Indian J Pediatr (April 2013) 80(4):326–333
DOI 10.1007/s12098-013-0987-x
'
SYMPOSIUM ON PGIMER MANAGEMENT PROTOCOLS IN GASTROINTESTINAL EMERGENCIES
Approach to a Child with Upper Gastrointestinal Bleeding
Sunit Singhi & Puneet Jain & M. Jayashree & Sadhna Lal
Received: 12 August 2012 / Accepted: 4 February 2013 / Published online: 17 March 2013
# Dr. K C Chaudhuri Foundation 2013
Abstract Upper gastrointestinal bleeding (UGIB) is a poten-
tially life threatening medical emergency requiring an appro-
priate diagnostic and therapeutic approach. Therefore, the
primary focus in a child with UGIB is resuscitation and
stabilization followed by a diagnostic evaluation. The differ-
ential diagnosis of UGIB in children is determined by age and
severity of bleed. In infants and toddlers mucosal bleed (gas-
tritis and stress ulcers) is a common cause. In children above
2 y variceal bleeding due to Extra-Hepatic Portal Venous
Obstruction (EHPVO) is the commonest cause of significant
UGIB in developing countries as against peptic ulcer in the
developed countries. Upper gastrointestinal endoscopy is the
most accurate and useful diagnostic tool to evaluate UGIB in
children. Parenteral vitamin K (infants, 1–2 mg/dose; chil-
dren, 5–10 mg) and parenteral Proton Pump Inhibitors
(PPI’s), should be administered empirically in case of a
major UGIB. Octreotide infusion is useful in control of
significant UGIB due to variceal hemorrhage. A tempo-
rarily placed, Sengstaken-Blakemore tube can be life
saving if pharmacologic/ endoscopic methods fail to
control variceal bleeding. Therapy in patients having
mucosal bleed is directed at neutralization and/or pre-
vention of gastric acid release; High dose Proton Pump
Inhibitors (PPIs, Pantoprazole) are more efficacious than
H2 receptor antagonists for this purpose.
Keywords Upper gastrointestinal bleeding . Endoscopy .
Variceal bleed . Octreotide
S. Singhi (*) : P. Jain : M. Jayashree
Department of Pediatrics Advanced Pediatrics Centre,
Post Graduate Institute of Medical Education and Research,
Chandigarh 160012, India
e-mail: sunit.singhi@gmail.com
S. Lal
Department of Gastroenterology,
Post Graduate Institute of Medical Education and Research,
Chandigarh 160012, India
Introduction
Upper gastrointestinal bleeding is usually defined as bleeding
from a site proximal to the ligament of Treitz at the level of
duodeno-jejunal flexure. Hematemesis is the cardinal sign
(vomiting of blood or coffee ground-like material) though
some children may present with malena (black, tarry stools).
Hematochezia (passage of bright red blood in stools) is usu-
ally a feature of lower gastrointestinal bleeding (GIB), but
some infants with UGIB can sometimes present with passage
of bright red blood from the rectum because of rapid gastro-
intestinal transit in a briskly bleeding child.
Etiology
The etiology of UGIB varies with age but considerable over-
lap exists between the different age groups [1]. Rate and extent
of bleeding is chiefly governed by the etiology of UGIB. In
India portal hypertension has been reported to be the com-
monest cause (95 %) in contrast to the developed countries
where non-variceal causes like peptic ulcer, esophagitis bleed-
ing are common (66 %). Extra-hepatic portal vein obstruction
(EHPVO) was the most common cause of variceal bleed in
Indian children [2, 3] (Table 1). While evaluating a child with
upper GI bleed it is important to keep the specific etiologies at
different ages in mind (Table 2).
Neonates
UGIB is rare in the first mo of life, but if seen must be
distinguished from swallowed maternal blood. Hemorrhagic
disease of the newborn due to vitamin K deficiency should be
considered in neonates not given vitamin K prophylaxis at
birth. Maternal idiopathic thrombocytopenia and maternal
NSAID use can also cause bleeding in the newborn. Other
causes include stress gastritis or ulcers, vascular anomalies,
coagulopathy caused by infection, liver failure, or a congenital
coagulation factor deficiency.
Indian J Pediatr (April 2013) 80(4):326–333 327

