patient with GI Bleeding
Hematemesis

  • Vomiting of fresh blood or “Coffee-grounds” (blood altered by gastric acid).

Hematochezia

  • Passage of stools containing red blood rather than tarry stools.

Melena

  • Refers to black tarry stools that usually result from upper GI bleeding.
  • Represent bleeding anywhere above the ileocecal valve.

Causes Of G.I. Bleeding

 Neonates

  • Most common causes :
    • Swallowed maternal blood
    • Bacterial enteritis
    • Milk protein allergies
    • Intussusception
    • Anal fissures
    • Lymphonodular hyperplasia.
  • Erosions of the esophageal, gastric, and duodenal mucosa
  • Some drugs:
    • NSAIDs, heparin, and tolazoline, used for persistent fetal circulation.
    • Indomethacin, used for patent ductus arteriosus in neonates
    • Maternal medications like Aspirin, cephalothin, and phenobarbital
    • Dexamethasone – Stress ulcers in newborns
  • Rarer causes of GI bleeding in a neonate include
    • Volvulus
    • Coagulopathies
    • Arteriovenous malformations
    • Necrotizing enterocolitis (especially in pre-term infants)
    • Hirschsprung enterocolitis
    • Meckel diverticulitis

Infants

  • GI mucosal lesions and irritations
    • includes esophagitis, gastritis, duodenitis, ulcers, colonic polyps, and anorectal disorders.
  • Intussusception
  • Other causes
    • Infectious diarrhea
    • Midgut volvulus
    • Meckel diverticulum
    • Arteriovenous malformation
    • GI duplication.
  • Rare causes
    • Foreign body ingestions
    • Variceal disease
    • Coagulation disorder(hemorrhagic disease of new born)

 

Children

Common Causes:

  • Bacterial enteritis
  • Anal fissure
  • Colonic polyps
  • Intussusception
  • Peptic ulcer/gastritis
  • Swallowed epistaxis 
  • Prolapse (traumatic) gastropathy 2° emesis
  • Mallory-Weiss syndrome

Rare Causes:

  • Esophageal varices
  • Esophagitis
  • Meckel diverticulum
  • Lymphonodular hyperplasia
  • Henoch-Schönlein purpura
  • Foreign body
  • Hemangioma, arteriovenous malformation
  • Sexual abuse
  • Hemolytic-uremic syndrome
  • Inflammatory bowel disease
  • Coagulopathy

Adults

Common Causes

  • Bacterial enteritis
  • Inflammatory bowel disease
  • Peptic ulcer/gastritis
  • Prolapse (traumatic) gastropathy 2° emesis
  • Mallory-Weiss syndrome
  • Colonic polyps

Rare causes

  • Hemorrhoids 
  • Esophageal varices
  • Esophagitis
  • Telangiectasia-angiodysplasia
  • Graft versus host disease

Adolescents

  • The most common causes of upper GI bleeding are duodenal ulcers, esophagitis, gastritis, and Mallory-Weiss tears.
  • Lower GI bleeding most likely is caused by inflammatory bowel disease, colonic polyps, hemorrhoids, anal fissures, or infectious diarrhea

Other causes

  • Gastroesophageal reflux disease (GERD)
  • Stress ulcers
  • Sexual trauma

History

Ask both age- and etiology-specific questions.

  • Acuteness or chronicity of bleeding
  • Color and quantity of the blood in stool or emesis
    • Massive UGI bleeding can produce bright red blood per rectum if GI transit time is rapid
  • Antecedent symptoms
  • History of straining, abdominal pain, or trauma.
  • Bloody diarrhea and signs of obstruction suggest volvulus, intussusception, or necrotising enterocolitis, (ex-premature infant)
  • Recurrent or forceful vomiting, Mallory-Weiss tears.
  • Sudden onset of bright color hematemesis and melena of large amount Esophageal varices
  • Gradual onset chronic, mild hematemesis and melena Acid peptic disease
  • Acid regurgitation, nausea, vomiting, water brash, retrosternal pain Reflux oesophagitis
  • H/o antepartum hemorrhage Swallowed maternal blood
  • Anorexia, nausea, vomiting and epigastric pain with relation to food Peptic ulcer
  • Bloody diarrhea, vomiting, abdominal pain, fever Dysentery
  • History of drug intake: NSAIDS, corticosteroids, Mucosal irritants, iron preparation
  • Risk factors for portal HTN- umbilical sepsis / catheterization, jaundice, liver disease Esophageal varices
  • H/o Fatigue, weakness, pallor or dyspnea
  • Ask questions that may reveal underlying but yet undiagnosed organ dysfunction.
  • H/o
    • Bleeding diathesis
    • Medications (NSAIDs, Aspirin, warfarin, hepatotoxins)
  • For complaints of bloody stool, make sure to elicit on history foods or drugs that may give a stool bloody appearance

