Clinical Approach to Neonatal Jaundice Dr. Siddeeg Addow Pediatric Resident Khartoum, Sudan

CONTENTS: INTRODUCTION PATHOPHYSIOLOGY DIFFERENTIAL DIAGNOSIS HISTORY EXAMINATION INVESTIGATION

INTRODUCTION Bilirubin is the end product of heme degradation Most of the daily production comes from the breakdown of RBCs in the RES Heme biliverdin bilirubin Bilirubin is released & bound to serum albumin Bilirubin is uptake & conjugated with glucuronic acid Finally conjugated bilirubin is excreted in bile

PATHOPHYSIOLOGY Tightly compounded to s. albumin Non toxic UNCONJUGATED B. CONJUGATED B. Tightly compounded to s. albumin Normally very small amount is present as albumin free Insoluble in water can not be excreted in urine Toxic Non toxic Water soluble Loosely bound to albumin. Delta fraction

Both conjugated & unconjugated bilirubin may accumulate systemically & deposit in tissues Normally s. bilirubin level vary b/w 0.3 & 1.2mg/dl. The rate of systemic bilirubin production is = to the rate of hepatic uptake, conjugation & biliray excretion . Jaundice becomes evident when the s.bilirubin levels rise above 2.0 to 2.5mg/dl

Levels as high as 30 to 40mg/dl can occur with sever disease Jaundice occurs when the = b/w bilirubin production &clearance is disturbed by one or more of the following mechanisms: Excessive production of bilirubin Reduced hepatic uptake Impaired conjugation Decreased hepatocellular excretion Impaired bile flow

PRDOMINATLY DIRECT HYPERBILIRUBINEMIA CAUSES OF JAUNDICE PRDOMINATLY DIRECT HYPERBILIRUBINEMIA PRDOMINATLY INDIRECT HYPERBILIRUBINEMIA

Excessive production of bilirubin PRDOMINATLY INDIRECT HYPERBILIRUBINEMIA Excessive production of bilirubin hemolytic anemia's resorption of blood from internal hemor. ineffective erythropoiesis

Reduced hepatic uptake: drugs some cases of Gilbert syndrome

Impaired bilirubin conjugation: physiologic jaundice breast milk jaundice genetic deficiency of glcuronosyl transferase decreased expression of glcuronosyl transferase diffuse hepatocellular diseases

Decrease excretion of conjugated bilirubin: PREDOMINATLY DIRECT HYPERBILIRUBINEMIA Decrease excretion of conjugated bilirubin: deficiency in canalicular membrane transport drug induced canalicular membrane dysfunction hepatocelluler damage or toxicity

Decreased intrahepatic bile flow : inflammatory destruction of intrahepatic bile ducts

Extra hepatic biliary obstruction: gall stone obstruction of biliary tree extra hepatic biliary atresia biliary stricture & choledochal cyst primary sclerosing cholangitis liver fluke infestation carcinoma

HISTORY onset / duration pain nausea & vomiting loss of weight itching color of stool color of urine past history ttt &family history

EXAMINATION color of skin severity of jaundice anemia liver spleen gall bladder ascites

INVESIGATION CBC LFT Prothrombin time Alfa feto proteins UG SG U/S ERCP & PTC Liver biopsy

The End