Medical toxicology
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Methanol and ethylene glycol poisonings share many characteristics both clinically and biochemically. Both alcohols are metabolised via alcohol dehydrogenase to their toxic metabolites. Methanol is slowly metabolised to formaldehyde which is rapidly metabolised to formate, the metabolite mainly responsible for methanol toxicity. ⋯ Presence of ethanol will therefore inhibit formation of toxic metabolites from methanol and ethylene glycol. Due to competition for the enzyme, the therapeutic ethanol concentration depends on the concentration of the other two alcohols, but a therapeutic ethanol concentration around 22 mmol/L (100 mg/dl) is generally recommended. Most patients are, however, admitted at a late stage to hospitals not capable of performing analyses of these alcohols or their specific metabolites on a 24-hour basis.(ABSTRACT TRUNCATED AT 400 WORDS)
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By applying a sensible toxicological approach to the general principles of intensive care, an optimum setting for the treatment of poisoning is created. The intensive care unit (ICU) can perform the necessary close observation and monitoring, and thus facilitate rapid detection of symptoms, and the institution of early appropriate treatment. Diagnosis may be complex in poisoning and require continuous qualified interpretation of clinical and analytical data. ⋯ The capacity of the ICU to counteract various toxic effects in a nonspecific way and to provide optimum symptomatic and supportive care is crucial. However, the ongoing toxic effects on the body must always be considered and allowed to guide symptomatic treatment. Thus, clinical toxicology appears to be a specialised branch of intensive care medicine.
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Methaemoglobin is haemoglobin with the iron oxidised to the ferric (Fe ) state from the normal (or reduced) ferrous (Fe++) state. Methaemoglobinaemia refers to the presence of greater than the normal physiological concentration of 1 to 2% methaemoglobin in erythrocytes. Methaemoglobin is incapable of transporting oxygen. ⋯ An intense 'chocolate brown' coloured blood and central cyanosis unresponsive to the administration of 100% oxygen suggests the diagnosis. A simple bedside test using a drop of the patient's blood on filter paper helps to confirm the clinical suspicion. Methaemoglobin can be quantitated rapidly by a spectrophotometric method.(ABSTRACT TRUNCATED AT 250 WORDS)
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This review examines the various clinical options used to elicit gastric emptying, viz. drug-induced emesis, mechanical pharyngeal stimulation, gastric lavage, and catharsis. Apomorphine and syrup of ipecac are the 2 drugs most frequently used for induction of emesis. Both agents act centrally and, in addition, syrup of ipecac has a peripheral action. ⋯ They elicit an osmotic reaction in the small intestine which results in increased intraluminal fluid bulk, hyperperistalsis, and subsequent propulsion of contents. Cathartics have also been shown to stimulate the secretion of cholecystokinin, which is thought to have similar effects on the intestine. Cathartics have not been shown to significantly enhance drug elimination from the gastrointestinal tract.(ABSTRACT TRUNCATED AT 400 WORDS)
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Deaths from tricyclic antidepressant (TCA) overdose are usually due to arrhythmias and/or hypotension. Tricyclic antidepressant toxicity is due mainly to the quinidine-like actions of these drugs on cardiac tissues. Slowing of phase 0 depolarisation of the action potential results in slowing of conduction through the His-Purkinje system and myocardium. ⋯ However, administration of hypertonic sodium bicarbonate is beneficial even when blood pH is normal. Lignocaine (lidocaine) may be useful in treating ventricular tachycardia but should be administered cautiously to avoid precipitating seizures. Ventricular bradyarrhythmias are due to impaired automaticity or depressed atrioventricular conduction and can be treated by placement of a temporary pacemaker, or with a chronotropic agent, e.g. isoprenaline (isoproterenol), with or without concomitant vasoconstrictors.(ABSTRACT TRUNCATED AT 400 WORDS)