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than 4 days or outdated reagents or cards.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.
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
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.
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.
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.
