Jornal de Pediatria - Vol. 76, Supl.

2, 2000 S135

0021-7557/00/76-Supl.2/S135

Jornal de Pediatria
Copyright 2000 by Sociedade Brasileira de Pediatria

REVIEW ARTICLE

Gastrointestinal bleeding
Elisa de Carvalho,1 Miriam H. Nita,2 Liliane M.A. Paiva,2 Ana Aurlia R. Silva2

Objective: to present an analysis of the occurrence of gastrointestinal bleeding in children and

emphasize: i) diagnostic methods; ii) the organized use of different therapeutic approaches in upper
gastrointestinal bleeding; iii) the review of concepts, classifications and techniques used in endoscopy,
which are important to the practice of clinical pediatrics.
Methods: literary review of chapters selected from textbooks, pertinent articles obtained through the
Medline system and active search, as well as personal archives belonging to the authors.
Results: the differential diagnosis of gastrointestinal bleeding in children varies according to the age.
The causes of upper gastrointestinal bleeding are subdivided into variceal and nonvariceal. Nonselective
beta-blockers are recommended to prevent variceal bleeding. Vasoactive drugs, such as somatostatin,
octreotide, and glypressin may be used, showing good results in both variceal and nonvariceal acute
bleeding. Both sclerotherapy and variceal ligation can be used in children to achieve variceal eradication.
Cyanoacrylate is effective and presents the lowest complication rate related to gastric variceal bleeding.
The presence of hemorrhage stigmata, such as active bleeding and visible vessel in ulcers is indicative of
a higher risk for recurrent bleeding, suggesting the need for endoscopic hemostasis. Proton pump inhibitors
are more efficacious than H2-receptor antagonists to promote the peptic ulcer healing.
Conclusion: the correct etiologic diagnosis of gastrointestinal bleeding in children is fundamentally
important to adopt the adequate therapeutic approach, whose main advances concern the pharmacological
and the endoscopic treatment.
J Pediatr (Rio J) 2000; 76 (Supl.2): S135-S146: upper gastrointestinal bleeding, digestive bleeding,
digestive endoscopy.

Introduction
Gastrointestinal bleeding constitutes an important topic,
once it is a medical emergency in every age group. It is still
associated with expressive morbidity and mortality indexes,
as well as with high-cost hospitalizations.

The discussion about gastrointestinal bleeding in children

presents differences and similarities when compared to
adults. The greatest discrepancy concerns the differential
diagnosis. Some pathologies, especially the ones that reflect
congenital malformations, such as intestinal duplication
and Meckels diverticulum, are the most common in
childhood, while neoplasias are seen more frequently among
adults. Regardless of the clinical differences, the diagnostic
and therapeutic approaches are usually similar to those used
among adults.1

1. Preceptor, Pediatric Gastroenterology Residency Program, Hospital de

Base do Distrito Federal.
2. Physician, Pediatric Gastroenterology Sector, Hospital de Base do Distrito
Federal.

S135

S136 Jornal de Pediatria - Vol. 76, Supl.2, 2000

The development of the fibroendoscope, commercially

available since 1960, has revolutionized the diagnostic
approach for diseases of the gastrointestinal tract. 2 In the
70s, the first esophagogastroduodenoscopies were
performed in children,3 and, in 1989, Tam and Saing
reported their 13-year experience in pediatric endoscopy,
documenting the efficacy and safety of the procedure.4
Parallelly to the advances obtained with endoscopic
hemostasis techniques, there were important progresses
concerning the pharmacological treatment of gastrointestinal
bleeding, which is defined as blood loss originating in the
gastrointestinal tract and adnexa. It may be manifested as:
Hematemesis: indicates that the bleeding origin is above
the Treitz angle, i.e., that it constitutes an upper
gastrointestinal bleeding (UGIB);
Melena: in 90% of the cases, it is associated with upper
gastrointestinal bleeding, but it may be originated in the
small intestine or in the proximal colon;
Hematochezia or enterorrhagia: evacuations with bright
red blood, generally originated in the colon, rectum or
anus. However, upper bleeding, either extensive or
associated with intestinal transit speed, may also be
manifested this way;
Occult blood in feces: reflects the blood loss through the
feces, being macroscopically imperceptible. In general,
these bleedings are originated in the small intestine or in
the upper segments.5

Differential diagnosis
Five factors provide important information for the
etiologic diagnosis: age, location of the hemorrhagic site,
color and severity of the bleeding, presence or absence of
pain and diarrhea.1 Table 1 shows the main cases for
gastrointestinal bleeding in childhood, correlating the
different pathologies with the age group and with the
presence of other signs and symptoms.
Generally, in childhood, lower gastrointestinal bleeding
is more frequent, but it is usually less severe than the upper.6
This study will focus specially on diagnostic and therapeutic
methods used in children with UGIB.

