Severe and chronic pain including that caused by trigeminal neuralgia may be relieved by injection of alcohol close to the nerve.

Alcohol is given intravenously in the treatment of acute poisoning from methanol.

Severe pain including trigeminal neuralgia

0.2ml, for a small nerve root to a maximum of 10ml for blockade of the coeliac ganglion. Injected into the individual nerve root or ganglion. The needle tip should ideally be located by radiographic or fluoroscopic means prior to dose delivery.

Methanol poisoning

A loading dose of 600 – 800mg/kg should be given. If used parenterally this should be in the form of 7.5ml/kg of a 10% infusion of Ethanol in 5% Glucose Solution for Infusion. The infusion should be given over 30minutes preferably via a central venous catheter.

The standard maintenance dose, for an average patient is 120-138mg of 100% ethanol/kg/hr (1.38ml of 10% ethanol/kg/hr) by the IV route.

Blood monitoring should occur every 1-2hours until a concentration of 1-1.5g/L is reached and thereafter at 2-4hourly intervals. After the loading dose maintenance concentrations should be reduced dependant on the normal drinking habits of the patient and any other concomitant treatments.

Patients treated with Ethanol require close monitoring preferably in a critical care area because of the risk of CNS and respiratory depression.

Ethanol can be added to peritoneal dialysate at a concentration of 1-2g/L of dialysate.

Known hypersensitivity to alcohol.

Women and the elderly may be more susceptible to the adverse effects of alcohol ingestion. Unpleasant reactions, similar to those occurring with disulfiram may occur when alcohol is taken concomitantly with chlorpropamide, metronidazole, and some cephalosporins. Alcohol may cause hypoglycaemic reactions in patients receiving sulphonylurea (antidiabetic agents) or insulin, and may cause orthostatic hypotension in patients taking drugs with vasodilator action.

It may also aggravate peptic ulcer disease or hepatic impairment.

Alcohol may enhance the acute effects of drugs which depress the central nervous system, such as hypnotics, antihistamines, muscle relaxants, opioid analgesics, antiepileptics, antidepressants, and tranquillisers.

Alcohol is also known to interact with the following medicines or group of medicines: antihypertensive agents such as ACE inhibitors, adrenergic neurone blockers, beta-blockers, antidiabetic agents (see section 4.4), alpha blockers, angiotensin II receptor antagonists, Bromocriptine, calcium channel blockers, oral coagulants such as Coumarins, phenindione, cycloserine, antifungal agents, Hyoscine, diuretics, metronidazole, nabilone, and procarbazine.

Studies indicate the oral use of alcohol during first and second trimesters can have serious effects upon the foetus, including low birth weight. Use of alcohol during third trimester can cause withdrawal syndrome in babies. To minimise these risks, pregnant women are advised to limit their intake to 1-2 drinks/week (8 or 16g of ethanol). The volume of alcohol used in nerve blocks is of such a small amount, it is extremely unlikely the foetus would be affected. The risk to the foetus from significant methanol poisoning exceeds that of the appropriate treatment.

Alcohol is freely secreted in breast milk in concentrations slightly below those in blood. In all cases the benefit must be weighed against the potential risk prior to using alcohol during pregnancy or lactation.

All processes requiring judgement and co-ordination are affected by alcohol and these include the driving of any form of transport and the operating of machinery.

Effects of alcohol at higher concentrations may include; nausea, vomiting, headache, dizziness and tremor. Alcohol depresses medullary action causing lethargy, amnesia, hypothermia, hypoglycaemia (especially in children), stupor, coma, respiratory depression cardiomyopathy, hypotension or hypertension and cardiovascular collapse.

At low to moderate concentrations, alcohol acts as a stimulant depresses cortical function causing loss of judgement, emotional lability, muscle incoordination, visual impairment, slurred speech, ataxia, dysarthia and nystagmus.

Symptoms: Acute toxicity is primarily one of CNS depression.

Treatment:

In acute poisoning the stomach may be emptied by aspiration and lavage if indicated. If respiration is depressed, assisted respiration may be necessary. It is important to provide good supportive treatment and to keep the patient warm. Fluid balance should be maintained by the use of suitable electrolyte solution, and glucose may be needed for the treatment of hypoglycaemia.

Primary and continuous depressant of the central nervous system. It has a depressant action on the vasomotor-centre.

Subcutaneous tissues:

Alcohol injected hypodermically causes considerable pain followed by anaesthesia. If the injection is made close to the nerves, neuritis and nerve degeneration may occur. Injections in or near nerves are deliberately used to cause anaesthesia of protracted or even permanent character in the treatment of severe pain, for example, in tic doulourex.

Peripheral Nerves:

Alcohol blocks conduction in peripheral nerve by decreasing the maximal values of both the sodium and potassium conductances. The resting potential usually becomes slightly less negative.

Alcohol is rapidly distributed throughout the body. It readily crosses the placenta.

Alcohol is mainly metabolised in the liver and is converted by alcohol dehydrogenase to acetaldehyde and is then further oxidised to acetate. A hepatic microsomal oxidising system is also involved. About 90% to 98% of alcohol is oxidised and the remainder is excreted unchanged by the kidneys and the lungs and also in breast milk, saliva, sweat and other secretions.

There are no additional data of relevance to the prescriber.

Not applicable

None stated

60 months (unopened)

None stated

Colourless ampoules of neutral glass packed into cartons of 10 ampoules, containing 2ml, 5ml, 10ml, 20ml, or 50ml of solution.

None stated.