Anticholinesterase poisoning/intoxication

Poisoning - In anticholinesterase poisoning from exposure to insecticides, give large doses of at least 2 to 3 mg parenterally repeat until signs of atropine intoxication appear. 

In contrast to the beneficial effects of treatment with oximes in cases of OP intoxication, reports in the literatnre suggest that treatment of poisoning with certain anticholinesterase carbamates with some oximes should be avoided because they may actually potentiate carbamate action. Other oximes decrease carbamate toxicity. The effects observed are, in general, correlated with changes in the rates of carbamylation and decarbamylation in the presence of the various oximes . ... 

On these grounds, one could expect that the treatment effectiveness of the well-known antidotes against OPC (safolen-31, safolen-58, afin) would be very low on poisonings by substance 1, even for its intravenal application. In fact, these treatment preparations removed or considerably suppressed the effects, determined by the specific anticholinesterase and the direct damages, only during the phase of the acute intoxication by this poisonous substance. In perspective, in a delayed period of time, the development of secondary pathology resulted in high lethality of the animals (Table 4). 

AN-a(s) has been reported to be responsible for the fatal intoxications of ducks and swine (Cook et al., 1989). AN-a(s) was also implicated in the deaths of nine dogs at Richmond Lake, SD, USA in 1985 (Mahmood et al., 1988). One of the first reports of this toxin outside North America was when it was identified in the stomach contents of poisoned birds from a lake in Denmark (Henriksen et al., 1997 Onodera et al., 1997). There have been other suspected occurrences of AN-a(s), including in Brazil (Molica et al., 2005), based on observed anticholinesterase activity but the lack of a commercially available standard and the toxin s labihty render absolute confirmation difficult. AN-a(s) readily loses the methyl phosphate moiety on storage to produce a nontoxic product. 

Key findings that have been reported include significant hypoxia, acidosis, and carbon dioxide retention (Sofer et al., 1989). Also, hyperglycemia, hypokalemia, and leukocytosis were observed in a case series of OP exposures (Levy-Khademi et al., 2007). A study done on 17 children with typical OP or carbamate poisoning looked at laboratory abnormalities that are associated with acute pancreatitis. Five of the patients (30%) had laboratory values consistent with pancreatitis with elevated immunoreac-tive trypsin, amylase, and serum glucose. None of the patients had hypocalcemia, renal dysfunction, or acidosis, and all experienced complete recovery of pancreatic function. The authors concluded that acute pancreatihs, due to anticholinesterase (anti-AChE) intoxication, is not xmcommon in the pediatric population (Weizman and Sofer, 1992). Pancreatitis has been described in adult exposures, and the association has been investigated in animal studies (Weizman and Sofer, 1992). 

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