1

CHAPTER I
INTRODUCTION
1.1 Background
Central to human digestive health are both the production of bile by
hepatocytes and cholangiocytes in the liver and the excretion of bile through the
biliary tree. By volume, conjugated bilirubin is a relatively small component of bile,
the yellowish-green liquid that also contains cholesterol, phospholipids, organic
anions, metabolized drugs, xenobiotics, and bile acids. In most cases, the elevation of
serum-conjugated bilirubin is a biochemical manifestation of cholestasis, which is the
pathologic reduction in bile formation or flow.1
Complex mechanisms exist for the transport of bile components from serum
into hepatocytes across the basolateral cell surface, for the trafficking of bile
components through the hepatocyte, and finally for movement of these bile
components across the apical cell surface into the bile canaliculus, which is the
smallest branch of the biliary tree. From the bile canaliculus, bile then flows into the
extrahepatic biliary tree, including the common bile duct, before entering the
duodenum at the ampulla of Vater. Isolated gene defects in proteins responsible for
trafficking bile components can lead to cholestatic diseases.1
Cholestasis is condition which secretion and excretion of bile from the liver to
duodenum is disrupted. So, substance which is excreted with bile is restrained in
liver. The parameter of cholestasis is serum conjugated bilirubin >1 mg/dl if total
bilirubin < 5mg/dl, or conjugated bilirubin >20% of total bilirubin when total
bilirubin >5mg/dl.2
Cholestasis can be due to infectious, genetic, metabolic, or undefined
abnormalities giving rise to mechanical obstruction of bile flow or to functional

impairment of hepatic excretory function and bile secretion. Mechanical lesions

include stricture or obstruction of the common bile duct; biliary atresia is the
prototypic obstructive abnormality. Functional impairment of bile secretion can result
from congenital defects or damage to liver cells or to the biliary secretory apparatus.3
In the early neonatal period, jaundice caused by physiologic unconjugated
hyperbilirubinemia or human milk jaundice is impossible to distinguish from jaundice
caused by cholestasis based on physical appearance alone. Indeed, physiologic
unconjugated hyperbilirubinemia and cholestasis can coexist in early infancy. A
critical time point for establishing the diagnosis of cholestasis is at the 2-week wellchild visit. Persistent jaundice at 2 weeks after birth should alert the care provider to
the possibility of cholestasis. The diagnosis is made by obtaining a conjugated
bilirubin level or direct bilirubin fraction, whichever is available locally. If the
infant appears well otherwise, a second option is to see the infant back in 1 week. If
the jaundice persists at 3 weeks after birth, laboratory evaluation is mandatory.1
The serum aspartate aminotransferase (AST) and alanine aminotransferase
(ALT) levels typically are elevated to a variable degree, but are not specific for the
cause of cholestasis. The gamma glutamyltransferase (GGT) level usually is elevated
in cholestasis. Normal or low GGT levels in the setting of cholestasis have been
associated with bile acid synthesis defects, some cases of hypopituitarism, and
progressive familial intrahepatic cholestasis types 1 and 2 (PFIC1, PFIC2).1
Abnormalities in hepatic synthetic function, such as a prolonged prothrombin
time, elevated ammonia level, low serum albumin concentration, or hypoglycemia,
suggest advanced hepatic injury and should prompt immediate referral to a pediatric
tertiary care facility. A urinalysis and urine culture will assess for urinary tract
infection, and the presence of reducing substances in the urine suggests
galactosemia.1

Cholestatic jaundice affects approximately 1 in every 2,500 infants (1,2), and is

