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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. n most cases, the elevation ofserum-conjugated bilirubin is a biochemical manifestation of cholestasis, which is the
pathologic reduction in bile formation or flow.!
Complex mechanisms exist for the transport of bile components from serum
into hepatocytes across the basolateral cell surface, for the traffic"ing 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. #rom the bile canaliculus, bile then flows into the
extrahepatic biliary tree, including the common bile duct, before entering the
duodenum at the ampulla of $ater. solated gene defects in proteins responsible for
traffic"ing bile components can lead to cholestatic diseases.!
Cholestasis is condition which secretion and excretion of bile from the liver to
duodenum is disrupted. %o, substance which is excreted with bile is restrained in
liver. &he parameter of cholestasis is serum conjugated bilirubin '! mg(dl if total
bilirubin ) *mg(dl, or conjugated bilirubin '+ of total bilirubin when total
bilirubin '*mg(dl.+
Cholestasis can be due to infectious, genetic, metabolic, or undefined
abnormalities giving rise to mechanical obstruction of bile flow or to functional
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impairment of hepatic excretory function and bile secretion. echanical lesions
include stricture or obstruction of the common bile duct/ biliary atresia is the
prototypic obstructive abnormality. #unctional impairment of bile secretion can result
from congenital defects or damage to liver cells or to the biliary secretory apparatus.0
n the early neonatal period, jaundice caused by physiologic unconjugated
hyperbilirubinemia or human mil" jaundice is impossible to distinguish from jaundice
caused by cholestasis based on physical appearance alone. ndeed, physiologic
unconjugated hyperbilirubinemia and cholestasis can coexist in early infancy. 1
critical time point for establishing the diagnosis of cholestasis is at the +-wee" well-child visit. 2ersistent jaundice at + wee"s after birth should alert the care provider to
the possibility of cholestasis. &he diagnosis is made by obtaining a conjugated
bilirubin level or 3direct4 bilirubin fraction, whichever is available locally. f the
infant appears well otherwise, a second option is to see the infant bac" in ! wee". f
the jaundice persists at 0 wee"s after birth, laboratory evaluation is mandatory.!
&he serum aspartate aminotransferase 51%&6 and alanine aminotransferase
517&6 levels typically are elevated to a variable degree, but are not specific for the
cause of cholestasis. &he gamma glutamyltransferase 588&6 level usually is elevated
in cholestasis. 9ormal or low 88& levels in the setting of cholestasis have been
associated with bile acid synthesis defects, some cases of hypopituitarism, and
progressive familial intrahepatic cholestasis types ! and + 52#C!, 2#C+6.!
1bnormalities 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. 1 urinalysis and urine culture will assess for urinary tract
infection, and the presence of reducing substances in the urine suggests
galactosemia.!
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Cholestatic jaundice affects approximately ! in every +,* infants 5!,+6, and is
thus infrequently seen by most providers of medical care to infants. :owever,
distinguishing jaundice caused by cholestasis from noncholestatic conditions is
critical because cholestatic jaundice is much more li"ely to have a serious etiology
that needs prompt diagnosis and therapy. &he most common causes of cholestatic
jaundice in the first months of life are biliary atresia and neonatal hepatitis, which
account for most cases. 9eonatal hepatitis has referred to a histologic appearance of
widespread giant cell transformation. 1lthough giant cell transformation isrecognized 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. 1lpha-! antitrypsin deficiency causes another * to !*
of cases. &he 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/ 1lagille syndrome/ infection/ and other rare disorders.;
nfants with cholestatic jaundice caused by bacterial sepsis, galactosemia,
hypopituitarism, or gallstone often appear acutely ill. &hese disorders require early
diagnosis and urgent treatment. :owever, many infants with cholestatic jaundice
appear otherwise healthy and grow normally. &he 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 ! in !, to !
