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Chapter 5: Disorders of the liver 197

Investigations encephalopathy. However, long-term sequelae, e.g. cir-
Liver function tests show hyperbilirubinaemia, high rhosis or chronic hepatitis is rare in survivors.
serum transaminases, abnormal coagulation profile.
Liver ultrasound may be of value to show underlying
chronic liver disease. Specific tests depend on the sus- Complications of chronic
pected underlying cause, e.g. viral serology, paracetamol liver disease
levels.Othertestsincludefullbloodcount,ureaandelec-
trolytes, glucose, calcium, phosphate and magnesium Portal hypertension
levels.
Definition
Management Raised portal venous pressure is usually caused by in-
Treatment is supportive as the liver failure may resolve: creased resistance to portal venous blood flow and is a
Specialisthepatologyinputisessential,ideallypatients
common sequel of cirrhosis. When the portal venous
should be managed in a specialist liver unit. Position- pressure is consistently above 25 cm H 2 O, serious com-
ing at a 20˚ head up tilt can help ameliorate the ef- plications may develop.
fects of cerebral oedema. Monitoring of intracranial
pressure may be necessary in severe encephalopathy. Aetiology
Whilst adequate nutrition is essential the protein in- By far the most common cause in the United Kingdom
take should be restricted to 0.5 g/kg/day or less. Lac- is cirrhosis of the liver. Causes may be divided into those
tulose and phosphate enemas may be used to empty due to obstruction of blood flow, and rare cases due to
the bowel and minimise the absorption of nitroge- increased blood flow (see Fig. 5.5).
nous substances. Oral neomycin can decrease enteric
bacteria. Sedatives should be avoided.
Anytreatable cause, e.g. paracetamol overdose should
Pathophysiology
Venous blood from the gastrointestinal tract, spleen and
be managed appropriately.
pancreas (and a small amount from the skin via the pa-
Complications should be anticipated and avoided

raumbilical veins) enters the liver via the portal vein. As
wherever possible. Regular monitoring of blood glu-
the portal vein becomes congested, the pressure within
cose and 10% dextrose infusions are used to avoid
it rises and the veins that drain into the portal vein be-
hypoglycaemia. Other electrolyte imbalances should
come engorged. If the portal pressure continues to rise
be corrected. Coagulopathy should be treated with in-
travenous vitamin K (although this may not be effec- the flow in these vessels reverses and blood bypasses the
tive due to poor synthetic liver function), fresh frozen liver through the porto-systemic anastamoses (paraum-
plasma should be avoided unless active bleeding is bilical,oesophageal,rectal).Thisportosystemicshunting
present or prior to invasive procedures as it can pre- eventually results in encephalopathy.
cipitate fluid overload. Antisecretory agents, e.g. H 2
antagonists or proton pump inhibitors may reduce Clinical features
the risk of gastrointestinal haemorrhage. Renal sup- The presenting symptoms and signs may be those of
port may be necessary. the underlying disease, (most commonly cirrhosis), of
Systemic antibiotics and antifungals may be used to reduced liver function or features of portal hyperten-

prevent sepsis. sion. Portal hypertension causes oesophageal varices,
Liver support using cellular and non-cellular systems splenomegaly, distended paraumbilical veins (caput

areunderdevelopment;however,livertransplantation medusa), ascites and encephalopathy.
remains the treatment of choice if the patient fails to
improve.
Complications
Prognosis Oesophageal varices can cause acute, massive gastroin-
Outcome is dependent on the degree of encephalopa- testinal bleeding in approximately 40% of patients with
thy. There is over 80% mortality for those with grade IV cirrhosis.Anorectalvaricesarecommon,butrarelycause