Table 1 Causes of UGIB among Indian children presenting to a the setting of trauma, liver biopsy, and acute/chronic pancrea-
hospital (adapted from reference 2 & 3)
titis. Henoch-Schönlein purpura and vasculitis such as poly-
Cause Yachha et al. 1996 Mittal et al. 1994 arteritis nodosa are rarer causes of UGIB in this age group.

Varices 95 % 39.4 %
Esophagitis - 23.7 % Key Issues
Gastritis 1.3 % 7.2 %
Gastric ulcer - 1.2 % Initial Assessment and Stabilization
Duodenal ulcer - 0.42 %
Esophageal ulcer - 0.42 % As for any other emergency the first priority should be to
Henoch Schönlein purpura 1.3 % - assess the airway, breathing and circulation of a patient
ITP 1.3 % - presenting with UGIB. The most important aspect of the
Gastroduodenal artery 1.3 % - evaluation is to determine the degree and rapidity of blood
aneurysm loss. Orthostatic changes in blood pressure (more than
Unknown - 27.5 %
10 mm of Hg) suggest a moderate bleed (15–20 % of blood
loss) and warrant a more aggressive approach to manage-
Infants and Toddlers ment. Presence of signs of shock (tachycardia, prolonged
capillary refill time, cold-clammy skin, supine hypotension)
Stress ulcers and gastritis in a sick infant or toddler, peptic ulcers, indicates severe bleed of more than 25–30 % of blood loss
variceal bleeding in children with portal hypertension and vas- and a need for immediate volume expansion and stabiliza-
cular malformations can cause major bleeds in this age group. tion before proceeding to a diagnostic algorithm (Fig. 1).
Reflux esophagitis, esophageal or gastrointestinal foreign body, Once the patient is stable the following issues should be
communicating duplication cysts, NSAIDS and corrosive injury addressed before more elaborate diagnostic workup:
can cause non life threatening bleeds. History of a choking
episode, even if it was transient or occurred days or even weeks 1. Whether actual blood or ingested substances
before the bleeding episode, is an important clue for a foreign The first consideration in evaluating children who have
body. new-onset “bleeding” is to determine whether the material
passed is actual blood. A number of substances may
Older Children and Adolescents simulate bright red blood (food coloring, colored gelatin
or children’s drinks, red candy, beets, tomato skins, rifam-
Causes of UGIB in older children and adolescents are similar pin, phenytoin, antibiotic syrups) or malena (bismuth or
to those seen in adults. Varices, peptic ulcers, Dieulafoy’s iron preparations, charcoal, spinach, blueberries, grapes,
lesions and vascular malformations can cause major bleeds. licorice). For detecting blood in vomitus or nasogastric
Reflux esophagitis, Drug induced gastritis, Mallory Weiss aspirate, the Gastroccult® test is more accurate [4]. The
tears, communicating duplication cysts, stromal tumors, lym- test uses Gastroccult slides, sealed in special wrapper, and
phomas (rarely), Crohn’s disease and portal hypertensive gas- stored at room temperature (15–30 °C). One drop of
tropathy can cause minor bleeds. Haemobilia or bleeding from gastric sample is placed to the occult blood test area of
the pancreas (splenic artery aneurysm) should be considered in the slide and two drops of Gastroccult Developer is applied

Table 2 Age wise distribution

of etiology of UGIB in children
(Adapted from reference 1)
Age group Well appearing Ill appearing
Neonates Swallowed maternal blood Hemorrhagic gastritis
Hemorrhagic disease of newborn Necrotizing enterocolitis
Drugs- heparin, indomethacin Gastric stress ulcers
Thrombocytopenia, platelet dusfunction Disseminated intravascular coagulation
Infants Reflux esophagitis Hemorrhagic gastritis
Reactive gastritis Gastric stress ulcers
Arteriovenous malformation
Children Mallory-Weiss tear Esophageal varices ( liver disease)
Reflux esophagitis Hemorrhagic gastritis
Reactive gastritis Stress ulcers
328 Indian J Pediatr (April 2013) 80(4):326–333

