The symptom called ‘Jaundice’ refer to yellow appearance of the skin, sclera and the mucous membranes resulting from the increased bilirubin concentration in body fluids. It is detectable while the plasma bilirubin exceeds 50µm o1/1(3mg/dl). The internal tissues and the body fluids are colored yellow but not the brain since bilirubin does not cross blood-brain barrier other than in immediate neonatal period.
Cholestasis is the failure of bile flow, and the cause may lie anywhere between hepatocyte and duodenum. The jaundice becomes gradually severe in the unrelieved cholestasis because the conjugated bilirubin is unable to enter bile canaliculi and passes back into blood. It happens also because there is the failure of the clearance of un-conjugated bilirubin arriving in liver cells.
Aetiology: - Cholestasis may be because of failure of the hepatocytes to generate the bile flow, to the obstruction to bile flow in bile ducts in portal tracks, or to the obstruction to bile flow in extra-hepatic bile ducts between porta hepatic and papilla of Vater. The cause of cholestasis may operate at more than one of these levels. Those confined to extra-hepatic bile ducts can be amenable to the surgical correction.
Clinical Feature: - The clinical features in the cholestasic jaundice include those to the cholestasis itself and to the development of the cholangitis consequent on biliary obstruction. Jaundice is very variable. It may be static or may fluctuate. If it is prolonged and severer; it may give the skin a greenish look. Stools are pale or clay colored for the deficiency of pigment derived from bilirubin. The urine is dark from renal excretion of conjugated bilirubin. Many patients may have pruritus generated and the accessible parts of the body may also show scratch marks. The lipid deposits may develop in skin during prolonged cholestatic jaundice. Most of them are xanthelasmas on eyelids but sometimes xanthomas also occur. Prolonged cholestasis may also cause marked mal absorption leading to weight loss, severe steatorrhoea, and hemorrhagic tendency because of Vitamin K deficiency associated with the calcium and vitamin D deficiency. Clinical and biochemical evidence of the biliary cirrhosis and hepatocellular failure occur eventually. Cholangitis, due to the infection with or without rigors and the coincident pain and the hepatic tenderness may indicate the development of the hepatic abscess. None of the features are pathognomonic of any particular cause, but are more likely to be in some diseases than the others.
Investigation & Treatment: - Examinations in individual patients are determined by clinical findings. But where there is no obvious cause for cholestasis, initial efforts are directed to identifying efforts for biliary obstructions. In all cases ultra-sonography should be carried out. Test for anti-mitochondrial antibody should be performed. ERCP is a better investigation when the biliary tract is dilated particularly if dilatation extends to lower common bile duct. PTC is used where ERCP is not available. ERCP is appropriate when ultra-sonography does not show the dilated bile ducts, if there is no clinical clue to the cause of cholestasis or if conditions like sclerosing, cholangitis arise or ulcerative colitis is present. Liver biopsy is strongly recommended as this type of jaundice is a major manifestation of liver diseases such as the spider telangiectasias.
(Abbreviations Used:- ERCP: - endoscopic retrograde cholangiopancreatography; PTC: - percutaneous transhepatic cholangiography)
