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