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conditions that cause cholestasis may also lead to better outcomes because better
support of the infant may avoid complications of liver disease.;
Aespite these data showing that early diagnosis is potentially life saving,
referral for evaluation of cholestatic jaundice frequently occurs after ;* to ? days of
age 5!+6. n recognition of this, and noting that no evidence-based guideline for its
evaluation currently exists, the Cholestasis 8uideline Committee was formed by the
9orth 1merican %ociety for 2ediatric 8astroenterology, :epatology and 9utrition
591%28:196 to develop a clinical practice guideline for the diagnostic evaluation
of cholestasis in infants.
;
1.2 Objectie
&his paper is completed in order to fulfill one of the requirements in the
%enior Clinical 1ssistance program in Aepartment of Child :ealth of :aji 1dam
ali" 8eneral :ospital, niversity of 9orth %umatera. n addition, this paper passes
the "nowledge of cholestasis and its management
http://journals.lww.com/jpgn/Fulltext/2004/08000/Guideline_for_the_Evaluation_of_Cholestatic.1#P84http://journals.lww.com/jpgn/Fulltext/2004/08000/Guideline_for_the_Evaluation_of_Cholestatic.1#P847/23/2019 Cholestasis Jaundice.docx
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CHAPTER II
THEOR!
2.1 De"inition
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.
&herefore, the clinical definition of cholestasis is any condition in which substances
normally excreted into bile are retained. &he serum concentrations of conjugated
bilirubin and bile salts are the most commonly measured.*
Conjugated hyperbilirubinemia is defined biochemically as a conjugated
bilirubin level of + mg(d7 and '+ of the total bilirubin.!
2.2 E#ide$io%og&
Sex
9o clear difference in the incidence of cholestasis between males and females
is observed. ncidence is equal in most genetic diseases leading to cholestasis.
:owever, several conditions have a female dominance, includingbiliary atresia,
drug-induced cholestasis, and of course, cholestasis of pregnancy.*
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Age
Cholestasis is observed in people of every age group. :owever, newborns and
infants are more susceptible and more li"ely to develop cholestasis as a consequence
of immaturity of the liver.*
Doung gestational age, low birth body weight, more sepsis episodes, and long
duration of parenteral nutrition are ris" factors associated with 2arenteral nutrition-
associated cholestasis.*
2.' Etio%og&1
Congenital infection
E Cytomegalovirus
E &oxoplasmosis
E Fubella
E :erpes simplex virus
E %yphilis
E :$
1cquired infection
E rinary tract infection
E %epsis
etabolic
E 1lpha-! antitrypsin deficiency
E Cystic fibrosis
E 8alactosemia
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E &yrosinemia
E Aefects in bile acid synthesis
E nborn errors of carbohydrate, fat, protein metabolism
Gbstructive
E Biliary atresia
E Choledochal cyst
E nspissated bile syndrome
E %pontaneous perforation of bile duct
Cholestatic syndromes
E 1lagille syndrome
E 2rogressive familial intrahepatic cholestasis
@ndocrinopathy
E :ypothyroidism
E :ypopituitarism
Arug or toxin induced
E 2arenteral nutrition
E Arugs
%ystemic disorder
E %hoc"
E Congenital heart disease(heart failure
2.(. )&$#to$* and )ign*
&he typical findings in an infant who has cholestasis are protracted jaundice,
scleral icterus, acholic stools, dar" yellow urine, and hepatomegaly. %ome infants
may have coagulopathy secondary to vitamin = malabsorption and deficiency and
present with bleeding or bruising. Coagulopathy may also be caused by liver failure,
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indicating either severe metabolic derangement of the liver 5as in respiratory chain
deficiency disorders6 or cirrhosis and end-stage liver disease 5as in neonatal
hemochromatosis6. %plenomegaly can be observed in infants who have cirrhosis and
portal hypertension, storage diseases, and hemolytic disorders. 9eurologic
abnormalities including irritability, lethargy, poor feeding, hypotonia, or seizures can
indicate sepsis, intracranial hemorrhage, metabolic 5including Hellweger syndrome6
and mitochondrial disorders, or severe liver dysfunction resulting in
hyperammonemia and encephalopathy. 7ow birth weight, thrombocytopenia,
petechiae and purpura, and chorioretinitis are often associated with congenital
infection. #acial dysmorphism may suggest a chromosomal abnormality or 1lagille
syndrome. 1 palpable mass in the right upper quadrant may indicate a choledochal
cyst. 1 cardiac murmur increases the li"elihood of 1lagille syndrome or B1.
