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Dr M.Sanjeevappa
M.D.(paeds)
Designated Associate Professor of
Paediatrics
G.M.C. , Ananthapuramu.
 MELENA: passage of black, tarry stools; suggests
bleeding proximal to the ileocecal valve.
 HEMATOCHEZIA: passage of bright or dark red
blood per rectum; indicates colonic source or
massive upper GI bleeding.
 HEMATEMESIS: passage of vomited material
that is black (“coffee grounds”) or contains frank
blood; bleeding from above the ligament of Treitz
 Bleeding proximal to the ligament of Treitz.
◦ Presents with:
 Hematemesis .
 Melena
 If massive then hematochezia.
◦ More blood loss than lower GI bleeding.
 Bleeding distal to the ligament of Treitz.
◦ Presents with:
 Hematochezia – bright red blood per rectum.
 Maroon stools – profuse bleed from distal
small bowel
Foods: tomatoes, cranberries, Beets ,
red fruit juices and gelatin.
Red-colored medications:
Acetaminophen
Amoxicillin
 Spinach, iron, and bismuth
often lead to black stools, which can be confused
with true melena.
◦ Employs a peroxidase-like activity of
hemoglobin to oxidize with the reagent
changing the color to blue.
◦ False positive: red meat, horseradish, turnips,
iron, tomatoes and fresh red cherries.
◦ False negatives: Vitamin C, storage for more
than 4 days or outdated reagents or cards.
 Swallowed maternal blood -Apt-Downey test
 Bleeding mouth lesions.
 Nasopharyngeal bleeds.
 Pulmonary hemorrhage.
 Vaginal bleeding in a newborn.
 Münchausen syndrome by proxy.
 One part of the bloody stool or gastric aspirate is
mixed with 5 parts of water to lyse the red blood
cells.
 After the mixture is centrifuged, 1 mL of
0.2 % sodium hydroxide is added to the
supernatant hemoglobin solution.
 After2 minutes, fetal hemoglobin, which resists
the alkaline reduction, remains pink, whereas
maternal hemoglobin turns yellow-brown.
NEWBORNS
Upper GI Bleeding
• Hemorrhagic disease of the newborn
• Gastritis
• Stress ulcer
• Esophagitis
Lower GI Bleeding
• Necrotizing enterocolitis
• Duplication
• Volvulus, malrotation
• Vascular malformations
• Milk allergy
• Infectious enteritis
• Anal fissure
INFANTS AND YOUNG CHILDREN
Upper GI Bleeding
• Esophagitis.
• Acid reflux.
• Esophageal foreign body.
• Mallory-Weiss tear.
• Gastro esophageal varices.
• Gastritis
Lower GI Bleeding
• Juvenile polyps
• Meckel diverticulum
• Intussusception
• Infectious enterocolitis
• Pseudomembranous colitis
• Vasculitis (HSP, HUS)
• Milk allergy
• Lymphonodular hyperplasia
• Anal fissure or trauma.
• Duplication
• Vascular malformation.
OLDER CHILDREN AND ADOLESCENTS
Upper GI Bleeding
• Esophagitis
• Mallory-Weiss tear
• Gastro esophageal varices
• Gastritis
• Aspirin, NSAIDs
• Helicobacter pylori
• Peptic ulcer disease
Lower GI Bleeding
• Polyps
• Infectious enterocolitis
• Inflammatory bowel disease
• Vasculitis
• Vascular malformation
• Meckel’s diverticulum
• Hemorrhoids
• Anal fissure
Goal of history :
 GI bleeding or not?
 If GI bleed ,then where is the source ?
 What is the severity of the blood loss ?
 What are the most likely causes?
Symptom or sign Location of bleeding lesion
Effortless bright red blood
from mouth
Nasopharyngeal or oral lesions , tonsillitis ,
Esophageal varices
Vomiting of bright red
blood or of coffee
grounds.
Lesion proximal to ligament of treitz
Melena Lesion proximal to ligament of treitz , upper
small bowel .
Blood loss >50 -100 ml /day
Bright red or dark red
blood in stools
Lesion in ileum or colon
Streak of blood on outside
of a stool
Lesion in the rectal ampulla or anal canal
 Vital signs.
 Skin: pallor, jaundice, ecchymosis, abnormal
blood vessels, hydration, cap refill.
 HEENT: nasopharyngeal injection, oozing,
tonsillar enlargement, bleeding.
 Abdomen: organomegaly, tenderness, ascites,
caput medusa.
 Perineum: fissure, fistula, induration.
 Rectum: gross blood, melena, tenderness
 CBC, ESR,CRP; PT, PTT in all cases
 Others as indicated:
◦ Blood grouping and cross match
◦ AST, ALT, bilirubin
◦ Albumin, total protein
◦ Stool for culture, ova and parasite
examination.