Assess airway , breathing and circulation :

If signs of shock, orthostatic changes in
blood pressure, impaired responsiveness

Maintain airway, start oxygen, support breathing and circulation

Insert 2 large bore I.V. cannula
Blood for group and cross match, Hematocrit/coagulogram
Monitoring of vitals, oximetry
Volume replacement by crystalloids, start blood as soon as possible
Correct coagulopathy-vitamin K, + fresh frozen plasma/platelets
Nasogastric tube placement – for lavage and monitoring of ongoing bleed
Acid suppression therapy

Suspect Variceal Bleed Suspect Mucosal Bleed/Ulcer

Features suggestive of portal (History of drug intake,
hypertension, chronic liver disease abdominal pain, dysphagia, etc)
(splenomegaly, hepatomegaly)

Acid suppression therapy- High dose PPIs

Start Octreotide infusion,
Pediatric Gastroenterology consult
Controlled Not controlled
Controlled Not controlled
- Elective Endoscopy Endoscopy
- Continue PPIs
Emergency Endoscopic - Test and treat Ulcer found
sclerotherapy(EST) H. pylori

Endoscopic Management
Endoscopic
Not controlled Injection therapy
sclerotherapy (EST) or
(adrenaline+saline)/
variceal ligation (EVL)
Mechanical hemostasis-
Endoclip/Themocoagulation
Balloon tamponade
Continue PPIs- Test and treat
H. pylori

Planned Controlled Not controlled

Not controlled No Ulcer/Lesion
EST/EVL

TIPSS (Cirrhotics) or
Devascularisation / Shunt Surgical/ Intervention
Surgery Radiologist consult

Fig. 1 Algorithmic approach to management of a patient with significant acute upper GI bleed