1lthough + of B1 patients will have other extrahepatic congenital malformations
5including cardiac anomalies, situs inversus, intestinal malrotation, midline liver, and
polysplenia or asplenia6, the majority of patients who have B1 are well appearing
during the first month after birth, and there is no single historical or physical
examination finding that uniquely suggests B1
2.+. Diagno*e
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+.*.! :istory
- 2regnancy and labor history 5&GFC: infection6
- Birth weight and gestational age
- :istory of administration vitamin =
- :istory of similar complaints in family
- :istory of current complaints I onset of jaundice, urine and feces>s color, history of
therapy, parenteral nutrition, bleeding, history of feeding, diarrhea or emesis
- blac" urine
- acholic feces
- growth disorders +
+.*.+. 2hysical examination
- jaundice
- acholic feces
- bleeding signs 5vitamin = deficiency6
- hepatomegaly or hepatosplenomegaly
- abdominal mass, ascites
- growth failure
- other signs about specific disease or syndrome I dysmorphic signs 5&risomy,
1lagille syndrome6/ murmur 51lagille syndrome, extrahepatic billiary atresia
5@:B166/ baby is sic", vital signs abnormal 5sepsis, :7:, congenital infection6/
micropenis 5panhipopituitarism6/ cataract 5rubella, galactosemia6/ situs inversus
5@:B16/ retina>s problem 5&GFC: infection, 1lagille syndrome6/ abdominal mass
5choledocus duct cyst6/ hemangioma cutaneus 5hepar hemangioma6/ white hair
5:emophagocytic lymphohistiocytosis(:7:6.+
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2.5.3. Diagnostic test
!. Foutine hematology profile for main screening
+. 7iver biochemical test I serum bilirubin fraction, aspartat aminotransferase
51%&6, alanin aminotransferase 517&6, 1l"aline phospatase 51726, and
8amma-glutamil transpeptidase 588&6
0. %ynthesis of liver function test I 2&, a2&&, albumin, cholesterol profile,
glucose profile
;. Bacteria culture I urine and(or blood, if considered severe infection
*. rinalysis, include %8 liver two phase 5fasting and post prandial6, liver
biopsy
?. #&; and &%: screening, to rule out(support presumption hypothyroidism
J. Fadiology I cholangiography 5gold standard for biliary atresia6+
Cholestasis 17&(1%& 172(88& Bilirubin
ntrahepatic KKK K KK
@xtrahepatic K KKKK KKK
Fecommendations
!. 1 detailed history and physical examination are essential
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+. ltrasound is the first-line non-invasive imaging procedure in order to differentiate
intra- from extrahepatic cholestasis
0. agnetic resonance cholangiopancreatography 5FC26 is the next step to be
considered in patients with unexplained cholestasis
;. @ndoscopic ultrasound 5@%6 is an alternative to FC2 for evaluation of distal
biliary tract obstruction
*. Aiagnostic endoscopic retrograde cholangiopancreatography 5@FC26 should be
reserved for highly selected cases 5-+(1!6. f the need for a therapeutic maneuver is
not anticipated, FC2 or @% should be preferred to @FC2 because of the morbidity
and mortality related to @FC2.J
2.,. -anage$ent
!. 8eneral edical anagement
ost infants with cholestasis are underweight and will need nutritional support. &he
goal is to provide adequate calories to compensate for steatorrhea and to prevent( treat
malnutrition. &he calorie requirement is approximately !+* of the recommended
dietary allowance 5FA16 based on ideal body weight. n breastfed infants,
breastfeeding should be encouraged and medium-chain triglyceride 5C&6 oil should
be administered in a dose of !-+ m7("g(day in +-; divided doses in expressed breast
mil". n older infants, a mil"-cereal-mix fortified with C& is preferred. 1dding
puffed rice powder and C& to mil" can ma"e feeds energy-dense. @ssential fatty
acids should constitute +- 0 of the energy provided. $egetable protein at +-0
g("g(day is recommended.L
%pecific treatment
n infants with pruritus due to severe cholestasis, the group recommended, in the
following orderI rsodeoxycholic acid 5AC16 5+ mg("g(d6, rifampicin 5*-!
