake in the right lower quadrant. (b) Intraoperative images of Meckel’s diverticulum encountered during surgical exploration

If bleeding is involved, treatment involves surgical resection of the diverticulum and inspection of the adjacent ileum. The presence of ulceration prompts bowel resection with primary anastomosis to avoid rebleeding.

Enteric Duplication Cysts

Duplication cysts are hollow, epithelium-lined structures attached to the wall of the gastrointestinal tract, usually with a common blood supply to the bowel. They are uncommon congenital malformations and may occur anywhere along the alimentary tract but most commonly in the ileum on the mesenteric border. Similar to a Meckel’s diverticulum, duplication cysts often contain ectopic gastric mucosa that may lead to ulceration and gastrointestinal bleeding. Other symptoms may include intussusception or obstruction. Duplication cysts are removed by complete resection of the cyst itself as well as the adjacent bowel and mesentery.

Hirschsprung’s Disease

Hirschsprung’s disease is an enteric nervous system disorder characterized by the absence of ganglion cells within the distal intestine. Neonates with delayed passage of meconium or abdominal distention with constipation should raise suspicions for Hirschsprung’s disease. Evaluation typically begins with a contrast enema, which typically demonstrates colonic dilation with a transition zone. If suspicious, this can be followed with a suction rectal biopsy, in which absent ganglion cells, hypertrophic nerve fibers, and positive acetylcholinesterase staining would confirm the diagnosis. Following this diagnosis, operative planning is initiated for removal of the aganglionic segment.

Patients may also present with Hirschsprung-associated enterocolitis (HAEC), particularly if the diagnosis of Hirschsprung’s disease is delayed. Symptoms include abdominal distention, explosive diarrhea, vomiting, fever, and lethargy. Rectal bleeding is an uncommon presentation of Hirschsprung’s disease, but may be seen in 6% of children with HAEC (Elhalaby et al. 1995). Treatment consists of aggressive resuscitation, broad spectrum antibiotics, and rectal irrigations.

Intussusception

Most commonly seen in children less than 2 years old, intussusception is an invagination of a portion of proximal intestine into a distal portion. Intussusception is one of the most common causes of pediatric bowel obstruction and may lead to necrosis and perforation. Patients present with sudden onset, colicky abdominal pain with vomiting. The classic sign of “currant red jelly” stools, the result of venous congestion with ischemia, may or may not be present. Diagnosis is made with ultrasound.

Intussusception is frequently treated with contrast or air enema, although pneumatic reduction has been shown to have higher rates of success due to higher intraluminal pressures. Contraindications to enema include peritonitis, perforation, or necrotic bowel, which would prompt surgical management. While recurrent intussusception may be treated with repeat enemas, persistent intussusception or failed reduction will also require operative management.

Polyps

Polyps are commonly seen in preschool- or school-aged children with painless rectal bleeding. The majority are solitary and found in the left colon. Polyps may be discovered by colonoscopy and require endoscopic removal for definitive diagnosis and to prevent sequelae (bleeding, intussusception) (Thakkar et al. 2012)

There are two types of polyps based on microscopic appearance: hamartomas and adenomas. The majority of polyps are hamartomatous, which are usually solitary and benign. The most common type of hamartomatous polyp are juvenile polyps, which represent 70–80% of polyps in children (Fox et al. 2010). However, multiple hamartomatous polyps may be found in premalignant conditions such as juvenile polyposis syndrome or Peutz-Jeghers syndrome.

In contrast to hamartomatous polyps, adenomatous polyps are dysplastic with malignant potential and so require frequent surveillance. They are rarely solitary in children. Familial adenomatous polyposis is the most common syndrome associated with adenomatous polyps. Turcot syndrome and Gardner syndrome are also examples of adenomatous polyposis syndromes.

Inflammatory Bowel Disease

Approximately 25% of all patients with inflammatory bowel disease are diagnosed before the age of 20, particularly between the ages of 10 and 16 (Vinton 1994). These patients often present with chronic bloody diarrhea with weight loss and abdominal pain. Laboratory signs may include anemia and hypoalbuminemia. Gastrointestinal bleeding occurs in almost all patients with ulcerative colitis and in 25% of patients with Crohn’s disease (Farmer 1991). Diagnosis may be made by colonoscopy and biopsy. In cases where colonoscopy is indeterminate, or if small bowel disease is suspected, either capsule or double-balloon enteroscopy may be necessary.

