Pediatric Gastrointestinal Bleeding

Overview
Presentation
DDx
Workup
Treatment
Medication
Updated: Oct 20, 2014

Background

Etiology
Epidemiology
Patient Education
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Multimedia Library
Tables
References

Background
Gastrointestinal (GI) bleeding in infants and children is a fairly
common problem, accounting for 10%-20% of referrals to
pediatric gastroenterologists. However, it is usually limited in
volume, allowing time for diagnosis and treatment.
The initial approach to all patients with significant GI bleeding is
to ensure patient stability, to establish adequate oxygen
delivery, to place intravenous access, to initiate fluid and blood
resuscitation, and to correct any underlying coagulopathies.
A juvenile polyp, one of the causes of GI bleeding, is seen in
the image below.

Go to Upper Gastrointestinal Bleeding for complete information

on this topic.

Intraoperative view of a
bleeding juvenile polyp.

Etiology
Age-specific etiologies for GI bleeding are discussed below for
the following groups:

Neonates
Children aged 1 month to 1 year
Children aged 1-2 years
Children older than 2 years

Neonates
Anal fissures are the most common cause of GI bleeding in
infants. They produce bright red blood that streaks the stool or
causes spots of blood in the diaper. The cause is a tear at the
mucocutaneous line, most commonly located dorsally in the
midline.
Most common causes of apparent neonatal GI bleeds include
bacterial enteritis,milk protein allergies, intussusception,

swallowed maternal blood, and lymphonodular hyperplasia.

Milk or soy enterocolitis, or allergic colitis, is a cause for
vomiting with blood staining after the introduction of these food
products into the diet.
Erosions of the esophageal, gastric, and duodenal mucosa are
also a frequent cause for true neonatal GI bleeding.
Presumably, this damage is caused by the dramatic increase in
gastric acid secretion and the laxity of gastric sphincters in
infants.
Maternal stress in the third trimester has been proposed to
increase maternal gastrin secretion and enhance infantile
peptic ulcer formation.
Neonatal peptic ulcer disease has not been associated with
mode of feeding or hyperalimentation.
Some drugs are implicated in neonatal GI bleeds. These
include NSAIDs, heparin, and tolazoline, which are used for
persistent fetal circulation.
Indomethacin, used for patent ductus arteriosus in neonates,
may cause GI bleeding through intestinal vasoconstriction and
platelet dysfunction.
Maternal medications can cross the placenta and cause
problems in the developing fetus and in the neonate on
delivery. Aspirin, cephalothin, and phenobarbital are well-known
causes of coagulation abnormalities in neonates.
Stress gastritis occurs in up to 20% of patients cared for in
neonatal intensive care units (ICUs). Prematurity, neonatal
distress, and mechanical ventilation are all associated with
stress gastritis.
Stress ulcers in newborns are associated with dexamethasone,
which can be used for fetal lung maturation.

Rarer causes of GI bleeding in a neonate include volvulus,

coagulopathies,arteriovenous malformations, necrotizing
enterocolitis (NEC; especially in preterm infants), Hirschsprung
enterocolitis, and Meckel diverticulitis.
Hemorrhagic disease of the newborn is a self-limited bleeding
disorder resulting from a deficiency in vitamin Kdependent
coagulation factors. levels of clotting factors II, VII, IX, and X
decline rapidly after birth, reaching their nadir at 48-72 hours of
life. In 0.25%-0.5% of neonates, severe hemorrhage may
result.

Upper gastrointestinal bleeding in children aged 1

month to 1 year
Peptic esophagitis caused by gastroesophageal reflux (GER) is
the most common cause of bleeding in this age group.
Gastritis is primary or secondary in etiology. Primary gastritis is
associated withHelicobacter pylori infection and is the most
common cause of gastritis in children. Other causes of primary
gastritis include steroidal and nonsteroidal anti-inflammatory
drug (NSAID) use, Zollinger-Ellison syndrome, and Crohn
disease.
Secondary gastritis occurs in association with severe systemic
illnesses that result in mucosal ischemia and produce diffuse
erosive and hemorrhagic gastric mucosa.

Lower gastrointestinal tract bleeding in children aged 1

month to 1 year
Anal fissures produce bright red blood that streaks the stool or
causes spots of blood in the diaper. The cause is a tear at the
mucocutaneous line, most commonly located dorsally in the
midline. (In older children, as in adults, refractory anal fissures
or those located off the midline should raise suspicion
for inflammatory bowel disease [IBD], specifically Crohn
disease.)

Intussusception is the most likely cause of lower GI bleeding in

infants aged 6-18 months.
Gangrenous bowel is another common cause of lower GI
bleeding. Causes include malrotation with volvulus,
omphalomesenteric remnant with volvulus, internal hernia with
strangulation, segmental small-bowel volvulus, and,
rarely, sigmoid volvulus.
Milk protein allergy causes a colitis that may be associated with
occult or gross lower GI bleeding. It is the most common allergy
observed in infancy and is caused by an adverse immune
reaction to cow's milk.

Upper gastrointestinal tract bleeding in children aged

1-2 years
In children older than 1 year, peptic ulcer disease is the most
common cause of hematemesis. The etiologies, which include
NSAID use, are similar to those mentioned in the above
discussion of gastritis.
When an ulcer not associated with H pylori infection is
diagnosed, a fasting plasma gastrin level is measured to
exclude Zollinger-Ellison syndrome.
Most of the peptic ulcers occurring in children of this age range
are secondary to other systemic diseases, such as burns
(Curling ulcer), head trauma (Cushing ulcer), malignancy, or
sepsis.

Lower gastrointestinal tract bleeding in children aged

1-2 years
Most polyps in persons of this age group are the juvenile type
and are located throughout the colon. These are benign
hamartomas and usually require no treatment, because they
autoamputate. (A juvenile polyp is seen below.)

Intraoperative view of a
bleeding juvenile polyp.

Meckel diverticulum (see the images below) occurs in 2% of the

population. The etiology of GI bleeding due to Meckel
diverticulum is ileal ulceration caused by acid secretion from
the ectopic gastric mucosa. Erosion into small arterioles leads
to painless, brisk rectal bleeding. The site of ulceration is
generally at the base of the diverticulum where the ectopic
mucosa and the normal ileum join. More rarely, the ulcer
appears distally in the ileum.

Intraoperative view of the

bleeding Meckel diverticulum. Note the ulceration at the base.

Radioactive tracer in
stomach, bladder, and the Meckel diverticulum in a 5-year-boy brought in
for lower gastrointestinal bleeding.

Upper gastrointestinal tract bleeding in children older

than age 2 years
Esophageal varices result can from portal hypertension,
regardless of the age group. The increased resistance to blood
flow through the portal system is due to prehepatic,
intrahepatic, and suprahepatic obstruction, but the most
common causes of portal hypertension in children include
portal vein thrombosis (prehepatic) and biliary
atresia (intrahepatic).
The most common causes of upper GI bleeding in children
older than 12 years are duodenal ulcers, esophagitis, gastritis,
and Mallory-Weiss tears.

Lower gastrointestinal tract bleeding in children older

than age 2 years
The most common cause of lower GI bleeding in children older
than 2 years is juvenile polyps, and this remains true until the
patients are teenagers.

Inflammatory bowel disease (IBD) also becomes a common

cause of GI bleeding in this age group. Bleeding is less
common in individuals with Crohn disease than in persons
with ulcerative colitis, but both may have bloody diarrhea as
part of the clinical scenario. These children generally have the
diagnosis of IBD well established before acute or chronic
bleeding necessitates intervention.
Infectious diarrhea is suspected when lower GI bleeding occurs
in association with profuse diarrhea. Recent antibiotic use
raises suspicion for antibiotic-associated colitis and Clostridium
difficile colitis. The 2 most common pathogens in infectious
diarrhea are Escherichia coli and species of Shigella.
Vascular lesions include a wide variety of malformations,
including hemangiomas,arteriovenous malformations, and
vasculitis.

Summary
The causes of upper and lower gastrointestinal bleeding,
according to age group, are summarized in the table below.
Table. Common Sources of Gastrointestinal Bleeding in
Pediatrics (Open Table in a new window)
Age Group

Neonates

Upper Gastrointestinal
Bleeding

Lower Gastrointestinal
Bleeding

Hemorrhagic disease of the

newborn

Anal fissure

Necrotizing enterocolitis
Swallowed maternal blood
Malrotation with volvulus
Stress gastritis

Coagulopathy

Anal fissure

Infants aged 1 month to 1

year

Esophagitis

Intussusception

Gastritis

Gangrenous bowel

Milk protein allergy

Peptic ulcer disease

Polyps

Gastritis

Meckel diverticulum

Infants aged 1-2 years

Polyps

Esophageal varices

Inflammatory bowel disease

Gastric varices

Infectious diarrhea

Children older than 2 years

Vascular lesions

Epidemiology
Severe GI bleeds are rare in the general pediatric population
and are therefore not well documented.

In the pediatric ICU population, 6-20% of the general pediatric

population has upper GI bleeds. The incidence of lower GI
bleeding has not been well established.
In one report, rectal bleeding alone accounted for 0.3% of the
chief complaints in more than 40,000 patients presenting to a
major urban emergency department.
An investigation into the epidemiology of GI bleeding in
hospitalized children in the United States reported that there
were 23,383 pediatric discharges with a diagnosis of GI
bleeding accounting for 0.5% of all discharges. Children with a
GI bleeding were more likely to be male (54.5% vs. 45.8%),
and older (children 11 years; 50.8% vs. 38.7%). Children 1115 years of age had the highest incidence of GI bleeding (84.2
per 10,000 discharges) and children less than 1 year of age the
lowest (24.4 per 10,000 discharges). The highest incidence of
GI bleeding was attributable to cases coded as blood in stool
(17.6 per 10,000 discharges) followed by hematemesis (11.2
per 10,000 discharges). The highest mortality rates associated
with GI bleeding were observed in cases with intestinal
perforation (8.7%) and esophageal perforation (8.4%).[1]

Patient Education
For patient education information, see
eMedicineHealth's Digestive Disorders Center, as well
as Gastrointestinal Bleeding, Abdominal Pain in
Children, Vomiting and Nausea, and Rectal Bleeding.
Proceed to Clinical Presentation

http://emedicine.medscape.com/article/1955984-overview#showall

Approach Considerations

Provide hydration and volume support in patients with

gastrointestinal (GI) bleeding. Transfusion may be required.
If an acute bleed is suspected and there is hemodynamic
instability, access with 2 large-bore intravenous (IV) catheters
must be obtained.
Patients with severe GI bleeds should be admitted to the
pediatric ICU.
For variceal bleeds, GI consultants may endoscopically control
active hemorrhage with sclerotherapy, an elastic ligature (for
esophageal varices or for hemorrhoids), or (in rare cases) a
transjugular intrahepatic portosystemic shunt (TIPS).
Failure to control bleeding may require the placement of a
Sengstaken-Blakemore balloon for temporary tamponade if
endoscopic treatment fails or is not possible at the time due to
the massive bleeding.
Significant GI bleeding that cannot be controlled (eg, due to
duodenal ulcers or varices in the proximal GI tract, vascular
malformations, nonreducible points of intussusception) by using
the previously mentioned techniques may require surgical
intervention, such as laparoscopy.
Patients with first-time occurrences of nonsignificant amounts
of bleeding who are discharged should be followed by their
primary care pediatrician for further episodes. Again, most of
these cases are benign and self-limiting.
Children who present with upper or lower GI hemorrhage to
hospitals without a pediatric ICU should be transferred to such
a facility when sufficiently stable.
Age-specific treatment and management strategies are
discussed below.

Go to Upper Gastrointestinal Bleeding for complete information

on this topic.

Upper gastrointestinal tract bleeding in neonates

Treatment for stress gastritis in neonates is supportive and
includes adequate resuscitation to reduce the underlying
hypoxemia, nasogastric suction, and IV H2 blockers or PPIs.
Studies have advocated identifying high-risk neonates and
treating them prophylactically with acid-reducing agents.
Extremely rarely, continued or massive hematemesis despite
medical therapy leads to operative interventions, such as
gastric resection, vagotomy and pyloroplasty, or antrectomy
and vagotomy.
Hemorrhagic disease of the newborn is a bleeding disorder
resulting from a deficiency in vitamin Kdependent coagulation
factors. Although it is normally self limited, in 0.25%-0.5% of
neonates, severe hemorrhage may result.
Prophylactic vitamin K administration in the newborn period
virtually eliminates hemorrhagic disease. If the disorder occurs,
IV administration of 1 mg of vitamin K generally stops the
hemorrhage within 2 hours. If the clinical condition warrants,
fresh frozen plasma and packed red blood cells are
administered in addition to the vitamin K.

