Hematemesis in Children- Beyond Infancy

Dr. Divya NairDNB PediatricsMahavir Hospital.

Gastrointestinal (GI) bleeding in children is a fairly common problem

In the pediatric ICU population, 6-20% have upper GI bleeds. The incidence of lower GI bleeding has not been well established

10-20% of referrals to pediatric gastroenterologists

Upper gastrointestinal (UGI) bleeding originating from esophagus, stomach or duodenum-proximal to the ligament of Treitz (aka duodenojejunal ligament)

Commonly presents with hematemesis (vomiting of blood or coffee ground-like material) and/or melena (black, tarry stools)

Etiology:A) Gastrointestinal causes

B) Systemic causes

C) Genetic causes

D) Spurious causes

A) Gastrointestinal causes:

1) Esophagitis:

GERD

Hiatus Hernia

Infection: e.g. Candida,

Aspergillus, CMV, HSV

Medications: e.g. tetracycline,

aspirin, NSAIDs, potassium chloride

“ erosive esophagitis"

2) Esophageal Rupture

Mallory-Weiss Syndrome (located at LES)

3) Gastritis: More common than ulcers Medications (e.g. NSAIDs, aspirin) Infections (e.g., Helicobacter pylori, CMV,

herpes) Crohn’s disease

4) Gastric Erosions:

Trauma, burn, shock or sepsis

This is usually superficial and occurs mainly in the

fundus of the stomach

5) Peptic Ulcer Disease

6) Zollinger-Ellison syndrome Gastrinoma Results in multiple

diffuse GI/ small bowel

ulcerations

Ulcer with red spot

Bleeding Ulcer

7)Portal hypertension: Esophageal varices Gastric varices Hypertensive gastropathy

Cirrhosis due to congenital

hepatitis, hepatic fibrosis,

cystic fibrosis

8) Extra-hepatic portal vein

obstruction

Esophageal varices

9) Vascular malformations:

Hemangiomas

Aorto-esophageal/-enteric fistulas

Dieulafoy ulcer (superficial defect of gastric mucosa which overlies an ectatic submucosal a.)

Watermelon stomach (gastric antral vascular ectasia)

Vasculitis eg: ITP

10) Tumors:

Polyps

Lipomas, leiomyoma

Adenocarcinoma

Lymphoma

Metastatic tumors,

Kaposi’s sarcoma, Barrett’s esophagus

Kasabach-Merritt synd (Hemangioma thrombocytopenia

syndrome)

11) Traumatic: Prolapsing gastropathy

Foreign body ingestion

Direct abdominal trauma

12) Iatrogenic- throat/nose Sx,

traumatic NG

13) Miscellaneous:

Hemobilia

Hemosuccus pancreaticus

Menetries’ Disease

Eosinophilic enteropathy

Munchausen by proxy syndrome

Barrett’s ulcer secondary to GERD

B) Systemic Causes:1) Coagulopathy (congenital/acquired): Hemophilia,

vWD

2) Sepsis, scarlet fever, malaria, leptospirosis

3) Burns, Sepsis ( Curling’s ulcer),

Raised ICT, Head injury, Encephalitis ( Cushing’s ulcer)

4) HUS, HSP

5) Malignancy- Leukemia

6) Poisonings- chemical, caustic

7) Drugs-aspirin, NSAIDS, anti-coagulants

8) Food (milk protein) allergy/ hypersensitivity

9) Idiopathic

NSAID induced Ulcers

C) Genetic conditions:Turner syndrome

Ehlers Danlos syndrome

( cutis hyperelastica)

Pseudoxanthoma elasticum

Klippel Trenaunay syndrome

Osler-Rendu-Weber syndrome

(hereditary hemorrhagic telangectesia)

Blue rubber bleb naevus syndrome

Hermansky-Pudlak syndrome

D) Spurious causes:

I) Hematememis: Bleeding from nose (epistaxis),

mouth, pharynx,

hemoptysis

II) Malena: Iron preparation, Bismuth, Lead,

spinach, beets,

blueberries

Grading of UGI BleedsMILD: presents as nausea, vomiting, abdominal discomfort & small

quantity of hematemesis/ malena

MODERATE: significant blood loss, tachycardia, cold sweat, hypo-

tension.

No ongoing blood loss; recovers with blood transfusion

SEVERE: more striking features of shock present, Hb falls to 8gm%

or less.

Requires multiple blood transfusions d/t ongoing blood loss

Takes longer time to recover; very high mortality unless treated

properly.

