JAUNDICE IN PREGNANCY

INCIDENCE IN INDIA – 1 IN 1000

CAUSES
 PREGNANCY INDUCED LIVER DISEASE
    HYPEREMESIS GRAVIDARUM OBSTETRIC CHOLESTASIS AFLP PREECLAMPSIA AND HELLP SYNDROME

 COINCIDENTAL LIVER DISEASE
 VIRAL HEPATITIS (Hep A MC World wide)  DRUG INDUCED JAUNDICE

 PREGNANCY SUPERIMPOSED ON C/C LIVER DISEASE
 CONGENITAL HYPERBILURUBINEMIA  CIRRHOSIS  C/C HEPATITIS

PHYSIOLOGY  RBC. .HAEME-BILIVERDIN-BILIRUBIN-Bound to aibumin-LIVER-Conjugated with 2 molecules of glucoronide(UDP transferase)canaliculi-extrahepatic bile duct-CBD-SITERMINAL ILEUM-bacterial actionUROBILINOGEN-Liver via enterohepatic circulation.

2. PREGNANCY.CLASSIFICATION  HEMOLYTIC JAUNDICE  HEMOLYSIS LEADS TO INCREASE IN UNCONJUGATED BILIRUBIN  MAINLY SEEN IN HEMOLYTIC ANEMIAS .  CONGENITAL HYPERBILIRUBINEMIA INCREASED UNCONJUGATED BILIRUBIN 1.. HELLP SYNDROME…. INTER CURRENT ILLNESS. IN GILBERT SYNDROME -DUE TO DECREASED LEVELS OF UDP TRANSFERASE. CRIGGLER NAJJAR SYNDROME -PRESENT AT . LFT NORMAL EXCEPT SERUM BILIRUBIN. FASTING CAUSES WORSENING OF JAUNDICE.

 MILD JAUNDICE 2.ABSENCE OF UDPT AD-DECREASED UDPT • CONJUGATED HYPER BILIRUBINEMIA 1.DUBIN JOHNSON SYNDROME .AR. ROTOR’S SYNDROME AD IN BOTH CONDITIONS .AR MUTATION IN MRP2 GENE. RESPONSIBLE FOR TRANSPORTING WIDE RANGE OF COMPOUNDS OUT OF THE HEPATOCYTE ACROSS THE CANALICULAR BORDER INCLUDING BILIRUBIN AND BILE SALT. BILIUBINURIA(+) .

DARK URINE.  (INTRAHEPATIC) OR THE CBD (EXTRAHEPATIC) DUE TO ACQUIRED DAMAGE OR OBSTRUCTION. ALCOHOL ABUSE. PL. PANCREATIC MALIGNANCY etc…. VIRAL HEPATITIS. OC.  DRUG REACTIONS. BILE SALT . BILIRUBIN . CIRRHOSIS.  PALE STOOLS. AFLP. etc ACCUMULATE IN BLOOD ALP INCREASES.SO CHOLESTEROL . HYPEREMESIS GRAVIDARUM  EXTRAHEPATIC CHOLESTASIS DUE TO OBSTRUCTION TO FLOW OF BILE AT ANY POINT BEYOND THE CANALICULUS SEEN IN GALL STONES. Eg. CONGENITAL HYPERBILIRUMINARIA. . CHOLESTATIC JAUNDICE  CHOLESTASIS IS DUE TO FAILURE TO EXCRETE BILE FROM HEPATOCYTES .  INTRA HEPATIC CHOLESTASIS DUE TO ABNORMALITIES AT CELLULAR LEVEL . BILIARY STRUCTURE. CANALICULUS.

PRENATAL  Identify the type of jaundice and its cause.  Interdisciplinary management depends on cause .MANAGEMENT PREPREGNANCY  Jaundice due to conditions with implications for pregnancy should be discussed.

.  Longterm management depends on the cause. POST NATAL  Confirm resolution of jaundice.LABOUR & DELIVERY  Plan early delivery if this will improve the outcome.  Avoid regional anaesthesia if coagulopathy present.

OBSTETRIC CHOLESTASIS AETIOLOGY  CHOLESTASIS EFFECT OF PREGNANCY DUE TO INCREASED LEVELS OF ESTROGEN. MORE COMMONLY IN THIRD TRIMESTER WHEN ESTROGEN LEVELS ARE HIGHEST .

SOLES AND TRUNK  RARELY JAUNDICE MAY FOLLOW PRURITUS AFTER 2-4 WKS.CLINICAL FEATURES  GENERALISED PRURITUS WITHOUT A RASH PREDILICTION FOR PALMS. .