Lower gastrointestinal tract bleeding in neonates

For neonates with NEC, the standard treatment is aggressive
medical resuscitation with bowel rest, antibiotics, total
parenteral nutritional, and nasogastric decompression.
Nonoperative management of NEC yields a 70-80% recovery
rate, but urgent laparotomy or drain placement is required in
neonates in whom conservative therapy is unsuccessful owing
to progressive sepsis, bowel perforation, or persistent bleeding.
Recurrent bleeding in a baby who has recovered from NEC

may indicate a second occurrence of the disease or an

enterocolitis stricture.

Upper gastrointestinal tract bleeding in children aged 1

month to 1 year
Peptic esophagitis caused by GER is the most common cause
of bleeding in this age group. Treatment begins with acidreducing agents, thickened feeds, upright positioning, and
prokinetic agents.
Antireflux procedures are rarely performed to control bleeding
but may be necessary to treat complications of GER (eg,
apnea, esophageal stricture, lung disease) that are refractory to
medical therapy.
Gastritis is primary or secondary in etiology. Primary gastritis is
associated withHelicobacter pylori infection and is the most
common cause of gastritis in children. Treatment is a
combination of H2 blockage, antibiotic therapy, and bismuth.
Secondary gastritis occurs in association with severe systemic
illnesses that result in mucosal ischemia and produce diffuse
erosive and hemorrhagic gastric mucosa. Correction of the
underlying metabolic derangements and acid reduction are
successful treatment measures in most patients.

Lower gastrointestinal tract bleeding in children aged 1

month to 1 year
Treatment for anal fissures consists of the administration of
stool softeners and the use of rectal dilation.
In patients with intussusception, barium, saline, and pneumatic
enema, while diagnostic, are potentially therapeutic as well.
Successful reduction in intussusception is achieved in up to
90% of cases. Unsuccessful enema necessitates laparotomy
and manual reduction or resection of the intussusception.

In cases of gangrenous bowel, laparotomy is usually necessary

for definitive treatment.
The symptoms of milk protein allergy generally resolve in 48
hours to 2 weeks after withdrawal of the offending milk product.

Upper gastrointestinal tract bleeding in children aged

1-2 years
Significant upper GI bleeding caused by peptic ulcers is
evaluated and treated with immediate endoscopy. Cautery,
epinephrine therapy, fibrin sealants, and Endoclips are
treatment options for ulcers, and biopsy samples are taken, if
warranted.
Therapy for peptic ulcer disease in children mimics that in
adults and centers around acid reduction and control of the
underlying condition. Obstruction and/or persistent bleeding are
indications for surgery.

Lower gastrointestinal tract bleeding in children aged

1-2 years
Most polyps in persons of this age group are the juvenile type
and are located throughout the colon. These are benign
hamartomas and usually require no treatment, because they
autoamputate. Colonoscopy, the diagnostic evaluation of
choice, can be used to excise bleeding polyps when they are
identified.
In Meckel diverticulum, bleeding may be brisk, and transfusion
is often required. However, the bleeding is usually self-limited
and resolves spontaneously with episodic recurrences.
The treatment of ulceration in Meckel diverticulum is surgical
resection after preoperative fluid resuscitation and adequate
transfusion. A right lower quadrant incision is used, and the
diverticulum is mobilized. (A bleeding, ulcerated Meckel
diverticulum is seen below.)

Intraoperative view of the

bleeding Meckel diverticulum. Note the ulceration at the base.

Careful visual inspection and palpation locate the ectopic

gastric mucosa and ulceration. If the ulcer is confined to the
diverticulum, diverticulectomy alone is performed and closed in
a transverse fashion with sutures or a stapling device.
If the diverticulum is broad based or the ulcer cannot be
included in the diverticulum specimen, segmental bowel
resection is necessary, with an end-to-end anastomosis. An
appendectomy is often performed with the resection.

Upper gastrointestinal tract bleeding in children older

than 2 years
Esophageal varices result from portal hypertension, regardless
of the age group. Once the diagnosis of gastric or esophageal
varices has been confirmed, treatment is initiated. Most
bleeding episodes stop spontaneously and respond to blood
products and careful monitoring.
Pharmacologic therapy, administered as necessary, is directed
at reducing portal venous blood flow. Vasopressin, octreotide,
and beta blockers have been used systemically to control
bleeding varices.
Balloon tamponade with a Sengstaken-Blakemore or
Minnesota tube has yielded up to an 80% success rate in

controlling bleeding varices, but rebleeding and serious

complications, such as pressure necrosis or misplacement,
make this technique less useful.
Endoscopic sclerotherapy with injection of sodium morrhuate
controls bleeding with a success rate of 90%-95%. Generally,
endoscopic sclerotherapy is repeated at 2- to 4-week intervals
after the acute bleed to prevent recurrence.
Variceal banding offers results at least comparable to
sclerotherapy but is more difficult to perform in children
because of the smaller size of the esophagus.
In the approximately 20% of cases in which conservative
management fails (defined by multiple transfusion requirements
or an inability to maintain hemodynamic stability) with combined
pharmacotherapy and endoscopic treatments, shunt and nonshunt surgeries are the definitive treatment.
For intrahepatic portal hypertension, TIPS provides temporary
decompression of the intrahepatic portal vein into the hepatic
veins. Surgical portosystemic or portoportal shunts are
reserved for refractory cases and/or when liver transplantation
is not an option.
Nonshunt operations include esophageal transaction and
devascularization of the gastroesophageal varices (Sugiura
procedure), but neither is commonly performed.

Lower gastrointestinal tract bleeding in children older

than 2 years
In patients with IBD, the occurrence of acute or persistent
bleeding with resultant anemia, despite the use of maximal
medical therapy, is considered to be an indication for surgery.
Therapy for ulcerative colitis is a total proctocolectomy with an
ileal pouchanal pull-through. The goal of surgical treatment in
Crohn disease is resection of all grossly diseased bowels with

primary anastomosis, provided previous surgery (or the current

resection) has not created a short-bowel situation.
Infectious diarrhea is suspected when lower GI bleeding occurs
in association with profuse diarrhea. Recent antibiotic use
raises suspicion for antibiotic-associated colitis and Clostridium
difficile colitis. The former should be self-limited and should
resolve after cessation of antibiotics, while Clostridium
difficile colitis requires therapy with oral metronidazole or
vancomycin. Escherichia coli and Shigellaspecies are the two
most common pathogens in infectious diarrhea. Treatment is
supportive with antibiotic therapy, as indicated.
Vascular lesions include a wide variety of malformations,
including hemangiomas, arteriovenous malformations, and
vasculitis. If these lesions are located in the colon, colonoscopy
may be diagnostic and therapeutic. However, brisk bleeding
may obscure the visual field, making localization of the bleeding
impossible. Arteriography assists in localizing the source and
embolizing the feeding vessel.
Surgery is necessary when bleeding cannot be controlled using
these techniques. Localization of hemorrhage in the small
bowel is a challenge to surgeons and may require
intraoperative endoscopy to find the lesion.

Further inpatient or outpatient care

Critically ill pediatric patients may benefit from receiving
prophylactic treatment to prevent upper gastrointestinal
bleeding. However, evidence to guide clinical practice remains
limited.[8]

Consultations
Direct consultation toward the discipline appropriate to the
diagnosis (eg, a radiologist for a barium enema study in
intussusception, a pediatric ICU specialist and a pediatric

surgeon for NEC, a gastroenterologist for presumed ulcer

disease).
http://emedicine.medscape.com/article/1955984-treatment#showall

History

A complete history can often identify a presumptive GI bleeding

source and direct an efficient workup. For example, NEC in
most neonates is diagnosed based on history and clinical
presentation.
Ask age- and etiology-specific questions. Ask about acuteness
or chronicity of bleeding, color and quantity of the blood in
stools or emesis, antecedent symptoms, history of straining,
abdominal pain, and trauma.
Melena, rather than bright red blood per rectum, is usually a
sign of bleeding that comes from a source proximal to the
ligament of Treitz. However, massive upper GI bleeding can
produce bright red blood per rectum if GI transit time is rapid.
Blood mixed in stool or dark red blood implies a proximal
source with some degree of digestion of the blood.
Intestinal malrotation is suspected with the sudden onset of
melena in combination with bilious emesis in a previously
healthy, nondistended baby.
For complaints of bloody stool, make sure to elicit a history of
foods consumed or drugs used that may give a stool bloody
appearance. This list includes certain antibiotics, iron
supplements, red licorice, chocolate, Kool-Aid, flavored gelatin,
or bismuth-containing products (eg, Pepto-Bismol).

A history of vomiting, diarrhea, fever, ill contacts, or travel

suggests an infectious etiology.
Bloody diarrhea and signs of obstruction
suggest volvulus, intussusception, ornecrotizing enterocolitis,
particularly in premature infants. Acute bloody diarrhea should
be considered a medical emergency.[2]
Recurrent or forceful vomiting is associated with Mallory-Weiss
tears.
Familial history or NSAID use may suggest ulcer disease.
Ingested substances, such as NSAIDs, tetracyclines, steroids,
caustics, and foreign bodies, can irritate the gastric mucosa
enough to cause blood to be mixed with the vomitus.[3]
Ask questions that may reveal underlying, but as yet
undiagnosed, organ dysfunction.
Recent jaundice, easy bruising, and changes in stool color may
signal liver disease.
Other evidence of coagulation abnormalities elicited from the
history may also point to disorders of the kidney or
reticuloendothelial system.
The rest of this section provides an age-specific discussion of
patient history.

Neonates
Milk or soy enterocolitis, or allergic colitis, is a cause for
vomiting with blood staining after the introduction of these food
products into the diet.

Some drugs are implicated in neonatal GI bleeds. These

include NSAIDs, heparin, and tolazoline, which are used for
persistent fetal circulation.
Indomethacin, which is used for patent ductus arteriosus in
neonates, may cause GI bleeding through intestinal
vasoconstriction and platelet dysfunction.
Maternal medications can cross the placenta and cause
problems in the developing fetus and neonate on delivery.
Aspirin, cephalothin, and phenobarbital are well-known causes
of coagulation abnormalities in neonates.
Prematurity, neonatal distress, and mechanical ventilation are
all associated with stress gastritis.

Lower gastrointestinal tract bleeding in children aged 1

month to 1 year
Episodic abdominal pain that is cramping in nature, vomiting,
and currant jelly stools are findings in children with
intussusception.
In milk protein allergy, the child displays, in addition to bleeding,
such symptoms as fussiness and increased frequency of bowel
movements; frank diarrhea is atypical.

Upper gastrointestinal tract bleeding in children aged 1-2

years
NSAID use is one of the factors in the development of peptic
ulcer disease in children older than 1 year. However, most of
the ulcers occurring in children aged 1-2 years are secondary
to systemic diseases, such as burns (Curling ulcer), head
trauma (Cushing ulcer), malignancy, or sepsis.

Lower gastrointestinal tract bleeding in children aged 1-2

years
Children with polyps are found to have painless bleeding per
rectum, which often streaks the stool with fresh blood.

Lower gastrointestinal tract bleeding in children older than

age 2 years
Bleeding is less common in individuals with Crohn disease than
in those withulcerative colitis, but persons with either disease
may have bloody diarrhea as part of the clinical scenario.
These children generally have the diagnosis of IBD well
established before acute or chronic bleeding necessitates
intervention.
Infectious diarrhea is suspected when lower GI bleeding occurs
in association with profuse diarrhea. Recent antibiotic use
raises suspicion for antibiotic-associated colitis and Clostridium
difficile colitis.

Physical Examination

Look for signs of shock, and document findings such as heart

rate, blood pressure, capillary refill, and orthostatic changes.
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.
Examine abdominal surgical scars and elicit the reason for the
surgery.

