Carbamates
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.
Toxicity Rating*:
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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