Acute Barbiturate Poisoning

ACUTE BARBITURATE POISONING

Mostly suicidal, sometimes accidental; infrequently encountered now due to in-availability of barbiturates. However, the principles of treatment apply to any CNS depressant poisoning.

Manifestations are due to excessive CNS depression—patient is flabby and comatose with shallow and failing respiration, fall in BP and cardiovascular collapse, renal shut down, pulmonary complications, bullous eruptions.

Lethal dose depends on lipid solubility. It is 2–3 g for the more lipid-soluble agents (short-acting barbiturates) and 5–10 g for less lipid-soluble phenobarbitone.

Treatment

1. Gastric lavage; leave a suspension of activated charcoal in the stomach to prevent absorption of the drug from intestines.

2. Supportive measures: such as, patent airway, assisted respiration, oxygen, maintenance of blood volume by fluid infusion and use of vasopressors— dopamine may be preferred for its renal vasodilating action.

3. Alkaline diuresis: with sodium bicarbonate 1 meq/ kg i.v. with or without mannitol is helpful only in the case of longacting barbiturates which are eliminated primarily by renal excretion.

4. Haemodialysis and Haemoperfusion (through a column of activated charcoal or other adsorbants) is highly effective in removing longacting as well as shortacting barbiturates.

There is no specific antidote for barbiturates. In the past, analeptics like metrazol, bemegride, etc. have been used in an attempt to awaken the patient. This is dangerous, may precipitate convulsions while the patient is still comatose—mortality is increased. The emphasis now is on keeping the patient alive till the poison has been eliminated.