Substances that Commonly Color Vomitus or Stools
Red

  • Candies
  • Red gelatin
  • Beet root
  • Tomato skin
  • Peach skin
  • Red cherries
  • Phenytoin
  • Rifampicin

Black

  • Bismuth
  • Activated charcoal
  • Iron
  • Spinach
  • Blueberries
  • Chocolate
  • Grape juice
  • Purple grapes

Past History

  • H/o previous GI problems, Blood transfusions, Coagulopathies, Iron deficiency

Family History

  • GI disorders (polyps, ulcers, colitis). In idiopathic peptic ulcer disease nearly 70% will have family history of ulcer disease.
  • Liver disease
  • Bleeding diathesis

Assessment of a child

  • One should first determine the amount of blood loss, and the site of bleeding.
  • The measurement of vital signs provides the only accurate assessment of blood loss (orthostatics, heart rate, complaints of weakness or dizziness, syncope).

Initial Evaluation

  • Performed concurrently with resuscitative measures regardless of the site of bleeding.

The questions that must be addressed are

  • Has the child been bleeding ?
  • Has the child had bleeding of sufficient magnitude to result in actual or impending circulatory collapse?
  • Is the child bleeding now?
  • What actions are required?

Physical examination

  • Vital signs :- PR, BP, RR, T, CRT
  • Acute losses of 10-25% of blood volume cause tachycardia, narrow pulse pressure and postural hypotension.
  • Earliest sign to increase is HR.
  • Supine Hypotension – >20% Blood loss.
  • Pallor, diaphoresis, confusion, obtundation, tachycardia, tachypnea → Shock.
  • Pallor
  • Icterus
  • Edema
  • Hydration status
  • Nutritional status- hematemesis/melena in a healthy thriving child Extra hepatic portal hypertension.
  • Ecchymosis, bluish nodules
  • Icterus with signs of liver failure like palmar erythrema, vascular telangiectasias, ascites liver disease.
  • CVS
    • Pulse rate, BP sitting & standing
    • Pulse pressure
    • Capillary filling
  • Abdomen
    • Distension, shiny skin, prominent veins (caput medusae)
    • Abdominal tenderness, with or without a mass, s/o intussusception or ischemia
    • Splenomegaly, Hepatomegaly
    • Evidence of free fluid
    • Hyperactive bowel sound
  • Inspection of the perianal area
    • fissures, fistulas, skin breakdown, or evidence of trauma.
    • Gentle digital rectal examination may reveal polyps, masses, or occult blood.
    • Looking for evidence of child abuse, such as perianal tearing, tags, or irregularities in anal tone and contour, is also important.
  • Examination of the skin
    • evidence of systemic disorders, such as inflammatory bowel disease, Henoch-Schönlein purpura, and Peutz-Jeghers polyposis.
  • Examination of the head, ears, eyes, nose, and throat
    • look for causes such as epistaxis, nasal polyps, and oropharyngeal erosions from caustics and other ingestions.
    • Color of stool
  • NG aspiration
    • A positive NG tube aspirate for blood usually signifies that the site of bleeding is proximal to the ligament of Treitz.
    • Assessing the activity and severity of upper GI bleeding