Diagnostic and therapeutic approach in children with

UGIB
Initially, false episodes of gastrointestinal bleeding have
to be excluded, for they may be caused by several factors,
such as: deglutition of breast milk, epistaxis, hemoptysis,
earlier use of drugs and foods that may color the feces, such
as iron, bismuth, berries, chocolate, beet, among others.
This way, the performance of invasive and unnecessary
procedures is avoided.7
The diagnostic and therapeutic approach of the child
with UGIB may be divided into three stages:

Gastrointestinal bleeding - de Carvalho E et alii

Stage I: general evaluation of the patient and

hemodynamic stabilization;
Stage II: etiologic diagnosis;
Stage III: specific treatment.
Stage I: General evaluation of the patient and
hemodynamic stabilization
In this phase, the pediatrician in charge of the patient
should rapidly evaluate three items: the permeability of
upper airways; the existence of active bleeding (intensity);
the patients hemodynamic conditions. Venous access,
resuscitation, adequate ventilation and control of pulse and
arterial pressure are essential for the patients good
evolution.8
The estimated blood loss is obtained through the
assessment of the exteriorized loss, of the arterial pressure,
pulse and hematocrit. However, the initial value of the
hematocrit may be deceiving, since it is only after 24 to 72
hours, with the reestablishment of the vascular space, that
the hematocrit reflects the actual loss volume.9
The observation of the volume and characteristics of the
drained material through a nasogastric catheter provides
information about the density of the bleeding. Besides
monitoring the loss, the drainage through a nasogastric
catheter promotes the gastric content cleaning. This way, it
eases the endoscopists work and decreases the risk for
aspiration of gastric content. For the performance of the
gastric lavage, the use of common water or physiological
serum at room temperature is recommended.10,11

Stage II: Etiologic diagnosis

In this phase, the attention is directed to the elucidation
of the etiologic diagnosis. UGIB is a symptom of digestive
problems, and not a disease by itself. It may be the result of
several heterogeneous affections, with different therapeutic
peculiarities. The differential diagnosis of UGIB in
childhood is showed in Table 2.
The following steps should be followed for the
elucidation of the etiologic diagnosis:
a) Clinical history
The complete and detailed clinical history is greatly
important, and does not have laboratorial substitutes. Chronic
pain, located (epigastric) or associated with clocking (to
wake up at night with pain), suggests the presence of peptic
disease. Hemorrhagic vomits and acute abdominal pain
after repetitive, initially non-hemorrhagic vomits suggest
diagnosis of Mallory-Weisss syndrome. Previous history
of gastroesophageal reflux corroborates the possibility of
complicated esophagitis. Other important data are: previous
history of umbilical catheterism, blood transfusions and use
of drugs, especially steroidal and nonsteroidal antiinflammatories.

Gastrointestinal bleeding - de Carvalho E et alii

Table 1 -

Jornal de Pediatria - Vol. 76, Supl.2, 2000 S137

Differential diagnosis of gastrointestinal bleeding in children

Age
0 - 2 years

> 2 - 12 years

> 12 years

Hematemesis

Peptic esophagitis
Mallory-Weiss syndrome
Gastritis
Duodenal ulcer
Gastric or duodenal duplication

Epistaxis
Peptic esophagitis
Caustic esophagitis
Mallory-Weiss laceration
Esophageal varices
Gastritis
Gastric ulcer
Duodenal ulcer
Telangiectasia
Hemobilia
Henoch-Schnlein purpura

Esophageal ulcer
Peptic esophagitis
Mallory-Weiss syndrome
Esophageal varices
Gastritis
Gastric ulcer
Duodenal ulcer
Telangiectasia
Hemobilia
Leiomyoma
Henoch-Schnlein purpura

Melena
(without
abdominal pain)

Duodenal ulcer
Duodenal duplication
Ileal duplication
Meckels diverticulum
Ectopic gastric mucosa