directly over the sample. The test is read within 60 s.
The development of any trace of blue color in the occult
blood test area is regarded as a positive for occult blood.
Simultaneously, functionality of test should be tested. For
this, one drop of Gastroccult Developer is added between
the positive and negative Performance Monitor areas and
results interpreted within 10 s. If the slide and developer are
functional, blue color will appear in the positive area, and
the negative area will remain colorless.
2. In a neonate- whether it is patient’s own blood or
swallowed blood
This is often applicable for neonates. The Apt-
Downey Test is used to differentiate between swallowed
maternal blood and patient’s blood.
Indian J Pediatr (April 2013) 80(4):326–333
3. Is there a pulmonary, oral or ENT source of bleed?
Bleeding from these sources may mimic GI bleed
especially when the blood is swallowed. It may be seen
in conjunction with epistaxis, sore throat or may follow
dental procedures or tonsillectomy. Hence these areas
must be explored to rule out in cases of doubt.
4. Level of bleeding
Vomiting of bright red or coffee ground vomitus is
the classic presentation of upper GI bleeding. Bloody
diarrhea and bright red blood mixed or coating normal
stool are the classic presentations of lower GI bleeding.
However, hematochezia, malena, or occult GI blood
loss could represent upper or lower GI bleeding. In case
of acute-onset hematochezia or malena, the level of
bleeding can be confirmed by passage of a nasogastric
tube. Presence of blood in the stomach and clearing of
nasogastric aspirate with lavage are diagnostic of UGIB.
Diagnostic Evaluation
Focused History
History is directed at finding the likely source and cause of
bleed. It should include the following:
& Recent or recurrent epistaxis: it raises the possibility of a
nasopharyngeal source of bleeding.
& Recent onset of jaundice and/or change in stool color:
may suggest underlying liver disease.
& History of easy bruising or bleeding: may suggests
a disorder of coagulation, platelet dysfunction, or
thrombocytopenia.
& History of any co-morbid illnesses: Personal or family
history of liver, kidney or heart disease, or coagulation
disorders.
& Epigastric pain, food pain relationship, may be an indi-
cator of gastritis, esophagitis or ulcer disease.
& Details of recent medications ingested as well as an
‘over the counter’ or ‘alternative’ drug history is impor-
tant to assess potential contributions from medications
that may induce ulceration (such as NSAIDs and corti-
costeroids). Even short-term use of ibuprofen can cause
gastric ulcers and hematemesis.
& History of previous bleeding episodes can point to
EHPVO, vascular malformations and duplication cysts.
Physical Examination
Focused physical examination, besides assessing the sever-
ity of bleed, should include a good inspection of skin (for
petechiae and echymoses, and vascular malformations) and
mucous membranes of the nose and throat (for bleeding),
329
and palpation of abdomen for localized tenderness and
organomegaly.
& The presence of hepatosplenomegaly and prominent
abdominal vessels and a protruding abdomen may indi-
cate portal hypertension and bleeding from esophageal
varices,
& Epigastric tenderness might suggest acute gastritis or
peptic ulcer disease.
& Vascular malformations like hemangiomas and telangi-
ectases should also be noted.
& Clinical evidences of bleeding diathesis like petechiae,
echymoses, purpura etc. should also be noted.
& Stigmata of chronic liver disease
Investigations
In an emergency setting only a few laboratory tests are
essential in the beginning to evaluate UGIB. These include
complete blood count, prothrombin time (PT) and partial
thromboplastin time (PTT), liver function tests and blood
grouping and cross matching if there is significant bleed.
Testing for H. pylori (urea breath test, stool antigen and
serological tests) is indicated in a patient with a probability
of peptic ulcer. Additional laboratory evaluation depends on
the result of the initial evaluation, the patient’s response to
treatment, and clinical suspicion of a particular diagnosis.
Radiographic Studies
Abdominal ultrasound is useful in patients where extra
hepatic portal hypertension, portal hypertension due to liver
disease, hemobilia, splenic artery aneurysm or large vascu-
lar anomalies are suspected. Doppler blood flow can identi-
fy evidence of cirrhosis and portal blood flow dynamics.
Endoscopy
Upper gastrointestinal endoscopy is the gold standard for
diagnosis and treatment of UGIB. It is the procedure of
choice for all patients with UGIB. In the hands of skilled
endoscopist, this procedure now can diagnose the etiology