 Upper GI series: dysphagia, odynophagia,
drooling.
 Barium enema: intussusception, stricture.
 Abdominal US: portal hypertension.
 Meckel’s scan: Meckel’s diverticulum.
 Sulfur colloid scan, labeled RBC scan,
angiography : obscure GI bleeding.
 Flexible sigmoidoscopy: hematochezia.
 Colonoscopy: hematochezia.
 Enteroscopy: obscure GI blood loss
 Supportive care: begin promptly
◦ IV fluids, blood products, pressors
 Specific care:
◦ Barrier agents (sucralfate)
◦ H2 receptor antagonists (cimetidine, ranitidine, etc.)
◦ Proton pump inhibitors (omeprazole, lansoprazole)
◦ Vasoconstrictors (somatostatin analogue, vasopressin)
 Somatostatin : dosage is one to three bolus injections
(250 μg/bolus)during first hour of therapy followed by
infusion of 250μg/hour of continuous infusion for 2–5
days.
 Terlipressin : IV injections (2 mg) every 4 hours till
bleeding free interval of 24–48 hours is achieved.
 Octreotide : It is a synthetic analog of somatostatin with
half-life of 90 minutes. In children the dose is 1–2 μg/kg
over 2–5 min, then 1–2 μg/kg per hour for 5 days.
 Balloon tamponade
 Endoscopic therapy:
stabilize and prepare patient first
Endoscopic variceal ligation
Endoscopic sclerotherapy :polydocanol, sodium
tetradecylsulfate,
Polypectomy.
A transjugular intrahepatic portosystemic shunt.
 Orthotopic liver transplantation represents a much better
therapy for portal hypertension resulting from intrahepatic
disease and cirrhosis.
 Long-term treatment with propranolol.
 Defined as an elevation of portal pressure
>10-12 mm Hg or a hepatic venous pressure
gradient >4 mm Hg.
Causes of Portal Hypertension :
EXTRAHEPATIC PORTAL HYPERTENSION :
 Portal vein agenesis, atresia, stenosis
 Portal vein thrombosis or cavernous transformation
 Splenic vein thrombosis
 Increased portal flow
 Arteriovenous fistula
Causes of Portal Hypertension :
INTRAHEPATIC PORTAL HYPERTENSION :
 Acute and chronic viral hepatitis
 Cirrhosis
 Congenital hepatic fibrosis
 Wilson disease
 α1 -Antitrypsin deficiency
 Glycogen storage disease type IV
 Parenteral nutrition
INTRAHEPATIC PORTAL HYPERTENSION :
 Biliary tract disease
 Extrahepatic biliary atresia
 Cystic fibrosis
 Choledochal cyst
 Sclerosing cholangitis
 Intrahepatic bile duct paucity
 Idiopathic portal hypertension
 Post sinusoidal obstruction
 Budd-Chiari syndrome
 Veno occlusive disease
Pathophysiology :
 Increased resistance to portal blood flow.
 Portosystemic shunting should decompress the portal
system.
 development of significant collaterals deviating portal
blood into systemic veins.
 A hyperdynamic circulation is achieved by tachycardia,
an increase in cardiac output, decreased systemic
vascular resistance, and increased splanchnic dilation.
 Collateral vessels can form prominently in areas in
which absorptive epithelium joins stratified epithelium
 Congestive gastropathy
Clinical Manifestations :
 Bleeding is the most common presentation of portal
hypertension in children.
 Splenomegaly is the second most common finding.
 Ascites is the presenting sign of portal hypertension
in 7–21% of children.
 Hepatopulmonary syndrome (HPS) and
portopulmonary hypertension (PP-HTN)
Diagnosis :
 patency of the portal vein, and Doppler flow
ultrasonography can demonstrate the direction of
flow within the portal system.
 Reversal of portal vein blood flow (hepatofugal flow)
is more likely to be associated with variceal
bleeding.
 presence of esophageal varices.
 Endoscopy is the most reliable method for
detecting esophageal varices and for identifying the
source of gastrointestinal bleeding.
Treatment :
 emergency treatment of potentially life-threatening
hemorrhage.
 A reasonable goal hemoglobin level after variceal bleed is
between 7 and 9 g/dL.
 Correction of coagulopathy by administration of vitamin K
and/or infusion of platelets or fresh-frozen plasma
 A nasogastric tube should be placed to document the
presence of blood within the stomach and to monitor for
ongoing bleeding.
 An H2 -receptor blocker or proton pump inhibitor should be
given intravenously to reduce the risk of bleeding from
gastric erosions.
 Intravenous antibiotics
Prognosis :
 Portal hypertension is usually progressive and is
often associated with deteriorating liver function.
