Cirrhosis and COMPLICATIONS of CIRRHOSIS with Treatment

Cirrhosis

Cirrhosis means there is irreversible liver dam­age with extensive fibrosis, and formation of re­generative nodules. There is hepatocyte necrosis with nodular regenera­tion of liver parenchyma. characterized pathologically by liver scarring with loss of normal hepatic architecture and areas of ineffective regeneration Cirrhosis represents a late stage of progressive hepatic fibrosis characterized by distortion of the hepatic architecture and the formation of regenerative nodules.

• This leads to jaundice, edema, coagulopathy, meta­bolic abnormalities, portal hypertension, gastroesoph­ageal varices, splenomegaly, ascites, and hepatic encephalopathy.
• Clinical symptoms of the disease result from loss of functioning liver cells and increased resistance to blood flow through the liver (portal hypertension).

Cirrhosis may be :

• 1. Alcoholic
• 2. Crypto~enic and posthepatitic
• 3. Biliary
• 4. Cardiac
• 5. Metabolic and inherited
• 6. Drug-relate’d.

COMPLICATIONS OF CIRRHOSIS

• Complications of cirrhosis are portal hypertension, splenomegaly, ascites, hepatic encephalopathy, spon­taneous bacterial peritonitis, hepatorenal syndrome, hepatocellular carcinoma.
• Congestive splenomegaly is seen in portal hyperten­sion.
• There is thrombocytopenia and pancytopenia.

PORTAL HYPERTENSION

• Portal hypertension is a common and important com­plication of cirrhosis of liver.

ASCITES

• Ascites is accumulation of excess fluid within the peri­toneal cavity. Common cause is cirrhosis.
• There is total body sodium and water excess leading to sequestration of fluid within the splanchnic vascu­lar bed due to portal hypertension.

Factors leading to ascites

• · Decreased intravascular volume leads to reten­tion of salt and water by kidneys.
• · There is peripheral arterial vasodilatation which causes hypotension, and release of vasoconstric­tors leading to increased cardiac output.
• · There is increased sympathetic outflow leading to decreased natriuresis due to activation of re~ . nin angiotensin system, decreased ANP (atrial < natriuretic peptide).
• · Increased hydrostatic pressure and ascites, are also due to portal hypertension.
• · Hypoalbuminemia also causes ascites.
• · Obstruction of hepatic sinusoids and Iymphatics lead to ascites.
• · Renal factors like failure to excrete water load also cause ascites.

Clinical Features

• There is increased abdominal girth, shortness of breath, shifting dullness, bulging offlanks, fluid wave or fluid thrill.

ASCITES Treatment

• Treatment of precipitating factors, liver disease, infections.
• Paracentesis is done with a small gauge needle for diagnostic purposes and also to relieve symp­toms due to excessive accumulation of fluid.
• 1 Kg/day of fluid is removed ideally.
• Salt restriction to 2 g NaCI / day.
• Fluid restriction 1 L /day.
• Diuretics like Frusemide, Spironolactone may be given.
• Albumin replacement IV.
• In refractory ascites, side-ta-side portacaval shunt may be done.
• Surgical implantation of a plastic Peritoneo­venous shunt.
• TIPS (Trans~ugular intrahepatic portosystemic shu nt).

SPONTANEOUS BACTERIAL PERITONITIS

• Treatment depends on source of infection. The prog­nosis is poor.

HEPATORENALSYNDROME

• This is a serious complication with azotaemia, sodiurTL retentior’l, oliguria. This is due to splanchnic vasodila­tation leading to severe renal vasoconstriction in cir­rhosis.
• It is precipitated by gastrointestinal bleeding, sepsis, diuretics, paracentesis. There is hypovolaemia lead­ing to acute tubular necrosis.
• Serum creatinine level is elevated.

HEPATORENALSYNDROME Treatment

• Salt-poor albumin is given for volume expansion Low dose dopamine IV
• Norepinephrine, Octreotide, Midodrine are help­ful
• Liver transplantation
• IV albumin infusion is especially helpful in spon­taneous bacterial peritonitis.

HEPATIC ENCEPHALOPATHY

• It is a complex neuropsychiatric syndrome.
• There is disturbance of consciousness and personal­ity changes.
• There is asterixis or flapping tremors.
• There is encephalopathy which may be acute or chronic.
• Coma and death may occur. Cause is unknown.
• There is severe hepatocellular dysfunction.
• Portal venous blood is shunted into the systemic cir­culation so that the liver is bypassed. So there is accumulation of toxic substances due to no detoxifi­cation by the liver.
• Ammonia affects the CNS.
• Others toxic metabolites are mercaptans, phenol, short-chain fatty acids, gamma amino butyric acid (GABA), benzodiazepines leading to encephalopathy.
• Gastrointestinal bleeding leads to increased produc­tion of ammonia.
• Increased protein intake leads to increased produc­tion of nitrogenous wastes.
• Diuretics, paracentesis, vomiting, leads to hypokale­mic alkalosis which precipitates encephalopathy.
• Acute infection can also trigger encephalopathy. Alcoholic hepatitis, surgery, cerebral edema can lead to coma and death.

Presentations of hepatic encephalopathy

• Euphoria or depression, confusion, slurred speech, lethargy, deep sleep, coma.
• Neurologic signs are asterixis (flapping tremors-non­rhythmic, asymmetric), rigidity, hyperrexlexia, exten­sor plantars, seizures, EEG signs – triphasic slow wave pattern .
• Fetor hepaticus is a unique musty odour of breath and urine due to mercaptans.

hepatic encephalopathy Treatment

• Supportive
• El i m ination of preci pitati ng factors Decrease protein intake
• Laxatives and enemas – Lactulose acts as os­motic laxative
• Lactulose acts as laxative and also results in acid pH which prevents absorption of ammo­nia as well as ammonia production
• Lactulose is given 30 – 60 ml every hour till diarrhoea occurs. Then it is given 30 ml three· times a day
• Flumazenil, a benzodiazepine antagonist is also useful
• Extra corporeal liver assist devices may be use­ful till liver transplantation
• Liver transplantation.

COAGULOPATHY

• · Thrombocytopenia
• · Reduced fibrinogen (factor – I), prothrombin (factor – II), factor V, VII, IX, X.

COAGULOPATHY Treatment

• Vitamin K may be given. Factor VII is given to correct prothrombin time.

HEPATOPULMONARYSYNDROME

• There is hypoxaemia, platypnea due to right – to ­left intrapulmonary shunt in cirrhosis.
• There is no specific treatment except liver transplan­tation.