Specifically include bowel-sound frequency in the abdominal

examination. Hyperactive bowel sounds are more common in
upper GI bleeding.
Abdominal tenderness, with or without a mass, raises the
suspicion of intussusception or ischemia.
Hepatomegaly, splenomegaly, jaundice, or caput medusa
suggests liver disease and subsequent portal hypertension.
Inspection of the perianal area may reveal fissures, fistulas,
skin breakdown, or evidence of trauma. Gentle digital rectal
examination may reveal polyps, masses, or occult blood.
Looking for evidence of child abuse, such as perianal tearing,
tags, or irregularities in anal tone and contour, is also important.
Examination of the skin may reveal evidence of systemic
disorders, such as IBD,Henoch-Schnlein purpura, and PeutzJeghers polyposis.
Anoscopy can be performed (if required in an infant) by gently
placing a lubricated red-top or purple-top test tube into the anus
to enable visualization of the inner anal anatomy.

Lower gastrointestinal tract bleeding in children aged 1

month to 1 year
Diagnosis of anal fissures is made by anal examination,
sometimes performed with a nasal speculum. Further tests are
unnecessary. (In older children, as in adults, refractory anal
fissures or those located off the midline should raise suspicion
for IBD, specifically Crohn disease.)
Symptoms of intussusception include a palpable, sausageshaped mass.

Children with a gangrenous bowel present with evidence of

bowel obstruction, abdominal distension, dehydration,
and peritonitis.
Previous
Proceed to Differential Diagnoses
http://emedicine.medscape.com/article/1955984-clinical#b3

Diagnostic Considerations

Aside from the disorders listed in the Differentials section,

below, other conditions to consider in pediatric patients with
symptoms of GI bleeding include the following:

NEC

Portal hypertension (variceal bleeding)

Caustic ingestions

Salmonella Infection

Sexual Assault

Epistaxis
Apt-Downey test
Maternal blood ingestion is the most common cause of
suspected GI bleeding. Blood can be swallowed during delivery
or while an infant is breastfeeding (from a fissure in the
mother's breast).
If a neonate is actively spitting up or vomiting blood, or if it is
significant enough to require placement of a nasogastric tube,
one can use the Apt-Downey test to differentiate between
maternal and fetal blood.
The blood is placed in a test tube; sterile water is added to
hemolyze the RBCs, yielding free hemoglobin.
This solution then is mixed with 1% sodium hydroxide. If the
solution turns yellow-brown, the hemoglobin is maternal or
adult hemoglobin, which is less stable than fetal hemoglobin.

If the solution remains the same color, it is the more stable fetal
hemoglobin; therefore, the newborn is the source of the
bleeding.
If the sample is taken from stool that has been exposed to air
longer than 30 minutes, even fetal hemoglobin has the yellowbrown color change of adult hemoglobin. In this situation, the
quantification of hemoglobin (fetal hemoglobin level >50%
points to a source in the child rather than maternal) can be
performed with a spectrophotometric assay.
Differential Diagnoses

Anal Fistulas and Fissures

Diaper Rash

Emergent Management of Pediatric Patients with Fever

Gastrointestinal Foreign Bodies

Hemolytic Uremic Syndrome in Emergency Medicine

Inflammatory Bowel Disease

Intussusception

Pediatric Dehydration

Pediatric Foreign Body Ingestion

Pediatric Gastroenteritis in Emergency Medicine

http://repository.unand.ac.id/18018/1/HUBUNGAN%20CARA%20PENYEDIAAN
%20SUSU%20FORMULA%20DENGAN%20KEJADIAN%20DIARE%20PADA%20BAYI
%200-6%20BULAN%20DI%20WILAYAH%20KERJA%20PUSKESMAS%20BALAI
%20SELASA.pdf

http://www.pps.unud.ac.id/thesis/pdf_thesis/unud-1340-544024934-tesis
%20eveline.pdf
http://perpustakaan.pom.go.id/KoleksiLainnya/Buletin%20Info%20POM/0108.pdf

http://spiritia.or.id/dokumen/pedoman-ims2011.pdf
http://jurnal-tip.net/jurnal-resource/file/5-Vol6No1Mar2013-%20Minarni%20%20Dessya%20Nanda%20Ariani.pdf
http://saripediatri.idai.or.id/pdfile/10-1-10.pdf

KONJUNGTIVITIS PURULENTA NEONATORUM

Kompetensi : 4
Laporan Penyakit : 1005 ICD X : H.00-H.01
Definisi
Radang konjungtiva yang terjadi pada bayi yang baru lahir.
Gejala muncul beberapa jam sampai 3 hari pasca lahir.
Penyebab
Bayi baru lahir tertular infeksi gonore oleh ibunya ketika melewati jalan lahir.
Gejala Klinis
Kelopak mata bengkak dan konjungtiva hyperemia hebat
Sekret mata purulen yang kadang bercampur darah.
Hasil pemeriksaan sekret atau kerokan konjungtiva dengan pewarnaan Gram
memperlihatkan banyak sekali sel polimorfonuklear. Kuman N.gonorrhoeae
khas tampak sebagai kokus gram negatif yang berpasangan seperti biji kopi,
tersebar di luar dan di dalam sel.
Diagnosis
Sekret purulen dengan riwayat ibu gonore.
Penatalaksanaan
Pengobatan harus segera diberikan dengan intensif karena gonore ini dapat
menyebabkan perforasi kornea yang berakhir dengan kebutaan.

Bayi ini harus diisolasi untuk mencegah penularan.

Mata dibersihkan dahulu kemudian diberi salep mata penisilin setiap 15 menit
Secara sistemik diberikan penisilin prokain i.m. dosis tunggal 50.000
IU/kgBB/hari selama 5 hari.
Kedua orang tua sebagai sumber infeksi juga harus diperiksa dan diobati.
Bila pemeriksaan sekret telah negatif 3 hari berturut-turut, maka penderita
boleh dipulangkan dan pemberian salep mata diteruskan 3 kali sehari. Seminggu
kemudian bila pemeriksaan sekret masih negatif pengobatan dihentikan.

http://www.gizikia.depkes.go.id/wp-content/uploads/downloads/2011/09/BukuSaku-Pelayanan-Kesehatan-Anak-di-RS.pdf

Konjungtivitis
Mata lengket dan konjungtivitis ringan
Perlakukan sebagai pasien rawat jalan.
Tunjukkan kepada ibu cara mencuci mata dengan air atau ASI dan cara
memberi salep mata. Ibu harus mencuci tangan sebelum dan sesudahnya.
Katakan kepada ibu untuk mencuci mata bayi dan memakai salep mata 4 kali
sehari selama 5 hari.
Beri ibu satu tube salep mata tetrasiklin ATAU salep mata kloramfenikol.
Evaluasi setelah 48 jam pengobatan.
Konjungtivitis berat (bernanah banyak dan/atau kelopak mata bengkak) sering
disebabkan oleh infeksi gonokokus. Rawat bayi di rumah sakit karena terdapat
risiko kebutaan dan perlu evaluasi dua kali sehari.
Cucilah mata untuk membersihkan nanah
sebanyak mungkin.
Berikan dosis tunggal sefotaksim
100 mg/kgBB, IV atau IM
JUGA gunakan seperti telah diuraikan
diatas :
Salep mata tetrasiklin ATAU
kloramfenikol
Obati ibu dan pasangannya untuk
penyakit kelaminnya: amoksisilin,
spektinomisin atau siprofloksasin
(untuk gonorhoea) dan tetrasiklin
(untuk khlamidia) tergantung pada
pola resistensi.

Background
Neonatal conjunctivitis presents during the first month of life. It
may be aseptic or septic.
Aseptic neonatal conjunctivitis most often is a
chemical conjunctivitis that is induced by silver nitrate solution,
which is used for prophylaxis of infectiousconjunctivitis.
Chemical conjunctivitis is less common owing to the use of
erythromycin ointment in place of silver nitrate solution for the
prophylaxis of infectious conjunctivitis. (See Etiology and
Treatment.)
Bacterial and viral infections are major causes of septic
neonatal conjunctivitis, withChlamydia being the most common
infectious agent. Infants may acquire these infective agents as
they pass through the birth canal during the birth process. (The
effects of gonococcal conjunctivitis are seen in the images
below.) (See Etiology.)

Severe purulent discharge

and eyelid edema in a newborn with gonococcal conjunctivitis (confirmed

with Gram stain and culture).

cornea without ulcer in neonatal gonococcal conjunctivitis.

See the following for more information:

Acute Hemorrhagic Conjunctivitis

Allergic Conjunctivitis
Atopic Keratoconjunctivitis
Bacterial Conjunctivitis
Emergent Treatment of Acute Conjunctivitis
Epidemic Keratoconjunctivitis
Giant Papillary Conjunctivitis
Keratoconjunctivitis Sicca
Superior Limbic Keratoconjunctivitis

Cloudy

Viral Conjunctivitis

Anatomy and pathology

The conjunctiva (a thin translucent mucous membrane) can be
divided into palpebral, bulbar, and fornical, based on the
location. The conjunctiva contains nonkeratinizing, squamous
epithelium and a thin, richly vascularized substantia propria
(containing lymphatic vessels and cells, such as lymphocytes,
plasma cells, mast cells, and macrophages). The conjunctiva
also has accessory lacrimal glands and goblet cells.
The pathology of neonatal conjunctivitis is influenced by the
anatomy of the conjunctival tissues in the newborn. The
inflammation of the conjunctiva may cause blood vessel
dilation, chemosis, and excessive secretion. This reaction tends
to be more serious due to the following: lack of immunity,
absence of lymphoid tissue in the conjunctiva, and absence of
tears at birth.

Patient education
Educate parents or care providers to wash their hands
frequently to prevent transmission of neonatal conjunctivitis.
Educate pregnant women on the importance of treating
sexually transmitted infections such as herpes simplex,
gonorrhea, and chlamydia in order to decrease the incidence of
neonatal conjunctivitis.
For patient education information, see the Eye and Vision
Center, as well asPinkeye.

Etiology
The etiology of neonatal conjunctivitis can be chemical or
microbial. Although several noninfectious and infectious agents
can inflame the conjunctiva, the more common causes of
neonatal conjunctivitis are silver nitrate solution and chlamydial,
gonococcal, staphylococcal, and herpetic infections.

Silver nitrate solution

Crede's method of instilling a drop of 2% silver nitrate into a
newborn's eyes was a major advance in preventing neonatal
conjunctivitis.[1]
Silver nitrate is a surface-active chemical, facilitating
agglutinate gonococci and inactivating them. Ironically, silver
nitrate was later found to be toxic to the conjunctiva, potentially
causing a sterile neonatal conjunctivitis.

Chlamydial conjunctivitis
Chlamydia trachomatis is an obligate intracellular parasite and
has been identified as the most common infectious cause of
neonatal conjunctivitis.[2]
The reservoir of the organism is the maternal cervix or urethra.
Infants who are born to infected mothers are at high risk
(approximately 25-50%) for developing an infection.[3]

Neisserial conjunctivitis
Neisseria gonorrhoeae is a gram-negative diplococcus and is
potentially the most dangerous and virulent infectious cause of
neonatal conjunctivitis. Similar to chlamydia, the reservoir of N
gonorrhoeae is the mother of the infant and is acquired during
birth.
Gonococci can penetrate intact epithelial cells and divide
rapidly inside them.
Gonococcal conjunctivitis must be absolutely excluded in every
case of neonatal conjunctivitis to avoid serious consequences.

Other bacteria
The most commonly identified gram-positive organisms
include Staphylococcus aureus,Streptococcus
pneumoniae,Streptococcus viridans, and Staphylococcus

epidermidis. These bacteria make up 30-50% of all cases of

neonatal conjunctivitis.[4]
Gram-negative organisms, such as Escherichia coli, Klebsiella
pneumoniae, Serratia marcescens, and Proteus,
Enterobacter, and Pseudomonas species, also have been
implicated. There has been 1 case report of neonatal
conjunctivitis being caused by Eikenella corrodens.[5]
Low birth weight and low gestational age among infants in the
neonatal intensive care unit (NICU) who have clinical signs of
conjunctivitis should raise the suspicion of a gram-negative
cause.[6]

Herpes simplex
Herpes simplex virus (HSV) can cause
neonatal keratoconjunctivitis, but it is rare (< 1% )[4] and can be
associated with a generalized herpes simplex infection.
Most infants with such an infection acquire the disease during
the birth process. Caesarean delivery is considered when
active genital disease is recognized at term since the risk of
transmitting HSV to the neonate during vaginal delivery is 2560%.[7]

Epidemiology
Occurrence in the United States
The incidence of infectious neonatal conjunctivitis ranges from
1-2%, depending on the socioeconomic character of the area.
The epidemiology of neonatal conjunctivitis changed when
silver nitrate solution was introduced in the 1800s to prevent
gonococcal ophthalmia.
Chlamydia is the most common infectious agent that causes
ophthalmia neonatorum in the United States (2-40% of
neonatal conjunctivitis is caused byChlamydia).[3]

In contrast, the incidence of gonococcal ophthalmia

neonatorum has been reduced dramatically and causes less
than 1% of cases of neonatal conjunctivitis.[8]

International occurrence
As in the United States, the incidence of ophthalmia
neonatorum in many other countries decreased after silver
nitrate solution came into use.
In Europe, the incidence fell from 10% of births to less than 1%.
The rates of neonatal conjunctivitis vary in different parts of the
world. In one hospital in Pakistan, the incidence of neonatal
conjunctivitis was reported at 17%.[9]

Race-, sex-, and age-related demographics

No published information is available on race- or sex-related
differences in the incidence of neonatal conjunctivitis.