mg("g(d6, and phenobarbitone 5*M! mg("g(d6. %ymptom chart should be made for
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pruritus. 1ppropriate antibiotics depending on the site of infection and culture
sensitivity reports need to be administered in patients with bacterial sepsis.L
=asai portoenterostomy
#or biliary atresia, which is a condition of extrahepatic biliary duct having
obstruction. &his condition need =asai 2@. =asai>s procedure if done early can give
good survival for + years, which is ?,*. But, the flow of bile will be hard to be
returned if the operation done after L wee"s old.+
7iver transplantation
7iver &ransplantation, the standard therapy for decompensated cirrhosis due to any
cause. 1ny baby, who has had =asai>s 2@ and the bilirubin remains '? mg(d7, three
months after surgery, should be referred to a transplant center. Babies with B1 who
present with decompensated cirrhosis 5low albumin, prolonged 9F, ascites6 are not
li"ely to improve with a =asai 2@ and should be referred for liver transplantation.
7iving related liver transplantation 5the vast majority of liver transplants in ndia are
living related6, performed at experienced centers, is associated with favorable
outcomes, with *- and !-year survival rates of
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CHAPTER III
CA)E REPORT
'.1 Ca*e
#1, a L months boy, with *.+ "g of BN and ?+ cm of B:, is a patient of
infection unit in 2ediatric Aepartment in Central 2ublic :ospital :aji 1dam ali"
edan on Gctober 0!st+!* at !
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9o family history of A and other diseases
Hi*tor& o" #arent/* $edicationI
nclear
Hi*tor& o" #regnanc&
&he gestation age was 0? wee"s. 9o history of complication, neonate and maternal
problem.
Hi*tor& o" birt0
Birth assisted by midwife spontaneously. &he baby was born pervaginal and she cried
immediately. Bluish was not found. Body weight 0
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:FI !0? bpm, FFI +L bpm
BNI *.+ "g
B:I ?+ cmanemic 5-6, icteric sclera 5K6, dyspnea 5-6, cyanosis 5-6, edema 5-6.
5oca%ied *tatu*
:ead I @yesI 7ight reflex K(K, icteric scleraK(K, isochoric
pupil,inferior conjunctiva palpebral pale K(K
@ars I Nithin normal range
9ose I Nithin normal range
outh I Nithin normal range
9ec" I 7ymph node enlargement 5-6
&horax I %ymmetrical fusiform, retraction 5-6, icteric 5K6:FI !0? bpm, regular, murmur 5-6FFI +L bpm, regular, rhonchi 5-(-6
1bdomen I Aistension 5K6, liverI palpable +cm below acrus costa,
7ienI schuffner -!$, post operation wound 5K6
@xtremities I cteric 5K6 2ulse !0? bpm regular, p(v adequate, warm
acral,CF& ) 04.
Di""erentia% diagno*i* I -
6orking diagno*i* I Cholestasis Paundice ec dd stenosis bilier dd atresia bilier
5aborator& "indingComplete blood analysis 5%eptember 0!st, +!*6
Te*t Re*u%t Unit Re"erra%
He$og%obin L.! g !+.-!;.;
Er&t0roc&te 0.J !?(mm0 ;.;-;.;L
5eucoc&te +;.L !0(mm0 ;.*-!0.*
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T0ro$boc&te +?* !0(mm0 !*-;*
He$atocrite +*.L 0J-;!
Eo*ino#0i% *.* !-?Ba*o#0i% .L -!
Neutro#0i% 0?.* 0J-L
5&$#0oc&te ;L.L +-;
-onoc&te L.; +-L
Neutro#0i% ab*o%ute ;.; !0(Q7 +.;-J.0
5&$#0oc&te ab*o%ute *.