Duodenal ulcer
Duodenal duplication
Ileal duplication
Meckels diverticuluml
Ectopic gastric mucosa

Duodenal ulcer
Leiomyoma

Melena
(with abdominal
pain or signs
of peritonitis
or perforation

Necrotic enterocolitis
Intussusception
Volvulus

Duodenal ulcer
Hemobilia
Intussusception
Volvulus
Ileal ulcer

Duodenal ulcer
Hemobilia
Ileal ulcer (Crohns disease)

Enterorrhagia
(with diarrhea
or abdominal pain)

Infectious colitis
Pseudomembranous colitis
Allergic colitis
Enterocolitis (Hirschsprung)

Infectious colitis
Pseudomembranous colitis
Ulcerous colitis
Granulomatous colitis
(Crohns disease)
Hemolytic-uremic syndrome
Henoch-Schnlein purpura
Lymphoid nodular hyperplasia

Infectious colitis
Pseudomembranous colitis
Ulcerous colitis
Granulomatous colitis
(Crohns disease)
Hemolytic-uremic syndrome
Henoch-Schnlein purpura

Enterorrhagia
(without diarrhea
or abdominal pain)

Anal fissure
Allergic colitis
Ectopic gastric mucosa (rectal)
Hemangiomas (colon)

Anal fissure
Rectal ulcer
Polyps
Lymphoid nodular hyperplasia

Anal fissure
Rectal ulcer
Hemorrhoid
Colonic arteriovenous
malformation

Source: Treem1

b) Physical examination
After the general evaluation of the patient and the
hemodynamic stabilization, a detailed clinical examination
should be carried out. The evaluation of vomit and evacuation
characteristics should be part of the physical examination of
UGIB patients. Some findings are important to the final
conclusion of the etiologic diagnosis: the presence of aphthae
suggests diagnosis of Crohns disease; the presence of
splenomegaly, spiders, ascites and hard consistency of the
liver are compatible with the diagnosis of portal hypertension;
the presence of ecchymoses in the lower members suggests

Henoch-Schonlein purpura; torticollis is part of the Sandifer

syndrome and is associated with reflux esophagitis, among
others.
c) Upper digestive endoscopy
The patient should be referred to endoscopic evaluation
after the hemodynamic and respiratory stabilization,
preferably in the first 12 hours after the hemorrhagic episode,
since the diagnostic index is higher, up to 95%, in
endoscopies performed early. Patients with solid losses,
who continue with active bleeding and hemodynamic

Gastrointestinal bleeding - de Carvalho E et alii

S138 Jornal de Pediatria - Vol. 76, Supl.2, 2000

Table 2 -

UGIB main etiologies in childhood

Variceal UGIB

Nonvariceal UGIB
Peptic

Nonpeptic

Esophagus

Esophageal varices

Esophagitis
Esophageal ulcer

Mallory-Weiss

Stomach

Gastric varices

Gastritis
Gastric ulcer

Dieulafoy lesion
PHG*

Duodenum

Duodenal varices

Duodenitis
Duodenal ulcer

Hemobilia

Variable location

Polyps
Crohns disease
Telangiectasia
Aortoenteric fistula

* PHG - Portal hypertensive gastropathy

instability even after reposition should be submitted to

endoscopic evaluation immediately, concomitantly with
the resuscitation and hemodynamic stabilization procedures,
and preferably in a intensive therapy unit.5 It is important to
remember that 70% to 80% of the patients present selflimited bleeding .12
Upper digestive endoscopy acts in three stages: on the
diagnosis, on the prognosis and during the treatment.
Diagnosis: upper digestive endoscopy is better than
radiographic studies to the localization of hemorrhagic
sites.13,14
Prognosis: hemorrhage stigmata, defined at Forrests
classification, were originally described more than two
decades ago and are worldwide accepted still in the present
days.15 They provide information about the prognosis,
since they present a correlation with the hemorrhagic
recidivism index.16 This way, they orient the endoscopist
and the pediatrician in terms of the adequate therapeutic
conduct, hospitalization time and necessary fasting time.
Forrests classification is specified in Table 3, and the
correlation between the bleeding stigmata and the rebleeding
indexes is shown in Table 4.

Table 3 -

Forrests classification

I.