GI BLEEDING IN CHILDREN

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GI BLEEDING IN CHILDREN

  • 1. Dr M.Sanjeevappa M.D.(paeds) Designated Associate Professor of Paediatrics G.M.C. , Ananthapuramu.
  • 2.  MELENA: passage of black, tarry stools; suggests bleeding proximal to the ileocecal valve.  HEMATOCHEZIA: passage of bright or dark red blood per rectum; indicates colonic source or massive upper GI bleeding.  HEMATEMESIS: passage of vomited material that is black (“coffee grounds”) or contains frank blood; bleeding from above the ligament of Treitz
  • 3.  Bleeding proximal to the ligament of Treitz. ◦ Presents with:  Hematemesis .  Melena  If massive then hematochezia. ◦ More blood loss than lower GI bleeding.
  • 4.  Bleeding distal to the ligament of Treitz. ◦ Presents with:  Hematochezia – bright red blood per rectum.  Maroon stools – profuse bleed from distal small bowel
  • 5. Foods: tomatoes, cranberries, Beets , red fruit juices and gelatin. Red-colored medications: Acetaminophen Amoxicillin  Spinach, iron, and bismuth often lead to black stools, which can be confused with true melena.
  • 6. ◦ Employs a peroxidase-like activity of hemoglobin to oxidize with the reagent changing the color to blue. ◦ False positive: red meat, horseradish, turnips, iron, tomatoes and fresh red cherries. ◦ False negatives: Vitamin C, storage for more than 4 days or outdated reagents or cards.
  • 7.  Swallowed maternal blood -Apt-Downey test  Bleeding mouth lesions.  Nasopharyngeal bleeds.  Pulmonary hemorrhage.  Vaginal bleeding in a newborn.  Münchausen syndrome by proxy.
  • 8.  One part of the bloody stool or gastric aspirate is mixed with 5 parts of water to lyse the red blood cells.  After the mixture is centrifuged, 1 mL of 0.2 % sodium hydroxide is added to the supernatant hemoglobin solution.  After2 minutes, fetal hemoglobin, which resists the alkaline reduction, remains pink, whereas maternal hemoglobin turns yellow-brown.
  • 9. NEWBORNS Upper GI Bleeding • Hemorrhagic disease of the newborn • Gastritis • Stress ulcer • Esophagitis Lower GI Bleeding • Necrotizing enterocolitis • Duplication • Volvulus, malrotation • Vascular malformations • Milk allergy • Infectious enteritis • Anal fissure
  • 10. INFANTS AND YOUNG CHILDREN Upper GI Bleeding • Esophagitis. • Acid reflux. • Esophageal foreign body. • Mallory-Weiss tear. • Gastro esophageal varices. • Gastritis
  • 11. Lower GI Bleeding • Juvenile polyps • Meckel diverticulum • Intussusception • Infectious enterocolitis • Pseudomembranous colitis • Vasculitis (HSP, HUS) • Milk allergy • Lymphonodular hyperplasia • Anal fissure or trauma. • Duplication • Vascular malformation.
  • 12. OLDER CHILDREN AND ADOLESCENTS Upper GI Bleeding • Esophagitis • Mallory-Weiss tear • Gastro esophageal varices • Gastritis • Aspirin, NSAIDs • Helicobacter pylori • Peptic ulcer disease
  • 13. Lower GI Bleeding • Polyps • Infectious enterocolitis • Inflammatory bowel disease • Vasculitis • Vascular malformation • Meckel’s diverticulum • Hemorrhoids • Anal fissure
  • 14. Goal of history :  GI bleeding or not?  If GI bleed ,then where is the source ?  What is the severity of the blood loss ?  What are the most likely causes?
  • 15. Symptom or sign Location of bleeding lesion Effortless bright red blood from mouth Nasopharyngeal or oral lesions , tonsillitis , Esophageal varices Vomiting of bright red blood or of coffee grounds. Lesion proximal to ligament of treitz Melena Lesion proximal to ligament of treitz , upper small bowel . Blood loss >50 -100 ml /day Bright red or dark red blood in stools Lesion in ileum or colon Streak of blood on outside of a stool Lesion in the rectal ampulla or anal canal
  • 16.  Vital signs.  Skin: pallor, jaundice, ecchymosis, abnormal blood vessels, hydration, cap refill.  HEENT: nasopharyngeal injection, oozing, tonsillar enlargement, bleeding.  Abdomen: organomegaly, tenderness, ascites, caput medusa.  Perineum: fissure, fistula, induration.  Rectum: gross blood, melena, tenderness
  • 17.  CBC, ESR,CRP; PT, PTT in all cases  Others as indicated: ◦ Blood grouping and cross match ◦ AST, ALT, bilirubin ◦ Albumin, total protein ◦ Stool for culture, ova and parasite examination.