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#osfatase 1l"ali 51726 ;;+ (7 );?+
1%&(%8G& !L* (7 )0L
17&(%82& !?J (7 );!
8O55O6 UP
Noe$ber91*t: 2nd2;1+
) Dellow all over body5K6, #ever5K6
O %ensorium I C, &empI 0J,* M 0J,
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7ienI schuffner -!$, post operation wound 5K6
@xtremities cteric 5K6 2ulse !0?x(i, regular, adequate volume and
pressure, warm acral, CF& ) 04.A Cholestasis Paundice dd biliary stenosis
dd biliary atresia
P -anage$ent
$ nj cefepime :cl +*mg(!+jam
rdafal" +x0mg
&heobron syr 0x R cth
$#A A* 9acl ,++* +gtt(i microP%anning
rine and #eaces test
Urine < "eace* te*t Re*u%t
9ormal
Noe$ber9 'rd: (t0 2;1+
) Dellow all over the body5K6, #ever 5-6
O %ensorium I C, &empI 0J,+ M 0?,!oC BBI *.+=g
:ead #ontanels within normal limit. 7ight reflexes 5K(K6, isochoric
pupil, icteric sclera K(K, inferior conjunctiva palpebral
pale K(K @ar, nose and mouth are normal
9ec" 7ymph node enlargement 5-6
&horax %ymmetry fusiformis. Fetraction 5-6.
:eart rate !0;x(i, regular, urmur 5-6,
Fespiratory Fate +?x(i, regular, ronchi 5-(-6
1bdomen Aistension 5K6, liverI palpable +cm below acrus costa,
7ienI schuffner -!$, post operation wound 5K6@xtremities cteric 5K6 2ulse !0;x(i, regular, adequate volume and
pressure, warm acral, CF& ) 04.
A Cholestasis K Bronchopneumonia
P -anage$ent
$#A A* 9acl ,++* +gtt(i mi"ro
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nj cefepime :cl +*mg(!+jam
rdafal" +x0mg
&heobron syr 0x R cth
Noe$ber9 +t0=,t02;1+
) Dellow all over the body5K6, Cough 5K6 #ever 5-6
O %ensorium I C, &empI 0J M 0?,JoC
:ead #ontanels within normal limit. 7ight reflexes 5K(K6, isochoric
pupil, icteric sclera K(K, inferior conjunctiva palpebral
pale K(K @ar, nose and mouth are normal
9ec" 7ymph node enlargement 5-6
&horax %ymmetry fusiformis. Fetraction 5-6.
:eart rate !!x(i, regular, urmur 5-6,
Fespiratory Fate +x(i, regular, ronchi 5-(-6
1bdomen Aistension 5K6, liverI palpable +cm below acrus costa,7ienI schuffner -!$, post operation wound 5K6
@xtremities cteric 5K6 2ulse !!x(i, regular, adequate volume and
pressure, warm acral, CF& ) 04.
A Cholestasis K Bron"opneumonia
P -anage$ent
$#A A* 9acl ,++* +gtt(menit mi"ro
nj cefepime :cl +*mg(!+jam
rdafal" +x0mg
&heobron syr 0x R cth
P%anning
%8 7iver
U)4 Re*u%t
:epatomegaly left lobe with minimal ascites
Noe$ber9 >t0 = ?t0 2;1+
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) Dellow all over the body5K6, Cough 5K6 #ever 5-6
O %ensorium I C, &empI 0J. M 0?,JoC BB I *.+"g
:ead #ontanels within normal limit. 7ight reflexes 5K(K6, isochoric
pupil, icteric sclera K(K, inferior conjunctiva palpebral
pale K(K @ar, nose and mouth are normal
9ec" 7ymph node enlargement 5-6
&horax %ymmetry fusiformis. Fetraction 5-6.
