Barbiturate poisoning

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. 

CaH,3N02. White flaky or crystalline powder, m.p. 126-128°C. Used in (he treatment of barbiturate poisoning, by intravenous injection. 

Analysis of alkaloids, barbiturates, and other drugs and poisons in forensic science 97AC123R. 

Death from overdose of barbiturates may occur and is more likely when more than 10 times the hypnotic dose is ingested. The barbiturates with high lipid solubility and short half-lives are the most toxic. Thus the lethal dose of phenobarbital is 6—10 g, whereas that of secobarbital, pentobarbital, or amo-barbital is 2-3 g. Symptoms of barbiturate poisoning include CNS depression, coma, depressed reflex activity, a positive Babinski reflex, contracted pupils (with hypoxia there may be paralytic dilation), altered respiration, hypothermia, depressed cardiac function, hypotension, shock, pulmonary complications, and renal failure. 

Barbiturates such as amobarbital inhibit NAD-hnked dehydrogenases by blocking the transfer from FeS to Q. At sufficient dosage, they are fatal in vivo. Antin cin A and dimercaprol inhibit the respiratory chain between cytochrome b and cytochrome c. The classic poisons H2S, carbon monoxide, and cyanide inhibit cytochrome oxidase and can therefore totally arrest respiration. Malonate is a competitive inhibitor of succinate dehydrogenase. 

The purpose of this paper is to give some of the results obtained in a study of the antidotal action of barbiturates in chlordan poisoning, and of the metabolic fate of chlordan. 

Table 1. Antidotal Action of Barbiturates in Chlordan Poisoning in Rabbits...

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. 

For cyanide and cyanogen, antidote should be administered as soon as possible. The Lilly Cyanide Antidote Kit contains amyl nitrite, sodium nitrite, and sodium thiosulfate. Cobalt edentate or 4-dimethylaminophenol are alternative antidotes for cyanide poisoning. Benzodiazepines or barbiturates may be required to control severe seizures. 

Furosemide is a highly effective and quick-acting diuretic whose action, hke all of the examined loop diuretics, is associated with blocking reabsorption of ions in the ascending bend of Henle s loop. It is used for edema syndrome of various origins, edema of the lungs and brain, chronic renal insufficiency, some forms of hypertonic crises, and poisoning by barbiturates and other compounds excreted mainly with urine. 

Mannitol (OsmitroL others) [Osmotic Diuretic] Uses Cerebral edema, T lOP/ICP, renal impair, poisonings Action Osmotic diuretic Dose Test dose 0.2 g/kg/dose IV over 3-5 min if no diuresis w/in 2 h, D/C Oliguria 50-100 g IV over 90 min T lOP 0.5-2 g/kg IV over 30 min Cerebral edema 0.25-1.5 g/kg/dose IV >30 min Caution [C, ] w/ CHF or volume overload Contra Anuria, dehydration, HE, PE Disp Inj SE May exacerbate CHF, N/V/D Interactions t Effects OF cardiac glycosides X effects OF barbiturates, imipramine, Li, salicylates EMS Monitor ECG for hypo-/hyperkalemia (T wave changes) OD May cause dehydration, t urine frequency/amount hypotension and CV collapse symptomatic and supportive... 

The principal disadvantages of barbiturates as hypnotics include the development of physical dependence, a relatively low therapeutic index (and the potential of poisoning, as in suicide), suppression of REM sleep, and possible hangover effects. As mentioned above, benzodiazepines (e.g., flurazepam or brotizolam) are hypnotics as effective as barbiturates and are much safer in terms of their therapeutic index, addiction potential, and REM sleep-deprivation effects. Thus benzodiazepines have displaced barbiturates as sedative hypnotics. 

An understanding of common mechanisms of death due to poisoning can help prepare the care-giver to treat patients effectively. Many toxins depress the central nervous system (CNS), resulting in obtundation or coma. Comatose patients frequently lose their airway protective reflexes and their respiratory drive. Thus, they may die as a result of airway obstruction by the flaccid tongue, aspiration of gastric contents into the tracheobronchial tree, or respiratory arrest. These are the most common causes of death due to overdoses of narcotics and sedative-hypnotic drugs (eg, barbiturates and alcohol). 

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