Clinical Consequences of Liver Disease
Vitamins A, D, E and K are all stored in the liver, as is vitamin B12. Therefore, in liver damage, you can’t store as many of these as you would like to.
Note that there are no valves in the portal circulation.
The portal supply is 70% of the blood that the liver receives. The other 30% is supplied by the hepatic artery.
The four main veins that contribute to the portal system are:
- Splenic vein
- Superior mesenteric
- Inferior mesenteric
- Portal Vein
Patterns of damage:
- Hepatocytes – hepatocellular – transaminases are raised
- Bile ducts – cholestatic –
- Blood vessels (vasculitis or autoimmune damage)
- Mixed damage
- Secondary (very common! Particualy with GI malignancy)
Patterns of injury
Acute – 80-99% will recover, 1-20% will develop fulminant liver disease.
Cirrhosis – effects
- Low albumin (due to protein synthesis problems)
- Bleeding – internal and external (bruising) – due to problems with clotting factor synthesis. Clotting factors 2, 7 9 and 10!!
- Encephalopathy – confusion – you test this with a piece of paper and 4 randomly numbered dots – the patient has to join these dots as soon as possible. If they are getting slower at doing this, they are getting more ill – if they are doing it quicker, then they are getting better.
- Portal hypertension
- Ascites (also has other causatory factors)
- Hepatocellular carcinoma – this arises in up to 1/3 of patients with cirrhosis
- Very common in patients with Hepatitis B – so very common in places where this is endemic.
Alcohol consumption in the EU in general is falling, but in the UK it is rising. As a result, death as a result of cirrhosis is also increasing in the UK and decreasing in the EU.
6 units a day for 4 weeks is enough to make a fatty liver! Fatty liver can lead to alcoholic hepatitis, which then leads to cirrhosis and possible hepatoma.
There are various scoring systems for how bad the liver damage is. The most widely used of these is the Childs-Pugh score.
Normal portal pressure is 6mmHg. In portal hypertension, this can be as high as 12mmHg.
Average life expectancy after ascites has developed is 2 years.
5-10% of patients with ascites as resistant to diuretic treatment
Average volume of ascites is 20L
The draining techniques is known as paracentisis.
Diuretics have slightly lower morbidity and mortality than paracentisis, although the difference is very small. Therefore you should try diuretics first, then try paracentisis.
Spontaneous bacterial peritonitis – can result when you drain ascitic fluid with paracentisis. You can reduce the risk of this by giving albumin when you take fluid.
Hepatorenal syndrome – renal failure secondary to liver failure.
The main treatment is glypressin. This reduces the risk of bleeding in the short term. In the longer term, you probably want to band the varices.
Basically, give patients lots of banding and secondary prophylaxis (beta-blockers, or if not tolerated, then give nitrates) and at the same time you should try sclerotherapy.