| ID | 7 |
|---|---|
| Name | JAUNDICE |
| Cause | A Due to intra-erythrocytic defect: a. Heriditary - Spherocytosis, Haemoglobinopathies, Disorders of glycolysis etc. b. Acquired - Red cells produced by dyserythro-poietic states e.g. vit. B12 and folate deficiency. B. Due to extra-erythrocytic abnormalities: a. Antibodies (autoimmune and isoimmune). b. Physical trauma (prosthetic heart valve), microangiopathic haemolytic anemia. c. Chemical trauma (drugs), d. Infections- malaria, clostridial infections, e. Toic factors associated with inflammatory or neoplastic disease and metabolic failure, f. Splenomegaly. 1. Acute parenchymal liver disease due to hepatitis viruses, toxins, drugs, or alcohol. 2. Immature bilirubin transport mechanism in the newborn especially Prematurity. 3. Congenital defects in bilirubin transport, and 4. Chonic hepatitis and cirrhosis. Cholestatic (Obstructive) Jaundice Cholestasis is failure of bile flow, and its cause may lie any where between the hepatocyte and duodenum. 1. Large duct obstruction : a. Inpaction of a gall-stone in the common bileduct. b. Carinomaof the head of the pancreas. c. Cacinoma of the ampulla of water or bile duct. d. Stricture of the bile duct. e. Sclerosing cholangitis. f. Metastatic tumour. g. Primary biliary cirrhosis. h. Parasitic infestation. 2. Small duct obstruction: a. Drugs and alcohol- which may exert their effects either on the liver cells or on the bile ducts, b. Viral hepatitis, c. Chronic active hepatitis, d. Cirrhosis of liver, e. Cholestasis of pregnancy, f. Following surgery, g. Severe bacterial infection, h. Hodgkins disesase. i. Widespread carcinoma of the liver etc. |
| Signs Symptoms | itching. dark urine. pale stools. loss of appetite. weight loss. fever. mental changes such as tiredness or confusion. abdominal pain. |
| Diagnosis | Bruising of the skin. Spider angiomas (abnormal collection of blood vessels near the surface of the skin). Palmar erythema (red coloration of the palms and fingertips) |
| Investigations | 1. Routine blood film: polychromatophiliaevidence of haemolytic anemia. 2. Reticulocyte count: 3. Bone marrow: hyperplasia. 4. Heptoglobin & hemopexin: or absent 5. Lactate dehydrogenase: 6. LFT : normal except billirubin Hepatocellular Jaundice Hepatocellular jaundice results from inability of the liver to transport bilirubin into the bile as a result of liver cell damage. In hepatocellular jaundice the concentration in the blood of both unconjugated and conjugated bilirubin increaseit might be due to variable way through which bilirubin transport is disturbed. Jaundice ranges from mild to very severe. A. Laboratory studies: Serum aminotransferase levels (AST, ALT)- ? (due to hepatocellular necrosis or inflammation. ALT is more specific for liver function than AST). Alkaline phosphatase- ? (elevation suggests cholestasis or infiltrative liver disease). B. Liver biopsy: percutaneous liver biopsy is the definitive study for determining the cause and extent of hepatocllular dysfunction or infiltrative liver disease. C. Imaging: USG, CT scan, & MRI can be used to demonstrate hepatomegaly, intrahepatic tumors, and changes of portal hypertension. If obstructive jaundice is suspected ERCP (endoscopic retrograde cholangiopancreatography) or PTC (percutaneous transhepatic cholangiography) can identify the cause, location and extent of biliary obstruction. Table: Comparative serum biochemical findings of three types of jaundice. Tests Normal Obstructive Hepatocellular Haemolytic Values Jaundice Jaundice Jundice 1 . Serum Bilirubin a. Total 0.3-l.Omg/dl Mostly Mostly Mostly 5-17 umol/1 Conjugated T Conjugated T Unconjugated T (varies) b. Direct 0.1-0.3mg/dl Incrased Incrased - c. Indirect 0.2-0.7mg/dl Incrased Incrased Incrased 2. Alkaline phosphatases (IU/L) 30-1 15 IU/L Incrased Incrased (+) Normal (++++) 3. Serum amino- ALT 5-35 IU/L Mininally Marked increase Normal transferase ASt 5-40 IU/L incrased in active state 4. Serum proteins - Usually Increased, Normal normal, y-globulin 5. Prothrombin time 12-20 Sees Increased Increased Normal 6. Flocculation test Negative Negative Positive usually Negative |
