drjanak
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Toxicology - Picrotoxin and Barbiturate Poisoning
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07.15.08 (1 month ago)
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Goodman & Gilman’s Manual of Pharmacology
and therapeutics 2008 McGraw-HillBARBITURATE POISONING
The lethal dose of barbiturate varies, but severe poisoning is likely to occur when more than 10 times the full hypnotic dose has been ingested at once. If alcohol or other depressant drugs also are present, the concentrations that can cause death are lower.The treatment of acute barbiturate intoxication is based on general supportive measures, which are applicable in most respects to poisoning by any CNS depressant. Hemodialysis or hemoperfusion is necessary only rarely, and the use of CNS stimulants is contraindicated because they increase the mortality rate (see Chapter 64).
Even the 9th Edition of Harrisson 1980 (28 years ago) mentions that “the modern” treatment of barbiturate intoxication does not include the use of picrotoxin or other analeptics because of their epileptogenic properties. It also says that treatment with Metrazol, picrotoxin and Megimide which enjoyed a brief period of popularity has been generally abandoned.
Using the Goodman Gilman Bibliography for references I found that the paper they have quoted extensively describes the use of Picrotoxin and parts of the paper are reproduced if you are interested.
PICROTOXIN FOR BARBITURATE POISONING
By Eldon M. Boyd, M.D. - Department of Pharmacology
, Queen's University, Kingston, Ontario
Picrotoxin does not directly neutralize the toxic effects of barbiturates: rather it keeps the patient alive until all or most of the depressant drug has beeni oxidized or eliminated from the body. Thus, for example, picrotoxin does not awaken the patient in barbiturate coma; that does not occur until the excess barbiturate has been taken care of by the body. What actually happens is that we superimpose picrotoxin poisoning upon barbiturate poisoning.
The picrotoxin solution is then injected at a rate just sufficienit to keep the patient breathing deeply with a good blood pressure and pulse and in a state of slight hyperreflexia. A useful guide as to dosage is to give enough picrotoxin so that the patient will twitch slightly when pinched, or tapped, or a needle point applied to the skin.
One not familiar with the Pharmacology
of picrotoxin may be tempted to discontinue use of the drug at the onset of a convulsion. On no account should picrotoxin administration be discontinued during a convulsion,
because if the drug is stopped, picrotoxin convulsions are followed by a deep coma, which, added to the barbiturate coma, may prove fatal.
A very practical point is that the administration of picrotoxin requires the constant attendance of a physician, keeping a continuous watch on the patient. If a very large dose of barbiturate has been taken by the patient, picrotoxin therapy may require 12, 18 or 24 hours, and arrangements should be made to have two or more physicians take shifts in watching the patient and administering the drug.
Interesting isn’t it? However the paper does not correlate the end of the treatment to monitoring of respiration or pulse or BP etc Hence your question remains unanswered.
Incidentally this paper was published in the Canadian M. A. J in May 1946!!
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