Prognosis
Neonatal conjunctivitis usually responds to appropriate
treatment, and the prognosis generally is good.
Antibiotics have significantly altered the prognosis of neonatal
conjunctivitis, especially with Neisseria gonorrhoeae infection.
Mortality associated with neonatal conjunctivitis is due to
systemic involvement of the infecting agent. No published
information is available on mortality.

Complications
If untreated, corneal ulceration may occur in N
gonorrhoeae infection and rapidly progress to corneal
perforation.

When unrecognized and not immediately

treated, Pseudomonas infection may lead to endophthalmitis
and subsequent death.
Pneumonia has been reported in 10-20% of infants with
chlamydial conjunctivitis.[10]
HSV keratoconjunctivitis can cause corneal scarring and
ulceration. Additionally, disseminated HSV infection often
includes central nervous system involvement.[7]
Proceed to Clinical Presentation
http://emedicine.medscape.com/article/1192190-overview#showall

History

Incubation period
Chemical conjunctivitis secondary to silver nitrate solution
application usually occurs in the first day of life, disappearing
spontaneously within 2-4 days.
Gonococcal conjunctivitis tends to occur 2-7 days after birth but
can present later.[4]
Chlamydial conjunctivitis usually has a later onset than
gonococcal conjunctivitis; the incubation period is 5-14 days.
The incubation period for other, nongonococcal, nonchlamydial
conjunctivitis is also 5-14 days.[4]
Herpetic conjunctivitis usually occurs within the first 2 weeks
after birth and has an incubation period of approximately 6-14
days.[4]

Clinical presentation of gonococcal conjunctivitis

Gonococcal conjunctivitis tends to be more severe than other

causes of ophthalmia neonatorum; there is a classic
presentation of bilateral purulent conjunctivitis.
Corneal involvement, including diffuse epithelial edema and
ulceration, may progress to perforation of the cornea and
endophthalmitis.
Patients also may have systemic manifestations (eg, rhinitis,
stomatitis, arthritis, meningitis, anorectal infection, septicemia).

Clinical presentation of chlamydial conjunctivitis

The presentation of chlamydial conjunctivitis may range from
mild hyperemia with scant mucoid discharge to eyelid swelling,
chemosis, and pseudomembrane formation.
Blindness, although rare and much slower to develop than in
gonococcal conjunctivitis, is not due to corneal involvement as
in gonococcal conjunctivitis; eyelid scarring and pannus (as in
trachoma) cause it.
A follicular reaction does not occur, because newborns have no
requisite lymphoid tissue present in the conjunctiva.
Like gonococcal conjunctivitis, chlamydial conjunctivitis also
may be associated with extraocular involvement, including
pneumonitis, otitis, and pharyngeal and rectal colonization.

Clinical presentation of neonatal conjunctivitis due to other

agents
Neonatal conjunctivitis due to other microbial agents is usually
milder.

Herpes simplex keratoconjunctivitis usually presents in infants

with generalized herpes simplex with corneal epithelial
involvement or vesicles on the skin (which surround the eye).
Serious systemic complications, such as encephalitis, may
occur in these neonates due to their poor immunologic
response.
Physical

Presentations for different organisms may vary. Typical findings

may include erythema and edema of the eyelids and palpebral
conjunctiva and/or purulent eye discharge during the external
eye exam. (Perform a Gram stain conjunctival smear in all
cases.) Eyelid edema and purulent discharge are seen in the
image below.

Severe purulent discharge

and eyelid edema in a newborn with gonococcal conjunctivitis (confirmed
with Gram stain and culture).

Chemical conjunctivitis
The clinical picture of chemical conjunctivitis is mild, transient
tearing and conjunctival injection.
If the 1% silver nitrate used for neonatal conjunctivitis is
provided in a large bottle, the solution can evaporate and
become concentrated over time. More concentrated silver
nitrate solution may result in more severe responses (eg, lid
edema, chemosis, exudate, membranes or pseudomembranes,
permanent damage to the conjunctiva or the cornea). This
problem is obviated by using sealed, single-use ampules.

Chemical conjunctivitis is becoming less common because of

the substitution of erythromycin ointment in place of silver
nitrate.

Chlamydial conjunctivitis
Patients typically present with unilateral or bilateral watery
discharge, which may become more copious and purulent later.
Although most cases are mild and self-limited, chlamydial
conjunctivitis occasionally may be severe. Pseudomembranes,
thickened palpebral conjunctiva, significant peripheral pannus,
and/or corneal opacification may be present.

Gonococcal conjunctivitis
This type of conjunctivitis is the most serious, usually occurring
24-48 hours following birth. Typically, patients develop a
hyperacute conjunctivitis, associated with marked lid edema,
chemosis, and purulent discharge.
A conjunctival membrane may be present.
Corneal ulcer may occur and rapidly progress to perforation if
treatment is delayed.

Other bacterial conjunctivitis

Various organisms (eg, gram-positive and gram-negative
bacteria) have been identified in neonatal conjunctivitis.
Classic clinical pictures are lid edema, conjunctival injection,
chemosis, and discharge, which are variable and often
indistinguishable from signs of other etiologies.
Although it rarely causes neonatal
conjunctivitis, Pseudomonas can lead to devastating
consequences, such as rapid progression to corneal ulceration
and perforation. (If left untreated, it even can lead to
endophthalmitis and subsequent death.)

Herpetic conjunctivitis
This type of neonatal conjunctivitis typically occurs within the
first 2 weeks after birth.
Ocular involvement may follow systemic herpes infection or
vesicular lesions on the skin or lid margins.
Patients may present with nonspecific lid edema, moderate
conjunctival injection, and nonpurulent and often
serosanguineous discharge, which may be unilateral or
bilateral.
Microdendrites or geographic ulcers, rather than typical
dendrites as seen in adults, are the most typical signs of
herpetic keratitis in newborns.
Conjunctival membrane may be present.
http://emedicine.medscape.com/article/1192190-clinical#b4

Approach Considerations
Specific treatment is available for the various causes of
neonatal conjunctivitis. Preliminary presumptive treatment
pending culture confirmation should be based on the clinical
picture and the findings on Gram, Giemsa, and Papanicolaou
stains.
Consider the risk of transmission of chlamydial, gonococcal,
herpetic, and streptococcal pathogens to the fetus during the
birth process. Obtain cervical cultures if indicated, and manage
appropriately.
To confirm the presence of a sexually transmitted disease in the
neonate, examine and treat the mother and her sexual
partner(s). If necessary, therapy can be modified when the
results of culture and sensitivity are known.

The treatment prior to laboratory results should include topical

erythromycin ointment and IV or IM third-generation
cephalosporin. Prompt treatment of gonococcal conjunctivitis is
important, since this organism can penetrate an intact corneal
epithelium and rapidly cause corneal ulceration. Because of the
rapid progression of gonococcal conjunctivitis, patients with
acute neonatal conjunctivitis should be treated for gonococcal
conjunctivitis until culture results are available; the treatment is
altered according to the laboratory results.
In cases of chlamydial conjunctivitis, systemic treatment is
necessary because of the significant risk for life-threatening
pneumonia.
Infants with a potentially sexually transmitted disease, such as
gonorrhea or chlamydia, should undergo evaluation for other
sexually transmitted diseases, such as syphilis and HIV,[13] as
should the mother and her sexual partner(s).
Newborns with conjunctivitis are at risk for secondary
infections, such as pneumonia, meningitis, and septicemia,
which can lead to sepsis and death and thus should be
admitted for full workup and treatment.
Bacterial conjunctivitis rarely fails to respond to treatment.
A consultation can be made with a pediatrician or pediatric
infectious specialist in neonatal conjunctivitis, and the patient
should be seen daily until response to treatment is confirmed.
Discharged patients should continue the treatment, according
to clinical presentations and available culture results. Treatment
may be modified later per culture results.
Avoid eye patching.
Treatment of neonatal chemical conjunctivitis is not necessary.
Lubrication with artificial tear preparations may ease mild
discomfort.

Neonatal Chlamydial Conjunctivitis

This infection is treated with oral erythromycin (50 mg/kg/d
divided qid) for 14 days.
Topical treatment alone is ineffective. Topical erythromycin
ointment may be beneficial as an adjunctive therapy.
Since the efficacy of systemic erythromycin therapy is
approximately 80%, a second course sometimes is required.
Systemic treatment is important in cases of chlamydial
conjunctivitis since topical therapy is ineffective in eradicating
the bacteria in the nasopharynx of the infant, which could cause
a life-threatening pneumonia if left untreated.

Treatment of Neonatal Herpetic Conjunctivitis

Neonates with a suspected herpetic simplex infection should be
treated with systemic acyclovir to reduce the chance of a
systemic infection.
An effective dose is 60 mg/kg/day IV divided tid.
The recommended minimal duration is 14 days, but a course as
long as 21 days may be required.
Infants with neonatal HSV keratitis should receive a topical
ophthalmic drug, most commonly 1% trifluridine drops or 3%
vidarabine ointment.
Topical antibiotics can also be considered to prevent secondary
bacterial infections in cases with significant epithelial defects.

Prophylaxis
According to the 2012 Red Book, topical 0.5% erythromycin
and 1% tetracycline are considered equally effective for
prophylaxis of ocular gonorrhea infection in newborn infants.
Each is available in single-dose tubes. Topical silver nitrate,

povidone-iodine, and erythromycin are all effective in the

prevention of nongonococcal nonchlamydial neonatal
conjunctivitis. There is no agent that is currently effective in
preventing the transmission of C trachomatis from mother to
baby.[14] This is a change from the 2009 Red Book which stated
that erythromycin or silver nitrate could prevent vertical
transmission.[8]
Povidone-iodine solution (2.5%) is effective in preventing
neonatal ophthalmia. Povidone-iodine is widely used outside of
the United States. It is approved by the US Food and Drug
Administration (FDA), but it is not commercially available in this
country.[14]
Silver nitrate is the best agent in areas where the incidence of
penicillinase-producing N gonorrhoeae (PPNG) is significant.[10]
The recommendations in the 2012 Redbook are for 2 drops of
1% silver nitrate or a 1 cm ribbon of antibiotic ointment (either
erythromycin or tetracycline) placed into the lower conjunctival
sac; both acceptable regimens for the prophylaxis of neonatal
conjunctivitis.[4] Erythromycin ointment is considered the best
regimen for prophylaxis against neonatal conjunctivitis because
of its efficacy against gonococcal, and nongonococcal
nonchlamydial pathogens, and due to its low incidence of
causing a chemical conjunctivitis.[10]
Proceed to Medication
http://emedicine.medscape.com/article/1192190-treatment#showall

Pengasuhan Anak
Keluhan Anak
Imunisasi
ASI
Review
Seputar Kesehatan Anak
ASI
23 AUGUST 2013

