Upper gastrointestinal

bleeding
Dr Henock Hailu (R2)
Outline
• INTRODUCTION
• EPIDEMIOLOGY
• ETIOLOGY
• DIFFERENCIAL DIAGNOSIS
• CLINICAL PRESENTATION
• LABORATORY EVALUATION
• IMAGING
• MANAGEMENT
INTRODUCTION
• Upper gastrointestinal bleeding commonly presents with
hematemesis (vomiting of red blood or coffee ground-like material)
and/or melena (black, tarry stools).

• In comparison, hematochezia (bright red or maroon-colored blood or

fresh clots per rectum) is usually a sign of a lower gastrointestinal
source.

• In general, the redder the blood, the more distal the site of bleeding
EPIDEMIOLOGY
• As much as 20 percent of all episodes of gastrointestinal bleeding in
children come from an UGI source .

• A population-based study from France estimated that UGI bleeding

occurred in 1 to 2 per 10,000 children per year and that exposure to
(NSAIDs) played a role in 36 % of these cases .

• A study conducted at ST.paul`s hospital in 2018

Varices is the most common causes of UGIB(46.1%) followed by
peptic ulcer disease (24.2%) and esophagitis(3.9%)
M to F ratio was 5:1 & Overall mortality was 17.2%
Gastrointestinal causes Systemic Causes:
Esophagitis Coagulopathy
Esophageal Rupture Sepsis
Gastritis Burns ( Curling’s ulcer)
Gastric Erosions HUS, HSP
Peptic Ulcer Disease Malignancy- Leukemia
Portal hypertension Poisonings- chemical, caustic
Extra-hepatic portal vein Drugs-aspirin, NSAIDS, anti-
obstruction coagulants
Vascular malformations Food (milk protein) allergy/
hypersensitivity
Tumors Idiopathic
Genetic conditions
Turner syndrome
Ehlers Danlos syndrome
Pseudoxanthomaelasticum
KlippelTrenaunay syndrome
Osler-Rendu-Weber syndrome
Blue rubber bleb naevus syndrome
Hermansky-Pudlak syndrome

Traumatic
Iatrogenic-
continued ...
• The most common causes of UGI bleeding in children vary depending
upon age and the geographic setting.

• In Western countries, the most common causes are gastric and

duodenal ulcers, esophagitis, gastritis, and varices .

• In India and some other parts of the world, variceal bleeding

predominates .

• Conditions associated with structural abnormalities of blood vessels

and congenital or acquired coagulopathies can produce bleeding at
any time of life.
Neonates
Swallowed maternal blood.

 Hemorrhagic disease of the newborn

Stress gastritis or ulcers

 Intestinal duplications or vascular anomalies

Coagulopathy caused by infection, liver failure, or a congenital

coagulation factor deficiency.

Milk protein intolerance

Risk factors
Neonate Infant Child or adolescent

Swallowed maternal blood Stress gastritis or ulcer Mallory-Weiss tear

Vitamin K deficient bleeding Acid-peptic disease Acid-peptic disease

Stress gastritis or ulcer Mallory-Weiss tear Gastric or esophageal varices

Esophagitis Esophagitis Esophagitis

Trauma (eg, nasogastric tube) Vascular anomalies Foreign body
Vascular anomalies Gastrointestinal duplications Caustic ingestion
Gastrointestinal duplications Gastric or esophageal varices Vasculitis (eg, Henoch-Schoenlein
purpura)
Coagulopathy (eg, associated with Duodenal or gastric webs Crohn's disease
infection)
Milk protein intolerance Bowel obstruction Bowel obstruction
Congenital coagulation factor Dieulafoy lesion
deficiency
Mallory-Weiss syndrome
• Longitudinal mucosal
lacerations in the distal
esophagus, usually developing
after forceful retching.

The bleeding is usually small

and self-limited, but
occasionally is severe.
Esophageal or GI foreign body
• Sharp, caustic, and lodged in the esophagus. Clinical clues include a
history of a choking episode,

 Rarely, ingestion of a button battery has led to severe UGI

hemorrhage due to aortoesophageal fistula, which can be fatal

• Esophagitis – usually is caused by gastroesophageal reflux disease or

eosinophilic esophagitis, and occasionally by caustic ingestion. Peptic
esophagitis also may develop after recurrent vomiting from other
causes.
Peptic ulcers and gastritis
• Occasionally occur in all age
groups, typically in the setting of
critical illness or use of (NSAIDs).

Gastritis or peptic ulcers also may

be related to H.pylori infection or
occasionally to a cytomegalovirus .
• Pill esophagitis – caused by direct injury to the esophageal
mucosa from prolonged contact with certain drugs, including
tetracyclines , NSAID or bisphosphonates.

The condition presents with pain with swallowing and may

progress to hematemesis.

• Infectious esophagitis – due to candida, cytomegalovirus, or

herpes simplex can cause similar symptoms as pill esophagitis.
• Esophageal varices – are caused by Portal vein hypertension, Clues
include splenomegaly and/or a history of thrombocytopenia.

Causes of portal hypertension include:

 Cirrhosis due to chronic liver disease (eg, cystic fibrosis-related liver disease , biliary atresia,
or intestinal failure-associated liver disease).

