bleeding from the intestinal tract and rarely from the biliary system (hemobilia) or pancreatic ductal system (hemosuccus pancreaticus). Occasionally, UGI bleeding will present as melena without vomiting. If there is mas- sive UGI bleeding and/or rapid intestinal transit (e.g., infants, short bowel), hematochezia may be seen. Finally, a severe bleed may present with hypovolemic shock before hematemesis or the passage of a bloody stool.
Depending on the etiology and severity of bleeding, chil- dren may appear completely asymptomatic or quite ill.
Lower GI Bleeding
Overt LGI bleeding can present as hematochezia or mel- ena depending on etiology and severity. The amount and character of blood loss (bright red, black, or currant jelly) is important in suggesting specifi c diagnoses and possible need for urgent intervention. Stool frequency and consistency (normal, large and hard, or loose) should be investigated. Streaks of red blood coating hard or normal stool suggest a distal source (e.g., anal fi ssure and polyp). Presence of abdominal or anal pain can also be helpful. Non-bloody vomiting may occur with certain etiologies (e.g., bowel obstruction and infl ammatory bowel disease). As with UGI bleeding, LGI bleeding can present with signs of severe blood loss before passage of a bloody stool.
DIFFERENTIAL DIAGNOSIS BASED ON PRESENTATION
Memorizing the differential diagnosis for UGI and LGI bleeding is less useful than a thoughtful approach based on the clinical presentation. Tables 6–4 and 6–5 provide a guide for hematemesis and hematochezia, respectively. It should be remembered that some diag- noses can have variable presentations and occur in dif- ferent age groups. Tables 6–6 and 6–7 list rare causes separately. Variables besides presentation may include the age of the patient, the type and character of bleed- ing, and the clinical status of the child. The key initial steps described above should be undertaken no matter the presentation.
APPROACH TO DIAGNOSIS AND MANAGEMENT
See Tables 6–8 and 6–9.
Hematemesis or Coffee Ground Emesis
Hematemesis or coffee ground emesis indicates an UGI bleed. An algorithm for approaching the child with UGI bleeding is shown in Figure 6–2. In the hemodynamically stable child, a controlled approach in the outpatient Etiology of Hematemesis or Coffee Ground Emesis by Age and Presentation
Age Ill Appearing
Well Appearing
High Rate Low Rate
Newborn (up to a couple of months)
Hemorrhagic gastritis Volvulus
Swallowed maternal blood Vitamin K defi ciency
Mallory–Weiss tear (e.g., pyloric stenosis) Vascular anomaly
Infants (<2 years) Hemorrhagic gastritis Esophageal varices
Volvulus or bowel obstruction
Esophageal varices Intestinal duplication
Acid peptic disease Mallory–Weiss tear
Swallowed blood (e.g., epistaxis) Food protein allergy
Child to adolescent Esophageal varices Caustic ingestion Hemorrhagic gastritis Bowel obstruction Crohn’s disease
Esophageal varices Mallory–Weiss tear Acid peptic disease Chemical gastritis Ingestion (caustic or
foreign body) Swallowed blood Vasculitis (e.g., HSP) Crohn’s disease
Swallowed blood may include: maternal blood, epistaxis, recent surgery (tonsillectomy, adenoidectomy, and dental work), and hemoptysis. Acid peptic disease includes:
erosive refl ux esophagitis, gastritis (including H. pylori), and gastric or duodenal ulcer. Hemorrhagic gastritis has the following risk factors: ICU admission, burns, trauma, mechanical ventilation, and multi-organ failure. Chemical gastritis has the following risk factors: NSAID use, alcohol, and bile refl ux.
Table 6–4.
setting may be appropriate. If the bleeding is signifi cant by history or the patient is hemodynamically unstable, an NG saline lavage can determine if there is still active bleed- ing. (Note: Room temperature saline should be used as iced saline lavage is no longer considered useful or safe.)