thus infrequently seen by most providers of medical care to infants. However,
distinguishing jaundice caused by cholestasis from noncholestatic conditions is
critical because cholestatic jaundice is much more likely to have a serious etiology
that needs prompt diagnosis and therapy. The most common causes of cholestatic
jaundice in the first months of life are biliary atresia and neonatal hepatitis, which
account for most cases. Neonatal hepatitis has referred to a histologic appearance of
widespread giant cell transformation. Although giant cell transformation is
recognized to be non-specific and may be associated with infectious, metabolic, and
syndromic disorders, this term is used to be consistent with the older literature
reviewed for this guideline. Alpha-1 antitrypsin deficiency causes another 5% to 15%
of cases. The remaining cases are caused by a variety of other disorders, including
extra-hepatic obstruction from common duct gallstone or choledochal cyst; metabolic
disorders such as tyrosinemia, galactosemia, and hypothyroidism; inborn errors of
bile acid metabolism; Alagille syndrome; infection; and other rare disorders.4
Infants with cholestatic jaundice caused by bacterial sepsis, galactosemia,
hypopituitarism, or gallstone often appear acutely ill. These disorders require early
diagnosis and urgent treatment. However, many infants with cholestatic jaundice
appear otherwise healthy and grow normally. The benign appearance of such an
infant may lull the parents or physician into believing that the jaundice is physiologic
or caused by breast-feeding, when in fact it may be caused by biliary atresia. Biliary
atresia occurs in 1 in 10,000 to 19,000 infants. Substantial observational evidence
suggests that earlier diagnosis and surgical repair lead to better outcomes for this
disorder. The Kasai portoenterostomy appears to have the greatest likelihood of reestablishment of bile flow and the longest term survival of the infants native liver
when performed before the age of 45 to 60 days. Early diagnosis of many of the other

conditions that cause cholestasis may also lead to better outcomes because better
support of the infant may avoid complications of liver disease.4
Despite these data showing that early diagnosis is potentially life saving,
referral for evaluation of cholestatic jaundice frequently occurs after 45 to 60 days of
age (12). In recognition of this, and noting that no evidence-based guideline for its
evaluation currently exists, the Cholestasis Guideline Committee was formed by the
North American Society for Pediatric Gastroenterology, Hepatology and Nutrition
(NASPGHAN) to develop a clinical practice guideline for the diagnostic evaluation
of cholestasis in infants.4

1.2 Objective
This paper is completed in order to fulfill one of the requirements in the
Senior Clinical Assistance program in Department of Child Health of Haji Adam
Malik General Hospital, University of North Sumatera. In addition, this paper passes
the knowledge of cholestasis and its management

CHAPTER II
THEORY
2.1 Definition
Cholestasis is defined as a decrease in bile flow due to impaired secretion by
hepatocytes or to obstruction of bile flow through intra-or extrahepatic bile ducts.
Therefore, the clinical definition of cholestasis is any condition in which substances
normally excreted into bile are retained. The serum concentrations of conjugated
bilirubin and bile salts are the most commonly measured.5
Conjugated hyperbilirubinemia is defined biochemically as a conjugated
bilirubin level of 2 mg/dL and >20% of the total bilirubin.1

2.2 Epidemiology
Sex
No clear difference in the incidence of cholestasis between males and females
is observed. Incidence is equal in most genetic diseases leading to cholestasis.
However, several conditions have a female dominance, including biliary atresia,
drug-induced cholestasis, and of course, cholestasis of pregnancy.5

Age
Cholestasis is observed in people of every age group. However, newborns and
infants are more susceptible and more likely to develop cholestasis as a consequence
of immaturity of the liver.5
Young gestational age, low birth body weight, more sepsis episodes, and long
duration of parenteral nutrition are risk factors associated with Parenteral nutritionassociated cholestasis.5

2.3 Etiology1
Congenital infection
Cytomegalovirus
Toxoplasmosis
Rubella
Herpes simplex virus
Syphilis
HIV
Acquired infection
Urinary tract infection
Sepsis
Metabolic
Alpha-1 antitrypsin deficiency
Cystic fibrosis
Galactosemia

Tyrosinemia
Defects in bile acid synthesis
Inborn errors of carbohydrate, fat, protein metabolism
Obstructive
Biliary atresia
Choledochal cyst
Inspissated bile syndrome
Spontaneous perforation of bile duct
Cholestatic syndromes
Alagille syndrome
Progressive familial intrahepatic cholestasis
Endocrinopathy
Hypothyroidism
Hypopituitarism
Drug or toxin induced
Parenteral nutrition
Drugs
Systemic disorder
Shock
Congenital heart disease/heart failure
2.4. Symptoms and Signs
The typical findings in an infant who has cholestasis are protracted jaundice,
scleral icterus, acholic stools, dark yellow urine, and hepatomegaly. Some infants
may have coagulopathy secondary to vitamin K malabsorption and deficiency and
present with bleeding or bruising. Coagulopathy may also be caused by liver failure,