TRANSAMINASE  SERUM BILIRUBIN MAY BE RAISED BUT USUALLY NOT MORE THAN 5 g/dl  ALP NONSPECIFIC .INVESTIGATIONS  ELEVATED SERUM BILE ACIDS.

MATERNAL AND FETAL RISK  MATERNAL RISK  PRURITUS CAN BE A VERY DISTRESSING SYMPTOM  MATERNAL MORBIDITY DUE TO MALABSORPTION AND Vit K DEFICIENCY LEADING TO PROLONGATION OF CLOTTING TIME AND PPH  IF THE SYMPTOMS / BIOCHEMICAL ABNORMALITIES PROLONG FOR >3 MONTHS POSTPARTUM. WOMAN SHOULD BE REFERRED TO A HEPATOLOGIST  90% RISK OF RECURRENCE  FETAL RISK  SPONTANEOUS PREMATURITY  FETAL DISTRESS ( MSAF/CTG ABNORMALITY )  IUD DUE TO ANOXIA ASSOCIATED WITH INCREASED SERUM BILE ACIDS ( >40 µmol/L )  RARELY FETAL COAGULOPATHY WITH Vit K DEFICIENCY .

. advise of recurrence risk of 90%  Obtain biliary tract USG to exclude other pathology PRENATAL  Confirm the diagnosis with S. ALT.AST measurement  Exclude viral infections including hep C .MANAGEMENT PREPREGNANCY  If previous history of OC . bile acid. autoimmune hep and other causes of biliary obstrn.

guargum Monitor fetal well being . though it does not predict at risk fetus . Treat maternal symptoms initially with simple      topical measures ( aqueous cream with menthol) Consider UCDA 500mg bid for women with severe symptoms Consider oral vit K to reduce the risk of PPH Dexamethasone 12mg daily x 7 days . with a gradual reduction in the dose over subsequent 3 days ( problem of possible fetal adverse neurological effects of repeated doses ) Cholestyramine .

.LABOUR AND DELIVERY  Consider elective delivery at 37 – 38 wks  Maintain vigilance for PPH POSTNATAL  Monitor biochemical resolution  Vit K supplement for baby  Use OCP only with close clinical and biochemical monitoring . 27% of cases have cyclical or OCP induced pruritus  Consider referral to to hepatologist if symptoms& biochemical abnormalities persists.

AFLP  RARE BUT DANGEROUS DISORDER  CLINICAL SYMPTOMS AND SIGNS ARE NOT SPECIFIC  DEFINED AS ACUTE LIVER FAILURE WITH REDUCED HEPATIC METABOLIC CAPACITY IN THE ABSENCE OF OTHER CAUSES  HISTOLOGICALLY THERE WILL BE PANLOBULAR MICROVESICULAR STEATOSIS AND INTRA HEPATIC CHOLESTASIS .

IN ADDITION THE WOMEN ARE HETEROZYGOUS FOR THIS DEFECT . PREECLAMPSIA . MALE FETUSES .AETIOLOGY  ASSOCIATE WITH FIRST PREGNANCY . MULTIPLE PREGNANCIES  MANY OF THESE WOMEN ARE CARRYING FETUSES WHO ARE HOMOZYGOUS FOR βFATTY ACID OXIDATION DEFECTS (LCHAD DEFICIENCY). MATERNAL OBESITY.

VOMITING ABDOMINAL PAIN POLYDIPSIA AND POLYURIA ENCEPHALOPATHY ELEVATED TRANSAMINASES (>42 IU/L) ELEVATED BILIRUBIN (>14µmol/L) HYPOGLYCEMIA (<4 mmol/L) ELEVATED URATE (340µmol/L) .DIAGNOSIS  SWANSEA CRITERIA PRESENCE OF MORE THAN 5 DIAGNOSTIC         .

      RENAL IMPAIREMENT (CREATININE > 150µmol/L) ELEVATED AMMONIA (>47µmol/L) LEUCOCYTOSIS COAGULOPATHY (PT > 14 sec. . apTT > 34 sec ) ASCITES/ BRIGHT LIVER ON ULTRASOUND SCAN MICROVESICULAR STEATOSIS ON LIVER BIOPSY ONE OF THE KEYS TO THE DIAGNOSIS OF AFLP IS THE RAPIDITY WITH WHICH LFT CAN DETERIORATE IN THE AGGRESSIVE PHASE OF THE DISEASE.

