Cholestasis Jaundice.docx

7/23/2019 Cholestasis Jaundice.docx

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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#P84


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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.*
http://emedicine.medscape.com/article/927029-overviewhttp://emedicine.medscape.com/article/927029-overview


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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


Noe$ber9 +t0=,t02;1+

) Dellow all over the body5K6, Cough 5K6 #ever 5-6

O %ensorium I C, &empI 0J M 0?,JoC






: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


A Cholestasis K Bron"opneumonia

P -anage$ent

$#A A* 9acl ,++* +gtt(menit mi"ro


rdafal" +x0mg


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






:eart rate !x(i, regular, urmur 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



P -anage$ent

$#A A* 9acl ,++* +gtt(menit mi"ro


rdafal" +x0mg


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


pupil, icteric sclera K(K, inferior conjunctiva palpebralpale K(K @ar, nose and mouth are normal



:eart rate !x(i, regular, urmur 5-6,


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7ienI schuffner -!$, post operation wound 5K6@xtremities cteric 5K6 2ulse !x(i, regular, adequate volume and



P -anage$ent

1moxicilin %yrup 0xcth

rdafal" 0x+mg


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






:eart rate !+x(i, regular, urmur 5-6,

Fespiratory Fate ++x(i, regular, ronchi 5-(-6


7ienI schuffner -!$, post operation wound 5K6@xtremities cteric 5K6 2ulse !+x(i, regular, adequate volume and



P -anage$ent



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rdafal" 0x+mg


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






: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



P -anage$ent


rdafal" 0x+mg


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

Cholestasis Jaundice.docx

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Pathology of Cholestasis

Infantile Cholestasis Metabolic and Genetic Cholestasis ...€¦ · Infantile Cholestasis Metabolic and Genetic Cholestasis : An Overview. PICTURE Current position: Paediatric Gastroenterologist

Neonatal Cholestasis Due to Biliary Sludge- Review and ... · PDF fileHerein we report a case of cholestasis secondary to ... report and review neonatal cholestasis due to biliary

Approach to cholestasis

Cholestasis of pregnancy –Where are we?...Intrahepatic cholestasis of pregnancy (“cholestasis”) • Commonest primary liver disorder in pregnant women: varies with ethnicity,

4 neonatal cholestasis

12 Gonzalez Cholestasis - ucsfcme.com

Extrahepatic Cholestasis

Neonatal Cholestasis

Intrahepatic cholestasis of pregnancy

Cholestasis of Pregnancy

Cholestasis Neonatus.doc

Neonatal Cholestasis - Khon Kaen UniversityNeonatal Cholestasis รศ.เพ ญศร โควส วรรณ ภาคว ชากม ารเวชศาสตร คณะแพทยศาสตร

Diagnosis and Management of Cholestasis

Guidelines Cholestasis

OBSTRUKSI JAUNDICE.docx

Intrahepatic Outline Cholestasis of Pregnancy

Infant Cholestasis Guidelines