For unstable patients, attention should be focused on supportive care (see the section “Key Initial Steps in the Evaluation of GI Bleeding”). Transfer to an intensive care setting and/or a tertiary care center with surgical and
endoscopic services should be initiated early. Surgical exploration is indicated for signs of obstruction or ongo- ing blood loss uncontrolled by medical therapy. Causes of severe UGI bleeding most often include: esophageal Hematochezia or Melena by Age and Presentation (Always Consider UGI Sources)
Age Ill Appearing
Well Appearing
High Rate Low Rate
All age groups Infectious colitis Anal fi ssure
Infectious colitis Newborn (up to a couple
of months)
Necrotizing enterocolitis Hirschsprung’s enterocolitis Volvulus
Swallowed maternal blood Benign rectal bleeding
(lymphoid hyperplasia) Allergic colitis
Infants (<2 years) Intussusception Meckel’s diverticulum Volvulus or bowel obstruction Hirschsprung’s enterocolitis
Meckel’s diverticulum Allergic colitis
Lymphonodular hyperplasia (LNH) Swallowed blood (e.g., epistaxis) Preschool (2–5 years) Meckel’s diverticulum
Bowel obstruction
Infl ammatory bowel disease
Meckel’s diverticulum Juvenile polyp with
autoamputation Ulcerative colitis
Juvenile polyp Swallowed blood Vasculitis (e.g., HSP) Infl ammatory bowel disease LNH
Child to adolescent Infl ammatory bowel disease Bowel obstruction
Ulcerative colitis Juvenile polyp with
autoamputation Meckel’s diverticulum
Juvenile polyp Swallowed blood Vasculitis (e.g., HSP) Infl ammatory bowel disease LNH
Infl ammatory bowel disease refers to either Crohn’s disease or ulcerative colitis. HSP = Henoch–Schoenlein purpura; LNH = lymphonodular hyperplasia.
Table 6–5.
Rare Causes of Hematochezia or Melena See rare causes of UGI bleeding in Table 6–6 Perianal group A beta-hemolytic streptococcus Hemorrhoids: internal or external
Vascular abnormalities: hereditary hemorrhagic telangiectasia, Turner syndrome (telangiectasias), angiodysplasia, Dieulafoy lesion, blue rubber bleb nevus syndrome
Polyposis syndromes: familial adenomatous polyposis, Peutz–
Jeghers syndrome, Gardner syndrome, Turcot syndrome Clotting disorders: hemophilia, von Wilebrand’s disease Vasculitis: lupus erythematosus, Churg-Strauss syndrome,
polyarteritis nodosa
Related to prior surgery: diversion colitis, perianastamotic ulcer Cancer related: colorectal carcinoma, GVHD, neutropenic
colitis (typhlitis)
Solitary rectal ulcer syndrome Abuse with traumatic anal fi ssures Intestinal duplication
Table 6–7.
Rare Causes of UGI Bleeding Radiation gastritis or esophagitis
Vascular abnormalities: hemangioma, hemangioendothelioma, arteriovenous malformations, Dieulafoy lesion,
aortoesophageal fi stula
Hemobilia (biliary bleeding) or hemosuccus pancreaticus (pancreatic bleeding)
Tumors: teratoma, leiomyosarcoma
Graft versus host disease (GVHD): common with bone marrow transplant
Munchausen syndrome by proxy: intentional poisoning, factitious bleeding
Table 6–6.
varices due to portal hypertension, hemorrhagic gastritis in the ICU setting (e.g., trauma, burns, and mechanical ventilation), and ischemic bowel injury (malrotation with volvulus, bowel obstruction, and intussusception).
Selected conditions leading to UGI bleeding Acid peptic disease Acid peptic disease is one of the more common causes of UGI bleeding in older children (⬎6–12 months) or those in a critical care setting. How- ever, it is important to remember that this is a common problem that does not usually present with overt GI bleeding, but rather with more typical symptoms (regurgitation, heartburn, acid brash, epigastric pain, and poor feeding). Refl ux esophagitis or gastritis is rare in infants ⬍6 months old in spite of the fact that over half of all infants have frequent spitting (physiologic refl ux of infancy). This is probably due to frequent milk
intake buffering gastric acid. However, it can occur, especially in older infants who eat less frequently with less milk intake. They are usually fussy and may have a decline in oral intake. Other conditions may contribute (e.g., eosinophilic esophagitis or food allergy).