 Portal vein thrombosis with a history of umbilical vein catheterization or sepsis during the
neonatal period.

 Hepatic vein obstruction (Budd-Chiari syndrome).

• Arterial bleeding – Rarely, severe acute UGI bleeding is from an artery, either
from an overlying peptic ulcer .
Esophageal varices
Differential diagnosis
• Swallowed maternal blood

• Epistaxis – Swallowed blood from the patient's nasopharynx

or respiratory tract

• Substances that resemble blood – Red food colorings and dyes

• Medical child abuse – Factitious illness caused by surreptitious

administration of blood or blood-like substance to simulate
UGI bleeding,
CLINICAL PRESENTATION
• Hematemesis – Bright red blood usually indicates brisk or very fresh bleeding.

 Coffee-ground-like material generally indicates slower rate of bleeding . This effect can be
altered with acid suppression therapy.

• Melena – Dark red stool produced by relatively small volumes of blood (50–100
mL) in the stomach.

 While lower gastrointestinal (LGI) bleeding tends to be associated with

hematochezia .

 However, these distinctions in stool color are not absolute because melena can be seen
with proximal LGI bleeding, and hematochezia can be seen with massive UGI bleeding.
Clinical features suggesting a severe UGI
bleed are:

• Melena or hematochezia
• Heart rate >20 beats per minute above the mean heart rate for age
• Prolonged capillary refill time
• Decrease in hemoglobin of more than 2 g/dL
• Need for fluid bolus
• Need for blood transfusion (given if hemoglobin <8 g/dL)
History

• GI symptoms including dyspepsia, heartburn, abdominal pain, dysphagia, and weight loss.

• Recent onset of jaundice, easy bruising, or change in stool color,

• Recent or recurrent epistaxis, to investigate the possibility of a nasopharyngeal source.

• History of easy bruising or bleeding, which suggests a disorder of coagulation, platelet

dysfunction, or thrombocytopenia.

• Personal or family history of liver, kidney, or heart disease, or coagulation disorders.

• Drug history (NSAIDs, corticosteroids,Tetracyclines)

Physical examination
• Vitals:- Heart rate, respiratory
rate, BP, capillary refill,
orthostatic changes

• Pallor

• During HEENT exam :

epistaxis, nasal polyps, and

oropharyngeal erosions from
caustics and other ingestions
• Examination of the skin and mucus membranes for bruising,
petechiae, or mucosal bleeding. eg, ITP , Trauma

• Signs of CLD: Jaundice, Clubbing, leukonychia, palmar erythema,

spider nevi, gynecomastia, etc.

• Vascular malformations: hemangiomas, telangiectasias or purpura

over skin.

• Peutz- Jeghers syndrome: pigmented lips, palms, soles

• Pseudoxanthomaelasticum: “Plucked chicken appearance” of skin.

Abdominal examination
• Tenderness, Hyperactive bowel sounds

• Caput medusa with ascites, shrunken liver

and splenomegaly Cirrhosis with PHT

• Extra-hepatic PHT will have splenomegaly

without hepatomegaly

• Spleen may contract following a massive

bleed and may not be palpable
Work up
• Complete blood count, coagulation studies, liver function test, renal function test

• The BUN result can be helpful for confirming the source of bleeding. An increase in BUN in the
absence of renal disease is consistent with an UGI source .

• For patients with epigastric abdominal pain, pancreatitis also should be ruled out with screening
amylase and lipase;

• For patients with clinically significant bleeding or known varices, a specimen should be drawn to
type and cross-match blood .

• Less extensive laboratory evaluation may be appropriate for patients with small amounts of blood
in the vomitus and a likely explanation.
Continued...
• Oesophago-gastro-duodenoscopy : most sensitive and specific for
diagnosis and provides therapeutic options

• Ultrasound with Doppler to assess liver disease and PHN

• In episodic or obscure bleeding : nuclear medicine radionucleotide

studies, arteriography, and wireless video capsule endoscopy are used

• Serum gastrin levels ( Zollinger Ellison syndrome)

• Peroxide based tests: Gastroccult for upper GI

Imaging
• Barium contrast studies- barium swallows, upper GI series,
small bowel follow-throughs, or barium enemas :
for non emergency bleeds, to point to foreign bodies, ulcers, IBD,
or polyps.
Endoscopy
• Patients with severe upper GI bleeding should receive endoscopy
within the first 12 hours of the hemorrhagic episode if they are
sufficiently stable,

• The site of upper GI bleeding can be identified in 90% of cases

when endoscopy is performed within 24 hours.

• This modality is also beneficial in predicting the likelihood of

continued bleeding.
Rockall risk assessment score
Glasgow-Blatchford score
 Continued...
• Angiography may be useful in patients with rapid bleeding in whom endoscopy is unsuccessful in finding a source.
For therapeutic purposes, standard angiography may be useful in treating some patients with vascular anomalies,
hemobilia, or some ulcers.