in 85– 90 % of cases. It is indicated to identify the site of the
bleeding, to diagnose the specific cause of the bleeding, and
to initiate therapeutic interventions when indicated. In case
the endoscopic appearance suggests esophagitis, gastritis or
duodenitis a biopsy should be obtained; in suspected peptic
ulcer disease antral biopsies for H. pylori work up (histo-
logical examination, rapid urease test, and culture) should be
taken. Though there is no definite time frame given, in all
cases of major upper GI bleed, an early endoscopy (within
first 24 h) is recommended by most of the reviews [5].
Endoscopy is contraindicated in hemodynamically unstable
330
patients; it should be considered only after stabilization
because early endoscopy (<6 h after presentation) in such
patients has not improved outcomes.
CT Angiography
CT angiography may help to delineate vascular malforma-
tions beyond the duodenum, in areas not accessed by routine
upper GI endoscope.
Nuclear Scintigraphy
In patients with persistent bleeding in whom endoscopy fails
to identify a bleeding site, radioisotope-tagged red blood
cell scans using technetium 99 m-sulfur colloid may be
capable of detecting the site of bleeding. This modality is
useful only if the rate of bleeding exceeds 0.1 ml/min.
However, this modality has significant false localization
and false-negative rates [1].
Angiography
Celiac/ Superior mesenteric artery angiography is used se-
lectively in children with non variceal massive bleeding,
e.g., from a peptic ulcer, that obscures endoscopic evalua-
tion and therapy. It is also very useful in Hemobilia, splenic
artery aneurysms and some types of vascular malformations.
Bleeding must be more than 0.5 ml/min to be detected by
angiography [6]. Angiography is not only helpful in making
the diagnosis but also facilitates embolic coil/fibric/glue
occlusion of the arterial branches supplying the lesion in
case of vascular malformation.
Some newer investigations are available in a few centres for
the evaluation of upper GI bleed from obscure areas beyond the
duodenum (Capsule Endoscopy/ Double Balloon Enteroscopy)
and in the liver or pancreas (Endosonography) in older children.
Management
The initial steps in management of severe acute GI Bleed
include assessment, resuscitation, re-evaluation, identifica-
tion of the cause and source of bleeding, and commencing
appropriate treatment (Fig. 1). This requires a multidisci-
plinary approach. Early consultation from pediatric gastro-
enterologist is recommended for patients who have active
ongoing bleed. The Interventional Radiologist and the Pe-
diatric Surgeon must be kept in the picture in case of the
failure/non-feasibility of endoscopic therapy, massive bleed-
ing, recurrent bleeding, bleeding associated with significant
abdominal pain. Care in the Pediatric Intensive Care setting
can be life saving in the early part of the management before
specific therapy can be instituted.
Indian J Pediatr (April 2013) 80(4):326–333
Resuscitation and Stabilization
Children presenting with symptoms and signs of upper GI
bleeding require prompt recognition during triage so that
timely resuscitation can be initiated and hemodynamic sta-
bility restored.
Airway Treatment should begin with airway protection. In-
tubation is indicated in obtunded patients or in those with
uncontrolled massive hemetemesis to prevent aspiration and
to facilitate upper endoscopy if it is necessary for bleeding
control.
Breathing Supplemental oxygen should be provided to all
patients. The adequacy of the breathing efforts must be
assessed and supported if needed.
Circulation Patients are assessed for hypovolemia and
shock to determine requirements for fluid infusion and
transfusion of packed erythrocytes. Large bore venous ac-
cess should be obtained to restore blood volume. Preferably
2 cannulae should be in place: one for fluid/blood resusci-
tation and the second for sampling and drugs. Peripheral
venous access may be difficult in a child with hypovolemic
shock due to peripheral vasoconstriction, therefore intraos-
seus access should be considered for large volume resusci-
tation. Subsequently central venous access may be
required. Fluid resuscitation should begin with crystalloids
(20 ml/ kg) while the blood is being arranged. The rate of
blood transfusion is determined by the severity of the
hypovolemia, continuing active bleeding, and presence of
co-morbidities. Blood transfusion is not needed in a
hemodynamically stable patient that has a hematocrit
above 24 % at presentation. Over transfusion (volume
overexpansion) should be avoided especially in variceal
bleed. Hematocrit should not exceed 30 %. This can