| Management | A. Haemolytic Jaundice: 1. Blood transfusion in case of severe anemia. 2. Treatment of underlying causesa. Incase of Autoimmune haemolytic anemiaprednisolone 60mg daily for 3-4 weeks. b. Hereditary spherocytosis- splenectomy. c. Thalassemia- blood transfusion, folic acid, bone marrow transplantation, splenectomy. B. Hepatocellular Jaundice: See below under the management of viral hepatitis. C. Cholestatic Jaundice: See in the surgical section- under the management of cholelithiasis/ choledocholithiasis |
| Introduction | Jaundice is a clinical manifestation referring to the yellow appearance of the skin, sclera and mucus membarane resulting from an increased bilirubin concentration in the body fluids. Normal bilirubin level is 0.2-1.2mg/dl and clinically, jaundice may not be recognisable until levels are above 3mg/dl (or 50umol/l); and from 1.2-3mg/dl is called ‘latent jaundice’. Pathophysiological mechanisms giving rise to jaundice fall into following groups: A. Haemolytic jaundice- (increased bilirubin production due to haemolysis). B. Congenital non-haemolytic hyperbilirubinaemia- (Unconjugated hyperbilirubinaemia- Gilbert’s syndrome, CriglerNajjar Type-1 & Type-11; Conjugated hyperbilirubinaemia- Dubin-Johnson syndrome, Rotor’s syndrome). C. Hepatocellular jaundice- (impaired conjugation of bilirubin due to hepatocellular failure). D. Cholestatic or obstructive jaundice- (impaired hepatic bilirubin transport due to post-hepatic obstruction). Type of Hyperbilirubinemia1 - 2 A. Unconjugated hyperbilirubinemia: 1. Hyperbilirubinemia due to Haemolysis- (increased bilirubin production due to red blood cell destruction). 2. Posthepatitis hyperbilirubinemia- (impaired bilirubin uptake and storage). 3. Congenital Unconjugated hyperbilirubinaemia- (impaired bilirubin uptake and storage- Gilbert’s syndrome & Crigler-Najjar syndrome). B. Conjugated hyperbilirubinemia: 1. Hyperbilirubinemia due to Hepatocellular dysfunctiona. Biliary epithelial damage- as in hepatitis, hepatic cirrhosis. b. Intrahepatic cholestasis- as in biliary cirrhosis, sepsis, postoperative jaundice, certain drugs. c. Hepatocellular damage or intrahepatic cholestasis resulting from various causes- e.g spirochetal infections, infectious mono nucleosis, cholangitis, sarcoidosis, lymphomas, industrial toxins. 2. Cholestatic (Obstructive) Jaundice- Biliary obstruction due to mechanical or infective causes (see below under cholestatic jaundice). 3. Congenital conjugated hyperbilirubinemia (hereditary cholestatic syndromes)- Faulty excretion of conjugated bilirubin, as in Dubin Johnson syndrome, Rotor’s syndrome. |
| History | _ |
| Etiology | Most common causes of various types of jaundices are due to1. Viral hepatitis 2. Bile duct obstruction from gall stones or carcinoma of the head of the pancreas 3. Drugs like salphonamides, PAS, rifampicin, methyldopa etc. 4. Secondary deposits of carcinoma in the liver. 5. Infectious mononucleosis. 6. Gilbert’s syndrome. 7. Less commonly- haemolytic anemia, congenital hyperbilirubinaemia etc. Haemolytic Jaundice This results from an increased rate of destruction of red blood cells or their precursors in the marrow causing the production of more bilirubin |
| Clinical Features | 1. The serum bilirubin is dominently unconjugated and rarely exceeds 85 umol (5 mg/100 ml). 2. Most patients have splenomegaly due to excessive reticuloendothelial activities, but not always. 3. Anemia is present. 4. More stercobilinogen and stercobilin in the stool leads to dark coloured. 5. The urine rapidly becomes deep yellow or dark on standing. 6. Other tests of liver function are normal. A. Due to cholestasisLate feature xanthelesma & xanthemas malabsorption weight loss steatorrhoea bleeding tendency Early feature jaundice, dark urine pale stools pruritus anorexia B. Due to cholangitisFever, rigor, pain, biliary infection, hepatic abscess |
| Preventions | _ |
| Treatment | Refer to Management |
| Complications | it can cause a condition called kernicterus. Kernicterus is a type of brain damage that can result from high levels of bilirubin in a baby's blood. It can cause athetoid cerebral palsy and hearing loss |
| Prognosis | _ |
| Types | _ |
| Classification | _ |
| Observation | _ |
| Pathology | _ |
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