indicating either severe metabolic derangement of the liver (as in respiratory chain
deficiency disorders) or cirrhosis and end-stage liver disease (as in neonatal
hemochromatosis). Splenomegaly can be observed in infants who have cirrhosis and
portal hypertension, storage diseases, and hemolytic disorders. Neurologic
abnormalities including irritability, lethargy, poor feeding, hypotonia, or seizures can
indicate sepsis, intracranial hemorrhage, metabolic (including Zellweger syndrome)
and

mitochondrial

disorders,

or

severe

liver

dysfunction

resulting

in

hyperammonemia and encephalopathy. Low birth weight, thrombocytopenia,

petechiae and purpura, and chorioretinitis are often associated with congenital
infection. Facial dysmorphism may suggest a chromosomal abnormality or Alagille
syndrome. A palpable mass in the right upper quadrant may indicate a choledochal
cyst. A cardiac murmur increases the likelihood of Alagille syndrome or BA.
Although 20% of BA patients will have other extrahepatic congenital malformations
(including cardiac anomalies, situs inversus, intestinal malrotation, midline liver, and
polysplenia or asplenia), the majority of patients who have BA are well appearing
during the first month after birth, and there is no single historical or physical
examination finding that uniquely suggests BA

2.5. Diagnose

2.5.1 History
- Pregnancy and labor history (TORCH infection)
- Birth weight and gestational age
- History of administration vitamin K
- History of similar complaints in family
- History of current complaints : onset of jaundice, urine and fecess color, history of
therapy, parenteral nutrition, bleeding, history of feeding, diarrhea or emesis
- black urine
- acholic feces
- growth disorders 2
2.5.2. Physical examination
- jaundice
- acholic feces
- bleeding signs (vitamin K deficiency)
- hepatomegaly or hepatosplenomegaly
- abdominal mass, ascites
- growth failure
- other signs about specific disease or syndrome : dysmorphic signs (Trisomy,
Alagille syndrome); murmur (Alagille syndrome, extrahepatic billiary atresia
(EHBA)); baby is sick, vital signs abnormal (sepsis, HLH, congenital infection);
micropenis (panhipopituitarism); cataract (rubella, galactosemia); situs inversus
(EHBA); retinas problem (TORCH infection, Alagille syndrome); abdominal mass
(choledocus duct cyst); hemangioma cutaneus (hepar hemangioma); white hair
(Hemophagocytic lymphohistiocytosis/HLH).2

10

2.5.3. Diagnostic test

1. Routine hematology profile for main screening
2. Liver biochemical test : serum bilirubin fraction, aspartat aminotransferase
(AST), alanin aminotransferase (ALT), Alkaline phospatase (ALP), and
Gamma-glutamil transpeptidase (GGT)
3. Synthesis of liver function test : PT, aPTT, albumin, cholesterol profile,
glucose profile
4. Bacteria culture : urine and/or blood, if considered severe infection
5. Urinalysis, include USG liver two phase (fasting and post prandial), liver
biopsy
6. FT4 and TSH screening, to rule out/support presumption hypothyroidism
7. Radiology : cholangiography (gold standard for biliary atresia)2