Air Susu Ibu dan Pengendalian Infeksi

Efektivitas ASI dalam mengendalikan infeksi dapat dibuktikan
dengan berkurangnya kejadian beberapa penyakit spesifik pada
bayi yang mendapat ASI dibanding bayi yang mendapat susu
formula. Penelitian oleh Badan Kesehatan Dunia (WHO)
membuktikan bahwa pemberian ASI sampai usia 2 tahun dapat
menurunkan angka kematian anak akibat penyakit diare dan infeksi
saluran napas akut.
Sistim kekebalan tubuh pada bayi saat lahir masih sangat terbatas
dan akan berkembang sesuai dengan meningkatnya paparan
mikroorganisme di dalam saluran cernanya. Berbagai faktor
perlindungan ditemukan di dalam ASI, termasuk antibodi IgA
sekretori (sIgA). Saat menyusui, IgA sekretori akan berpengaruh
terhadap paparan mikroorganisme pada saluran cerna bayi dan
membatasi masuknya bakteri ke dalam aliran darah melalui mukosa
(dinding) saluran cerna. Peran perlindungan ASI terdapat pada
tingkat mukosa. Pada saat ibu mendapat kekebalan pada saluran

cernanya, kekebalan di dalam ASI juga terangsang

pembentukkannya.
Keadaan ini yang menerangkan mengapa menyusui dapat
melindungi bayi baru lahir terhadap berbagai infeksi secara efektif.
Berbagai penelitian juga melaporkan bahwa ASI dapat mengurangi
kejadian dan beratnya penyakit diare, infeksi saluran napas, radang
telinga tengah (otitis media), radang selaput otak (meningitis),
infeksi saluran kemih, dan infeksi saluran cerna yang disertai
kematian jaringan (enterokolitis nekrotikan).
Perlindungan ASI terhadap infeksi bakteri
Imunoglobulin A yang terdapat di dalam ASI memiliki aktivitas
antitoksin terhadap enterotoksin (racun) yang dihasilkan oleh
bakteri E. Coli dan V. Cholerae, dan antibodi terhadap beberapa
tipe E. Coli. Hal tersebut dapat dibuktikan dengan ditemukannya
titer antibodi E. Coli yang tinggi pada tinja bayi yang mendapat ASI.
Suatu penelitian prospektif di Bangladesh menunjukkan kadar
antibodi kolera yang bervariasi di dalam kolostrum dan ASI. Adanya
hubungan antara kolonisasi, kejadian penyakit, dan antibodi dalam
ASI menunjukkan bahwa antibodi terhadap kolera tidak melindungi
anak dari kolonisasi V. cholerae, tetapi melindungi terhadap
terjadinya penyakit. Respons yang cepat dari kolostrum dan ASI
serta kemampuan melawan kuman melalui pertahanan tubuh nonspesifik juga ditemukan pada infeksi salmonella.
Strain (jenis) bakteri E. coli yang ditemukan pada tinja bayi
menyusui berbeda dengan bayi yang mendapat susu formula. Jenis
E. coli pada bayi menyusui lebih sensitif terhadap efek bakterisidal
(mematikan bakteri) serum manusia, meskipun kurang sensitif
terhadap reaksi spontan seperti yang terjadi pada tempat lain, yaitu

kemaluan atau saluran kemih. Hal ini merupakan salah satu cara
ASI melindungi tubuh terhadap infeksi.
Penelitian di Swedia menemukan bakteri E. coli jenis 0111 pada 6
anak yang mengalami diare; 2 diantaranya hanya mendapat ASI
dan memperlihatkan gejala klinis yang ringan. ASI ibu kedua anak
tersebut ternyata tidak mengandung antibodi terhadap E.coli 0111.
Hal ini menunjukkan bahwa masih ada faktor lain di dalam ASI yang
berperan melindungi bayi dari penyakit berat.
Perlindungan ASI terhadap infeksi virus
Air susu ibu mengandung antibodi terhadap berbagai jenis virus,
antara lain poliovorus, coxsakievirus, echovirus, influenza virus,
reovirus, respiratory syncytial virus (RSV), rotavirus dan rhinovirus.
Telah terbukti bahwa ASI menghambat pertumbuhan virus-virus
tersebut.
Kolostrum mempunyai aktivitas menetralisasi terhadap RSV. Virus
ini mengancam jiwa dan sering sebagai penyebab bayi dirawat di
beberapa negara berkembang. Bayi yang dirawat karena menderita
infeksi RSV jauh lebih sedikit pada kelompok yang mendapat ASI
dibanding bayi yang mendapat susu formula (7% vs 28%).
Penelitian prospektif tentang respon kekebalan terhadap RSV
memperlihatkan antibodi IgM dan IgG jarang ditemukan dalam
kolostrum atau ASI, tetapi IgA spesifik RSV ditemukan pada 4075% spesimen (contoh) ASI. Dua orang ibu yang terinfeksi RSV
memiliki IgG, IgM dan IgA di dalam serum dan sekresi
hidung/tenggorokannya, tetapi hanya IgA yang ditemukan dalam
ASInya. Keadaan ini membuktikan bahwa antibodi IgA spesifik
terhadap mikroorganisme patogen saluran napas terdapat dalam
ASI. Oleh karena RSV hanya bereplikasi (bertambah banyak) di
saluran napas, maka antibodi spesifik RSV yang terdapat di dalam

kelenjar payudara dapat berasal dari jaringan limfoid saluran napas

(bronkus).
Enterokolitis nekrotikan merupakan ancaman serius pada bayi
khusunya prematur. Penelitian prospekti terhadap bayi berat lahir
rendah di India dengan menggunakan ASI donor dari manusia,
didapatkan kejadian infeksi lebih sedikit secara bermakna dan tidak
terdapat infeksi berat pada kelompok yang diberi ASI manusia,
sedangkan bayi pada kelompok yang tidak mendapat ASI (kontrol)
banyak mengalami diare, pneumonia, sepsis dan meningitis.
Peran IgA sekretori di dalam ASI juga dapat dilihat pada kejadian
radang telinga tengah (otitis media purulenta). Kejadian otitis media
purulenta lebih sedikit pada kelompok bayi yang mendapat ASI
eksklusif dibanding bayi yang hanya mendapat susu formula.
Perlindungan ASI terhadap protozoa
Di dalam ASI terkandung bile salt stimulated lipase (BSSL) yang
diduga berperan sebagai mematikan protozoa. Walaupun demikian
mekanisme kerja secara pasti belum diketahui. Nonlipase (faktor
non-imunoglobulin) juga telah diidentifikasikan di dalam ASI dan
dapat menginaktivasi Giardia Lamblia.
Transmisi penyakit infeksi melalui air susu ibu
Air susu ibu memberikan perlindungan kepada bayi melalui
beberapa mekanisme, antara lain memperbaiki pertumbuhan
mikroorganisme non-patogen, mengurangi pertumbuhan
mikroorganisme patogen saluran cerna, merangsang
perkembangan barier mukosa saluran cerna dan napas, faktor
spesifik (IgA sekretori, sel kekebalan), mengurangi reaksi inflamasi

(peradangan), dan sebagai imunomodulator (perangsang

kekebalan).
Beberapa virus (HIV1, human T-limfofotrophic virus I/HTLV-I, CMV)
ditransmisi melalui ASI sehingga dapat menyebabkan infeksi pada
bayi dan anak. Meskipun jarang, bakteri Streptococcus grup B
dilaporkan dapat menginfeksi bayi melalui ASI. Walaupun demikian,
menyusui jarang menjadi kontra-indikasi saat ibu mengalami
infeksi. Segala keputusan tentang kemungkinan infeksi pada bayi
dan anak harus mempertimbangkan keuntungan ASI dan kerugian
risiko penularan penyakit.
Saat terjadinya infeksi pada ibu dan bayi dapat menentukan
mekanisme penularan. Infeksi saat persalinan dapat terjadi akibat
paparan darah/cairan tubuh atau kontak dengan mikrorganisme
patogen. Infeksi yang terjadi setelah persalinan melalui orang yang
merawatnya (misalnya orangtua, saudara, pengunjung, petugas
kesehatan) atau lingkungan (alat kedokteran, muntahan). Paparan
pada bayi umumnya terjadi sebelum penyakit pada ibu terdiagnosis
(misalnya campak, infeksi virus Coxakie) atau sebelum ibu tampak
sakit (cacar air, hepatitis). Oleh karena itu, menghentikan ASI tidak
akan mencegah infeksi pada bayi, bahkan akan mengurangi efek
ASI untuk membatasi penyakit pada bayi.
Beberapa penyakit ibu dengan gejala demam (misalnya payudara
membangkak, atelektasis (paru kempis), peradangan pembuluh
darah, dan infeksi saluran kemih) bukan merupakan alasan untuk
memisahkan bayi dari ibunya. Pertimbangan penting lain yang
berhubungan dengan ASI dan infeksi adalah kadar obat dalam ASI.
Kadar obat dalam ASI yang tertelan oleh bayi umumnya tidak
bermakna dibanding kadar obat yang diminum bayi secara
langsung.

Infeksi Bakteri
Infeksi bakteri sering terjadi pada neonatus dan bayi, dengan
frekuensi 1-5 episod per 1000 kelahiran. Saat terjadinya infeksi
dibagi menjadi early onset (sebelum usia 7 hari, terutama kurang
dari 24 jam), late onset (usia 7-30 hari), dan very late-onset (usia
lebih dari 30 hari). Mikroorganisme yang sering ditemukan pada
early onset adalah Streptococci group B dan E. Coli, disamping
beberapa mikroorganisme patogen lainnya, seperti Streptococci,
Enterococcus spp. Listeria spp, Haemophilus influenzae,
Streptococcus pneumoniae, Chlamydia spp, dan mikroorganisme
genital ibu. Mikroorganisme tersebut juga dapat menyebabkan
infeksi late- atau very late-onset. Transmisi mikroorganisme melalui
ASI sangat jarang terjadi dibanding penularan saat persalinan atau
melalui kontak langsung dengan lingkungan setelah melahirkan. .
Infeksi Clamydia merupakan infeksi yang ditularkan melalui
hubungan seksual. Kolonisasi yang terjadi saat bayi melalui jalan
lahir dapat menyebabkan konjungtivitis (infeksi pada mata) dan
pneumonitis (infeksi pada paru). Di dalam kolostrum dan ASI
terkandung IgA sekretori spesifik terhadap Clamydia. Sampai
sejauh ini, tidak ada bukti penularan infeksi Clamydia melalui ASI.
Escheria coli dapat menyebabkan bakteremia dan infeksi sistemik
pada neonatus. Meskipun E.coli sering ditemukan pada lingkungan
ibu dan bayi, belum pernah dilaporkan bahwa ASI sebagai sumber
infeksi E. Coli. Infeksi Haemophilus influenzae dapat terjadi melalui
kontak langsung atau droplet pernapasan. Begitu pula, belum ada
bukti transmisinya melalui ASI, bahkan dilaporkan ASI dapat
membatasi kolonisasi H. Influenzae di tenggorokan bayi. Neisseria
gonorrhoeae ditransmisi melalui jalan lahir dan jarang melalui
kontak setelah lahir. Risiko penularan melalui ASI tidak pernah
dilaporkan, sehingga ASI dapat terus diberikan.

Infeksi Staphylococcus sering terjadi lambat pada periode

neonatus. Empat puluh sampai sembilan puluh persen bayi yang
dirawat inap mengalami kolonisasi Staphylococcus aureus pada
hari ke-5 dengan sumber infeksinya adalah kontak dengan ibu,
petugas kesehatan, atau donor ASI yang terkontaminasi. Bakteri ini
sering pula sebagai penyebab mastitis (infeksi kelenjar payudara)
pada ibu.
Infeksi coagulase-negative staphylococcus menyebabkan infeksi
late-onset pada bayi. Prematuritas, berat lahir rendah/sangat
rendah, pengobatan invasif (infus, pembedahan, cuci darah),
pemakaian antibiotik dan perawatan yang lama merupakan faktor
risiko terjadinya infeksi ini. Tidak ada perbedaan kejadian infeksi
pada bayi yang mendapat susu formula dan ASI. Oleh karena itu,
ASI tetap diberikan dan diharapkan dapat memberikan manfaat dari
kandungan lainnya.
Streptococcus group B (GBS) ditransmisi terutama saat dalam
kandungan dan saat persalinan. American Academy of Pediatrics
merekomendasi pemberian antibiotik profilaksis intrapartum pada
bayi dengan risiko tinggi. Kolonisasi pada bayi terjadi saat pasca
persalinan dan menyebabkan penyakit GBS late-onset. Penelitian
menemukan GBS di dalam hidung, tenggorokan bayi, dan payudara
ibu pada saat yang sama. Penularan lebih disebabkan melalui
kontak. Ibu yang terinfeksi dan mendapat pengobatan, perlu
dipisahkan dari bayinya selama 24 jam dengan tetap memberikan
ASI perah untuk bayinya.
Begitu pula tidak ada bukti tentang penularan Clostridium botulinum
atau toksinnya melalui ASI. Pertumbuhan Clostridium botulinum di
dalam saluran cerna dapat dihambat dengan suasana asam yang
ditimbulkan akibat mengkonsumsi ASI.