Helicobacter pylori may cause gastritis but not usually ulcers as it may in adults. Gastritis may also be caused by frequent NSAID use, often for another chronic problem (e.g., headaches, juvenile rheumatoid arthritis, and cystic fi brosis). If an NSAID is prescribed as a daily medication for some of these problems, there are data that concurrent use of a proton pump inhibi- tor (PPI) reduces the incidence of gastritis or ulceration.
Mallory–Weiss tear Retching from any cause (e.g., viral gastroenteritis, pyloric stenosis, or anatomic Physical Exam Findings Suggestive of Specifi c Diagnoses
Portion of Exam Findings Suggested Diagnoses
Vital signs Impaired linear growth or weight gain;
weight loss
Crohn’s disease; Hirschsprung’s disease;
Turner syndrome
Fever Infectious colitis, IBD
Abdomen Hepatosplenomegaly, ascites, caput medusa Portal hypertension Rectal exam Midline anal fi ssures or tags; dilated rectal vault Constipation
Anal fi ssures or tags without constipation. Fissures not in midline. Abscess, fi stula
Crohn’s disease; chronic granulomatous disease
Rectal mass on a stalk Polyp
Circumscribed erythema Perianal group A streptococcus
Miscellaneous Jaundice, spider angioma, palmar erythema Cirrhotic liver disease
Pigmented oral or buccal lesions Peutz–Jeghers syndrome
Fingernail clubbing Cirrhotic liver disease, IBD
Arthritis IBD, HSP
Palpable purpura HSP
Table 6–8.
Laboratory Findings Suggestive of Specifi c Diagnoses
Laboratory Test Findings Suggested Diagnoses
CBC Microcytic anemia, elevated platelets IBD
Elevated WBC, no anemia Infectious colitis
Low platelets, leucopenia Portal hypertension
ESR, CRP Elevated ESR or CRP IBD, infectious colitis
Metabolic profi le Elevated transaminases, bilirubin Liver disease
Low albumin Liver disease, Crohn’s disease
Stool studies Culture, C. difficile toxin Infectious colitis
Urinalysis Positive for blood HSP
Table 6–9.
obstruction) can lead to mucosal tears and bleeding.
Coffee ground emesis in an infant under 4 months of age should prompt one to investigate for a history of progressively worsening retching during or after feeding (pyloric stenosis).
Esophageal varices Large-volume, bright red UGI bleeding is most commonly caused by esophageal variceal bleeding and may present as hematemesis or melena. Interruption or slowing of portal venous fl ow (portal hypertension, portal venous thrombosis, etc.) leads to shunting of blood to the systemic circulation (Figure 6–3). Flow is reversed through the left gastric vein into gastric and esophageal venous plexuses that then drain into the azygous vein. The engorged submu- cosal esophageal veins are most prominent near the gas- troesophageal junction and lower esophagus.
Although variceal bleeds frequently resolve spon- taneously, rebleeding is a common problem without prophylactic therapy. The history should investigate risk
factors for liver disease (neonatal history, family history, infectious exposure, blood transfusions, and jaundice) and portal vein thrombosis (omphalitis, sepsis, and umbilical catheter). The examination should focus on fi ndings consistent with portal hypertension and liver disease: hepatosplenomegaly, ascites, caput medusa, jaundice, and spider angiomata.
Ingestions Foreign body ingestion can cause bleed- ing if there is a sharp edge. A foreign body in the esophagus for over 24 hours may cause erosion and bleeding. A chronic foreign body in the stomach may cause an ulcer. Caustic ingestions may also cause UGI or LGI bleeding. This is usually a late occurrence for accidental ingestions (usually a small amount) after stricture formation. However, intentional ingestions (larger amounts with more signifi cant injury) may present as bloody vomiting.4 Similarly, overdose with certain medications (e.g., iron) can cause ulceration and bleeding.
Identify source
Suspect blood not GI
History & physical
Test vomitus or NG aspirate for blood
Reassurance Identify source
Hemodynamic status / bleeding severity
Is it the patient’s blood?