  • 18.  Upper GI series: dysphagia, odynophagia, drooling.  Barium enema: intussusception, stricture.  Abdominal US: portal hypertension.  Meckel’s scan: Meckel’s diverticulum.
  • 19.  Sulfur colloid scan, labeled RBC scan, angiography : obscure GI bleeding.  Flexible sigmoidoscopy: hematochezia.  Colonoscopy: hematochezia.  Enteroscopy: obscure GI blood loss
  • 20.  Supportive care: begin promptly ◦ IV fluids, blood products, pressors  Specific care: ◦ Barrier agents (sucralfate) ◦ H2 receptor antagonists (cimetidine, ranitidine, etc.) ◦ Proton pump inhibitors (omeprazole, lansoprazole) ◦ Vasoconstrictors (somatostatin analogue, vasopressin)
  • 21.  Somatostatin : dosage is one to three bolus injections (250 μg/bolus)during first hour of therapy followed by infusion of 250μg/hour of continuous infusion for 2–5 days.  Terlipressin : IV injections (2 mg) every 4 hours till bleeding free interval of 24–48 hours is achieved.  Octreotide : It is a synthetic analog of somatostatin with half-life of 90 minutes. In children the dose is 1–2 μg/kg over 2–5 min, then 1–2 μg/kg per hour for 5 days.
  • 22.  Balloon tamponade  Endoscopic therapy: stabilize and prepare patient first Endoscopic variceal ligation Endoscopic sclerotherapy :polydocanol, sodium tetradecylsulfate, Polypectomy. A transjugular intrahepatic portosystemic shunt.  Orthotopic liver transplantation represents a much better therapy for portal hypertension resulting from intrahepatic disease and cirrhosis.  Long-term treatment with propranolol.
  • 23.  Defined as an elevation of portal pressure >10-12 mm Hg or a hepatic venous pressure gradient >4 mm Hg.
  • 24. Causes of Portal Hypertension : EXTRAHEPATIC PORTAL HYPERTENSION :  Portal vein agenesis, atresia, stenosis  Portal vein thrombosis or cavernous transformation  Splenic vein thrombosis  Increased portal flow  Arteriovenous fistula
  • 25. Causes of Portal Hypertension : INTRAHEPATIC PORTAL HYPERTENSION :  Acute and chronic viral hepatitis  Cirrhosis  Congenital hepatic fibrosis  Wilson disease  α1 -Antitrypsin deficiency  Glycogen storage disease type IV  Parenteral nutrition
  • 26. INTRAHEPATIC PORTAL HYPERTENSION :  Biliary tract disease  Extrahepatic biliary atresia  Cystic fibrosis  Choledochal cyst  Sclerosing cholangitis  Intrahepatic bile duct paucity  Idiopathic portal hypertension  Post sinusoidal obstruction  Budd-Chiari syndrome  Veno occlusive disease
  • 27. Pathophysiology :  Increased resistance to portal blood flow.  Portosystemic shunting should decompress the portal system.  development of significant collaterals deviating portal blood into systemic veins.  A hyperdynamic circulation is achieved by tachycardia, an increase in cardiac output, decreased systemic vascular resistance, and increased splanchnic dilation.  Collateral vessels can form prominently in areas in which absorptive epithelium joins stratified epithelium  Congestive gastropathy
  • 28. Clinical Manifestations :  Bleeding is the most common presentation of portal hypertension in children.  Splenomegaly is the second most common finding.  Ascites is the presenting sign of portal hypertension in 7–21% of children.  Hepatopulmonary syndrome (HPS) and portopulmonary hypertension (PP-HTN)
  • 29. Diagnosis :  patency of the portal vein, and Doppler flow ultrasonography can demonstrate the direction of flow within the portal system.  Reversal of portal vein blood flow (hepatofugal flow) is more likely to be associated with variceal bleeding.  presence of esophageal varices.  Endoscopy is the most reliable method for detecting esophageal varices and for identifying the source of gastrointestinal bleeding.
  • 30. Treatment :  emergency treatment of potentially life-threatening hemorrhage.  A reasonable goal hemoglobin level after variceal bleed is between 7 and 9 g/dL.  Correction of coagulopathy by administration of vitamin K and/or infusion of platelets or fresh-frozen plasma  A nasogastric tube should be placed to document the presence of blood within the stomach and to monitor for ongoing bleeding.  An H2 -receptor blocker or proton pump inhibitor should be given intravenously to reduce the risk of bleeding from gastric erosions.  Intravenous antibiotics
  • 31. Prognosis :  Portal hypertension is usually progressive and is often associated with deteriorating liver function.