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Cirrhosis of the liver and its effects

Chronic Hepatitis C  (CHC) is one of the diseases that may lead to cirrhosis of the liver (the normal liver cells are irreversibly replaced by scar tissue). The loss of normal liver tissue increasingly slows the processing of nutrients, hormones, drugs, and toxins by the liver, as well as the production of proteins and other substances made by the liver. The scar tissue that forms in cirrhosis damages the structure of the liver, progressively making the flow of blood through the liver more difficult.

People with liver cirrhosis may develop other complications:

- When the liver is  heavily scarred, the blood cannot get through the liver at the normal pace because of the obstruction presented by the scar tissue, thus creating a higher than normal pressure in the portal vein - the main vein feeding the liver (portal hypertension).

- The portal hypertension often causes ascites, which is the accumulation of fluid in the abdominal cavity. If the ascites becomes tense, it can cause an umbilical hernia (a protruding belly button).

- The portal hypertension may lead to the formation of varices, when the  increased blood pressure causes the dilatation of the veins with thin walls (mainly the blood vessels around the oesophagus or around the anus); in certain conditions these varicose veins may burst, causing blood loss.

- Cirrhosis sometimes may lead to jaundice (a yellowing of the whites of the eyes and/or the skin) due to the accumulation of bilirubin in the blood. If the bilirubin is excreted in the urine, the urine may turn dark.

- Cirrhosis may also lead to hepatic encephalopathy, which manifests as fatigue or confusion , and is caused by ammonia and other by-products of protein digestion which are not cleared properly by the liver from the bloodstream .

- People with cirrhosis often bruise easily because the liver manufactures reduced amounts of clotting factors. Additionally, the level of platelets in the blood may be lower than normal if the spleen is enlarged.
 

 

Portal Hypertension 

Portal hypertention is a state in which the pressure within the hepatic portal vein is increased, causing enlargement of the spleen, enlargement of the veins in the oesophagus (gullet) (which may rupture to cause severe bleeding), and accumulation of fluid in the peritoneal cavity (ascites). The commonest cause is cirrhosis, but other diseases of the liver or thrombosis of the portal vein can also produce it.

Treatment is :

  
 
 
Ascites

Occurring in advanced cirrhosis, the accumulation of fluid in the abdominal cavity, or ascites, is related to portal hypertension, significant reduction in serum albumin, and renal retention of sodium. The volume of abdominal ascites in adults with cirrhosis may  sometimes reach levels of 10 to 12 liters (20 to 24 pints). Ascitic fluid may accumulate in the scrotum and in the chest cavity, where its presence, combined with the upward pressure on the diaphragm from the abdominal fluid, may affect breathing. Appetite also is often reduced by the abdominal distention.

Ascites is treated by the removal of fluid directly from the abdomen by needle puncture to ease discomfort and breathing. Patients are placed on diets low in salt, and they are given diuretic drugs to increase the output of water by the kidneys. If these measures do not control massive ascites, ascites can be drained internally into the general venous blood system by running a plastic tube from the abdominal cavity, under the skin of the chest, into the right internal jugular vein of the neck (peritoneovenous shunt of LeVeen). 


 
Varices

As said before, portal hypertension is the increased pressure in the portal vein and its tributaries resulting from increased resistance to the blood flow into the liver, and is usually caused by the scarring process of cirrhosis. The increased pressure causes varices, or dilatations of the veins tributaries to the portal vein. When varices are located in superficial tissues and have thin walls, they may rupture and bleed. The two main locations where bleeding is likely to occur are the lower oesophagus/upper stomach and the perianal region.

Oesophageal varices are likely to bleed most heavily, and this bleeding is sometimes associated with the onset of hepatic encephalopathy or coma. Because of their location at the lower end of the oesophagus and/or the upper portion of the stomach, bleeding from these varices is often difficult to control.

If discovered before bursting, or after successful emergency treatment, varices can be treated long term with beta blockers, which induce a reduction in the portal vein blood pressure.