Tuberkulosis kongenital dan mastitis tuberkulosis (TB) jarang

terjadi. Penularan TB setelah lahir dapat terjadi melalui droplet dari
ibu atau anggota keluarga lainnnya yang menderita TB aktif. Bayi
menyusui atau yang mendapat susu formula memiliki risiko yang
sama untuk tertular melalui saluran napas. Apabila ibu sudah
mendapat pengobatan yang adekuat dan sudah dinyatakan tidak
menular, maka ibu dapat kontak langsung dengan bayinya.
Pemantauan terhadap ibu dan bayi harus terus dilakukan sampai
ibu selesai mendapat pengobatan. Transmisi TB dari ASI belum
pernah dilaporkan pada kasus tanpa mastitis TB. ASI dapat
diberikan secara aman pada bayi, karena obat anti TB pun dapat
diberikan kepada bayi. Satu-satunya kontraindikasi pemberian ASI
adalah jika ibu menderita mastitis TB. Pengobatan profilaksis
isoniazid yang diberkan kepada bayi dapat mencegah terjadinya
infeksi TB. Apabila baik ibu maupun bayi mendapat terapi TB, maka
ibu dapat kontak langsung dengan bayinya.
Infeksi virus
Infeksi virus pada bayi dapat terjadi saat di dalam kandungan dan
saat persalinan. Transmisi infeksi melalui ASI telah dilaporkan pada
CMV, HIV1, dan HTLV-1. Cytomegalo virus merupakan infeksi
kongenital tersering di Amerika. Sekitar 1% bayi mengekskresi
CMV dari urinnya saat setelah lahir ( kurang dari usia 3 minggu).
Kurang lebih 5% bayi yang terinfeksi kongenital akan mengalami
gejala saat lahir dan 15% akan memperlihatkan gejala di kemudian
hari (seperti kehilangan pendengaran dan gangguan belajar).
Infeksi pada bayi dapat melalui kontak langsung atau cairan tubuh
saat melahirkan. Infeksi saat setelah lahir dapat terjadi melalui ASI
atau kontak dengan cairan tubuh dari individu yang terinfeksi.
Infeksi melalui ASI jarang menyebabkan penyakit pada bayi cukup

bulan. Antibodi pada ibu yang terinfeksi CMV dapat melalui

plasenta dan melindungi bayi cukup bulan dari infeksi CMV.
Infeksi primer CMV yang terjadi pada ibu saat melahirkan atau
selama laktasi jarang meningkatkan risiko penyakit pada bayi. Virus
ini dapat diidentifikasi dalam ASI ibu dengan CMV positif dengan
jumlah yang bervariasi. Penelitian melaporkan kejadian infeksi CMV
berkurang pada bayi prematur yang mengkonsumsi ASI dengan
CMV positif yang disimpan pada suhu -20OC atau dipasteurisasi.
Ibu dengan CMV positf dapat memberikan ASI kepada bayinya
yang cukup bulan dengan aman. Sebaliknya, bayi prematur dengan
CMV negatif harus dihindarkan dari ASI dengan CMV positif.
Virus hepatitis (A, B dan C), CMV, dan virus Epstein Barr
merupakan virus penyebab hepatitis terbanyak. Transmisi hepatitis
A (HAV) dalam ASI hanya dilaporkan pada satu kasus dan
paparan biasanya telah terjadi sebelum diagnosis pada ibu
ditegakkan. Oleh karena itu, tidak ada alasan untuk menghentikan
menyusui. Bayi dari ibu yang terinfeksi HAV harus mendapat
imunoglobulin dan imunisasi HAV.
Infeksi hepatitis B (HBV) kronis berkembang pada 90% bayi yang
terinfeksi saat dalam kandungan dan saat kelahiran. Meskipun
transmisi HBV dapat melalui ASI, (+40% ASI dari ibu HBsAg positif
juga menunjukkan HBsAg positif) tetapi tidak ada perbedaan
kejadian infeksi pada bayi yang mendapat susu formula maupun
ASI. Penelitian menggunakan mikroskop elektron memperlihatkan
hanya partikel HBsAg yang terkandung di dalam ASI ibu dengan
HBsAg positif (tidak ada partikel Dane); hal ini menandakan bahwa
ASI tidak menularkan penyakit hepatitis B.
Pemberian Imunoglobulin Hepatitis B (HBIg) dan vaksin HBV
segera setelah bayi lahir dari ibu penderita hepatitis B dapat

mencegah penularan pada lebih dari 95% kasus, tanpa

memandang bagaimana pemberian makanannya dan ASI dapat
terus diberikan.
Infeksi virus hepatitis C (HCV) dapat menjadi infeksi kronik pada
70%-85% kasus, tanpa memperhatikan kapan infeksi terjadi.
Menyusui bukan merupakan kontraindikasi bagi ibu dengan infeksi
HCV, walaupun diduga bahwa puting lecet atau berdarah dapat
meningkatkan risiko penularan.
Virus herpes simpleks tipe 1 dan 2 (HSV-1,HSV-2) dapat
menyebabkan infeksi saat dalam kandungan dan persalinan.
Penelitian melaporkan bayi yang mendapat ASI terinfeksi oleh HSV
dari ibu HSV positif akibat luka pada payudara. Menyusui atau ASI
perah tanpa ada lesi pada payudara ibu dan tanda lain infeksi HSV
dapat diberikan dengan menggunakan perlindungan yang aman,
seperti menutupi daerah lesi/luka, menggunakan baju khusus dan
rajin mencuci tangan.
Ibu dengan HIV-1 positif yang menyusui bayinya dapat
meningkatkan risiko penularan melalui ASI sebesar 4%-22%.
Walaupun demikian, menghentikan pemberian ASI pada negara
miskin justru akan meningkatkan angka kesakitan dan kematian
akibat asupan nutrisi yang kurang atau akibat infeksi lain. Beberapa
upaya dapat dilakukan untuk membatasi penularan HIV1 dari ibu ke
bayi, antara lain memenuhi kriteria AFASS menyusui eksklusif,
penghentian dini (6 bulan), edukasi untuk mengurangi terjadinya
mastitis atau lesi pada puting, terapi antivirus untuk ibu dan bayi,
mengurangi jumlah virus di ASI (dengan sinar ultraviolet,
pembekuan, dan thawing), menstimulasi sistim kekebalan tubuh
bayi dengan imunisasi. Semua upaya tersebut harus diuji kemampu
laksanaannya (feasibility), diterima oleh budaya setempat, manfaat
gizi, dan efikasi dengan efek terbaik. Virus HIV2 menyebabkan

penyakit dengan gejala klinis mirip dengan HIV1. Oleh karena

belum cukup data mengenai transmisi virus tersebut, maka
pedoman menyusui atau memberi ASI sama dengan infeksi HIV1.
Respiratory syncytial virus (RSV) sering menyebabkan penyakit
saluran napas akut pada bayi dan anak. Sampai sejauh ini tidak
ada bukti penularan RSV melalui ASI, sehingga menyusui pada ibu
yang terinfeksi RSV dapat dilanjutkan. ASI perah dapat digunakan
bila bayi mengalami kesulitan mengisap akibat adanya distres
pernapasan.
Infeksi virus varicella-zoster (VZV) menyebabkan varicella (cacar
air) pada infeksi primer dan Herpes Zoster pada infeksi reaktivasi.
Bayi yang menyusu pada ibu terinfeksi VZV mempunyai risiko
tertular yang sama dengan bayi yang mendapat susu formula. Bayi
harus dipisahkan dan dirawat oleh orang lain selama ibu masih
dalam periode menular. ASI perah dapat diberikan kepada bayi jika
tidak ada lesi kulit pada payudara atau setelah imunoglobulin
varicella-zoster telah diberikan kepada bayinya.
Virus rubella baik pada infeksi alamiah maupun pasca imunisasi
pada ibu, dapat ditularkan ke bayi melalui ASI tetapi tidak
menimbulkan efek yang membahayakan.
Virus dengue (serotipe 1-4) menyebabkan demam berdarah
dengue. Tidak ada bukti ilmiah adanya penularan virus dengue
melalui ASI. Ibu dengan penyakit dengue dapat tetap menyusui.
Human T Lymphoma virus (HTLV) yang dilaporkan dapat
menyebabkan leukemia dilaporkan ditransmisi melalui ASI.
Kesimpulan
Air susu ibu bukan merupakan tempat penularan dari sebagian
besar infeksi virus pada ibu, oleh karena itu meneruskan menyusui

merupakan tindakan terbaik bagi ibu dan bayi. Virus CMV, HIV, dan
HTLV-1 merupakan virus yang sering dilaporkan sebagai penyebab
infeksi pada bayi akibat penularan dari ASI. Infeksi bakteri pada ibu
jarang mengakibatkan penularan infeksi melalui ASI kepada bayi.
Pada sebagian kasus ibu menyusui dengan tersangka infeksi,
menghentikan menyusui hanya akan mengurangi masukan nutrisi
dan manfaat kekebalan dari ASI. Keputusan untuk menyusui harus
mempertimbangkan manfaat tak ternilai ASI dibanding risiko
tertularnya penyakit.

Sumber : Buku Bedah ASI IDAI

Penulis : Alan R. Tumbelaka dan Mulya R. Karyanti

http://idai.or.id/public-articles/klinik/asi/air-susu-ibu-dan-pengendalianinfeksi.html
http://idai.or.id/wp-content/uploads/2014/01/konsensus-tata-laksana-alergi-sususapi.pdf

Gastrointestinal (GI) perdarahan pada bayi dan anak-anak adalah masalah yang
cukup umum, akuntansi untuk 10% -20% dari arahan untuk Pencernaan anak.
Namun, biasanya terbatas dalam volume, sehingga waktu untuk diagnosis dan
pengobatan.
Pendekatan awal untuk semua pasien dengan perdarahan GI signifikan adalah
untuk memastikan stabilitas pasien, untuk mendirikan pengiriman oksigen yang
cukup, untuk menempatkan akses intravena, untuk memulai resusitasi cairan
dan darah, dan untuk memperbaiki koagulopati yang mendasari.
Polip remaja, salah satu penyebab dari perdarahan GI, terlihat pada gambar di
bawah.
Pergi ke Upper Gastrointestinal Perdarahan untuk informasi lengkap mengenai
topik ini.

Lihat intraoperatif dari polip remaja berdarah.

Etiologi
Etiologi-usia tertentu untuk perdarahan GI dibahas di bawah untuk kelompok
berikut:
Neonatus
Anak-anak berusia 1 bulan sampai 1 tahun
Anak-anak berusia 1-2 tahun
Anak-anak yang lebih dari 2 tahun
Neonatus
Anal fissures adalah penyebab paling umum dari GI perdarahan pada bayi.
Mereka menghasilkan darah merah terang yang garis-garis tinja atau
menyebabkan bercak darah di popok. Penyebabnya adalah air mata di garis
mukokutan, paling sering terletak dorsal di garis tengah.
Kebanyakan penyebab umum dari perdarahan GI jelas neonatal termasuk
enteritis bakteri, alergi protein susu, intususepsi, darah ibu menelan, dan
hiperplasia lymphonodular. Susu atau enterocolitis kedelai, atau kolitis alergi,
adalah penyebab muntah dengan pewarnaan darah setelah pengenalan produk
makanan ini ke dalam diet.
Erosi dari esofagus, lambung, dan mukosa duodenum juga sering menjadi
penyebab untuk benar neonatal perdarahan GI. Agaknya, kerusakan ini
disebabkan oleh peningkatan dramatis dalam sekresi asam lambung dan
kelemahan sfingter lambung pada bayi.
Stres ibu pada trimester ketiga telah diusulkan untuk meningkatkan sekresi
gastrin ibu dan meningkatkan infantil pembentukan ulkus peptikum.
Ulkus peptikum neonatal belum dikaitkan dengan modus pemberian makan atau
hiperalimentasi.
Beberapa obat yang terlibat dalam GI neonatal berdarah. Ini termasuk NSAID,
heparin, dan tolazolin, yang digunakan untuk sirkulasi janin persisten.
Indometasin, digunakan untuk paten ductus arteriosus pada neonatus, dapat
menyebabkan perdarahan GI melalui vasokonstriksi usus dan disfungsi
trombosit.
Obat ibu dapat melewati plasenta dan menyebabkan masalah pada janin yang
sedang berkembang dan dalam neonatus pengiriman. Aspirin, sefalotin, dan
fenobarbital yang penyebab kelainan koagulasi terkenal pada neonatus.

