Jaundice

Jaundice or icterus refers to the yellow pigmentation of the skin or sclera by bilirubin. Bilirubin pigment has high affinity for elastic tissue and hence jaundice is particularly noticeable in tissues rich in elastin content. Jaundice is the result of elevated levels of bilirubin in the blood termed hyperbilirubinaemia. Normal serum serum bilirubin concentration ranges from 0.2-0.8mg/dl, about 80% of which is unconjugated. Jaundice become clinically evident when th total serum billirubin exceeds 2mg/dl. A rise of serum bilirubin between normal and 2 mg/dl is generally not accompanied by visible jaundice and is called latent jaundice.

Classification and features of jaundice

Based on the pathophysiology, jaundice may result from one or more of the following mechanisms;

  1. Increased bilirubin production
  2. Decreased hepatic uptake
  3. Decreased hepatic conjugation
  4. Decreased excretion of bilirubin into bile

Accordingly, a simple classification of jaundice is to divide it into 3 predominant types

  1. Pre-hepatic(haemolytic)
  2. Hepatic
  3. Post-hepatic(cholestatic)

Predominantly unconjugated hyperbilirubinaemia

 

Increased bilirubin producton (haemolytic, acholuric or prehepatic jaundice)

Decreased hepatic uptake

Dereased biirubin conjugation

  • Intra-and extra vascular haemolysis
  • Ineffective erythropoiesis
  • Drugs
  • Prolonged starvation
  • Sepsis
  • Hereditary disorders (Gilbert’s syndrome, Crigler-Najjar syndrome)
  • Acquired defects(drugs, hepatitis, cirrhosis)
  • Neonatal jaundice

 

Predominantly conjugated hyperbilirubinaemia (Cholestasis)

 

Intrahepatic cholestasis (impaired hepatic excretion) Extrahepatic cholestasis (extrahepatic biliary obstruction)
  • Hereditary disorders or ‘pure cholestasis’ (Dubin Johnson syndrome, Rotor’s syndrome, fibrocystic disease of pancreas, benign familial recurrent cholestasis, intrahepatic atresia, cholestatic jaundice of pregnancy)
  • Acquired disorders or ‘hepatocellular cholestasis’ (viral hepatitis, drugs, alcohol induced injury, sepsis, cirrhosis)
 Mechanical obstruction (gallstones, inflammatory strictures, carcinoma head of pancreas, tumours of bile ducts,  sclerosing cholangitis, congenital atresia of extrahepatic ducts)

Hereditary non haemolytic hyperbilirubinaemia

These are a small group of uncommon familial disorders of bilirubin metabolism when haemolytic causes have been excluded. The commonest is Gilbert’s syndrome, while others are Crigler-Najjar syndrome, Dubin-Johnson syndrome, Rotor’s syndrome and benign familial recurrent cholestasis.

 

Neonatal jaundice

Jaundice appears in neonates when the total serum bilirubin is more than 3 mg/dl or more than 85 μmol/l (5 mg/dL) manifests clinical jaundice in neonates.  In newborns, jaundice is detected by blanching the skin with digital pressure so that it reveals underlying skin and subcutaneous tissue. Jaundiced newborns have an apparent icteric sclera, and yellowing of the face, extending down onto the chest.

Causes of neonatal jaundice

 

Unconjugated hyperbilirubinaemia

Conjugated hyperbilirubinaemia

  • Physiologic and prematurity jaundice
  • Haemolytic disease of newborn and kernicterus
  • Congenital haemolytic disorders
  • Perinatal complication (haemorrhage, sepsis)
  • Gilbert’s syndrome
  • Crigler-Najjar syndrome
  • Hereditary (Dubin-Johnson syndrome, Rotor’s syndrome)
  • Infections (hepatitis B, hepatitis C, rubella, coxsackievirus, cytomegalovirus, echovirus, herpes simplex, syphilis, toxoplasma, gram-negetive sepsis)
  • Metabolic (galactosaemia, alpha-1-antitrypsin deficiency, cystic fibrosis, Niemann-Pick disease)
  • Idiopathic (neonatal hepatitis, congenital hepatic fibrosis)
  • Biliary atresia (intrahepatic and extrahepatic)
  • Reye’s syndrome

Classification of neonatal Jaundice

Physiological

Pathological

Most infants develop visible jaundice due to elevation of unconjugated bilirubin concentration during their first week. This common condition is called physiological jaundice. This pattern of hyperbilirubinemia has been classified into two functionally distinct periods

Phase one

  1. Term infants – jaundice lasts for about 10 days with a rapid rise of serum bilirubin up to 204 μmol/l (12 mg/dL).
  2. Preterm infants – jaundice lasts for about two weeks, with a rapid rise of serum bilirubin up to 255 μmol/l (15 mg/dL)

Phase two – bilirubin levels decline to about 34 μmol/l (2 mg/dL) for two weeks, eventually mimicking adult values.

  1. Preterm infants – phase two can last more than one month.
  2. Exclusively breastfed infants – phase two can last more than one month.

 

 

 

  1. Clinical jaundice appearing in the first 24 hours or greater than 14 days of life.
  2. Increases in the level of total bilirubin by more than 8.5 μmol/l (0.5 mg/dL) per hour or (85 μmol/l) 5 mg/dL per 24 hours.
  3. Total bilirubin more than 331.5 μmol/l (19.5 mg/dL) (hyperbilirubinemia).
  4. Direct bilirubin more than 34 μmol/l (2.0 mg/dL).

 

 

 

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