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CLINICAL SOLVING PROBLEM PATIENT WITH JAUNDICE AND ASCITES

ASCITES
DEFINITION Pathological accumulation of fluid in the peritoneal cavity. AETIOLOGY Abdominal Malignancy * C - Mesothelionia - Metastatic spread from tumours

Infections esp. TB * Albumin eg. Nephrotic syndrome Congestive cardiac failure C Constrictive pericarditis Pancreatitis * Myxoedema Cirrhosis P C Budd Chiari syndrome * P

IVC or portal vein thrombosis P Meigs syndrome Portal nodes P 30 g/l in diseases marked * Ascites with portal hypertension P Common causes C

PATHOGENESIS
Two theories have been proposed. Underfilling theory: this suggests that the primary abnormality is inappropriate sequestration of fluid within the splanchnic vascular bed due to portal hypertention. This results in a decrease in intravascular volume and the kidney responds by retaining salt and water.

The overflow theory: the primary abnormality is inappropriate retention of salt and water by the kidney in the absence of volume depletion.

MECHANISMS OF ASCITES FORMATION


Combination of liver failure and portal hypertension. Liver failure decreases renal blood flow, resulting in retention of salt and water. Secondary hyperaldosteronism due to increased renin release and decreased metabolism of aldosterone by the liver. Decreased metabolism of antidiuretic hormone

Hypoalbuminaemia which decreases colloid oncotic pressure. Lymphatic obstruction resulting in a weeping liver Over production of nitric oxide.

CLINICAL FEATURES
History Abdominal distention Symptoms pain in the abdomen (spontaneous bacterial peritonitis, malignancy). Heart failure, renal failure, or liver disease TB(peritoneal tuberculosis) Malignancy ? Primary tumour

EXAMINATION(SIGNS)
Look for stigmata of underlying disease. Eg. Cirrhosis, cardiac failure, renal failure or malignancy. Full flanks and umbilicus Presence of shifting dullness and or fluid thrill.

INVESTIGATION
Diagnostic paracentesis for proteins - albumin - cell count - cell type - cytology Ultrasonography of the abdomen Peritoneal biopsy Laparascopy

Serum ascitic albumin gradient - Serum albumin conc- ascitic fluid albumin conc. -Correlates directly with portal pressure -Gradient > 1.1 g/dl = portal hypertension.

COMPLICATIONS
Respiratory embarrassment may complicate large amounts of ascites. Spontaneous bacterial peritonitis -ascitic fluid leucocyte count of 500 cells per l - > 250 polymorrphonuuclear cells per l - Rx with non nephrotoxic antibiotics

MANAGEMENT
The most important treatments are: Sodium restriction Diuretics Sodium restriction to 88 mmol per day Fluid restriction is usually not necessary unless the serum sodium cooncentration drops below 120 mmol/l When the patient has tense ascites, 5 liters or more of ascitic fluid should be removed to release shortness of breath.

To diminish early satiety. To prevent pressure related leakage of fluid from the site of a previous paracentesis.

DIURETIC THERAPY
The most effective diuretic regimen is a combination of spironolactone and furosenide > 90% of patients respond to this therapy. Diuretic resistant ascites ie when patients do not respond to diuretic therapy- 300 mg spironolactone or 120 mg furosemide/day Therapeutic paracentesis with infusion of salt free albumin. This decreases hospital stay.

Peritoneovenous shunting- limited by high rate of infection and DIC. Transjugular intrahepatic portosytemic stent shunt (TIPS) -Non- surgical side to side shunt -Consists of a stented channel between a main branch of the portal vein and the hepatic vein. Extracorporeal ultrafiltration of ascitic fluid with reinfusion. Liver transplantation.

PROGNOSIS
Ascites indicates decompensation of previously asymptomatic chronic liver disease. It is a poor prognostic sign.

JAUNDICE
DEFINITION Yellow pigmentation of skin, sclera and mucosae due to plasma bilirubin. Visible at Bilirubin > 35mol/L Classified by: a) the site of the problem Prehepatic Hepatocellular Cholestatic / obstructive
b)The type of circulating bilirubin -conjugated or unconjugated.

UNCONJUGATED HYPERBILIRUBINAEMIAS
Overproduction haemolysis eg. Drugs antimalarials. Impaired hepatic uptake - drugs contrast agents - Rifampicin - congestive cardiac failure Impaired conjugation- glucoronyl tansferase deficiency

- Gilberts syndrome - Crigler Najjar syndrome

CON JUGATED HYPERBILIRUBINAEMIA


Hepatocellular dysfunction -There is hepatocyte damage usually with some cholestasis.

-Causes: 1) Viruses Hepatitis A,B,C,D,E - CMV - EBV

2) Drugs Paracetamol overdose - Isoniazid, rifampicin, pyrazinamide - Monoamine oxide inhibitors 3) Alchoholic hepatitis 4) Liver metastases 5) Abscesses 6) Autoimmune hepatitis 7) Septicaemia

8) Leptospirosis 9) alpha1 antitrypson deficiency 10) Budd- Chiari 11) Rotor syndrome 12) Toxins eg. Carbon tetrachloride 13) Fungi (Amanita phalloides)

Impaired hepatic excretion -Primary biliary cirrhosis -Extrinsic compression of bile duct. -Drug induced cholestasis Flucloxacillin- may occur weeks after treatment Co- amoxiclav Steroids (anabolic, the pill ) Sulphonylureas Prochloperazine Chlorpromazine

Common bile duct gall stones Pancreatic cancer Lymph nodes at the porta hepatis Choledochal cyst Biliary atresia Mirrizis syndrome obstructive jaundice from common bile duct compression by a gall stone impacted in the cystic duct often associated with cholangitis.

Associated with dark urine - pale stools - intractable pruritus

CLINICAL FEATURES
History: Blood transfusions Intravenous drug use Body piercing, tattoos Sexual activity, travel abroad. Jaundicel contacts Family history Alcohol consumption Drugs

Tests: Urine Prehepatic Bilirubin absent : acholuric jaundice -Urobilinogen abscent in obstructive jaundice Haematology FBC - Clotting - Blood film - Reticulocyte count - Coombs test

Biochemistry U and E - LFT US Scan dilated bile ducts > 6 mm obstruction Liver biopsy CT MRI

CAUSES OF JAUNDICE IN PATIENTS WITH ASCITES DUE TO CIRRHOSIS.

Sepsis (UTI, pneumonia, peritonitis) Malignancy eg. HCC Alcohol Drugs