Stres gastritis terjadi pada sampai dengan 20% dari pasien dirawat di unit
perawatan intensif neonatal (ICU). Prematuritas, kesusahan neonatal, dan
ventilasi mekanik semua yang berhubungan dengan stres gastritis.
Ulkus stres pada bayi baru lahir yang berhubungan dengan deksametason, yang
dapat digunakan untuk pematangan paru janin.
Penyebab jarang dari GI perdarahan pada neonatus yang meliputi volvulus,
koagulopati, malformasi arteri, necrotizing enterocolitis (NEC, terutama pada
bayi prematur), Hirschsprung enterocolitis, dan Meckel divertikulitis.
Penyakit hemoragik pada bayi baru lahir adalah gangguan perdarahan diri
terbatas akibat kekurangan vitamin K tergantung faktor koagulasi. tingkat
pembekuan faktor II, VII, IX, dan X penurunan cepat setelah lahir, mencapai titik
nadir mereka di 48-72 jam kehidupan. Dalam 0,25% -0.5% dari neonatus,
perdarahan berat dapat terjadi.

Age Group

Upper Gastrointestinal
Bleeding

Lower Gastrointestinal
Bleeding

Hemorrhagic disease of the

newborn
Anal fissure
Swallowed maternal blood
Necrotizing enterocolitis
Neonates
Stress gastritis
Malrotation with volvulus
Coagulopathy

Anal fissure

Infants aged 1 month

to 1 year

Esophagitis

Intussusception

Gastritis

Gangrenous bowel

Milk protein allergy

Peptic ulcer disease

Polyps

Gastritis

Meckel diverticulum

Infants aged 1-2 years

Polyps

Esophageal varices
Children older than 2
years

Gastric varices

Inflammatory bowel
disease

Infectious diarrhea

Vascular lesions

1. Ilyas, S. Ilmu penyakit mata. Edisi 3. Jakarta: fakultas kedokteran universitas

Indonesia. 2009. Pp 122-123
2. Kemenkes RI. Pedoman nasional penanganan infeksi menular seksual. 2011. Pp 58-59
3. Emily, A. Neonatal conjungtivitis. Emedicine. 2014. Diakses dari
http://www.emedicine.com/conj.neonatal/1192190-overview.htm
4. Kemenkes RI. Buku panduan: tatalaksana bayi baru lahir di rumah sakit. 2010

http://www.kalbemed.com/Portals/6/29_215Teknik-Teknik%20Operasi
%20Labiopalatoskizis.pdf

History of the Procedure

Chinese physicians were the first to describe the technique of
repairing cleft lip. The early techniques involved simply excising
the cleft margins and suturing the segments together. The
evolution of surgical techniques during the mid-17th century
resulted in the use of local flaps for cleft lip repair. These early
descriptions of local flaps for the treatment of cleft lip form the
foundation of surgical principles used today.
Tennison introduced the triangular flap technique of unilateral
cleft lip repair, which preserved the Cupid's bow in 1952. The
geometry of the triangular flap was described by Randall, who
popularized this method of lip repair. Millard described the
technique of rotating the medial segment and advancing the
lateral flap; thus, preserving the Cupid's bow with the philtrum.
[1]
This technique has resulted in improved outcomes in cleft lip
repair. See the image below.

Cleft lip.

Problem
Cleft lip is among the most common of congenital deformities.
The condition is due to insufficient mesenchymal migration
during primary palate formation in the fourth through seventh
week of intrauterine life. This results in disfigurement and
distortion of the upper lip and nose. Cleft lip may be associated
with syndromes that include anomalies involving multiple
organs. Patients may have impaired facial growth, dental
anomalies, and speech disorders (if a cleft palate is present),
and they may experience late psychosocial difficulties.
A study by Datana et al indicated that the prevalence of upper
cervical vertebrae anomalies is more than three times greater
in persons with cleft lip/palate than in those without the
condition. The prevalence was 20.3% in the cleft group overall,
compared with 6.4% in the control group. In patients with
unilateral cleft lip and palate, the prevalence was 22.2%, while
in those with bilateral cleft lip and palate, the prevalence was

19.1%, and in patients with cleft palate only, the prevalence of

upper cervical vertebrae anomalies was 16.6%. The study
involved 128 patients with cleft lip/palate and 125 controls.[2]

Epidemiology
Frequency
The incidence of cleft lip in the white population is
approximately 1 in 1000 live births. The incidence in the Asian
population is twice as great, whereas that in the black
population is less than half as great. Male children are affected
more often than female children. A study by Michalski et al
found that among isolated, noncardiac birth defects, cleft lip
had one of the highest male-to-female ratios. The study
involved 25,952 infants from the National Birth Defects
Prevention Study (1997-2009), with male preponderance
among isolated, noncardiac birth defects being greatest for
craniosynostosis (2.12), cleft lip with cleft palate (2.01), and
cleft lip alone (1.78).[3]
Isolated unilateral clefts occur twice as frequently on the left
side as on the right and are 9 times more common than
bilateral clefts. Combined cleft lip and palate is the most
common presentation (50%), followed by isolated cleft palate
(30%), and isolated cleft lip or cleft lip and alveolus (20%).
Fewer than 10% of clefts are bilateral.
For parents with cleft lip and palate or for a child with cleft lip
and palate, the risk of having a subsequent affected child is
4%. The risk increases to 9% with 2 previously affected
children. In general, the risk to subsequent siblings increases
with the severity of the cleft.

Etiology
Little evidence exists that links isolated clefts to exposure to
any single teratogenic agent. The exception is the
anticonvulsant drug, phenytoin. The use of phenytoin during
pregnancy is associated with a 10-fold increase in the
incidence of cleft lip. The incidence of cleft lip in infants born to
mothers who smoke during pregnancy is twice that of those
born to nonsmoking mothers. Syndromic clefts are those
associated with malformations in other developmental regions,
with reported frequencies ranging from 5-14%.
The most commonly recognized syndrome associated with
clefts of the lip and palate is Van der Woude syndrome. This
syndrome is an autosomal dominant disorder characterized by
clefts of the lip and/or palate and blind sinuses, or pits, of the
lower lip. Clefts of the secondary palate alone are far more
likely to be associated with syndromes than are clefts involving
the lip alone or the lip and palate. Most cases of lip clefts are
nonsyndromic and believed to be either multifactorial in origin
or the result of changes at a major single-gene locus.

Pathophysiology
Development of the upper lip is characterized by fusion of the
maxillary prominences with the lateral and medial nasal
prominences. This process starts during the fourth week of
gestation and is completed by the seventh week. Failure of
mesenchymal migration to unite one or both of the maxillary
prominences with the medial nasal prominences results in a
unilateral or bilateral cleft of the lip, respectively.

Classification

No universally accepted classification scheme exists for clefts

of the lip and palate. Veau categorized clefts into 4 classes, as
follows:
1. Clefts of the soft plate alone
2. Clefts of the soft and hard palate
3. Complete unilateral clefts of the lip and palate
4. Complete bilateral clefts of the lip and palate
This classification scheme does not provide a means of
classifying clefts of the lip alone and ignores incomplete clefts.
The Kernahan strippedY classification allows the description
of the lip, the alveolus, and the palate. In this classification, the
incisive foramen defines the boundary between clefts of the
primary palate (lip and premaxilla) and those of the secondary
palate.

Presentation
Clefts of the lip may manifest as microform, incomplete, or
complete clefts. Microform clefts are characterized by a vertical
groove and vermilion notching with varying degrees of lip
shortening. Unilateral incomplete lips manifest varying degrees
of lip disruption associated with an intact nasal sill or Simonart
band (a band of fibrous tissue from the edge of the red lip to the
nostril floor). Complete clefts of the lip are characterized by
disruption of the lip, alveolus, and nasal sill.
Bilateral clefts are almost always associated with cleft palate,
with 86% of patients with such clefts of the lip presenting with
palatal clefts. Unilateral clefts of the lip are associated with
palatal clefts in 68% of cases. Nasal regurgitation during
suckling may indicate an associated cleft of the palate. All

infants with clefts of the lip should have a complete head and
neck examination, including careful examination of the palate
as far as the tip of the uvula. The presence of a bifid uvula, a
translucent central zone in the velum, and a detectable notch of
the posterior border of the hard palate indicate submucosal
palatal cleft.
All patients with clefts are best referred to multidisciplinary cleft
lip and palate centers. Persistent otitis media and middle ear
effusions are associated with palatal clefts and warrant regular
follow-up care. Depending on the preference of the surgical
centers, the otolaryngologist may elect to perform myringotomy
before or after definitive cleft lip and palate repair.
Most cases of lip clefts are nonsyndromic. Parents should be
reassured and advised sensitively. At the initial visit, review
feeding techniques carefully. For the infant, breastfeeding and
the capacity to suck are difficult. However, breastfeeding may
be possible with isolated clefts of the lip and the alveolus. For
infants with palatal clefts, a variety of special bottles and
nipples are available. Crosscut soft nipples made for premature
infants facilitate feeding of infants with cleft palate. At the
conclusion of the initial consultation, the parents and the infant
should be comfortable with the feeding method.

Indications
Clefts of the lip are usually repaired in early infancy. Reassure
and advise the parents that operative intervention is best
carried out at age 2-3 months. The rule of 10 serves as a safe
guideline, ie, body weight should be approximately 10 lb, the
hemoglobin concentration 10 g/dL, and age greater than 10
weeks.

Relevant Anatomy
The typical unilateral complete cleft lip deformity results from
both a deficiency and a displacement of the soft tissues, the
underlying bony structures, and cartilaginous structures. An
imbalance of the normal muscular forces acting upon the
maxilla results in an outward rotation of the premaxillarybearing medial segment and posterolateral displacement of the
smaller lateral segment.
The inferior edge of the anterior nasal septum is displaced out
of the vomerine groove into the noncleft nostril, and the anterior
septum leans laterally over the cleft. The overlying columella
invariably is short on the cleft side and distorted by the
displaced caudal septum. In the nasal tip, the alar cartilage is
characteristically deformed, and the medial crus is displaced
posteriorly. The dome is separated from that of the noncleft
side, and the lateral crus is flattened and stretched across the
cleft. The axis of the nostril on the cleft side is characteristically
oriented in the horizontal plane. This position is in contrast to
the normal vertical axis of the nostril on the opposite side.
The muscular fibers of the orbicularis oris do not decussate
transversely as in the normal lip; rather, they course obliquely
upward, paralleling the cleft margin toward the alar base on the
lateral side of the cleft and toward the base of the columella
medially. The philtrum on the cleft side is short, and the
presumptive Cupid's bow peak is displaced superiorly. The
vermilion is deficient on the cleft side of the medial element.
Complete bilateral clefts of the lip result from failure of the
premaxillary segment to fuse with the lateral maxillary
segments. Subsequent forward growth of the premaxilla,
attached only to the vomer above, leads to its projection

beyond the lateral segments. Within the isolated prolabium, the

skin is foreshortened vertically, the white roll is
underdeveloped, and the vermilion is deficient. The prolabium
lacks muscle fibers, and the philtral ridges, the central philtral
dimple, and Cupid's bow are absent. The bilateral cleft nasal
deformity is characterized by flaring of the alar bases and wide
separation of the domal segments of the alar cartilages. The
columella is markedly shortened, causing the nasal tip to be
depressed.

Contraindications
Coexisting medical conditions that would result in
cardiopulmonary complications, bleeding disorders, infection,
and/or malnutrition are all contraindications to surgery.
Proceed to Workup
Sejarah Prosedur
Dokter Cina adalah yang pertama untuk menggambarkan teknik memperbaiki bibir sumbing.
Teknik-teknik awal terlibat hanya excising margin sumbing dan menjahit segmen bersamasama. Evolusi teknik bedah selama abad pertengahan ke-17 mengakibatkan penggunaan flaps
lokal untuk perbaikan bibir sumbing. Ini deskripsi awal flaps lokal untuk pengobatan bibir
sumbing membentuk dasar dari prinsip-prinsip bedah yang digunakan saat ini.

