GI Bleeding in Children Maria Christina H. Ventura, MD, DPPS July 8, 2010

Bleeding may occur anywhere along the GI tract Identification of the site may be challenging

The least likely site of bleeding Small intestine Except in Meckel’s diverticulum wherein there is painless bleeding

The most common cause of bleeding Erosive damage to the mucosa of the GI tract Variceal bleeding secondary to portal hypertension also occurs frequently.

Rare cause of bleeding in children Vascular malformations

Clinical Definition HEMATEMESIS HEMATOCHEZIA MELENA When bleeding originates in the esophagus, stomach or duodenum, it may cause hematemesis. When the blood is exposed to the gastric or intestinal juices, blood quickly darkens to resemble coffee grounds. Massive bleeding is likely to be red. Red or maroon blood in the stools signifies either a distal bleeding site ofr massive hemorrhage above the distal ileum. When there is moderate to mild bleeding from sites above the distal ileum, this would cause tarry black stools known as melena Major hemorrhages in the duodenum or above can cause melena.

Upper vs. Lower GI Bleeding Acute Upper GI bleeding usually presents with hematemesis or the passage of melena Acute Lower GI bleeding usually presents with hematochezia Severe Acute GI bleeding may present with hematochezia because the blood is not altered during the very rapid transit the digestive tract.

Children with profuse upper and lower GI bleeding can present with hypovolemia and shock.

CLUES History Physical Examination Laboratory and Radiographic techniques

Clinical Algorithm Infants and Neonates Common Causes Bacterial Enteritis Milk protein allergy Intussusception Swallowed maternal blood Anal Fissure Lymphonodular hyperplasia

Infants and Neonates Rare Causes Volvulus Necrotizing enterocolitis Meckel diverticulum Stress ulcer, stomach Coagulation disorder ( Hemorrhagic Disease of the Newborn )

Clinical Algorithm Children Common Causes Bacterial enteritis Anal Fissure Colonic Polyps Intussusception Peptic Ulcer/ Gastritis Swallowed epistaxis Mallory Weiss Syndrome

Children Rare Causes Esophageal varices Esophagitis Meckel Dicerticulum Lymphonodular hyperplasia HSP Foreign body Hemangioma, AV Malformation Sexual abuse HUS IBD Coagulopathy

ADOLESCENT Common Causes Bacterial enteritis IBD Peptic Ulcer/ Gastritis Mallory Weiss Syndrome Colonic Polyps

Adolescent Rare causes Hemorrhoids Esophageal varices Esophagitis Telangiectasia- angiodysplasia Gay bowel disease Graft versus Host disease

Indirect Imaging Arteriography Scintigraphy CT Scan MRI

UPPER GI Causes Vascular lesions in the small bowel Peptic Ulceration Meckel’s diverticulum Esophageal varices Malignancy

Peptic Ulceration Ulcers and gastritis are classified as primary ( peptic) or secondary caused by factors known to affect the intergrity of the gastric or duodenal mucosa. Primary : chronic, duodenal and related to H. pylori gastritis Secondary : usually acute and gastric

Peptic Ulcer ULCER : a disruption of the intestinal epithelium exposed to acid or pepsin EROSION : superficial ulcer Ulcers are usually 1 cm of less in diameter Gastritis : inflammation of the gastric mucosa without disruption of the mucosa A fibrinous coat of leukocytes and red cells covers a zone of fibrinoid necrosis surrounded by an infiltration of acute and chronic inflammatory cells.

Factors in the development of gastritis mediators of mucosal inflammation of the gastric mucosa :Oxygen free radicals, lymphokines and monokines Mucosal defense mechanisms: surface water-unstirred water layer intestinal and pancreatobiliary sources of bicarbonate

surface active hydrophobic phospholipids in the mucosal area mucosal blood flow rapid rate of cell replacement enhanced by factors ( EGF)

Duodenal Ulcers Increased acid secretion Acid secretion does not correlate with with ulcer size or duration of symptoms. Family history : 20 -25% Partially due to the known clustering of H. pylori in families

OTHER FACTORS Blood Type O cigarette smoking climatic conditions dietary habits ( consumption of alcohol) emotional stress

Factors related to acid are more important in duodenal ulcers Tissue resistance is of more importance in gastric ulcers