Cholestasis

ALT/AST

ALP/GGT

Bilirubin

Intrahepatic

+++

++

Extrahepatic

++++

+++

Recommendations
1. A detailed history and physical examination are essential

11

2. Ultrasound is the first-line non-invasive imaging procedure in order to differentiate

intra- from extrahepatic cholestasis
3. Magnetic resonance cholangiopancreatography (MRCP) is the next step to be
considered in patients with unexplained cholestasis
4. Endoscopic ultrasound (EUS) is an alternative to MRCP for evaluation of distal
biliary tract obstruction
5. Diagnostic endoscopic retrograde cholangiopancreatography (ERCP) should be
reserved for highly selected cases (II-2/A1). If the need for a therapeutic maneuver is
not anticipated, MRCP or EUS should be preferred to ERCP because of the morbidity
and mortality related to ERCP.7
2.6. Management
1. General Medical Management
Most infants with cholestasis are underweight and will need nutritional support. The
goal is to provide adequate calories to compensate for steatorrhea and to prevent/ treat
malnutrition. The calorie requirement is approximately 125% of the recommended
dietary allowance (RDA) based on ideal body weight. In breastfed infants,
breastfeeding should be encouraged and medium-chain triglyceride (MCT) oil should
be administered in a dose of 1-2 mL/kg/day in 2-4 divided doses in expressed breast
milk. In older infants, a milk-cereal-mix fortified with MCT is preferred. Adding
puffed rice powder and MCT to milk can make feeds energy-dense. Essential fatty
acids should constitute 2- 3% of the energy provided. Vegetable protein at 2-3
g/kg/day is recommended.8
Specific treatment
In infants with pruritus due to severe cholestasis, the group recommended, in the
following order: Ursodeoxycholic acid (UDCA) (20 mg/kg/d), rifampicin (5-10
mg/kg/d), and phenobarbitone (510 mg/kg/d). Symptom chart should be made for

12

pruritus. Appropriate antibiotics depending on the site of infection and culture

sensitivity reports need to be administered in patients with bacterial sepsis.8

Kasai portoenterostomy
For biliary atresia, which is a condition of extrahepatic biliary duct having
obstruction. This condition need Kasai PE. Kasais procedure if done early can give
good survival for 20 years, which is 60,5%. But, the flow of bile will be hard to be
returned if the operation done after 8 weeks old.2
Liver transplantation
Liver Transplantation, the standard therapy for decompensated cirrhosis due to any
cause. Any baby, who has had Kasais PE and the bilirubin remains >6 mg/dL, three
months after surgery, should be referred to a transplant center. Babies with BA who
present with decompensated cirrhosis (low albumin, prolonged INR, ascites) are not
likely to improve with a Kasai PE and should be referred for liver transplantation.
Living related liver transplantation (the vast majority of liver transplants in India are
living related), performed at experienced centers, is associated with favorable
outcomes, with 5- and 10-year survival rates of 98% and 90%, respectively.8

13

CHAPTER III
CASE REPORT
3.1 Case
FA, a 8 months boy, with 5.2 kg of BW and 62 cm of BH, is a patient of
infection unit in Pediatric Department in Central Public Hospital Haji Adam Malik
Medan on October 31st 2015 at 19.30. His chief complaint was yellow all over body.
History of disease:
FA, a boy, 8 months old, came to Haji Adam Malik Hospital on October 31st 2015
with yellow all over body as the chief complaint. The patient have been experienced
since 1 week ago and got worst two days back. Discontinuous high fever (+) since 6
days ago with the temperature of 39C and reduced by taking anti pyretic drugs. The
patient has acholic stools since four days ago. The convulsion history (-), Diarrhea(-),
Cough(-), Sneezing(-), Dysphagia(-), Defecation (+) acholic stools, Urination (+)
Normal
History of previous illness:
The patient was already treated under Gastroanterohepatology at 5 months old.
Patient was done laparotomy due to infection ec hernia incarcerata. Then when the
patient was 6.5 months laparotomy was done in left side.
History of medication:
Sanmol, nystatin drops
History of family:

14

No family history of DM and other diseases

History of parents medication:
Unclear
History of pregnancy:
The gestation age was 36 weeks. No history of complication, neonate and maternal
problem.
History of birth:
Birth assisted by midwife spontaneously. The baby was born pervaginal and she cried
immediately. Bluish was not found. Body weight 3900 gram, body length 50 cm, and
head circumference was not measured.
History of feeding:
Breast feeding from born till now, additional food since 2 months old.
History of immunization:
Completed until 8 months of age
History of growth and development:
According to age
Physical Examination:

General status:
Body weight: 5.2 kg, Body length: 62 cm,
Z scores in Height for age boys: Z < -3
Z scores in Weight for age boys: Z < -3
Z scores in weight for height boys : -3 < Z< -2

Present status:
Level of consciousness: GCS 15 (E4 V5 M6)
Body temperature: 37.4C
BP: 160/100 mmHg