(Apt-Downey test)
Active bleeding (consider octreotide)
EGD: Diagnosis and therapy
No active bleeding
Approach depends upon likely diagnoses Stable / mild to moderate
Labs +/– radiography
NG aspirate if significant bleeding Unstable / severe
(octreotide & IV PPI or H2 blocker)
Resuscitation (fluid and/or blood)∗
Remains unstable after ~85 ml/kg blood transfusion
Emergent surgical exploration and/or endoscopy in OR
–
+ No
Yes
FIGURE 6–2 ■ Approach to hematemesis, coffee ground emesis, or rectal bleeding with positive NG aspirate. (*) The unstable or actively bleeding patient should be resuscitated (IV access, fl uid, and/or blood) while obtaining key laboratory and radiographic data if possible. The goal is to stabilize for controlled evaluation and possible transfer to the ICU and/or a facility with surgical and endoscopic services. Endoscopy is technically challenging with active bleeding but can be therapeutic (e.g., esophageal varices).
Malrotation with intermittent midgut volvulus Crying or screaming in infants before vomit- ing blood and/or bile is worrisome for obstruction, especially malrotation with volvulus (twisting of midgut that usually obstructs the superior mesenteric artery and blood fl ow to almost the entire small bowel). This is a surgical emergency as it can lead to necrosis of the entire small bowel and part of the colon. Patients will appear ill, often with distension, diminished bowel sounds, tachycardia, and poor perfusion. The highest risk for volvulus is in the fi rst few months of life but can occur at any age. Diagnosis is often confi rmed at surgery if the child is not stable for radiographic studies.5 Hemorrhagic gastritis In critically ill patients, shock (e.g., sepsis or heart failure) can commonly lead to isch- emic injury causing gastritis or stomach ulcers. However, signifi cant UGI bleeding is uncommon (⬍2%) even in this setting.6 Major risk factors include mechanical ven- tilation, burns, trauma, and multi-organ failure.
Coagulopathy Although coagulopathy alone does not usually cause GI bleeding, hemorrhagic disease of the newborn (vitamin K defi ciency) or other bleeding dis- orders (e.g., von Willebrand’s disease) can present this
way. Fat malabsorption (e.g., cystic fi brosis or other pancreatic insuffi ciency, and cholestasis) leading to vita- min K defi ciency in infancy is rare.
Food protein allergy Food allergies can occasionally present with gastritis and hematemesis although blood- streaked stools are much more common.7
Other causes Crohn’s disease can involve any part of the intestinal tract with ulcerations causing GI bleeding.
Upper tract involvement is not common in children.
This will usually be accompanied by other signs and symptoms such as growth impairment, abdominal pain, iron defi ciency anemia, and hypoalbuminemia. Other causes of overt UGI bleeding in children are rare:
Henoch–Schoenlein purpura, vascular anomalies (e.g., Dieulafoy lesion and aortoesophageal fi stula), hemo- succus pancreaticus, and gastric polyps or tumors.
Hemangiomas are common skin lesions but rarely symptomatic when present in the gut. Skin lesions are usually obvious when intestinal hemangiomas are pres- ent and can be a clue. As with skin lesions, gut heman- giomas often fade with time. Intestinal duplications are a rare cause of UGI bleeding if there is gastric mucosa present.
Inferior vena
cava Aorta
Hepatic vein
Portal vein
Left gastric vein
Middle rectal vein Levator ani muscle Inferior rectal vein
Superior rectal vein Sigmoid vein Left colic vein Inferior mesenteric vein Middle colic
vein Right colic vein
Lieocolic vein
Cecum Appendix Superior mesenteric vein
Esophagus
Esophagus
Veins in wall
Veins in stomach wall Stomach
Stomach Dilated veins in wall
Dilated veins in stomach wall
Azygous vein Esophageal vein
Splenic vein
FIGURE 6–3 ■ Portal hypertension and development of esophageal varices. The portal vein is formed by the junction of the superior mesenteric and splenic veins. The left gastric vein inserts into the portal vein. Impeded fl ow in the portal vein may lead to systemic shunting (e.g., to azygous vein via left gastric vein to gastric and esophageal veins) and development of esophageal varices. These develop distally and propagate upwards. Less commonly seen are caput medusa (abdominal wall veins) and hemorrhoids.