:eart rate !x(i, regular, urmur 5-6,
Fespiratory Fate +x(i, regular, ronchi 5-(-6
1bdomen Aistension 5K6, liverI palpable +cm below acrus costa,7ienI schuffner -!$, post operation wound 5K6
@xtremities cteric 5K6 2ulse !x(i, regular, adequate volume and
pressure, warm acral, CF& ) 04.
A Cholestasis K Bron"opneumonia
P -anage$ent
$#A A* 9acl ,++* +gtt(menit mi"ro
nj cefepime :cl +*mg(!+jam
rdafal" +x0mg
&heobron syr 0x R cth
Noe$ber9 @t0=1;t02;1+
) Dellow whole body5K6, #ever 5-6, Cough 5-6
O %ensorium I C, &empI 0?.LoC BB I *.+"g
:ead #ontanels within normal limit. 7ight reflexes 5K(K6, isochoric
pupil, icteric sclera K(K, inferior conjunctiva palpebralpale K(K @ar, nose and mouth are normal
9ec" 7ymph node enlargement 5-6
&horax %ymmetry fusiformis. Fetraction 5-6.
:eart rate !x(i, regular, urmur 5-6,
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Fespiratory Fate +x(i, regular, ronchi 5-(-6
1bdomen Aistension 5K6, liverI palpable +cm below acrus costa,
7ienI schuffner -!$, post operation wound 5K6@xtremities cteric 5K6 2ulse !x(i, regular, adequate volume and
pressure, warm acral, CF& ) 04.
A Cholestasis K Bron"opneumonia
P -anage$ent
1moxicilin %yrup 0xcth
rdafal" 0x+mg
&heobron syr 0x R cth
Noe$ber9 11t0=12t02;1+
) Dellow whole body5K6, #ever 5-6, Cough 5-6
O %ensorium I C, &empI 0?.< M 0J,!oC BB I *.+"g
:ead #ontanels within normal limit. 7ight reflexes 5K(K6, isochoric
pupil, icteric sclera K(K, inferior conjunctiva palpebral
pale K(K @ar, nose and mouth are normal
9ec" 7ymph node enlargement 5-6
&horax %ymmetry fusiformis. Fetraction 5-6.
:eart rate !+x(i, regular, urmur 5-6,
Fespiratory Fate ++x(i, regular, ronchi 5-(-6
1bdomen Aistension 5K6, liverI palpable +cm below acrus costa,
7ienI schuffner -!$, post operation wound 5K6@xtremities cteric 5K6 2ulse !+x(i, regular, adequate volume and
pressure, warm acral, CF& ) 04.
A Cholestasis K Bron"opneumonia
P -anage$ent
1moxicilin %yrup 0xcth
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rdafal" 0x+mg
&heobron syr 0x R cth
CHAPTER (
DI)CU))ION
Noe$ber9 1't02;1+
) Dellow whole body5K6, #ever 5-6, Cough 5-6,acholic feces 5K6
O %ensorium I C, &empI 0?,JoC BB I *.+"g
:ead #ontanels within normal limit. 7ight reflexes 5K(K6, isochoric
pupil, icteric sclera K(K, inferior conjunctiva palpebral
pale K(K @ar, nose and mouth are normal
9ec" 7ymph node enlargement 5-6
&horax %ymmetry fusiformis. Fetraction 5-6.
:eart rate !!?x(i, regular, urmur 5-6,
Fespiratory Fate ++x(i, regular, ronchi 5-(-6
1bdomen Aistension 5K6,liverI palpable +cm below acrus costa,7ienI schuffner -!$, post operation wound 5K6
@xtremities cteric 5K6 2ulse !!?x(i, regular, adequate volume and
pressure, warm acral, CF& ) 04.
A Cholestasis K Bron"opneumonia
P -anage$ent
1moxicilin %yrup 0xcth
rdafal" 0x+mg
&heobron syr 0x R cth
P%anning
2atient was discharged with regular chec" up
nj vitamin = !mg((! times a month
rdafal" 0x+mg
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n the theory is stated that prevalence of cholestasis jaundice is No clear
diference in the incidence o cholestasis !et"een #ales and e#ales is
o!ser$ed. %holestasis is o!ser$ed in &eo&le o e$er' age gro(&. &he
etiology can be from congenital or acquired infection, metabolic disorder, obstructive,
cholestatic syndrome, endocrinopathy, drug or toxin, and systemic disorder.