Primary Peptic ulcers Manifestations : pain. vomiting and chronic gastrointestinal blood loss and a strong familial incidence Primary gastritis due to H pylori usually occurs with primary peptic ulcers 1st month of life : gastrointestinal bleeding and perforation

Primary Peptic ulcers Between the neonatal period and 2 years old : recurrent vomiting slow growth gastrointestinal hemorrhage

Primary Peptic ulcers Preschool children periumbilical postprandial pain is often elicited vomiting and hemorrhage

Primary Peptic ulcers After 6 years old : similar symptoms in children epigastric abdominal pain acute or chronic GI blood loss often leading to IDA predominantly male

Secondary Peptic Ulcers Usually due to sepsis in infants Respiratory or cardiac insufficiency Trauma or dehydration Stress ulcers and erosions associated with burns are Curling ulcers Associated with normal gastric secretions ; Common in burn patients (>25 % BSA)

Secondary Peptic Ulcers Cushing ulcers Follows head trauma or surgery Associated with gastric hypersecretion Most are aysmptomatic May be associated with severe hemorrhage or perforation

ANAL Causes Hemorrhoids Fissure Perianal abscess/ fissure Anal carcinoma

Hemorrhoids Usually uncommon in children Usually benign When seen, must suspect portal hypertension Avoidance of chronic constipation, fecal impaction or other irritating local factors

Anal Fissure Small laceration of the mucocutaneous junction of the anus. Acquired lesion secondary to the forceful passage of a hard stool, mainly seen in infancy. Fissures appear to be the consequence and not the cause of constipation.

Anal Fissure Usually a history of constipation is elicited. painful bowel movement Patient retains the stool voluntarily to avoid a painful bowel movement Bright red blood on the surface of the stool

Anal Fissure Inspection of the Anal area Infant’s hips are put in acute flexion Buttocks are separated to expand the folds of the perianal skin Fissure becomes evident as a minor laceration (+) TAG Peripheral to the laceration, the patient might be seen to have a small skin appendage that represents epithelialized granulomatous tissue secondary to chronic inflammation

Anal Fissure The most important element in the treatment is for the parents to understand the origin of the laceration and the mechanism of the cycle of constipation. Goal of the treatment : REVERSE the CYCLE soft stools to avoid overstretching

Anal Fissure Stool softener Avoid hard stools and diarrhea Treat the primary cause of constipation

Perianal Abscess and Fistula Two different groups of pediatric patients Infants without predisposing conditions Older children with predisposing conditions

Infants relatively common usually boys < 2 years old benign self-limited condition the abscess has a communication with one of the crypts of the pectinate line of the anal canal It is believed that the crypts are the source of infection although the exact mechanism is unknown.

Infants The abscess eventually drains through an orifice in the perianal area Then inflammation subsides But, a fistula remains that communicates with the affected crypt to the perianal external orifice Fistula becomes chronic but usually disappears spontaneously before 2yrs.

Infants low grade fever, mild rectal pain, area of perianal cellulitis No evidence indicates that antibiotics are useful in these patients When the patient is extremely uncomfortable, the abscess can be drained under local anesthesia Once a chronic fistula forms, it is recommended that a fistulotomy under general anesthesia is done.

Children Children >2 years old with perianal or perirectal abscess and with a predisposing illness. Drug-induced or autoimmune neutropenia, leukemia, AIDS, DM, Crohn disease, prior rectal surgery, immunosuppresant drugs More serious condition

Children Prognosis is related to the predisposing disease Abscess may be deep and may rapidly expand

RECTAL Causes Polyp Carcinoma Proctitis

Juvenile Colonic Polyp MOST COMMON childhood bowel tumor 3-4% in less than 21 years old Rarely appear before 1 yr. of age Mostly between 2-10 years old Usually proximal in the descending colon

Bright red painless rectal bleeding during or immediately after a bowel movement Colonoscopy Removal of the polyp

Familial Polyposis Syndromes Familial Adenomatous Polyposis Coli Gardner Syndrome Peutz-Jeghers Syndrome

COLONIC Causes Polyp Cancer Diverticular diseases Colitis ( Inflammatory, Infective or Ischemic) Angiodysplasia