Henoch-Schonlein Purpura

Henoch-Schonlein purpura is a small vessel vasculitis characterized by purpura, arthritis, abdominal pain, and hematuria. An upper respiratory tract infection generally precedes symptoms. Gastrointestinal symptoms occur in 43–75% of cases and manifest as colicky abdominal pain, vomiting, and bloody stools (Robson and Leung 1994). The disease is most commonly seen in children aged 2–10 years and is self-limiting with supportive treatment.

Infectious Causes of Gastrointestinal Bleeding

Patients with infectious colitis may also present with acute (<1 week) gastrointestinal bleeding, often in the form of bloody diarrhea, with abdominal pain and tenderness. While most cases will resolve, patients should be hospitalized to ensure appropriate resuscitation as well as halt secondary spread of the pathogen.

The most common bacterial causes include Salmonella, Shigella, Campylobacter jejuni,

Yersinia enterocolitica, Clostridium difficile, and E. coli O157:H7. These pathogens may be identified through stool cultures. Entamoeba histolytica may be a parasitic source of colitis, while rotatvirus and Norwalk virus may also cause bloody diarrhea. In an immunocompromised child, CMV, adenovirus, and Cryptosporidium may also be suspected.

Special consideration should be given to patients who have symptoms suspicious for E. coli O157:H7, as early recognition and management may have a significant impact upon outcome. E. coli O157:H7 begins with non-bloody diarrhea that becomes bloody after 1–3 days and abdominal pain that is worse on defecation. In addition to sending for a stool culture, these patients should be aggressively hydrated. However, practitioners should abstain from using antibiotics, as antibiotics in children with E. coli O157:H7 have been shown to increase risk of hemolytic uremic syndrome (HUS) (Bell et al. 1997).

HUS is the most feared complication from E. coli O157:H7 and is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. HUS may also lead to gastrointestinal bleeding from small vessel occlusion and mucosal ischemia.

Vascular Malformations as Causes of Gastrointestinal Bleeding

Several uncommon pediatric conditions can lead to vascular malformations that may cause gastrointestinal bleeding. The anomalies themselves can be classified based on whether they are venous, arterial, or arteriovenous. Klippel-Trenaunay, blue rubber bleb nevus, and Proteus syndromes are all associated with gastrointestinal venous malformations with bleeding potential (Dubois, Rypens et al. 2007). Patients with blue rubber bleb nevus syndrome (Fig. 2) can present with multiple venous malformations throughout their GI tract causing bleeding and anemia that, given its diffuse nature, can be difficult to manage. In such patients, a case series has shown successful eradication of bleeding in nine of ten patients with extensive intraoperative endoscopy and resection of malformations (Fishman et al. 2005).
Fig. 2

Intraoperative images of a pediatric patient with gastrointestinal bleeding from blue rubber bleb nevus syndrome

Hereditary hemorrhagic telangiectasia, or Rendu-Osler-Weber disease, is an autonomic dominant inherited disease associated with mucosal telangiectasias and arteriovenous malformations in the nasopharynx and GI tract. Patients may present with recurrent epistaxis or GI bleeding. The malformations are predominantly located in the stomach and small intestine and can be seen from the mucosal surface on endoscopy (Canzonieri et al. 2013). Various medical and interventional treatments exist for controlling bleeding from these lesions, including progesterone/estrogen therapy, bevacizumab, endoscopic cautery or laser treatment, and surgical excision (McDonald et al. 2011).

Conclusion and Future Directions

The differential diagnosis of gastrointestinal bleeding is wide ranging from benign and self-limiting etiologies to life-threatening bleeds that require emergent intervention. Identification of the bleed requires diligent review of the patient’s history and physical exam, which helps guide the appropriate diagnostic tests and treatment options. Management of GI bleeds may require of multidisciplinary approach of gastroenterologists, radiologists, as well as surgeons. In future, randomized clinical trials are needed to assess various modalities of treatment for upper and lower gastrointestinal bleeding.

Cross-References

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Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature 2020

Authors and Affiliations

  • Pamela Choi
    • 1
  • Josh Sommovilla
    • 1
  • Brad Warner
    • 1
  1. 1.Washington UniversitySt LouisUSA

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