2022 Oxford Handbook of Anaesthesia Oxford Press 5th Edition Export
2022 Oxford Handbook of Anaesthesia Oxford Press 5th Edition Export
2022 Oxford Handbook of Anaesthesia Oxford Press 5th Edition Export
Perioperative considerations
Premedication
PPIs or H2 antagonists should be used preoperatively. RSI will further re-
duce the risks of gastric aspiration. Sedative medication may precipitate or
worsen encephalopathy.
Monitoring
Standard monitoring should be used, with consideration given to invasive
arterial and CVP monitoring. CVP monitoring is controversial but allows
for centrally administered vasopressors and venous access. Perioperative
haemodynamic instability can worsen hepatic function; MAP should be
maintained within 10–20% of preoperative levels. Hepatic blood flow and
O2 delivery should be maintained; CO monitoring may be useful, although
transthoracic echocardiography or oesophageal Doppler may be contra-
indicated in varices.
Drug effects
Even in severe liver disease, the problem is usually one of exaggerated ef-
fects on the CNS, rather than poor liver metabolism. Hepatic blood flow is
altered by anaesthetic drugs (e.g. α- and β-agonists/antagonists), positive
pressure ventilation, PEEP and surgical technique. In most cases, anaesthesia
reduces hepatic blood flow. (See % Drug metabolism and liver disease,
p. 211.) Desflurane best preserves hepatic blood flow, is least metabolised
and has a quicker emergence time, but sevoflurane and isoflurane are also
acceptable volatiles to use.
Regional techniques
Can be useful adjuncts, but neuraxial techniques are contraindicated in the
presence of coagulopathy. Most LAs are metabolised by the liver.
Cardiovascular
Low SVR and arterial pressure, i HR and volume expansion 2° to an acti-
vated renin–angiotensin system seen in both ALF and CLD. Vasopressors
may be required; maintain MAP >75mmHg. Portosystemic, pulmonary and
cutaneous shunting (spider angiomata) contributes to a hyperdynamic, high
CO state, often i by up to 50%. Alcohol excess is associated with car-
diomyopathy; cirrhosis is associated with a high incidence of cardiac dys-
function (‘cirrhotic cardiomyopathy’), and concurrent smoking is a risk
factor for CAD. Preoperative assessment, including echo, where indicated.
Propranolol to reduce portal pressures.
Respiratory
Hypoxia is common and multifactorial in CLD. Ascites causes splinting of
the diaphragm, basal atelectasis and collapse. Excess PEEP will increase
hepatic venous pressure and ICP. Tense ascites may affect respiratory
mechanics; consider percutaneous drainage.
Pulmonary hypertension
Consider echo if suspicion of pulmonary hypertension (see % pp. 139–44).
Encephalopathy
This may be precipitated by sedatives, GI bleeding, infection, surgical op-
erations, trauma, hypokalaemia, constipation or acute severe liver failure.
Coagulopathy
Very common in liver disease; the liver synthesises all clotting factors,
except factor VIII. Coagulopathy is attributed to several mechanisms (d
synthesis of clotting factors and clearance of activated clotting factors,
quantitative and qualitative platelet abnormalities and hyperfibrinolysis).
Consider vitamin K. Reversal of coagulopathy with FFP, cryoprecipitate and
platelets directed by thromboelastography (TEG®)or similar point-of-care
testing (POCT). Ensure adequate provision is made for cross (X)-matched
blood and clotting products.
Renal
CO monitoring/goal-directed fluid therapy (GDFT) may be useful. Tense
ascites may impair renal blood flow and give a falsely high CVP. Avoid hypo-
tension and nephrotoxic drugs, and aim for urine output >1mL/kg/h.
Portal hypertension
Use of oesophageal Doppler/TOE/oesophageal temperature probes is
contraindicated. Treatment with β-blockers may contribute to periopera-
tive hypotension. A low CVP may reduce the risk of variceal or GI bleeding.
Ascites
Consider draining preoperatively as hypotension, hypoventilation and as-
piration are all i with tense ascites.
Hypoglycaemia
Patients with liver disease have impaired hepatic glycogen storage and are
prone to hypoglycaemia. Check blood glucose levels regularly. Give 10%
glucose infusions if <2mmol/L, and monitor plasma K+.
Immune function
Infections of the respiratory and urinary tracts are common. In the pres-
ence of ascites, spontaneous bacterial peritonitis may cause significant
sepsis—have a low index of suspicion. Intraoperative antibiotic prophylaxis
should be given where indicated.
Fluid resuscitation
Sodium chloride 0.9% is recommended 1st line, and sodium bicarbonate
may be considered if significant acidosis. Addition of glucose-containing
fluids if hypoglycaemic. Caution is required as over-resuscitation with crys-
talloid may worsen cerebral oedema.
Other considerations
IM and SC injections risk haematoma formation if coagulopathic or
thrombocytopenic. Care with positioning; the skin may be fragile. Muscle
wasting may leave patients prone to neuropraxia and pressure damage.
Postoperative considerations
• Patients with advanced liver disease will need postoperative intensive
care or high dependency care.
• Postoperative decompensation of CLD carries a high mortality.
• Constipating analgesics, such as opioids, should be prescribed with
concurrent lactulose to prevent encephalopathy.
• Postoperative ileus may also precipitate encephalopathy in cirrhotic patients.
• Complications include delayed wound healing, sepsis, renal impairment
and bleeding.