increase the portal venous pressure and aggravate the
UGIB.
Reassessment and Monitoring Vitals should be monitored
every 10 min –15 min till the child is stabilized and then
hourly for 24 h after stoppage of bleeding or stabilization.
Nasogastric Aspiration
Nasogastric aspiration and saline lavage are indicated in all
patients with UGIB to confirm the presence of intragastric
blood; to determine the rate of gross bleeding; to check for
ongoing or recurrent bleeding; to clear gastric field for endo-
scopic visualization; to prevent aspiration of gastric contents;
to prevent hepatic encephalopathy in patients of cirrhosis.
Lavage with iced or cooled solutions has not shown any
recognized advantage over room temperature solutions.
Indian J Pediatr (April 2013) 80(4):326–333
Some observers believe that solutions at 32 °C may interfere
with local coagulation mechanisms [7].
Correction of Coagulopathies
Parenteral vitamin K should be administered empirically
even when results of coagulogram are pending (infants,
1–2 mg/dose; children, 5–10 mg/ dose). Coagulopathy
with an international normalized ratio (INR) higher than
1.5 or abnormal partial thromboplastin time (PTT) should
be corrected with fresh frozen plasma (10 ml/kg initially);
cryoprecipitates may be tried in the face of severe coa-
gulopathy especially if volume of fluid has to be restrict-
ed; Factor VIIa has little additional advantage, even in
chronic liver disease, and is not routinely recommended;
Platelets transfusion is also not recommended unless there
is active bleeding with low platelet counts. All these
products should be included in the calculated resuscitation
fluids.
Pharmacotherapy
Variceal Bleed
Pharmacological therapy has the advantages of being gen-
erally applicable and capable of being initiated as soon as a
diagnosis of variceal hemorrhage is suspected. A meta-
analysis comparing emergency sclerotherapy and pharma-
cological treatment shows a similar efficacy with fewer side
effects with the latter thereby suggesting that pharmacolog-
ical therapy should be considered first-line treatment of
variceal bleeding [8].
Octreotide is a somatostatin analog that decreases splanch-
nic blood flow and has fewer hemodynamic adverse effects
than vasopressin. Pediatric studies have shown that it controls
UBIG in up to 70 % of children [9]. It is the drug of choice for
variceal bleeds and initiated as a bolus injection of 1 mcg/kg
(up to a maximum of 50 mcg) followed by continuous infu-
sion of 1 mcg/kg per h, which may be increased hourly by
1 mcg/kg per h up to 4 mcg/ kg per h [1]. Infusion should be
continued for at least 24–48 h after the bleeding has stopped to
prevent recurrence. The major adverse effect of octreotide is
hyperglycemia.
Vasopressin and Terlipressin Vasopressin use has largely
been replaced by octreotide and now by Terlipressin. The
usual dose is 0.002 to 0.005 units/kg per min for 12 h, and
then tapered over 24 to 48 h (maximum, 0.2 units/min) [1].
Its use is limited by the side effects of vasoconstriction.
Nitroglycerin has also been used to decrease portal pressure
and, when used in conjunction with vasopressin, may ame-
liorate some of its untoward effects. Vasopressin has been
replaced by its longer acting and safer analogue Terlipressin
331
which has been found to be as effective as Octreotide in
adults. Experience with Terlipressin in children is limited
though it is expected to be equally effective. An advantage
is intermittent 4–6 hourly dosing.
Somatostatin is also used for control of active bleed, in a
dose of 250 mcg/kg IV bolus followed by 250 mcg/kg/h
continuous infusion. In case of response, the infusion can be
maintained for 2 to 5 d, while frequently monitoring for
hyperglycemia [1]. Side effects include abdominal discom-
fort, flushing, nausea, bradycardia, steatorrhoea and
dyspepsia.
Prokinetic Agents Erythromycin has been used as a prokinetic
agent to clear the stomach of blood prior to emergent endos-
copy. Metoclopramide has also been used to act as a prokinetic
for similar reasons besides acting as a ‘pharmacologic tampo-
nade’ – it increases the lower esophageal sphincter tone.
Mucosal Bleeds
Mucosal bleeding is most common type of upper GI bleed in
critically ill children. Therapy in these groups of patients is
directed at neutralizing and/or preventing the release of acid.
The various agents used include:
Proton Pump Inhibitors (PPIs) are more efficacious
than H2 receptor antagonists. Pantoprazole is used for
control of active bleed. Dosage in children are: for body
weight <40 kg: 0.5 to 1 mg/kg per day IV once daily;
>40 kg: 20 to 40 mg once daily (maximum,
40 mg/d). These can be started empirically as it is