Diagnosis:

History Quantity, frequency, type of blood

(bright red vs coffee ground)

Nausea, vomiting, recurrent abdominal pain s/o PUD

Dysphagia/ odynophagia, chest pain/burning,

hematochezia, melena, bruising, bleeding, repeated retching f/b vomiting of

blood

Weight loss, early satiety s/o malignancy

Psychiatric symptoms

Drug ingestion

Bleeding sites- skin, mucosa, GUT, joints

Recurrent epistaxis

H/O Jaundice, stool color

Severe and diffuse upper GI ulcerations with chronic diarrhea usually : Zollinger Ellison syndrome or gastrinoma

Birth history: lines placed (umbilical lines can result in clotting of portal vein)

Past history: History of liver disease,

history of pancreatitis, GI surgeries

H/O Bleeding disorders in family

Medications: NSAID use, aspirin use

Diet history: Formula intolerance, food

allergies

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

Pallor

During 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

Signs of Chronic Liver Disease: Jaundice, Clubbing, leukonychia, palmar erythema, spider nevi, gynecomastia, etc.

Vascular malformations: hemangiomas, telangiectasias or purpura over skin

Peutz- Jeghers syndrome: pigmented lips, palms, soles

Pseudoxanthoma elasticum: “Plucked chicken appearance” of skin

Per Abdomen:Tenderness, Hyperactive bowel sounds

Caput medusa with ascites, shrunken liver and

splenomegaly s/o Cirrhosis with Portal Hypertension

Extra-hepatic PHT will have splenomegaly without hepatomegaly

Spleen may contract following

a massive bleed and may

not be palpable (Smith

Howard Syndrome)

Work up:

CBP, PCV, RBS

Coagulation studies

LFT to r/o cirrhosis

RFT

Type and cross-match of several units of blood

Oesophago-gastro-duodenoscopy : If active bleeding, most sensitive and specific for diagnosis and provides therapeutic options

Ultrasound with Doppler to assess liver disease and portal hypertension

In episodic or obscure bleeding : nuclear medicine radionucleotide studies, arteriography, and wireless video capsule endoscopy are used to assist in identifying the site of blood loss

Special tests:

Serum gastrin levels ( Zollinger Ellison syndrome)

Peroxide based tests: Gastroccult for upper GI bleed

Gastroccult : only test designed specifically for detecting gastric occult blood and determining gastric pH

It includes a convenient pH comparison chart for the Clinically relevant range which is important in monitoring antacid prophylaxis

Certain ingestions such as red meat, iron, and peroxidase-containing vegetables (eg: turnips, horseradish, broccoli, cauliflower, and cantaloupe), can give false-positive results

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, because early endoscopy improves the diagnostic index

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

The Forress classification divides endoscopic findings into the following 3 categories:

I - Active hemorrhage (Ia = bright-red bleeding,

Ib = slow bleeding)

II - Recent hemorrhage (IIa = non-bleeding visible vessel,

IIb = adherent clot on base of lesion,

IIc = flat pigmented spot)

III - No evidence of bleeding

Arteriography :

used to localize lesions when endoscopy has failed

or when the patient cannot cooperate

Detects vascular lesions in esophagus, stomach,

hepatic aneurysms & pseudo-

cysts of pancreas

The modality can be helpful

for bleeding that is distal to

the ligament of Treitz

Management:Initial approach

to ensure patient stability,

to establish adequate oxygen delivery,

to place intravenous access,

to initiate fluid and blood resuscitation,

to correct any underlying coagulopathies

Children at low risk for recurrent or life-threatening hemorrhage may be suitable for early hospital discharge or even outpatient care

All patients with hemodynamic instability/ active bleeding should be admitted in ICU for resusitation and close observation

ICU Requirements:

Pediatric Intensivist, Pediatric Surgeon, Pediatric Gastroenterologist,

Invasive monitors, Ventilators, Attached blood bank, Trained nursing

staff

i) Big bore canula (IV/ IO)

Hydration-NS/ RL

SOS Transfusion

ii) ICU care, invasive monitoring in unstable patients

Cardiorespiratory monitor, intake- output chart,

catheterization to monitor UO

CVP monitoring helps to guide replacement therapy

Inj Vit K 5mg to be given in case of hepatocellular

failure, cholestatic jaundice.

iii) NG aspiration:

Every ½ to 1 hourly for next 24 hours

If significant blood loss estimated; as it ascertains fresh

blood, decreases aspiration risk and aids in visualization via

endoscope

Gastric lavage with normal saline

Iced saline does not stop bleeding and may even cause

central hypothermia in a small child.

iv) Endoscopic therapy including:

1. Sclerotherapy (EST): The best Em/El procedure

Acts by producing intimitis thrombosis fibrosis of

the vessels

Sclerosants: Ethanolamine oleate 5%

Sodium morrhuate 5%

Sodium tetradecylsulphate 1.5%

Cx: Esophageal ulceration, stricture, Broncho-

esophageal fistula, thoracic duct damage,

recurrance of varices, transient bacteremia

2. Variceal banding: became popular b’cos of Cx of

EST, but it is difficult in children

Elastic band occludes the varix and it is necrosed &

sloughed off in 5-10 days

3. Heater probe and bipolar coagulation for ulcers

v) Sengstaken Blakemore tube/ Minnesota tube:

Mechanical Tamponade by balloons which

compresses esophageal & gastric varices

Has 3 lumens- for gastric and esophageal balloons

& for aspiration of gastric contents

Effectively controls acute bleeding, but assosiated

with significant no. of Cx

and rebleeding when tube

is removed

vi) Transjugular Intrahepatic Porto-systemic Shunt (TIPSS):

Percutaneous technique that creates a shunt in the

liver between the portal & hepatic veins

Indications: Refractory variceal h’age

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

vii) Selective embolization

viii) Laparoscopy/ Laparotomy

Surgical repair rarely indicated:

1) Pt with EHPHT is from a remote area without facilities for EST/

blood transfusions

2) Pt continues to bleed from ectopic varices/ persistent esophageal

varices, despite EST

3) Hypersplenism

Surgeries done for PHT: Decompressive Shunts

Devascularization

Liver Transplantation

Pharmacotherapy:ix) Antacids:

H2 blockers, Proton pump inhibitors: used as common causes of GI bleed

are gastritis and peptic ulcer disease.

Aluminium & Magnesium hydroxide

x) Children known to have cirrhosis should receive Antibiotics,

prefrebly before endoscopy, as bacterial infections are present

in upto 20% of these patients

Treat infections including triple therapy (antibiotics and proton pump

inhibitor) for H. pylori

Remove allergen in case of allergy

xi) Hormones/ hormone analogues (reduces splanchnic blood

flow for variceal bleeding by vasoconstriction) :

1) Somatostatin- polypeptide,

inhibits release of vasodialatory GI peptides

eg glucagon, VIP & sustance P

Dose: 250microgm IV bolus f/b 250microgm/hr

infusion

Disadvn: very short ½ life

2) Octreotide-synthetic analogue of somatostatin,

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

infusion

Dose: 1microgm/kg IV infusion over 30min f/b

0.5microgm/kg/hour

Disadvn: Exorbitant cost

Nausea, flatulence, malabsorbtion (supresses GI

motility & secretion)

Bowel ischemia in high doses

3) Vasopressin-non peptide, derived from posterior pituitary gland

Splanchnic vasoconstriction, constricts lower

esophageal sphincter

Dose: 0.33unit/kg over 20min f/b IV infusion of

0.33units/kg/hour

S/E: CVS-myocardial ischemia/infarction, VF (can

be decreased by combining it with Nitroglycerine)

Cerebral H’age, Respiratory arrest,

Bowel ischemia & necrosis

4) Terlipressin (Triglycyl-lysine vasopressin)

Synthetic analogue of vasopressin

Long duration of action & less cardiac S/E

Dose: 2mg IV q6h until bleeding stops f/b 1mg q6h for next

24hrs

5) Miscellaneous Drugs:

Clonidine (α2 agonist)

Ketanserine & Ritanserine (5HT2 receptor antagonists)

Molsidomine (venodialator)

Prophylaxis Against Bleed From Variceal

Hemorrhage and Ulceration

Primary prophylaxis is indicated because of high rate of

bleeding from esophageal varices and the high mortality

associated with bleeding

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

kg) or Nadolol therapy are the only cost-effective ones

No role of prophylactic EST/ EVL

Prophylaxis against stress ulcers are indicated in ICU patients with any of the following charecteristics:

1) Coagulopathy/ on anti-coagulants

2) Mechanical ventilation > 2 days

3) History of GI ulceration/ bleeding within the

past year

4) Two or more of the following risk factors-

sepsis, ICU admission lasting > 1 week, occult

GI bleeding > 6 days, glucocorticoid therapy

Effective identification and antibiotic treatment of

H.Pylori infections is also crucial in preventing

complications including upper GI bleeding

Prevention of NSAID related peptic ulcer disease and

complicating UGI bleed in patients at high risk

In such patients COX-2 selective inhibitor/ non-selective

NSAID + PPI/ Misoprostol is indicated

Patients with history of uncomplicated/ complicated

PUD should be tested for H.pylori prior to beginning a

NSAID/ low dose aspirin

If H.pylori present it should be treated with appropriate

therapy, even if it is believed that PU was due to NSAIDs

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