15

HR: 136 bpm, RR: 28 bpm

BW: 5.2 kg
BH: 62 cm
anemic (-), icteric sclera (+), dyspnea (-), cyanosis (-), edema (-).
Localized status:
Head
: Eyes: Light reflex +/+, icteric sclera+/+, isochoric
pupil,inferior conjunctiva palpebral pale +/+
Ears

: Within normal range

Nose

: Within normal range

Mouth : Within normal range

Neck
Thorax

: Lymph node enlargement (-)

: Symmetrical fusiform, retraction (-), icteric (+)
HR: 136 bpm, regular, murmur (-)
RR: 28 bpm, regular, rhonchi (-/-)
Abdomen
: Distension (+), liver: palpable 2cm below acrus costa,
Lien: schuffner III-1V, post operation wound (+)
Extremities : Icteric (+) Pulse 136 bpm regular, p/v adequate, warm
acral,CRT < 3.

Differential diagnosis

:-

Working diagnosis

: Cholestasis Jaundice ec dd stenosis bilier

dd atresia bilier

Laboratory finding

Complete blood analysis (September 31st , 2015)

Test
Hemoglobin
Erythrocyte
Leucocyte

Result
8.10
3.07
24.80

Unit
g%
106/mm3
103/mm3

Referral
12.0-14.4
4.40-4.48
4.5-13.5

16

Thrombocyte
Hematocrite
Eosinophil
Basophil
Neutrophil
Lymphocyte
Monocyte
Neutrophil absolute
Lymphocyte absolute
Monocyte absolute
Eosinophyl absolute
Basophyl absolute
MCV
MCH
MCHC
RDW
Morphology:

265
25.80
5.50
0.800
36.50
48.80
8.40
4.40
5.90
1.01
0.67
0.10
80.80
26.40
32.70
23.00

103/mm3
%
%
%
%
%
%
103/L
103/L
103/L
103/L
103/L
fL
Pg
g%
%

150-450
37-41
1-6
0-1
37-80
20-40
2-8
2.4-7.3
1.7-5.1
0.2-0.6
0.10-0.30
0-0.1
81-95
25-29
29-31
11.6-14.8

Erythrocyte: normokrom normositer, anisopoikilositosis

Leukocyte: normal in shape, leukocytosis
Trombocyte: normal

Clinical Chemistry
Test

Result

Unit

Referral

117.00

mg/dL

< 200

Natrium

137

mEq/L

135-155

Kalium
Chloride
Liver Function Test

4.4
105

mEq/L
mEq/L

3.6-5.5
96-106

Bilirubin Total
Bilirubin Direk

9.43
30.0

mg/dL
mg/dL

<1
0 - 0.2

Carbohydrate Metabolism
Blood Glucose
Electrolite

17

Fosfatase Alkali (ALP)

442

U/L

<462

AST/SGOT

185

U/L

<38

ALT/SGPT

167

U/L

<41

FOLLOW UP
November,1st 2nd 2015
S
O

Yellow all over body(+), Fever(+)

Sensorium : CM, Temp: 37,5 37,9o C
Head

Fontanels within normal limit. Light reflexes (+/+), isochoric

pupil, icteric sclera +/+, inferior conjunctiva palpebral
pale +/+ Ear, nose and mouth are normal

Neck

Lymph node enlargement (-)

Thorax

Symmetry fusiformis, Retraction (-),

Heart rate 136x/i, regular, Murmur (-),
Respiratory Rate 28x/i, regular, ronchi (-/-)

Abdomen

Distension (+),liver: palpable 2cm below acrus costa,

18

Extremities

Lien: schuffner III-1V, post operation wound (+)

Icteric (+) Pulse 136x/i, regular, adequate volume and

pressure, warm acral, CRT < 3.