Aiagnosing cholestatic jaundice is from the typical findings are protracted jaundice,
scleral icterus, acholic stools, dar" yellow urine, and hepatomegaly and the diagnostic
test is liver biochemical test 51%&, 17&, 172, 88&6, synthesis of liver function test,
%8 liver, biopsy liver, and radiology. anagement of cholestasis jaundice can be
general management and specific treatment such as =asai portoenterostomy and liver
transplantation.
n this patient a boy L months was referred to 1dam ali" 8eneral :ospital to
receive adequate treatment. Chief complaint was jaundice. n this patient do the
diagnostic test using history ta"ing, typical findings 5icteric, hepatomegaly, acholic
stools6, diagnostic test 5liver function test, %8 liver6. )anage#ent in hos&ital is
gi$en 1moxicilin %yrup 0xcth , rdafal" 0x+mg, &heobron syr 0x R cth
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)U--AR!
#1, a boy, L months old, came to :aji 1dam ali" :ospital on Gctober 0!st
+!*
with yellow all over body as the chief complaint. &he patient have been experienced
since ! wee" ago and got worst two days bac". Aiscontinuous high fever 5K6 since ?
days ago with the temperature of 0C and reduced by ta"ing anti pyretic drugs. &he
patient has acholic stools since four days ago. 2atient treated with $#A A* 9acl
,++* +gtt(i micro, nj cefepime :cl +*mg(!+jam, rdafal" +x0mg, &heobron
syr 0x R cth.
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RE8ERENCE)
!. Aavid Brumbaugh, Cara ac". Conjugated :yperbilirubinemia in Children.
2ediatrics in Feview Puly +!+, $G7@ 00 ( %%@ J. 1vailable at
httpI((pedsinreview.aappublications.org(content(00(J(+
+. &anto Chris, 7iwang #rans, :anifati %ona, 2radipta @"a 1dip, =apita %ele"ta
=edo"teran, +!;. $olume !.
0. =liegman, Behrman, Penson, %tanton. 9elson &extboo" of 2ediatrics !Lth ed.
+J.
;. oyer, $irginia A, 2:/ #reese, Aeborah =. A/ Nhitington, 2eter #. A/
Glson, 1lan A. A/ Brewer, #red A/ Colletti, Fichard B. A/ :eyman,
elvin B. A, 2:. 8uideline for the @valuation of Cholestatic Paundice in
nfantsI Fecommendations of the 9orth 1merican %ociety for 2ediatric8astroenterology, :epatology and 9utrition. Augu*t 2;;( = 7o%u$e '@ = I**ue 2
= ## 11+=12?. 1vailable at.
httpI((journals.lww.com(jpgn(#ulltext(+;(L(8uidelineTforTtheT@valuationT
ofTCholestatic.
*. :isham 9azer, B, BCh, #FC2, , A&U:. Cholestasis. edscape. 1vailable at
httpI((emedicine.medscape.com(article(
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httpI((www.msdmanuals.com(professional(pediatrics(perinatal-problems(neonatal-
cholestasis
L. $idyut Bahtia, 1shish Bavde"ar, Pohn atthai, Dogesh Nai"ar, and 1nupam
%ibal. anagement of 9eonatal CholestasisI Consensus %tatement of the 2ediatric
8astroenterology Chapter of ndian 1cademy of 2ediatrics. 1vailable at I
httpI((indianpediatrics.net(mar+!;(+0.pdf
http://www.msdmanuals.com/professional/pediatrics/perinatal-problems/neonatal-cholestasishttp://www.msdmanuals.com/professional/pediatrics/perinatal-problems/neonatal-cholestasishttp://www.msdmanuals.com/professional/pediatrics/perinatal-problems/neonatal-cholestasishttp://www.msdmanuals.com/professional/pediatrics/perinatal-problems/neonatal-cholestasis