Investigations

  • Blood
    • CBC, coagulation profile (PT, APTT, Platelets).
    • Blood grouping and cross matching of blood.
    • BUN
  • LFT and RFT
    • To stratify risk in case invasive intervention is required.
  • Stool
    • Occult blood
  • Apt test
    • To differentiate between maternal and fetal blood.
  • Localization Studies
    • Definitive management depends upon localization of its source and underlying cause.
  • Esophagogastroduodenoscopy
    • Allows prompt diagnosis and the ability to guide or perform therapy to hasten cessation of bleeding.
    • within the first 12 hours of the hemorrhagic episode if they are sufficiently stable because early endoscopy improves the diagnostic index.
    • The source of bleeding can be identified in 90% of cases if endoscopy is done within the first 24 hours.
    • Infants and children with anemia and positive stool occult-blood, even in the absence of melena, hematemesis or hematochezia, often need upper GI endoscopy examination.
    • Preferred method of Diagnosis and treatment.
  • The Forress classification divides endoscopic findings into 3 categories
    • I – Active hemorrhage (Ia = bright red bleeding, Ib = slow bleeding)
    • II – Recent hemorrhage (IIa, = nonbleeding visible vessel, IIb = adherent clot on base of lesion, IIc = flat pigmented spot)
    • III – No evidence of bleeding
  • Colonoscopy: For lower GI bleeds, can reveal the source of bleeding more effectively than barium enema, and it has 80% sensitivity.
    • Colonoscopy should be performed only when the patient is stable and when blood and feces will not conceal proper visualization.
    • The yield of finding a potential bleeding source in the colon is greatest if colonoscopy is performed within the initial 24 hours of presentation.
  • USG abdomen
    • Suspected portal HTN.
    • For suspected intussusception, color Doppler ultrasonography can be used. Its sensitivity is 98-100%, and its specificity is 89-100%, but these rates are operator dependent.
  • Tc 99m – labeled RBC scan
    • Can localize sites with bleeding rates of 0.1ml/min.
  • Meckel scan uses technetium-99m pertechnetate to highlight the ectopic gastric mucosa.
  • GI contrast studies
    • Contraindicated with active bleeding as the contrast can obscure endoscopic and angiographic studies.
    • To point to foreign bodies, esophagitis, inflammatory bowel disease, or polyps.
    • For neonates with malrotation with midgut volvulus, it may show a corkscrew of small bowel or a bird’s beak if complete obstruction is present
  • Angiography
    • Useful if endoscopy is not definitive.
    • Allows rapid localization and potential therapy of GI bleeding, extravasation of the dye into the intestine when bleeding rates > 0.5ml/min.
    • May also delineate the anatomy of bleeding lesion.
    • Offers the possibility of Rx – e.g., embolization, vasopressin infusion.
  • Nasopharyngoscopy and CT scan of PNS
    • If the source of bleeding is thought to be from sinuses or nasopharynx.
  • CXR
    • To r/o causes of hemoptysis e.g cystic fibrosis, bronchiectasis
  • Plain abdominal radiography:
    • Patients with suspected obstruction
    • May also be helpful in those neonates in whom necrotizing enterocolitis is a possibility;
    • the images may show free air, pneumatosis intestinalis (bubbles in the bowel wall), or portal air

Management

  1. Initial Resuscitation
    • Airway protection
      • Endotracheal intubation – to prevent aspiration- considered in situations in which diminished mental status (shock, hepatic encephalopathy), massive hematemesis or active variceal hemorrhage is +nt.
    • Restoration of intravascular volume
      • Large bore IV line – esp. 2.
      • CVP should be established in overt GI bleeding.
      • NS, RL or hemaccel.
      • Blood- best for volume replacement in severe blood loss.
      • O-ve blood can be used in emergency
    • Correction of coagulopathy
      • Discontinue offending anticoagulant.
      • Fresh blood.
      • Infusion of FFP if possible.
      • Vitamin K in  PT in patients on warfarin Rx or with hepatobiliary diseases → total 3 doses.
      • Platelet infusion if < 50,000/mm3.
  2. Specific management
    • Peptic ulcer – barrier agents (sucralfate), H2-antagonists (cimetidine, ranitidine, famotidine), H+-pump inhibitors (omeprazole, lansoprazole).
    • Coagulation – cautery, heater probe, laser.

Management of Variceal bleeding

  • Fluid resuscitation- crystalloids, packed RBCs, whole blood.
  • Coagulopathy- Vit K, FFP.
  • H2- blocker (ranitidine) – decrease bleeding from gastric erosion.
  • Pharmacologic Rx
    • To decrease portal pressure and if there is continuous bleeding.
  • Vasopressin
    • Splanchnic vascular tone and ↓ portal blood flow.
    • Bolus 0.33U/Kg over 20mins, then same dose/hr infusion (or 0.2U/1.73m2/min).
    • Causes vasoconstriction.
  • Nitroglycerine skin patches
    • ↓ portal pressure.
  • NTG + vasopressin
    • may ameliorate some of its side effects
  • Octreotide
    • ↓es splanchnic blood flow and reduces portal pressure.
  • Non-selective β – blockers
    • g. Propranolol, timolol
    • Lower cardiac output (β1 blockade) and portal pressure (β2 blockade).
    • Used extensively in adults.
    • In adults – evidence shows that it ↓es the incidence of variceal hemorrhage and improve long term survival.
    • Therapeutic effect – pulse rate ↓ed by at least 25%.
  • Endoscopy
    • Sclerosis
    • Elastic band ligation – safer, more effective.
  • Sengstaken – Blakemore tube
    • If pharmacologic and endoscopic measures fail.
    • Mechanically compress esophageal and gastric varices.
  • Endoscopy
    • Sclerosis
    • Elastic band ligation – safer, more effective.
  • Sengstaken – Blakemore tube
    • If pharmacologic and endoscopic measures fail.
    • Mechanically compress esophageal and gastric varices.
  • Surgery
    • Portocaval shunt – to divert portal blood flow.
  • TIPSS (Transjugular intrahepatic portosystemic shunting)
    • Shunt placed between hepatic veins and the portal vein.
  • Liver transplantation
    • In chronic liver diseases or post sinusoidal veno-occlusive diseases.