.
Management

Initial approach

Ensure patient stability,

Establish adequate oxygen delivery,
Place intravenous access,
Initiate fluid and blood resuscitation,
Correct any underlying coagulopathies.
Continued...
• For Hemodynamically stable patients with small amounts of blood in
the vomitus with a likely explanation eg Mallory-Weiss tear

supportive care with observation generally is sufficient,

usually with acid suppression with oral administration of a PPI such as

omeprazole or esomeprazole to treat any peptic component and reduce the risk for
rebleeding.
Hemodynamically unstable
1) Big bore canula (IV/ IO) Hydration-NS/ RL and blood Transfusion

2) ICU care Cardiorespiratory monitor

Intake- output chart
Catheterization to monitor UO
 CVP monitoring
Vit K 5mg injection to be given
3) NG tube aspiration:

• Every ½ to 1 hourly for next 24 hours If significant blood loss estimated

• For Unexplained gastrointestinal bleeding that is clinically significant

• Decreases aspiration risk and Determine if the bleeding is ongoing.

• Aids in visualization via endoscope

• Gastric lavage with normal saline remove particulate matter, fresh blood, and
clots
The lavage
may be performed with either water or normal saline, at room
temperature.

if the lavage returns fresh blood or coffee grounds, it confirm an

UGI (or nasopharyngeal) source of bleeding.

if lavage is negative, that there is no active UGI bleeding or

bleeding has ceased or arises beyond a closed pylorus.

The presence of bilious fluid suggests that the pylorus is open and if
lavage is negative, that there is no active UGI bleeding.
Survey
• In a national (USA)survey of UGI bleeding in adults, Gilbert et al.
reported that a bleeding source was identified in 16% of patients with
a negative gastric aspirate

• The American Society for Gastrointestinal Endoscopy, therapeutic

endoscopic intervention is recommended

for all active bleeding

for nonbleeding visible vessels in the bed of an ulcer
4) Endoscopic therapy :

A) Sclerotherapy : Acts by producing intimitis - thrombosis -fibrosis of

the vessels.

Sclerosants: Ethanolamine oleate 5%

Sodium morrhuate 5%
Sodium tetradecylsulphate 1.5%

• Cx: Esophageal ulceration, stricture, Bronchoesophageal fistula,

thoracic duct damage, recurrance of varices, transient bacteremia
Continued...
B) Variceal banding: Elastic band occludes the varix and it is necrosed &
sloughed off in 5-10 days

 but use of this technique in small children is limited by the small

diameter of the esophagus .

C) Heater probe and bipolar coagulation for ulcers

D) Mechanical clipping
 Surgical repair :
• Pt with EHPHT is from a remote area without facilities for EST/ blood
transfusions,

• Pt continues to bleed from ectopic varices or persistent esophageal varices,

despite EST,

• Hypersplenism,

• Decompressive Shunts for Portal Hypertention,

• Liver Transplantation.
5) TransjugularIntrahepatic Porto-systemic Shunt(TIPSS):
• Creates a shunt in the liver between the portal & hepatic veins.

Indications: Refractory variceal hemorrage

Refractory ascites
Hepatorenal syndrome

• CI: Polycystic liver disease, Right Heart Failure, Systemic Infections, PV

thrombosis, Biliary obstruction, severe hepatic encephalopathy.

• Cx: Acute thrombosis or Delayed stenosis of shunt, Hepatic Encephalopathy

Pharmacotherapy
A) Antacids:
• proton pump inhibitor (eg, esomeprazole or pantoprazole) or histamine
2 receptor antagonist (eg, ranitidine, famotidine or cimetidine)

used as common causes of GI bleed are gastritis and

peptic ulcer disease.
to treat or prevent any peptic component of the underlying
disorder

• Aluminium& Magnesium hydroxideIV preparation .

B) Hormones/ hormone analogues
reduces splanchnic blood flow for variceal bleeding by
vasoconstriction

1) Somatostatin- inhibits release of vasodilatory GI peptides such as

glucagon, VIP &sustance P

Dose: 250microgm IV bolus followed by 250microgm/hr infusion

Disadvn: very short half-life

2) Octreotide- synthetic analogue of somatostatin,

• has much longer ½ life & hence can be given as bolus or infusion

• Dose: 1microgm/kg IV infusion over 30min followed by

0.5microgm/kg/hour

• Disadvn: Nausea, flatulence, malabsorbtion (supresses GI motility &

secretion)
:Bowel ischemia in high doses
:Bradycardia and hyperglycemia
3) Vasopressin-non peptide,

• Splanchnic vasoconstriction, constricts lower esophageal sphincter

• Dose: 0.33unit/kg over 20min followed by IV infusion of

0.33units/kg/hour

• S/E: CVS-myocardial ischemia/infarction, Cerebral Hemorrage,

Respiratory arrest, Bowel ischemia & necrosis.
Prophylaxis
• Indicated because of high rate of bleeding from esophageal varices
and the high mortality rate.

Prophylactic Propranolol (most commonly used, 1-2mg/kg)

Nadolol therapy

• No role of prophylactic EST/ EVL

Reference
• Nelson text book of pediatrics 21 th edition
• Uptodate 2018
• Medscape
• The American Society for Gastrointestinal Endoscopy guideline.
THANK
YOU,,