Tennison memperkenalkan teknik lipatan segitiga unilateral cleft lip perbaikan, yang
diawetkan busur Cupid di tahun 1952. geometri flap segitiga digambarkan oleh Randall, yang
mempopulerkan metode ini perbaikan bibir. Millard menggambarkan teknik berputar segmen
medial dan memajukan flap lateral yang; dengan demikian, menjaga busur Cupid dengan
philtrum itu. [1] Teknik ini telah mengakibatkan hasil yang lebih baik dalam perbaikan bibir
sumbing. Lihat gambar di bawah ini.

Bibir sumbing.
Bibir sumbing.

Masalah
Bibir sumbing adalah salah satu yang paling umum dari cacat bawaan. Kondisi ini
disebabkan migrasi mesenchymal cukup selama pembentukan langit-langit utama dalam
keempat melalui minggu ketujuh kehidupan intrauterin. Hal ini menyebabkan cacat dan
distorsi dari bibir dan hidung bagian atas. Bibir sumbing dapat berhubungan dengan sindrom
yang mencakup anomali yang melibatkan beberapa organ. Pasien mungkin memiliki
gangguan pertumbuhan wajah, anomali gigi, dan gangguan bicara (jika sumbing hadir), dan
mereka mungkin mengalami kesulitan akhir psikososial.

Sebuah studi oleh Datana et al menunjukkan bahwa prevalensi anomali tulang leher bagian
atas lebih dari tiga kali lebih besar pada orang dengan celah bibir / langit-langit dibandingkan
pada mereka tanpa kondisi. Prevalensi adalah 20,3% pada kelompok sumbing secara
keseluruhan, dibandingkan dengan 6,4% pada kelompok kontrol. Pada pasien dengan bibir
sumbing dan langit-langit unilateral, prevalensi adalah 22,2%, sedangkan pada mereka
dengan bibir sumbing bilateral dan langit-langit, prevalensi adalah 19,1%, dan pada pasien
dengan sumbing langit-langit saja, prevalensi anomali tulang leher bagian atas adalah 16,6%.
Penelitian ini melibatkan 128 pasien dengan sumbing bibir / langit-langit dan 125 kontrol. [2]

Epidemiologi
Frekuensi
Insiden bibir sumbing pada populasi putih adalah sekitar 1 dari 1000 kelahiran hidup. Insiden
pada populasi Asia dua kali lebih besar, sedangkan pada populasi kulit hitam kurang dari
setengah besar. Anak laki-laki lebih sering terkena daripada anak-anak perempuan. Sebuah
studi oleh Michalski et al menemukan bahwa di antara terisolasi, cacat lahir noncardiac, bibir
sumbing memiliki salah satu rasio laki-perempuan yang tertinggi. Penelitian ini melibatkan
25.952 bayi dari Cacat Lahir Nasional Pencegahan Studi (1997-2009), dengan dominan lakilaki di antara terisolasi, cacat lahir noncardiac menjadi terbesar untuk craniosynostosis (2.12),
bibir sumbing dengan celah langit-langit (2,01), dan bibir sumbing saja (1,78 [3]).

Celah unilateral terisolasi terjadi dua kali sering di sisi kiri seperti pada kanan dan 9 kali lebih
umum daripada celah bilateral. Gabungan bibir sumbing dan langit-langit adalah presentasi
yang paling umum (50%), diikuti oleh sumbing terisolasi (30%), dan terisolasi bibir sumbing
atau celah bibir dan alveolus (20%). Kurang dari 10% dari celah bilateral.

Bagi orang tua dengan bibir sumbing dan langit-langit atau untuk anak dengan bibir sumbing
dan langit-langit, risiko memiliki anak yang terkena berikutnya adalah 4%. Risiko meningkat

menjadi 9% dengan 2 anak-anak yang terkena sebelumnya. Secara umum, risiko untuk
saudara selanjutnya meningkat dengan tingkat keparahan sumbing tersebut.

Etiologi
Sedikit bukti bahwa link terisolasi celah paparan agen teratogenik tunggal. Pengecualian
adalah obat antikonvulsan, fenitoin. Penggunaan fenitoin selama kehamilan dikaitkan dengan
peningkatan 10 kali lipat dalam kejadian bibir sumbing. Insiden bibir sumbing pada bayi
yang lahir dari ibu yang merokok selama kehamilan adalah dua kali lipat dari mereka yang
lahir dari ibu yang merokok. Celah sindrom adalah mereka yang berhubungan dengan
malformasi di daerah perkembangan lainnya, dengan frekuensi dilaporkan berkisar 5-14%.

Sindrom yang paling umum dikenal terkait dengan celah bibir dan langit-langit adalah Van
der sindrom Woude. Sindrom ini adalah gangguan dominan autosomal yang ditandai dengan
celah bibir dan / atau langit-langit dan sinus buta, atau lubang, bibir bawah. Celah langitlangit sekunder saja jauh lebih mungkin untuk dihubungkan dengan sindrom daripada celah
yang melibatkan bibir saja atau bibir dan langit-langit. Sebagian besar kasus celah bibir yang
nonsyndromic dan diyakini baik multifaktorial di asal atau hasil dari perubahan pada lokus
gen tunggal utama.

Patofisiologi
Pengembangan bibir atas ditandai dengan fusi tonjolan maksila dengan tonjolan hidung
lateral dan medial. Proses ini dimulai pada minggu keempat kehamilan dan selesai pada
minggu ketujuh. Kegagalan migrasi mesenchymal untuk menyatukan satu atau kedua
tonjolan maksila dengan medial prominences hidung hasil dalam sumbing unilateral atau
bilateral dari bibir masing-masing.

Klasifikasi
Tidak ada skema klasifikasi yang diterima secara universal ada untuk celah bibir dan langitlangit. Veau dikategorikan celah menjadi 4 kelas, sebagai berikut:

Celah plat lembut saja

Celah dari langit-langit lunak dan keras
Celah sepihak lengkap dari bibir dan langit-langit
Celah bilateral lengkap dari bibir dan langit-langit

Skema klasifikasi ini tidak menyediakan sarana mengklasifikasikan celah bibir saja dan
mengabaikan celah tidak lengkap. The Kernahan klasifikasi dilucuti-Y memungkinkan
deskripsi bibir, alveolus, dan langit-langit. Dalam klasifikasi ini, foramen tajam
mendefinisikan batas antara celah-celah langit-langit utama (bibir dan premaxilla) dan orangorang dari langit-langit sekunder.

Presentasi
Celah bibir dapat bermanifestasi sebagai microform, tidak lengkap, atau celah lengkap. Celah
microform ditandai dengan alur vertikal dan vermilion bentukan dengan berbagai tingkat
bibir shortening. Derajat yang berbeda-beda bibir lengkap sepihak nyata dari gangguan bibir
terkait dengan hidung utuh sill atau Simonart band (band dari jaringan fibrosa dari tepi bibir
merah untuk lantai lubang hidung). Celah lengkap bibir yang ditandai dengan gangguan bibir,
alveolus, dan sill hidung.

Celah bilateral hampir selalu dikaitkan dengan sumbing langit-langit, dengan 86% dari pasien
dengan celah seperti bibir menyajikan dengan celah palatum. Celah sepihak bibir
berhubungan dengan celah palatum di 68% kasus. Regurgitasi nasal selama menyusui
mungkin menunjukkan celah terkait langit-langit mulut. Semua bayi dengan celah bibir harus
memiliki kepala yang lengkap dan pemeriksaan leher, termasuk pemeriksaan yang cermat
dari langit-langit sejauh ujung anak lidah. Kehadiran uvula bifida, zona sentral tembus di
velum, dan takik terdeteksi batas posterior palatum keras menunjukkan submukosa sumbing
palatum.

Semua pasien dengan celah yang terbaik disebut multidisiplin bibir dan langit-langit sumbing
pusat. Persistent otitis media dan efusi telinga tengah berhubungan dengan celah palatum dan
menjamin tindak lanjut perawatan rutin. Tergantung pada preferensi pusat bedah,
otolaryngologist dapat memilih untuk melakukan miringotomi sebelum atau setelah bibir
sumbing definitif dan perbaikan langit-langit.

Sebagian besar kasus celah bibir yang nonsyndromic. Orang tua harus diyakinkan dan
menyarankan sensitif. Pada kunjungan awal, meninjau teknik menyusui dengan hati-hati.
Untuk bayi, menyusui dan kapasitas untuk menghisap sulit. Namun, menyusui dapat dibuat
dengan celah terisolasi dari bibir dan alveolus. Untuk bayi dengan celah palatum, berbagai
botol khusus dan puting tersedia. Puting potong lembut dibuat untuk bayi prematur
memfasilitasi makan bayi dengan bibir sumbing. Pada kesimpulan dari konsultasi awal, orang
tua dan bayi harus nyaman dengan metode makan.

Indikasi
Celah bibir biasanya diperbaiki pada awal masa bayi. Yakinkan dan menyarankan orang tua
bahwa intervensi operasi paling dilakukan pada usia 2-3 bulan. Aturan 10 berfungsi sebagai
pedoman yang aman, yaitu, berat badan harus sekitar 10, konsentrasi hemoglobin 10 g / dL,
dan usia lebih dari 10 minggu.

Anatomi relevan
Khas sepihak lengkap hasil sumbing bibir cacat dari kedua kekurangan dan perpindahan
jaringan lunak, struktur yang mendasari tulang, dan struktur tulang rawan.
Ketidakseimbangan kekuatan otot yang normal yang bekerja pada hasil rahang dalam rotasi
luar dari segmen medial premaxillary-bantalan dan perpindahan posterolateral dari segmen
lateral yang lebih kecil.

Tepi inferior septum hidung anterior dipindahkan keluar dari alur vomerine ke lubang hidung
noncleft, dan septum anterior bersandar lateral lebih sumbing tersebut. The atasnya
Columella selalu pendek di sisi sumbing dan terdistorsi oleh septum ekor pengungsi. Di
ujung hidung, tulang rawan alar yang bersifat cacat, dan crus medial dipindahkan posterior.
Kubah dipisahkan dari yang dari sisi noncleft, dan crus lateral diratakan dan membentang di
celah tersebut. Sumbu lubang hidung di sisi sumbing khas berorientasi pada bidang
horisontal. Posisi ini berbeda dengan sumbu vertikal normal lubang hidung di sisi
berlawanan.

Serat otot orbicularis oris tidak decussate melintang seperti pada bibir normal; bukan, mereka
tentu saja miring ke atas, paralel margin sumbing menuju dasar alar di sisi lateral sumbing
dan menuju dasar Columella medial. The philtrum di sisi sumbing pendek, dan puncak busur
dugaan Cupid dipindahkan superior. Vermilion yang kekurangan di sisi celah dari elemen
medial.

Celah bilateral lengkap dari hasil bibir dari kegagalan segmen premaxillary menyatu dengan
segmen rahang atas lateral. Pertumbuhan ke depan berikutnya dari premaxilla, melekat hanya
pada vomer atas, mengarah ke proyeksi luar segmen lateral. Dalam prolabium terisolasi, kulit
foreshortened vertikal, roll putih terbelakang, dan vermilion yang kekurangan. Prolabium
kekurangan serat otot, dan punggung philtral, lesung philtral pusat, dan busur Cupid absen.
Deformitas hidung sumbing bilateral ditandai dengan pembakaran basis alar dan pemisahan
macam segmen domal dari kartilago alar. Columella yang nyata dipersingkat, sehingga
menyebabkan ujung hidung tertekan.

Kontraindikasi
Hidup bersama kondisi medis yang akan mengakibatkan komplikasi cardiopulmonary,
perdarahan gangguan, infeksi, dan / atau kekurangan gizi semua kontraindikasi untuk operasi.

Lanjutkan ke hasil pemeriksaan

http://old.pediatrik.com/pkb/20060220-g2wryu-pkb.pdf
http://repository.usu.ac.id/bitstream/123456789/6185/1/07004512.pdf
http://saripediatri.idai.or.id/pdfile/13-1-1.pdf
http://saripediatri.idai.or.id/pdfile/5-4-6.pdf
http://download.portalgaruda.org/article.php?article=154422&val=5502&title=TERAPI
%20%20MEDIKAMENTOSA%20BAYI%20DENGAN%20BERAT%20BADAN
%20LAHIR%20RENDAH%20(BBLR)