Active hemorrhage
Ia. Bright severe bleeding (jet)
Ib. Slow bleeding (dribbling)

II.

Recent hemorrhage
IIa. Nonbleeding visible vessel
IIb. Adherent clot on the base of the lesion
IIc. Flat pigmented spotsFlat pigmented spots

III. No evidence of bleeding (clean base)

Source: Forrest 15

Table 4 -

Frequency of endoscopic stigmata and of rebleeding

incidence

Stigmata

Incidence

Rebleeding

Bleeding in jet
Visible vessel (red)
Adherent clot
Slow bleeding
Flat clot
Clean base

8 to 15%
26 to 55%
10 to 18%
10 to 20%
12%
36%

>90%
30 to 51%
25 to 41%
20 to 30%
0 to 5%
0 to 2%

Source: Luna5

Treatment: therapeutic upper digestive endoscopy

presented important advancements in the 80s, and it is
considered the first option in hemostatic treatment.
d) Other diagnostic methods
These other methods may also be useful for the diagnostic
elucidation:
Intestinal transit, especially when there is a clinical
suspicion of Crohns disease;
Abdominal scintigraphy, examination of choice for the
identification of Meckels diverticulum;
Arteriography;
Explorative laparotomy.
Stage III: Specific treatment
The different affections that may go along with UGIB in
childhood, listed in Table 2, require specific treatments.

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Jornal de Pediatria - Vol. 76, Supl.2, 2000 S139

Variceal hemorrhage
Bleeding resulting from the rupture of gastroesophageal
varices is the most serious complication of portal
hypertension, and it is responsible for 10 to 15% of UGIB
in childhood.17 The different therapeutic options used for
the hemostasis of variceal UGIB are listed in Table 5 and
will be discussed below.
Pharmacological treatment
Prophylactic treatment
Propranolole is used as a prophylactic medicine for the
prevention of either the first hemorrhagic episode or the
hemorrhagic recidivism.18 In general, it is well tolerated by
the pediatric population, with minimal side effects. The
dosage should be adjusted so that it reduces the original
cardiac frequency at 25%. It is contraindicated for asthmatic
patients and for those with cardiac blockade.19
Treatment of the acute phase
Vasoactive drugs, such as vasopressin, somatostatin,
octreotide and glypressin (terlipressin) are effective in
controlling variceal hemorrhage. Vasopressin, widely used
in the past, has been substituted for somatostatin or for its
synthetic analog, octreotide, which, for acting in a selective
way in the splanchnic vasoconstriction, present high efficacy
in the control of acute bleeding and minor side effects.
Octreotide presents a longer average life than somatostatin.20
and it is as efficacious as sclerotherapy in the control of
bleeding due to variceal rupture. 21 The preconized
dosages22-24 are shown in Table 6. The octreotide infusion
should be maintained until the control of the bleeding, for
48 hours on average, and the dosage reduction should be
started 24 hours after the bleeding interruption. The weaning
should be progressive, reducing half a dosage every 12
hours. Higher dosages may be used in selected cases, and
the increase should be progressive (every 8 hours). Side
effects are more frequent in high-dosage infusions. During
the use of the drug, even during weaning, glucemia should
be controlled. Since octreotide presents a longer average
life, it may be administrated subcutaneously every 8 hours22
In the department of Pediatric Gastroenterology, at Hospital
de Base do Distrito Federal (Braslia, DF, Brazil), we
started the continuous infusion with 0.25 mg/kg/hour, and
increased it every 2 hours, progressively (0.25 mg/kg/hour,