important to raise the gastroduodenal pH to maintain
clot stability. High dose PPI infusion has been found
to decrease the need for endoscopic therapy.
H2 Receptor Antagonists are used for control of active
bleed and prevention of rebleeds. E.g. Ranitidine can be
used as either continuous or bolus infusion; in the
former 1 mg/kg is given initially followed by infusion
of 2 to 4 mg/kg per day while in the latter 3 to 5 mg/kg
per day is divided into every 8 hourly infusions.
Treatment for H. pylori infection with a H2 blockers or
PPIs plus any two antibiotics (mainly nitromidazoles-
metronidazole/tinidazole, macrolides- clarithromycin,
amoxicillin and beta-lactames) for 10–14 d is recom-
mended in patients with peptic ulcer disease positive for
H. pylori or with no identifiable cause. American Col-
lege of Gastroenterology recommends four specific
drug regimens that use above referred combination of
three medications [10] or Bismuth- containing quadru-
ple therapy Bismuth subsalicylate, metronidazole, tet-
racycline all in 4 daily doses, and ranitidine or PPI
332
twice a day for 10–14 d. These combinations are
expected to cure 70 % to 85 % of infections [10].
Endoscopic Techniques
Variceal Bleed
Upper gastrointestinal endoscopy should be performed as
soon as possible after initial stabilization. Endoscopic ther-
apy should be done if variceal source of hemorrhage is
confirmed. A meta-analysis has shown that endoscopic var-
iceal ligation (EVL) is superior to sclerotherapy in the initial
control of bleeding. However EVL cannot be performed in
infants and toddlers due to the large size of available devi-
ces; EST is the mainstay of therapy in this group. Combi-
nation of pharmacological and endoscopic therapy is the
most rational approach in the treatment of acute variceal
hemorrhage [11]. Endoscopic injection of ‘tissue glue’ is
effective for controlling bleeding gastric varices. Argon
Plasma Coagulation can be used for bleeding portal hyper-
tensive gastropathy lesions, e.g., GAVE- Gastric Antral
Vascular Ectasias.
Non Variceal Ulcer Bleeds
In case of peptic ulcers with stigmata indicating high risk
of rebleed (spurting or oozing vessel in ulcer base/
adherent clot), any of the following endoscopic therapy
may be given: Injection therapy with adrenaline and
saline, mechanical hemostasis (Endoclip Devices) with
or without adrenaline, or thermocoagulation with or with-
out adrenaline.
Balloon Tamponade
In patients with variceal bleed who continue to bleed despite
pharmacologic and endoscopic methods, a Sengstaken-
Blakemore tube can be placed to stop hemorrhage by me-
chanically compressing esophageal and gastric varices.
However, its use is associated with potentially lethal com-
plications such as aspiration, migration, and necrosis/perfo-
ration of the esophagus with mortality rates as high as 20 %
[12]. The tube should never be kept inflated for durations
exceeding 12 h in children.
Surgical Treatment
Consultation with a pediatric surgeon and interventional
radiologist is necessary for children with massive bleed-
ing, ongoing significant blood loss, and failed endoscopic
procedure. Approaches to manage refractory variceal
hemorrhage include insertion of transjugular intrahepatic
porto-systemic shunt stents (in sinusoidal and post
Indian J Pediatr (April 2013) 80(4):326–333
sinusoidal portal hypertension), selective or non-selective
surgically created portosystemic shunts, and nonshunt
procedures aimed at interrupting and ligating varices
directly (devascularization) [13]. Non variceal bleed can
be tackled by transcatheter embolization by an interven-
tion radiologist. If this is not technically feasible or
expertise is unavailable, surgical ligation / resection can
be resorted to.
Key Points
& Upper GI bleeding is often a medical emergency.
& Specific etiologies at different ages should be kept in
mind while assessing pediatric patients.
& Variceal bleed is the most common cause of significant
upper GI bleeding in children.
& Immediate stabilization should be given priority before
proceeding to diagnostic algorithm.
& Upper GI endoscopy is the gold standard for diagnosis
and treatment of UGIB.
& Therapy in patients with mucosal bleeds is directed at
neutralization and/or prevention of the gastric acid re-
lease. Proton Pump Inhibitors (PPIs) are more effica-
cious than H2 receptor antagonists.
& Octreotide and terlipressin are useful in control of sig-
nificant UGIB especially due to variceal hemorrhage.
& Refractory variceal hemorrhage or non-variceal hemor-
rhage requires multidisciplinary approach.
Conflict of Interest None.
Role of Funding Source None.
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