Cholestasis Jaundice dd biliary stenosis
dd biliary atresia

Management
IV Inj cefepime Hcl 250mg/12jam
Urdafalk 2x30mg
Theobron syr 3x cth
IVFD D5% Nacl 0,225% 20gtt/i micro
Planning
Urine and Feaces test
Urine & feaces test Result

Normal
November, 3rd 4th 2015
S
Yellow all over the body(+), Fever (-)
O Sensorium : CM, Temp: 37,2 36,1o C BB: 5.2Kg
Head

Fontanels within normal limit. Light reflexes (+/+), isochoric

pupil, icteric sclera +/+, inferior conjunctiva palpebral
pale +/+ Ear, nose and mouth are normal

Neck

Lymph node enlargement (-)

Thorax

Symmetry fusiformis. Retraction (-).

Heart rate 134x/i, regular, Murmur (-),
Respiratory Rate 26x/i, regular, ronchi (-/-)

Abdomen

Distension (+), liver: palpable 2cm below acrus costa,

Lien: schuffner III-1V, post operation wound (+)
Extremities
Icteric (+) Pulse 134x/i, regular, adequate volume and
A
P

pressure, warm acral, CRT < 3.

Cholestasis + Bronchopneumonia
Management
IVFD D5% Nacl 0,225% 20gtt/i mikro

19

Inj cefepime Hcl 250mg/12jam

Urdafalk 2x30mg
Theobron syr 3x cth
November, 5th-6th 2015
S
O

Yellow all over the body(+), Cough (+) Fever (-)

Sensorium : CM, Temp: 37 36,7o C
Head

Fontanels within normal limit. Light reflexes (+/+), isochoric

pupil, icteric sclera +/+, inferior conjunctiva palpebral
pale +/+ Ear, nose and mouth are normal

Neck

Lymph node enlargement (-)

Thorax

Symmetry fusiformis. Retraction (-).

Heart rate 110x/i, regular, Murmur (-),
Respiratory Rate 20x/i, regular, ronchi (-/-)

Abdomen

Distension (+), liver: palpable 2cm below acrus costa,

Lien: schuffner III-1V, post operation wound (+)
Extremities
Icteric (+) Pulse 110x/i, regular, adequate volume and
A
P

pressure, warm acral, CRT < 3.

Cholestasis + Bronkopneumonia
Management
IVFD D5% Nacl 0,225% 20gtt/menit mikro
Inj cefepime Hcl 250mg/12jam
Urdafalk 2x30mg
Theobron syr 3x cth
Planning
USG Liver
USG Result
Hepatomegaly left lobe with minimal ascites
November, 7th - 8th 2015

20

S
O

Yellow all over the body(+), Cough (+) Fever (-)

Sensorium : CM, Temp: 37.0 36,7o C BB : 5.2kg
Head

Fontanels within normal limit. Light reflexes (+/+), isochoric

pupil, icteric sclera +/+, inferior conjunctiva palpebral
pale +/+ Ear, nose and mouth are normal

Neck

Lymph node enlargement (-)

Thorax

Symmetry fusiformis. Retraction (-).

Heart rate 100x/i, regular, Murmur (-),
Respiratory Rate 20x/i, regular, ronchi (-/-)

Abdomen

Distension (+), liver: palpable 2cm below acrus costa,

Lien: schuffner III-1V, post operation wound (+)
Extremities
Icteric (+) Pulse 100x/i, regular, adequate volume and
A

pressure, warm acral, CRT < 3.

Cholestasis + Bronkopneumonia

Management
IVFD D5% Nacl 0,225% 20gtt/menit mikro
Inj cefepime Hcl 250mg/12jam
Urdafalk 2x30mg
Theobron syr 3x cth
November, 9th-10th 2015

Yellow whole body(+), Fever (-), Cough (-)

Sensorium : CM, Temp: 36.8o C

Head

BB : 5.2kg

Fontanels within normal limit. Light reflexes (+/+), isochoric

pupil, icteric sclera +/+, inferior conjunctiva palpebral
pale +/+ Ear, nose and mouth are normal

Neck

Lymph node enlargement (-)

Thorax

Symmetry fusiformis. Retraction (-).