Table 5 -

0.50 mg/kg/hour, 0.75 mg/kg/hour, 1.00 mg/kg/hour). This

scheme is also used by the Pediatric Gastroenterology and
Nutrition Division, at the Childrens Hospital Medical
Center, Cincinnati, EUA.
Endoscopic treatment
Endoscopic hemostasis is indicated for the control of
acute hemorrhage and also for the prevention of hemorrhagic
recidivism.
Sclerotherapy is not usually indicated for the prevention
of the first episode of variceal hemorrhage25 However, a
study performed by the North Italian Endoscopic Club
(NIEC) established prognostic criteria for the risk for
bleeding, with an estimated variation of 6.8 to 68.9%. The
three variables with prognostic significance were: Childs
classification, the caliber of the varices, and the presence of
red stains on their surface. Based on these criteria, some
authors preconize the prophylactic endoscopic treatment
for the obliteration of esophageal varices in patients with a
high risk for bleeding.26 Although this index is not ideal for
the pediatric population, it is still the most accepted one.
Endoscopic sclerotherapy of esophagogastric varices
In the present days, several types of sclerosants are
available, and the ethanolamine oleate is the most commonly
used for the sclerosis of esophageal varices, with intra and
paravasal injections,27 as shown in Figure 1. Esophageal
varices are more common and present a better response to
sclerotherapy. Gastric varices present a higher caliber,
bleed more abundantly and are associated with a higher
mortality rate.28 It is worthwhile to stand out that the control
of hemorrhage resulting from the rupture of gastric varices
is more efficacious and associated with a lower index of
complications when cyanoacrylate is used.29
In children, the sclerotherapy of esophageal varices is
greatly successfully, presenting low incidence of
complications and low mortality rate. It is usually considered
the first option in hemostatic treatment.30,31
Elastic ligature
The elastic ligature of esophageal varices32 (Figure 2)
uses the same technique of the treatment of hemorrhoids,
and it was proposed as an alternative for the eradication of

Therapeutic methods used in variceal UGIB

Pharmaceutics

Endoscopic

Mechanical

Shunt
(nonsurgical)

Surgical

Propanolol
Vasopressin
Somatostatin
Octreotide
Glypressin

Sclerotherapy
Elastic ligature

Balloon

TIPS*

Esophageal transection
Esophageal
devascularization
Portosystemic shunt
Liver transplantation

*TIPS - Transjugular intrahepatic portosystemic shunt

S140 Jornal de Pediatria - Vol. 76, Supl.2, 2000

Gastrointestinal bleeding - de Carvalho E et alii

of reduction of the bleeding after adolescence, as a

consequence of the recanalization of the portal vein and of
the development of collateral portosystemic in other areas.40
Additional measures
After the sclerotherapy sessions, the use of H2 blockers
or sucralfate is indicated, aiming to decrease the incidence
of complications, such as ulcers and stenoses. Antibiotics
are indicated for the prophylaxis of bacterial endocarditis in
risk patients.41 The use of omeprazole promotes the
efficacious cicatrization of the post-sclerosis ulcer.30

Figure 1 - Endoscopic sclerotherapy of esophageal varices.

A. Intravasal injection. B. Paravasal injection
Source: Terblanche27

esophageal varices in 1986.33 Its utilization was more

accepted after the development of multiple league
applicators, which allow the collocation of up to 10 leagues
in one only passage of the endoscope.34 Good results are
obtained with the ligature in children.35-38
Cost and availability
Sclerotherapy is the most used technique, since it offers
easy execution, low cost and availability in several centers.
The elastic ligature is associated with a lower index of
complications, but its availability is more restrict, and its
cost is more elevated.39
Independently on the method used, the long-term survival
depends especially on the hepatopathy stage, that is, on the
hepatocellular dysfunction level. In children presenting
portal hypertension without hepatocellular dysfunction
(example: thrombosis of the portal vein), there is a tendency

Figure 2 - Scheme of elastic ligatures in esophageal varices

Source: Stiegmann32

Combined pharmacological and endoscopic treatment

Vasoactive drugs, indicated for the treatment of the
acute phase, may be administrated in UGIB cases right after
the patients admission, still in the emergency room, even
before the endoscopic evaluation. The co-operating
treatment (endoscopic and pharmacological) is more
effective. The decrease of the hemorrhagic flux eases the
visualization of the lesion, favors the endoscopic treatment,
reduces the need for blood transfusion, and decreases the
risk for aspiration of hemorrhagic gastric content during
endoscopy.42
Mechanical treatment: Sengstaken-Blakemore balloon
Indications
Still in the present days, the temporary tamponade is
useful. It is obtained with the installation of the SengstakenBlakemore balloon,43 shown in Figure 3. The main
indications are: failure of the endoscopic treatment or
impossibility of visualization at the bleeding area (severe
bleeding).
Installation
After the introduction of the balloon catheter, certify
that the gastric balloon is placed with one end in the
stomach. Then, the partial insufflation of the gastric probe
should be done, and right after this, a radiograph of the
upper abdomen should be performed, in order to confirm
the position of the gastric balloon (below the diaphragm). If
the gastric balloon is well placed, its insufflation should be
completed, and the balloon catheter should be pulled and
fixed, so that the gastric balloon gets adjusted to the
gastroesophageal junction. Then, the esophageal probe
may be insufflated in order to maintain the pressure at 30 to
40 mmHg. The cleanness of the gastric cavity and the
intermittent aspiration of secretions from the hypopharynx
and esophagus are important to avoid aspiration. The
esophageal balloon should not remain insufflated for more
than 24 hours, due to the risk for ischemia of the esophageal
mucosa. After the fixation of the gastric balloon, it is
possible to leave it only insufflated for a period of 4 to 6
hours, since only this measure may be sufficient for the
hemorrhage control, with the decrease of the flux to the