If varices burst, they can be obliterated using endoscopically placed rubber bands or injections with a drug that turns the varices into sclerotic tissue. If the bleeding is heavy, a rubber baloon may be placed at the lower end of the esophagus or the upper portion of the stomach, and is then inflated, in order to stop the bleeding by pressure. If treatment via endoscopy fails to stop the bleeding, a TIPS (Transjugular Intrahepatic Portosystemic Shunt) can be created by inserting a short metal mesh tube through a neck vein into the liver, redirecting part of the blood flow from the portal vein to another vein in the liver. Another possibility is to surgically redirect some of the blood flow from the portal vein around the liver.

Some physicians consider the occurence of bleeding oesophagial varices as a condition more serious than a heart attack. It is vital that the patient is taken without delay to a hospital at the first signs of bleeding. The symptoms are vomiting up blood and/or passsing of dark, almost liquid, bowel motions (melena).
 


 
Hepatic encephalopaty

Hepatic encephalopathy refers to the changes in the brain that occur in patients with advanced acute or chronic liver disease. If liver cells are damaged, certain substances that are normally cleansed from the blood by the healthy liver are not removed (ammonia mainly, and other toxins). A patient with chronic hepatic encephalopathy may develop progressive loss of memory, disorientation, untidiness, and muscular tremors, leading to a form of chronic dementia. The ingestion of protein invariably aggravates these symptoms.

The treatment of hepatic encephalopathy involves, first, the removal of all drugs that require detoxification in the liver and, second, the reduction of the intake of protein. Restricting the amount of protein in the diet will generally lower the levels of aminoacids and ammonia in the bloodstream and brain. Most physicians advise their patients with this condition to eat only about 40 grams of protein a day, and will prescribe lactulose or neomycin to lower amino acid production. Non-meat proteins, such as those found in vegetables and milk, are preferred. Certain amino acids are used in treatment, since they are considered less likely to cause mental impairment. A dietary supplement rich in these amino acids is used at many liver treatment centers.
 

 

The Child-Pugh classification system

The Child-Pugh classification is a scoring system used to determine the prognosis with cirrhosis.

Scoring is based upon several factors: albumin, ascites, total bilirubin, prothrombin time, and encephalopathy, as follows:
 

 

Score: 
1 point

Score: 
2 points

Score: 
3 points

Serum Albumin (g/dL)

>3.5 

3.0 - 3.5 

<3.0

Serum Bilirubin (mg/dL) 

<2.0 

2.0 - 3.0 

>3.0 

Prothrombin time (seconds) 

1 - 4 

4 - 6 

>6  

Ascites 

none 

moderate 

severe

Encephalopathy 

none 

mild 

severe 

>3 means higher than 3
<3 means lower than 3

The three classes and their scores are:

Patients with a score of 10 or more (in the Class C category) have a prognosis with 1-year survival being about 50%. Patients with Class A or B have a better prognosis of 5-years, with a survival rate of 70%- 80%.

Additional poor prognistic indices include refractory ascites, albumin < 3.2 gm/l, and a recent episode of SBP (spontaneous bacterial peritonitis). All individually are associated with a one-year survival of 50% or less.

Example of how this score is calculated:
Let's assume that someone has the following test results (these are imaginary results, just for the purpose of the exercise, therefore they may well not be encountered in real life):

Serum Albumin (g/dL)   4.1
Serum Bilirubin (mg/dL)    3.3
Prothrombin time (seconds)    5
Ascites    none
Encephalopathy    none

We look in the scoring table above, and find the number of points corresponding to each test result, as follows:

For Serum Albumin higher than   4.1 g/dL   we find in the scoring table   1 point
For Serum Bilirubin higher than   3.3 mg/dL   we find in the scoring table   3 points
Prothrombin time ()    5 seconds   we find in the scoring table   2 points
Ascites    none   we find in the scoring table   1 point
Encephalopathy    none   we find in the scoring table   1 point
        T O T A L points:   8 points

According to the Child-Pugh classification system, this score of 8 points would place the patient in Class B.


Webmaster & Author:  Daniel Dimitriou      

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