Acute barbiturate poisoning

Acute barbiturate poisoning is mostly suicidal but sometimes accidental. There is no specific antidote for barbiturate poisoning. Earlier analeptics such as pentylenetetrazol (Metrazol) and bemegride have been used for the treatment of poisoning. 

Vaccines and sera are biological products that impart active immunity. A foreign substance acts as an antigen, which specifically produces antibodies when administered to an individual. They are two types of immunization 

Cholera vaccines are produced by inactive bacteria and are administered subcutaneously, intramuscularly, or intradermally. Cholera vaccines should not be administered intradermally in children less than 5 years of age. The vaccination is particularly indicated for people living in highly endemic areas, as well as laboratory and medical personnel exposed to Vibrio cholerae. Diphtheria tetanus pertussis (DTP) vaccine can be made either as toxoids or inactivated whole bacteria. Hemophillus influenzae vaccine is a bacterial polysaccharide conjugated to proteins and is given as one intramuscular dose. A booster dose is not recommended. This vaccine is given to all children in cases such as plenia and other at-risk condiUons. 

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Lassen, N. A. Treatment of severe acute barbiturate poisoning by forced diuresis and alkalinisation of the urine. The LancetII, 338 (1960). 

Severe oliguria or anuria may occur in acute barbiturate poisoning, largely as a result of the marked hypotension. 

Acute barbiturate toxicity is characterized by automatism, or a state of drug-induced confusion, in which patients lose track of how much medication they have taken and take more. Death results from respiratory failure. The treatment of poisoning consists of supporting the respiration, preven-... 

Acute barbiturate toxicity is characterized by automatism, or a state of drug-induced confusion, in which patients lose track of how much medication they have taken and take more. Death results from respiratory failure. The treatment of poisoning consists of supporting respiration, prevention of hypotension, as well as diuresis, hemodialysis and, in the event of phenobarbital poisoning, the administration of sodium bicarbonate. Tolerance does not develop from lethal doses. The abrupt withdrawal from barbiturates may cause tremors, restlessness, anxiety, weakness, nausea and vomiting, seizures, delirium, and cardiac arrest. 

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 hertwperfusion is necessary only rarely, and the use of CNS stimulants is contraindicated because they increase the mortality rate (see Clmpter 64). 

Bumetanide is used in the treatment of renal insufficiency and, in conditions which warrant forced diuresis regimens for the control and management of acute drug poisoning e.g., barbiturate poisoning in attempted suicide cases. It is also employed in the treatment of oedema. 

The antidotal action of the barbiturates is probably limited to the effects of chlordan on the nervous system. They most likely have no beneficial antagonistic action against the delayed parenchymatous degenerative changes produced by chlordan (4). Therefore, they are primarily only of possible value in acute poisoning in which severe stimulation of the central nervous system may be the primary cause of death. 

Chlorpromazine has sometimes been used to treat amfetamine psychosis, for example due to acute poisoning in children who did not respond to barbiturates (14). 

SAFETY PROFILE Poison by ingestion, intraperitoneal, rectal, subcutaneous, and intravenous routes. Human systemic effects by intraarterial route acute arterial occlusion by rectal route respiratory depression, body temperature decrease, general anesthetic. An experimental teratogen. Experimental reproductive effects. An intravenous anesthetic. When heated to decomposition it emits toxic fumes of NOx and Na20. See also PENTOTHAL and BARBITURATES. 

Barbiturates have Uttle effect on the pupils. However, in acute or chronic poisoning a sluggish pupillary light reaction is common. 

Toxicology S. is rapidly absorbed after oral uptake, is metabolized mainly in the liver, and rapidly eliminated. Symptoms of intoxication are initial restlessness, anxiety, vomiting, then convulsions of the extensor muscles (1 or more/minute), the convulsions are again triggered by external stimuli. Therapy for acute poisoning gastrolavage and administration of activated charcoal - for severe poisoning barbiturate narcosis and administration of muscle relaxants. 

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