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Jornal de Pediatria - Vol. 76, Supl.2, 2000 S141

Figure 3 - Sengstaken-Blakemore balloon

Source: Terblanche43

esophageal varices. The use of the balloon in children

usually requires sedation.29,40,44

pathy.47 TIPS may be used in children, with good results,

for the treatment of the portal hypertension complications.48

Withdrawal
The probe is removed after the balloon deinsufflation;
initially, the esophageal balloon is deflated, and 24 hours
later, the gastric one.29,44

Surgery
The surgical treatment is indicated in cases of failure of
the already mentioned therapeutic alternatives. The surgical
options are: portosystemic shunts (nonselective and
selective), transection and esophageal devascularization,
and hepatic transplantation.49

Results and complications

The use of the balloon is effective in the control of acute
hemorrhage, with good results in children as well40. The
main limitations of its use are: high index of complications,
especially lesions of the esophageal mucosa and acute
respiratory insufficiency, due to the aspiration or even
migration of the balloon. Besides, it does not act in the
prevention of rebleeding.29,44
Transjugular intrahepatic portosystemic shunt (TIPS)
The TIPS is a percutaneous, non-surgical shunt. A
prosthesis, placed through the hepatic parenchyma, unites
the hepatic vein and the portal vein, as shown in Figure 4.
The TIPS are effective in the control of the variceal
hemorrhage, even in case of gastric varices.46 However,
they are associated with an increased risk for encephalo-

Figure 4 - Scheme of installation of TIPS. A. The needle reaches

the portal vein through the liver. B. Dilatation of the
hepatic parenchyma with catheter balloon. C.
Placement of a metallic stent in the transhepatic
tract, uniting the hepatic and the portal veins

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S142 Jornal de Pediatria - Vol. 76, Supl.2, 2000

Nonvariceal hemorrhage
Ulcers
Ulcers are classified according to their location
(esophageal, gastric or duodenal) and etiology (primary or
secondary). Secondary ulcers, associated with systemic
diseases or ulcerogenic drugs, are usually silent until the
arousal of complications, such as UGIB, with a higher index
of morbidity and mortality than in primary ulcers.50
Deep gastric ulcers, located in the lesser curvature, and
duodenal ulcers, located at the posterior-inferior wall of the
bulb, present a higher risk for massive bleeding, due to their
proximity with the large vessels.51
The different therapeutic options used for nonvariceal
UGIB hemostasis are now going to be discussed.
Pharmacological treatment
The use of proton pump blockers, indicated in the
treatment of hemorrhagic ulcer, is associated with the
decrease of the rebleeding rate, of the need for blood
transfusion, as well as of the surgical treatment. It should be
associated with endoscopic hemostasis in cases of active
bleeding.52 The omeprazole dosage for children53 is
described in Table 6. Vasoactive drugs, such as somatostatin
and octreotide, are efficacious in the control of nonvariceal
digestive bleeding.52,54
Endoscopic treatment
The need for endoscopic hemostasis in hemorrhagic
ulcerous lesions depends on the aspect of the ulcer base,
since the bleeding stigmata are especially important for the
prediction of the hemorrhagic recidivism, as shown in
Table 4. The hemostatic endoscopic treatment is indicated
in lesions that present endoscopic signs associated with a
high index of hemorrhagic recidivism, such as active bleeding

Table 7 -

Table 6 -

Drugs used in the treatment of the digestive

hemorrhage

Ranitidina
(Rodgers23)