MATERNAL AND FETAL PROGNOSIS  MATERNAL DEATH MAY BE DUE TO FULMINANT HEPATIC FAILURE DIC ENCEPHALOPATHY  IN SEVERE DISEASE FETAL PROGNOSIS IS POOR.  IF THE FETUS SURVIVE IT MAY DEVELOP RYE LIKE SYNDROME OF HEPATIC ENCEPHALOPATHY AND SEVERE HYPOGLYCEMIA DUE TO DEFECT IN BETA FATTY ACID OXIDN .

in which case. resuscitate  Intensive care / high dependency setting  Provide supportive therapy  Plan delivery or end pregnancy . start home testing for urinary protein from 24 wk .  Consider screening for LCHAD deficiency  PRENATAL  If previous AFLP. check LFT’s . monitor BP every 2 wk. confirm previous diagnosis.  Establish diagnosis . unless previous pregnancy is affected.MANAGEMENT OF ACUTE FATTY LIVER SYNDROME  PREPREGNANCY  None.advise risk of recurrence. check baseline LFT : advise to report any new symptoms.

vaginal delivery preferable  Maintain meticulous hemostasis .LABOUR AND DELIVERY  maternal resuscitation by correction of hypoglycemia fluid balance coagulopathy  Use multidisciplinary approach ideally in liaison with liver unit to manage liver failure  Use intensive fetal monitoring  Perform urgent delivery when maternal condition is stabilised .

POSTNATAL  Continue intensive care management  Watch for postpartum wound hematoma formation and sepsis . PPH  Recurrence risk is difficult to estimate perhaps as high as 10 to 20%  Support contraceptive measures  Full hepatic recovery expected without further sequelae . occasionally emergency liver transplant needed  Paediatricians to consider screening baby for LCHAD deficiency .

PSYCHOLOGICAL 5. PYLORI 3.INFECTIONS.5-1%  AETIOLOGY 1.UPPER GI DYSMOTILITY DUE TO SMOOTH M RELAXN EFFECT OF PROGESTERONE.LIVER DYSFUNCTION 6.HYPEREMESIS GRAVIDARUM  SEVERE NAUSEA & INTRACTABLE VOMITING.ALTERED LIPID METABOLISM 7.  0.DUE TO INCREASED hCG 2.IMMUNOLOGICAL . 4.ENDOCRINE.H.

HYPOKALEMIA &HYPOCHLOREMIA.PATHOLOGY 1. 3.HAEMATOLOGICAL HEMOCONC DUE TO DEHYDRN .HYPOVITAMINOSIS & FINALLY HEP DYSFUN 2.METABOLIC CHANGES STARVATION-GLYCOGEN DEPLETION& MOBILISN OF FAT STORES-INCREASE IN KB.HYPO PROTEINEMIA.BIOCHEMICAL VOMITING &DEHYDRN CAN LEAD TO HYPONATREMIA. INCREASED PROTEIN METABOLISM-î BUN IF PROLONGED – HYPOGLYCEMIA.

UREA HYPONATREMIA.HEMATOLOGICAL & BIOCHEMICAL INCREASE IN HAEMATOCRIT .î SP.GRAVITY.URINE ANALYSIS OLIGURIA. ACIDIC PH 2. Î IN KB.USG CONFIRMS A VIABLE I/U GESTN R/O MOLAR & MULTIPLE PREGNANCY .INVESTIGATIONS 1.B.HYPOKALEMIA ABN LFT 3.

LIVER DYSFUN 2. SEVERE GASTRO ESOPHAGEAL REFLUX D/S 4. PSYCHOLOGICAL PROBLEMS . PEPTIC ULCER 3.DIFF DIAGNOSIS 1.

VIT K DEFICIENCY. KORSAKOFF’S PSYCHOSIS.  FETAL IUGR .COMPLICATIONS  MATERNAL ELECTROLYTE IMBALANCE LIVER DYSFUN RENAL ABNORMALITIES STRESS ULCERS IN STOMACH MALLORY WEISS TEARS IN ESOPHAGUS VITAMIN DEFICIENCY.WERNICKE ENCEPHALOPATHY.PERIPHERAL NEURITIS.

MANAGEMENT PREPREGNANCY  Discuss recurrence risk  Give advise on treatment options and provide psychological support at an earlier stage  Give folate supplements PRENATAL  Remember alternative diagnosis  Rehydrate with IVF and electrolyte therapy  Supplement nutrients and vit ( thiamine) .

. Consult dietician . provide parenteral nutrition in extreme cases  Provide psychological and social support  Provide thromboprophylaxis if needed  Treatment  First line – conventional anti emetics  Alternative agents – corticosteroids 5-HT3 antagonist if no response  Provide fetal growth surveillance LABOUR AND DEIVERY  Woman on corticosteroids prenatally should have IV hydro cortisone to cover labour / delivery .

POSTNATAL  Review nutritional status  Wean off steroids  Discuss contraception .

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