Heart rate 100x/i, regular, Murmur (-),

21

Respiratory Rate 20x/i, regular, ronchi (-/-)

Abdomen

Distension (+), liver: palpable 2cm below acrus costa,

Lien: schuffner III-1V, post operation wound (+)
Extremities
Icteric (+) Pulse 100x/i, regular, adequate volume and
pressure, warm acral, CRT < 3.
A

Cholestasis + Bronkopneumonia

Management
Amoxicilin Syrup 3xcth I
Urdafalk 3x20mg
Theobron syr 3x cth

November, 11th-12th 2015

S

Yellow whole body(+), Fever (-), Cough (-)

Sensorium : CM, Temp: 36.9 37,1o C

Head

BB : 5.2kg

Fontanels within normal limit. Light reflexes (+/+), isochoric

pupil, icteric sclera +/+, inferior conjunctiva palpebral
pale +/+ Ear, nose and mouth are normal

Neck

Lymph node enlargement (-)

Thorax

Symmetry fusiformis. Retraction (-).

Heart rate 120x/i, regular, Murmur (-),
Respiratory Rate 22x/i, regular, ronchi (-/-)

Abdomen

Distension (+), liver: palpable 2cm below acrus costa,

Lien: schuffner III-1V, post operation wound (+)
Extremities
Icteric (+) Pulse 120x/i, regular, adequate volume and
pressure, warm acral, CRT < 3.
A

Cholestasis + Bronkopneumonia

Management
Amoxicilin Syrup 3xcth I

22

Urdafalk 3x20mg
November, 13th 2015

Theobron syr 3x cth

S

Yellow whole body(+), Fever (-), Cough (-),acholic feces (+)

Sensorium : CM, Temp: 36,7o C

Head

BB : 5.2kg

Fontanels within normal limit. Light reflexes (+/+), isochoric

pupil, icteric sclera +/+, inferior conjunctiva palpebral
pale +/+ Ear, nose and mouth are normal

Neck

Lymph node enlargement (-)

Thorax

Symmetry fusiformis. Retraction (-).

Heart rate 116x/i, regular, Murmur (-),
Respiratory Rate 22x/i, regular, ronchi (-/-)

Abdomen

Distension (+),liver: palpable 2cm below acrus costa,

Lien: schuffner III-1V, post operation wound (+)
Extremities
Icteric (+) Pulse 116x/i, regular, adequate volume and
pressure, warm acral, CRT < 3.
A

Cholestasis + Bronkopneumonia

Management
Amoxicilin Syrup 3xcth I
Urdafalk 3x20mg
Theobron syr 3x cth
Planning
Patient was discharged with regular check up
Inj vitamin K 1mg/IM/1 times a month
Urdafalk 3x20mg
CHAPTER 4
DISCUSSION

23

In the theory is stated that prevalence of cholestasis jaundice is No clear

difference in the incidence of cholestasis between males and females is
observed. Cholestasis is observed in people of every age group . The

etiology can be from congenital or acquired infection, metabolic disorder, obstructive,

cholestatic syndrome, endocrinopathy, drug or toxin, and systemic disorder.
Diagnosing cholestatic jaundice is from the typical findings are protracted jaundice,
scleral icterus, acholic stools, dark yellow urine, and hepatomegaly and the diagnostic
test is liver biochemical test (AST, ALT, ALP, GGT), synthesis of liver function test,
USG liver, biopsy liver, and radiology. Management of cholestasis jaundice can be
general management and specific treatment such as Kasai portoenterostomy and liver
transplantation.
In this patient a boy 8 months was referred to Adam Malik General Hospital to
receive adequate treatment. Chief complaint was jaundice. In this patient do the
diagnostic test using history taking, typical findings (icteric, hepatomegaly, acholic
stools), diagnostic test (liver function test, USG liver). Management in hospital is
given Amoxicilin Syrup 3xcth I , Urdafalk 3x20mg, Theobron syr 3x cth

24

SUMMARY
FA, a boy, 8 months old, came to Haji Adam Malik Hospital on October 31st 2015
with yellow all over body as the chief complaint. The patient have been experienced
since 1 week ago and got worst two days back. Discontinuous high fever (+) since 6
days ago with the temperature of 39C and reduced by taking anti pyretic drugs. The
patient has acholic stools since four days ago. Patient treated with IVFD D5% Nacl
0,225% 20gtt/i micro, Inj cefepime Hcl 250mg/12jam, Urdafalk 2x30mg, Theobron
syr 3x cth.

25

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