4 a 6 mg/kg/dia, 2x/dia, VO*/EV

Infuso contnua (EV): 0,10 a 0,25 mg/kg/hora

Ranitidine
Rodgers 23

4 to 6 mg/kg/day, twice a day, O*/E

Continuous infusion (E): 0.10 to 0.25 mg/kg/hour

Omeprazole 0.7 to 3.3 mg/kg/day, O*/EV

Israel 53
Propanolol 1 mg/kg/day, three times a day, O*
Shashidhar19 (progressive increase up to 25% of
the original CF )
Vasopressin Bolus (E): 0.33 U/kg (20 minutes)
Mowat24
Infusion (E): 0.33 U/kg/hour
Somatostatin Bolus (E): 1 to 2 g/kg (2 to 5 minutes)
Infusion (E): 1 to 2 g/kg/hour
Rodgers23
Octreotide
Siafakas22

* Orally

Teenagers and adults:

Bolus (E): 50 mg (5 minutes)
Infusion (E): 50 g/hour
Younger children:
Bolus (E): 1 g/kg (5 minutes)
Infusion (E): 1 g/kg/hour

Intravenously

Cardiac frequency

and visible vessel. Hemostasis is not indicated in ulcers with

a clean base or flat pigmented spots, due to the low frequency
of rebleeding. The conduct in lesions with an adherent clot
is no longer a consensus in literature, since the removal of
the clot may cause digestive bleeding again. In services
where thermal methods are not available, an injection of
adrenaline should be carried out on the base of the lesion,
and then, the clot should be removed, and the hemostatic
therapy should be performed according to the aspect of the
base of the lesion.16

Therapeutic methods used in nonvariceal UGIB

Nonthermal

Thermal

Injection

Mechanical

Topic

With contact

Without contact

Adrenaline
- Pure (1:10,000
or 20,000)
- With NaCl
- With sclerosants
- Associated with
thermal methods

Elastic ligature
Hemoclip
Sutures
Balloon
Endoloop

Tissue adhesives
Coagulation factors
Vasoconstrictors

Heater probe
Electrocoagulation
(mono and multipolar)

Laser
Coagulation with
argon gas

Absolute alcohol
Ethanolamine (1 to 5%)
Polidocanol (1%)
Thrombin
Fibrin glue
Cyanoacrylate

Gastrointestinal bleeding - de Carvalho E et alii

The several modalities of endoscopic hemostasis

available in the present days for the control on nonvariceal
hemorrhage are shown in Table 7. The injection therapy is
still the most commonly used, since it offers efficacy, low
cost, easy transportation, and handling.55,56
Dismissal
Patients that carry lesions associated with a low risk for
rebleeding may be dismissed on the same day, while highrisk patients should stay at the hospital for at least 72 hours,
period in which the hemorrhagic recidivism is more
frequent.57
Fasting
Fasting should be maintained for at least 48 hours in
children with a high risk for hemorrhagic recidivism, because
of the reasons mentioned before.58

Esophagitis
Hemorrhage is considered a complication of esophagitis,
which in childhood is usually associated with
gastroesophageal reflux (GER). So, in most cases, the
treatment should be directed both to esophagitis and GER.
In hemorrhagic esophagitis, proton-pump blockers are more
efficacious than H2-blockers to promote the lesion
cicatrization.53

Table 8 -

Jornal de Pediatria - Vol. 76, Supl.2, 2000 S143

Mallory-Weiss syndrome
In the Mallory-Weiss syndrome, the UGIB results from
the laceration of the esophageal mucosa. The clinical
treatment includes: volemic replacement, antacids,
antiemetics, and, if necessary, blood transfusion. Endoscopic
hemostasis is indicated in cases of active bleeding or visible
vessel close to the laceration. Other therapeutic options are:
vasoconstrictor pharmaceutics, such as octreotide;
embolization of the left gastric artery; or surgical correction
(gastronomy with suture of the fissure or fundoplication). 59
Gastritis and gastropathy
Different types of gastritis and gastropathy may
accompany UGIB in childhood. The classification of gastritis
through Sydneys system,60 used in adults, has a limited
value for the pediatric population, since it focuses especially
on the severity of chronic gastritis, atrophy, and intestinal
metaplasia, more common in adults. It does not classify
noninflammatory lesions either. A proposal to classify
gastritis and gastropathy in children was published in 1999,61
and is described in Table 8.
In the section of Pediatric Gastroenterology, at Hospital
de Base do Distrito Federal, we indicate the use of pump
blockers in the treatment of hemorrhagic gastritis. However,
H2 blockers may also be used. In the presence of Crohn
disease, celiac disease, and others, specific measures should
be instituted.

