Cirrhosis of liver refers to formation of nodules in liver parenchymal tissue which on later stages impair the functioning of liver. It is important to manage cirrhosis of liver in initial stages so as to prevent later complications.
What Are The Final Stages Of Cirrhosis Of The Liver?
Final stage of cirrhosis of liver includes fibrosis and scarring of liver. The final stage of cirrhosis has multiple complications which includes portal hypertension, ascites, hepatorenal syndrome, coagulopathy, bone disease (osteopenia, osteoporosis and osteomalacia), anemia, thrombocytopenia, gastroesophageal varices.
Clinical Presentation of Terminal Stage of Cirrhosis
The final stage usually presents with portal hypertension, which refers to elevation of venous pressure gradient to more than 5 mm of Hg. The major cause of portal hypertension is due to increased intrahepatic resistance to blood flow. As there is fibrosis of liver, there is usually difficult passage of flow of blood through the liver and thus this leads to increase in portal pressure. The second cause of portal hypertension is due to increase in splanchnic blood flow. If portal pressure is not controlled it may lead to ascites and variceal bleeding.
Other complication include oesophageal varices which in almost one third of the patient with portal hypertension. The risk varies from person to person. The treatment for varices includes endoscopic variceal ligation, balloon tamponade with Sengstaken- Blakemore tube which compresses the bleeding varices. Octreotide a direct splanchnic vasoconstrictor can also be used. In some cases sclerotherapy is used when all medical treatment fails.
Another complication of cirrhosis which occurs in last stages includes ascites, which refers to accumulation of fluid within the peritoneal cavity. The portal hypertension is the main cause of ascites. Due to increase intrahepatic resistance there is increase in portal pressure. This along with increase splanchnic blood flow leads to formation of ascites.
The treatment of choice is draining of fluid.
Another complication includes development of hepatorenal syndrome. The etiology is unknown but it is observed that along with liver disease renal symptoms also appears. This condition is also seen in cases of refractory ascites (when ascites persist even after giving large doses of diuretics in patient who are following proper guidelines, which includes low intake of salt). The midodrine is considered the best choice for treating such patients.
Hepatic encephalopathy is another complication which develops in end stage of cirrhosis. There is alteration in mental status of the patient and impaired cognitive function. The liver is responsible for removing gut derived neurotoxin, which is not removed in cases of liver cirrhosis. Thus ammonia levels are elevated which get deposited in brain and precipitate neurological symptoms. Patient may exhibit change in personality and at time many electrolyte changes are even seen. Asterixis can be elicited in such patients. Patient who have encephalopathy have liver flap that is sudden forward movement of wrist. The diagnosis of hepatic encephalopathy is made by expert’s clinician.
The treatment is correction of electrolyte imbalance. Lactulose should be used. The alternative treatment is use of metronidazole which decreases the chance of encephalopathy in patient of liver cirrhosis.
In last stages patient suffers from various coagulation related disorders. There is deficiency of vitamin K and clotting factors thus patient is prone for excessive bleeding. Apart from bleeding disorders there occur many metabolic problems. Osteoporosis is common in patient due to malabsorption of vitamin D and decrease calcium ingestion. Various other hematological manifestations occur in patient of cirrhosis.
Ascites and portal hypertension should be dealt in early stages else chance of variceal bleeding and peritonitis increases. Once sepsis occurs the condition of patient worsens. Thus timely management is important step in management of cirrhosis.
Histopathological finding shows extensive scarring and fibrosis. In later stages it is difficult to identify the hepatocyte in microscopy due to extensive fibrosis.
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