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 µl

- > 250 polymorrphonuuclear cells per µl

- 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 > 35µmol/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

- Gilbert’s 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 hepatitis4) Liver metastases5) Abscesses6) Autoimmune hepatitis7) 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 Mirrizi’s 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

- Coomb’s 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