Cirrhosis and COMPLICATIONS of CIRRHOSIS with Treatment


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).
Alcoholic Liver Disease3

Cirrhosis and COMPLICATIONS of CIRRHOSIS with Treatment

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 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 is a common and important com­plication of cirrhosis of liver.


  • 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).


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


  • 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.


  • 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.


  • 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.


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


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


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


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