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Factors affecting treatment under GA and sedation

Agents such as sedatives and general anaesthetics are potentially dangerous in liver disease mainly due to impairment of detoxification.

In the case of halothane, a hepatitis may follow its use especially in the obese, in smokers and in middle aged females and if a halothane anaesthetic has been given in the last 3 months. The precise mechanism is not known. The newer agents e.g. enflurane, sevoflurane are less hepatotoxic and as a result the use of halothane has waned.

 

A patient with a history or signs suggestive of a liver disorder or a high alcohol intake which might potentially cause liver damage should have blood taken for liver function tests (LFT's) and clotting studies.

These should be carried out prior to GA or surgery. Severe bleeding can occur after dental extractions in patients with chronic liver disease so the clotting status must be tested.

Relative analgesia is preferred to sedation with a benzodiazepine. A specialist anaesthetist is required even if GA is acceptable.

 

In many liver diseases brain metabolism is altered and it therefore becomes more sensitive to certain drugs. Encephalopathy can be triggered by sedatives or opiates. In obstructive jaundice, the main risk is bleeding due to vitamin K malabsorption.

If surgery is required in such patients, intravenous vitamin K may be required for several days beforehand to correct any bleeding tendency.

Any patient with jaundice has an increased risk of bleeding excessively following any surgical procedure including dental extractions. A peri-operative infusion of fresh frozen plasma will often be required.

If the patient is severely jaundiced a GA may precipitate renal failure, the Hepato-Renal Syndrome. The risk is decreased if the patient is well hydrated with intravenous fluids and given the osmotic diuretic mannitol to ensure a good urine flow pre, per and post-operatively.

 

Local anaesthesia is not entirely safe in patients with hepatic impairment.

Most of the amide local anaesthetics used in dental practice undergo biotransformation in the liver. Articaine is metabolised partly in plasma and prilocaine receives some metabolism in the lungs.9

However, the liver is the main site of metabolic activity.

All of an injected dose of local anaesthetic will eventually reach the circulation and if metabolism is affected the concentration in plasma will slowly increase. Only about 2% of the drug will be excreted unchanged. This may lead to signs of CNS toxicity with relatively low doses of the anaesthetic, as little as two cartridges in an adult patient may be too much if liver disease is severe.

 

If possible a full dental assessment should be carried out prior to a liver transplant particularly since post-operatively the patient will be immunosuppressed. Invasive dental treatment should only be carried out after consultation with the patient's physician. After transplantation no elective dental treatment should be carried out for the first three months. GA, if needed, must be carried out in units with the required expertise.

 

Dental sedation should only be performed in specialist units for patients with significant liver disease as small doses can lead to coma.

 

 

Ref: British Dental Journal 26 July 2003; Volume 195, No. 2