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Carbamates are as popular as organophosphates in their role as insecticides (and fungicides) and share a number of similari-ties. Only the differentiating features will be discussed. Indian brands are listed in Table 28.3.
The following are extremely toxic (LD50: 1 to 50 mg/kg), or highly toxic (LD50: 51 to 500 mg/kg)—
Aminocarb, Bendiocarb, Benfuracarb, Carbaryl, Carbofuran, Dimetan, Dimetilan, Dioxacarb, Formetanate, Methiocarb, Methomyl, Oxamyl, Propoxur.
The following are moderately toxic (LD50: 501 to 5000 mg/kg), or slightly toxic (LD50: more than 5000 mg/kg)—Aldicarb, Bufencarb, Isoprocarb, MPMC, MTMC, Pirimicarb.
Carbamates (like organophosphates) are inhibitors of acetyl-cholinesterase, but carbamylate the serine moiety at the active site instead of phosphorylation. This is a reversible type of binding and hence symptoms are less severe and of shorter duration. As a result both morbidity and mortality are limited when compared to organophosphate poisoning. Also, since carbamates do not penetrate the CNS to the same extent as organophosphates, CNS toxicity is likewise much less. With respect to all other clinical manifestations, there is general similarity between carbamates and organophosphates.
Carbamates are rapidly metabolised. They are rapidly hydrolysed by liver enzymes to methyl carbamic acid and a variety of low toxicity phenolic substances. These metabolites may sometimes be measured in urine as long as 2 to 3 days after significant pesticide absorption.
Miosis, a muscarinic effect, is characteristic of severe and moderately severe poisonings, but may appear late. Pupil dila-tion may occur as a nicotinic effect and may be present in up to 10% of patients.
Sinus tachycardia with ST segment depression may occur early in the course of poisoning. Repolarisation abnormalities may occur and are generally transient.
Dyspnoea is a common manifestation of carbamate expo-sure.
Chest tightness, bronchospasm, increased pulmonary secre-tions, and rales may develop secondary to muscarinic effects. Acute lung injury (pulmonary oedema) is a potential clinical manifestation of severe carbamate poisoning and is attributed to the muscarinic action of the insecticide. Contributing factors to the development of pulmonary oedema include bradycardia and weakened cardiac contraction from an accumulation of acetylcholine on the cardiovascular system. Hypoxia may develop due to increasing capillary permeability.
Headache, dizziness, blurred vision, tremor, paresis, mental depression, coma, delayed neuropathies, various dystonias, weakness, muscle twitching, and convulsions have all been reported with carbamate poisoning. Children may be more likely to develop CNS depression, convulsions, and hypotonia than the typical cholinergic syndrome. Absence of classic muscarinic effects has been reported in several children intoxicated with carbamate insecticides. The presence of either a cardiac arrhythmia or respiratory failure is associated with a higher incidence of fatal poisoning.
Various peripheral neuropathies have been reported after carbamate use. The symptoms are similar to those seen with organophosphates. Acute pancreatitis has been reported with propoxur.
In the case of carbamate poisoning, measurement of cholinest-erase activity in blood may be misleading due to in vitro reac-tivation of carbamylated enzyme. In vitro decarbamylation has been found to be promoted by dilution of the sample. The carbamylated sample should be stored undiluted and refriger-ated or frozen. Carbamylated cholinesterase activity follows a non-linear kinetic pattern over time, whereas phosphorylated enzyme activity is linear. At inhibition of greater than 40%, the non-linear pattern characteristic of carbamates is easily mapped.
One technique for assessing absorption of the principal N-methyl carbamate compounds is measurement of specific phenolic metabolites in urine, e.g. carbaryl (alpha-naphthol), carbofuran (carbofuranphenol) propoxur (isopropoxyphenol).
Chest X-ray should be obtained in all symptomatic patients. The major cause of morbidity and mortality in carbamate insecticide poisonings is respiratory failure and associated pulmonary oedema.
An important differentiating point from organophosphates is that oximes are generally not recommended, while atropine can be given. Especially in carbaryl poisoning, oxime therapy can lead to the production of a carbamylated oxime which may be a more potent acetylcholinesterase inhibitor than carbaryl itself. With other carbamate insecticides (particularly aldicarb), oximes may be a useful adjunct to atropine therapy. In 1986, a consensus of international experts concluded that pralidoxime can be used in conjunction with atropine for specific indica-tions as follows:
■■ Life-threatening symptoms such as severe muscle weak-ness, fasciculations, paralysis, or decreased respiratory effort.
■■ Continued excessive requirements of atropine.
■■ Concomitant organophosphate and carbamate exposure. In all cases, administer atropine in repeated doses intrave-nously until atropinisation is achieved (indicated by drying of pulmonary secretions). Adult dose—2 to 4 mg IV every 10 to 15 minutes. Paediatric dose—0.05 mg/kg IV every 10 to 15 minutes.
Convulsions can be controlled with a benzodiazepine (diazepam or lorazepam). If they persist or recur, administer phenobarbitone.
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