Classification of the gastrites and gastropathies in children

Erosive and/or
hemorrhagic gastrites or gastropathies

Non-erosive gastrites or gastropathies

Stress gastropathy
Neonatal gastropathy
Traumatic gastropathy
Gastropathy due to aspirin and other NSAI* drugs
Portal hypertensive gastropathy
Uremic gastropathy
Varioliform chronic gastritis
Biliary gastropathy
Gastropathy: Henoch-Schnlein purpura
Corrosive gastropathy
Gastropathy or exercise gastritis
Radiation gastropathy

Nonspecific gastritis
Gastritis due to H. pylori
Gastritis related to Crohns disease
Allergic gastritis
Gastropathy due to proton pump inhibitor
Gastritis related to celiac disease
Gastritis related to chronic granulomatous disease
Gastritis related to cytomegalovirus
Eosinophilic gastritis
Collagenous gastritis
Graft x host disease
Menetrier disease
Pernicious anemia
Gastritis associated with autoimmune disease
Other granulomatous gastrites
Emphysematous gastritis
Other infectious gastrites

* NSAI - Nonsteroidal anti-inflammatory

Source: Dohil61

S144 Jornal de Pediatria - Vol. 76, Supl.2, 2000

Portal hypertensive gastropathy

Portal hypertensive gastropathy is responsible for 10 to
50% of the UGIB cases in patients with portal hypertension.62
The classic therapy for gastritis does not improve the
bleeding significantly. During the acute phase of the bleeding,
vasoconstrictor drugs, such as somatostatin, octreotide, or
glypressin, are indicated. Propanolol, as a prophylactic, is
also indicated.63
Dieulafoy lesion
The Dieulafoy lesion deserves to be mentioned, even
though it is not one of the most common causes of UGIB in
childhood, since it is responsible for episodes of massive
hemorrhage. Early upper digestive endoscopy favors the
etiologic diagnosis. The bleeding occurs through a
punctiform, nonulcerous lesion, usually located at the upper
part of the stomach fundus, corresponding to rupture of the
caliber artery, which goes in an anomalous way up to the
submucosa, probably consisting of a congenital variation.
The methods of endoscopic hemostasis already described
may be used. Surgical treatment is indicated only in refractory
cases.59,64
Duodenitis
Duodenitis may be:
peptic;
parasitic (Ascaris lumbricoides, Ancylostoma
duodenale, Giardia lamblia, Strongyloides stercoralis
and Schistosoma mansoni);
associated with Crohn disease;
associated with granulomatous diseases (tuberculosis);
associated with the immunoproliferative small intestine
disease.
For the etiologic diagnosis, the description of the
macroscopic aspect and the collection of material are
important for the study: duodenal liquid for the investigation
of larvae, and biopsy for histological and histochemical
studies.65 The treatment of hemorrhagic duodenitis is similar
to that described for hemorrhagic gastritis.

Prevention of UGIB in childhood

It is important to avoid the abusive use of antiinflammatories, frequently used without a precise indication.
Up to the present moment, there are no evidences that the
nonhormonal anti-inflammatories reduces the inflammatory
process when associated with acute respiratory diseases.
They are the pharmaceutics most frequently used in the
world, generating an excessive index of hospitalization,
high cost, and important rates of morbidity and
mortality.66-68
The treatment of H. pylori in patients that carry primary
gastric or duodenal ulcers prevents rebleeding. 52,69

Gastrointestinal bleeding - de Carvalho E et alii

Another preventive measure is the performance of

elucidation campaigns, in order to prevent the abusive use
of alcohol among teenagers.
Finally, regarding the prophylaxis of stress ulcers, respect
to the serious patients pain and stress is important. At this
point, special scope should be given to humanization in
pediatric intensive therapies, as well as to analgesia and
gastric alkalization. The use of sucralfate or ranitidine is
efficacious for the prevention of UGIB resulting from stress
gastropathy.62,70,71

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Correspondence:
Dra. Elisa de Carvalho
HIGS 705, bloco A, casa 67
CEP 70350-701 Braslia, DF, Brazil
Phone:+ 55 61 4430.844 / 9984.4058
Fax: + 55 61 443.5082
E-mail: trevizoli@zaz.com.br