When there is decompensated cirrhosis, the liver has too many scars and stops working properly. Decompensated cirrhosis patients end up developing many life-threatening symptoms and complications.
What Are The Symptoms Of Decompensated Cirrhosis?
Patients with decompensated cirrhosis develop a variety of symptoms such as fatigue, lack of appetite, nausea, jaundice (yellowish coloration of skin and mucous), weight loss, stomach pain, impotence, bruising and bleeding and other life-threatening problems.
Because the liver stops performing its multiple tasks, many other complications can begin to emerge. The Complications Of Cirrhosis Can Be:
- The accumulation of fluids in the body due to a combination of factors, such as portal hypertension, albumin shortage and renal dysfunction. Ascites is the accumulation of fluid in the abdominal cavity. Edema is the accumulation of fluid in the extremities, especially in feet and legs.
- Hemorrhages (coagulopathy) that are triggered when the liver stops producing clotting factors. In addition, the concentration of platelets (necessary for coagulation) decreases as a result of dilation of the spleen.
- As the disease progresses, there is a loss of bone mass and density.
- Under normal conditions, the spleen stores white and red blood cells and platelets. The enlarged spleen is a consequence of the forced introduction of blood into the organ when portal hypertension occurs. When the spleen is dilated, it loses the ability to store red and white blood cells and platelets.
- Liver hardening due to destruction of hepatocytes, which can be palpated with a physical examination.
- The damaged liver cannot regulate the production and breakdown of some female and male hormones. In women, this can cause menstrual irregularities, and in men, gynecomastia (increase in breast size).
- Mental alterations are due to several factors. The toxic substances that normally filter the liver, such as ammonia, reach the brain. Symptoms of encephalopathy include personality changes, alterations in sleep pattern, violent behavior, and clumsiness of movements, feeling dizzy, confusion, stupor, and coma.
- Itching (pruritus) that can be debilitating. The cause of pruritus seems to be blocking the bile flow complicated by jaundice.
- Renal function deteriorates when there is decompensated cirrhosis, which contributes to fluid retention (ascites, edema) and various kidney disorders.
- The weakening of the muscles can appear because of the inability of the liver to metabolize proteins, which can make cirrhotic patients more prone to bone fractures.
- Scar tissue in the liver restricts blood flow and causes portal hypertension, which may end up causing ascites, spontaneous bacterial peritonitis, varicose veins, and other life-threatening complications.
- Spontaneous bacterial peritonitis occurs when the body’s natural bacteria enter the ascites fluid and cause a serious infection.
- The veins of the stomach, esophagus and rectum stretch and dilate in such a way (due to portal hypertension) that varicose veins appear with the potential to cause internal bleeding.
When the liver becomes completely mismatched and fails to perform its function, it leads to terminal liver disease. The objective in this stage is to control the complications derived from the deterioration of the liver. The treatment of people with decompensated cirrhosis usually consists of administering interferon and drugs without ribavirin. If patients are treated at this stage, it is usually done in a transplant center to monitor them closely.
The results of some small studies on anti-Hepatitis C Virus treatment in infected people awaiting a liver transplant have shown some success in achieving a sustained virological response and even a modest improvement in liver function. In addition, some studies have shown that eliminating HCV before liver transplantation prevents reinfection after transplantation. Currently, the only potentially effective remedy during the terminal stage is liver transplantation.
Conclusion
The clinical course of decompensated hepatic cirrhosis is very variable and depends on several factors: the ability of hepatic synthesis (also called liver reserve), the cause of cirrhosis, the possibility of stopping or slowing the process of liver damage and the development of hepatocellular cancer. As the disease progresses, the portal pressure increases and the liver function decreases, bringing serious consequences.
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