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