Respiratory Failure of Acute Organophosphate and Carbamate Poisoning: Discussion (4)
Pneumonia developed in about a quarter of our patients, and in all of them it occurred within 96 hours. This time of onset can almost exclude the etiology of hospital-acquired infection. Because in acute organophosphate poisoning there is depressed consciousness and cough reflex, accompanied by large amount of respiratory secretions and emesis, as well as the gastric lavage used in the first aid, aspiration is most likely the main cause of pneumonia. The patients who had pneumonia, of course, had a higher risk for RF. Around 80 percent of the patients with pneumonia developed RF in our series; this finding was similar to 76 percent reported by Bardin et al.
The dosage of atropine used for treatment in the first 24 hours was significantly different between patients with different degrees of severity of poisoning in our series. This finding suggested that the clinical signs of atropinization (mydriasis, pupils size <3 mm; tachycardia, heart rate >100/min; flushing; xerostomia; anhydrosis; etc) were rather reliable criteria for the judgment for dosage of atropine therapy. ventolin inhalers
Pralidoxime is a biochemical antidote for organophosphate poisoning; its beneficial effects include reactivation of cholinesterase by cleavage of phospho-rylated active sites, direct reaction and detoxification of unbounded organophosphate molecules, and an endogenous anticholinergic effect. Pralidoxime reversed the effects of cholinergic nicotinic stimulation that are unaffected by the use of atropine alone. Pralidoxime was used in most of our patients but it did not seem to work to reduce the incidence of RF in organophosphate poisoning. Although pralidoxime treatment in carbamate poisoning is still equivocal, five of our 13 patients with carbamate poisoning treated with it had no adverse outcome.