JAUNDICE Lana Bourhan Tashtoush. Jaundice a yellowish pigmentation of the skin, the conjunctiva membranes over the sclerae, and other mucous membranes. caused by hyperbilirubinemia. Normal conc. Of bilirubin is 0.2 – 1.2 mg/dL. 1.5 mg/dL (>26µmol/L), three times the usual value of approximately 0.5 mg/dL, for the coloration to be easily visible. Jaundice comes from the French word jaune, meaning yellow. How dose it happen Bilirubin is normaly produced as by product of hemoglobin metabolism. When red blood cells have completed their life span of approximately 120 days, or when they are damaged, their membranes become fragile and prone to rupture. Cellular contents, including hemoglobin, are subsequently released into the blood. The hemoglobin is phagocytosed by macrophages, and split into its heme and globin portions. The globin portion, a protein, is degraded into amino acids and plays no role in jaundice. the heme is then turned into unconjugated bilirubin in the macrophages of the spleen. this unconjugated bilirubin is not water soluble then it bound to albumin and sent to liver. in the liver it is conjugated with glucuronic acid making it soluble in water. Much of it goes into the bile, and thus out into the small intestine. Types of jaundice : Prehepatic (haemolytic) jaundice. Hepatocellular jaundice. Post hepatic jaundice ( obstructive jaundice ). Prehepatic (haemolytic) jaundice. Excessive destruction of red cells. Unconjugated hyperbilirubinaemia. most important to surgeons is hereditary spherocytosis, in which splenectomy may be necessary. Hepatocellular jaundice Failure to remove bilirubin from blood stream. Medical rather than surgical conditions. Surgical intervention may aggravate hepatocellular injury. Post-Hepatic (Obstructive) Jaundice blockage of any duct (intrahepatic or extrahepatic) that carries bile from the liver to the gallbladder or to the small intestine, which prevent excretion of conjugated Bilirubin jaundice due to biliary obstruction; This can occur at various levels within the biliary system. may result from Obstruction within the lumen, Pathology in the wall or External compression ( EC ). etiology of obstructive jaundice The most Common are : Common bile duct stones, LO (most common). Carcinoma of the head of pancreas, EC (2ed most common). Malignant porta hepatis lymph nodes, EC Metastatic tumors (usually from the gastrointestinal tract or the breast). Biliary obstruction can be intra or extrahepatic. Intrahepatic causes: Hepatitis; is inflammation of the liver with diffuse or patchy necrosis. Causes of hepatitis include viruses, drugs, and alcohol. Cirrhosis; results from chronic inflammation of the liver e.g. Alcoholic hepatitis or chronic hepatitis B. or PBC is a chronic, autoimmune progressive, granulomatous destruction of the intrahepatic ducts, more common in females. Drugs; such as anabolic steroids ,chlorpromazine and ceftriaxone directly cause cholestasis. Extra hepatic causes are subdivided into intraductal and extraductal. 1. -Intraductal causes include neoplasms, stone disease, biliary stricture, parasites, primary sclerosing cholangitis, AIDS-related cholangiopathy, and biliary tuberculosis. 2. Extraductal obstruction caused by external compression of the biliary ducts may be secondary to neoplasms, pancreatitis, or cystic duct stones with subsequent gallbladder distension. Gallstones may pass through the CBD and cause obstruction, larger stones can become lodged in the CBD and cause complete obstruction. Mirizzi syndrome is the presence of a stone impacted in the cystic duct or the gallbladder neck, causing inflammation and external compression of the common hepatic duct and thus biliary obstruction. Neoplasms Periampullary carcinomas, gallbladder carcinomas & cholangiocarcinomas. Metastatic tumors and the secondary adenopathies in the porta hepatis. Approach to jaundice 1-HISTORY. 2-PHYSICAL. 3-INVESTIGATIONS. 4-TREATMENT. History: - Jaundice, pale stools, dark urine and pruritus. - pain : (intermittent and severe, dull ache, backache, no pain ) - episodes of indigestion or dyspepsia. - loss of appetite and weight. - general malaise and breathlessness. History: Abdominal pain may be misleading; some patients with CBD stones have painless jaundice, whereas others with hepatitis have pain in the RUQ . History: - Age ,sex , occupation. - drugs, alcohol intake. - Hx of injections , infusions. - Hx of recent travel , blood transfusion ,contact with other jaundice patient. History History of anemia, previous malignancy. known GS disease, previous biliary surgery, hepatitis. Physical Examination: On physical examination signs of jaundice (skin, sclera , mucos membranes). - A high fever and chills suggest a coexisting cholangitis. - Enlarged liver or shrunken liver. - Needle tracks (over the limbs). Physical: Features of cirrhosis & liver failure: - Changes in Mental state for example loss of concentration. - spider naevi. - Ascites and collateral circulation, caput medusae. - Palmar erythema, bruising & oedema. - Dupuytrens, testicular atrophy, Gynaecomastia. - Finger clubbing & leuconychia. Physical: Neoplastic features: Courvoisier sign(palpable GB): when the gallbladder is palpable and the patient is jaundice, the bile duct is unlikely to be obstructed by a stone because previous attacks of inflammation will have caused the gallbladder to become thick-walled, fibrotic and non-distensible. it may be associated with pancreatic malignancy. Physical: Scratch marks over the limbs suggest prolonged cholestasis or high-grade biliary obstruction. Early signs of liver failure Body hair loss Spider naevi “ more than 9 indicates a state of a progressive disease Palmer erythema “Thenar and hypothenar” Dupuytrens contracture Leukonychia Clubbing Late signs: Ill looking, wasted patients. Jaundice. Gynaecomastia. Testicular atrophy. Ascitis. Liver flap. Encephalopathy with cogwheel limb rigidity. Disorientation. Intellectual change. Convulsions & coma.
Pages to are hidden for
"Jaundice Part1"Please download to view full document