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CASE REPORT |
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Year : 2016 | Volume
: 9
| Issue : 2 | Page : 244-245 |
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D-transallethrin: An unusual agent for accidental poisoning
Vinod Kedari, Rajesh Kulkarni, Chhaya Valvi, Aarti Kinikar, Sandhya Khadse
Department of Pediatrics, B. J. Govt. Medical College, Pune, Maharashtra, India
Date of Web Publication | 1-Mar-2016 |
Correspondence Address: Rajesh Kulkarni Department of Pediatrics, B. J. Govt. Medical College, Pune - 411 001, Maharashtra India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0975-2870.168008
D-trans allethrin, a pyrethroid, is commonly used as a coil mosquito repellant. There are very few reports of human toxicity due to D-trans allethrin. We present the case of an 11-month-old boy who presented to us with excessive salivation, altered sensorium and convulsions following alleged accidental ingestion of a coil containing D-transallethrin. He required mechanical ventilation for a brief period and made a full recovery. Although rare, the possibility of pyrethroid poisoning should be kept in mind in children who present with sudden onset unconsciousness or convulsions. Keywords: Children, d-transallethrin, insecticide, poisoning
How to cite this article: Kedari V, Kulkarni R, Valvi C, Kinikar A, Khadse S. D-transallethrin: An unusual agent for accidental poisoning. Med J DY Patil Univ 2016;9:244-5 |
Introduction | |  |
Pyrethroids are widely used as commercial and domestic insecticides. D-trans allethrin is a type 1 pyrethroid compound used as a coil mosquito repellant. Traditionally, pyrethroids have been considered as having relatively low toxicity, particularly when compared with organophosphate insecticides. Despite extensive use, there are few reports of human pyrethroid poisoning. Most case reports of pyrethroid toxicity earlier reported were adult cases who developed toxicity after ingestion of prallethrin or cypermethrin. [1],[2],[3],[4] Our case is unique because of the patient's age (11 months) and the pyrethroid involved (D-transallethrin).
Case Report | |  |
An 11-month-old male child was referred from a private hospital in intubated state with a history of alleged consumption of mosquito repellant coil (maxo coil® ). The child had allegedly consumed the coil in the morning; h later mother noticed that the child became excessively sleepy with excessive salivation and sweating. He was taken to a hospital, where he had one episode of generalized tonic-clonic convulsion for 5 min, followed by unconsciousness. Child was intubated in view of gasping respiration, started on bag and tube ventilation, given one dose of atropine IV 0.05 mg/kg (as he had constricted pupils), midazolam and phenytoin loading dose (10 mg/kg for convulsion) and referred to our hospital. At the time of admission to our pediatric intensive care unit (3 h after consumption), child was in altered sensorium with no spontaneous breathing and pupils were mid dilated with sluggish reaction to light. Mechanical ventilation was initiated.
Other vital parameters (heart rate, capillary refill time, blood pressure) were normal for age. Electrocardiogram was normal. Repeat doses of atropine were not given as there was a clear history of ingestion of maxo coil and as serum cholinesterase levels (sent from the referring hospital) were normal. After 6 h of mechanical ventilation, child started to have spontaneous breathing and limb movements. After 18 h of consumption of coil, child was extubated as a child was fully conscious and had good spontaneous breathing efforts with no repeat convulsions. We continued phenytoin for 3 days at a dose of 2.5 mg/kg/dose twice daily and discontinued it before discharge as there were no convulsions in our hospital and in view of the normal neurological examination at discharge.On follow-up after 1-month, the child was asymptomatic with no abnormal neurological findings.
Discussion | |  |
Maxo® coil contains 0.1% D-trans allethrin, a synthetic insecticide chemically related to pyrethroids. Pyrethroids are used as insecticides. They are about 2250 times more toxic to insects than to mammals due to increased sodium channel sensitivity, smaller body size and lower body temperature in the former. Poor absorption through the skin and rapid metabolism to inactive metabolites protects the mammals. The main toxic effects of pyrethroids are on voltage-gated sodium channels by delaying their closure. At higher concentration, pyrethroids can also act on g-aminobutyric acid-gated chloride channel, which causes seizure activity after toxicity. [5] Lethal dose of pyrethroids in humans is not known.
Ingestion of pyrethroid causes nausea, vomiting, abdominal pain, dizziness, headache, fatigue, palpitation, tightness in chest and blurring of vision. Coma, convulsions and pulmonary edema are uncommon, but can occur in severe poisoning. [6] Our patient had convulsions and coma. These signs and symptoms of pyrethroid are very similar to those of organophosphate poisoning which made the referring hospital use atropine prior to a diagnosis being made. The possibility that pyrethroids also induce hypersensitivity reactions, which may be fatal when the respiratory tract is involved, has been debated 2 occupational toxicity occurs through dermal absorption resulting in paraesthesia, which recovers spontaneously in a few hours. [7]
There is no specific antidote for pyrethroid toxicity; therefore management is only symptomatic and supportive. Following ingestion of large amount of pyrethroids, gastrointestinal decontamination may be done if patients report to the hospital within a few hours. [7] Occupational toxicity resulting in paraesthesia is treated by skin decontamination.
Conclusion | |  |
The signs and symptoms of pyrethroid toxicity are similar to those of organophosphate poisoning. It is essential to differentiate between the two as inappropriate atropine use (for organophosphorous poisoning) can be avoided in pyrethroid poisoning. Clinicians should be aware of the possibility of pyrethroid toxicity, its manifestations and treatment.
References | |  |
1. | Ardhanari A, Srivastava U, Kumar A, Saxena S. Management of a case of prallethrin poisoning-an unusual agent for suicidal ingestion. Sri Lankan J Anaesthesiol 2011;19:51-2. |
2. | Chandra A, Dixit MB, Banavaliker JN. Prallethrin poisoning: A diagnostic dilemma. J Anaesthesiol Clin Pharmacol 2013;29:121-2.  [ PUBMED] |
3. | Bhaskar EM, Moorthy S, Ganeshwala G, Abraham G. Cardiac conduction disturbance due to prallethrin (pyrethroid) poisoning. J Med Toxicol 2010;6:27-30. |
4. | Das RN, Parajuli S. Cypermethrin poisoning and anti-cholinergic medication - A case report. Internet J Med Update 2006;1:42-4. |
5. | Soderlund DM, Clark JM, Sheets LP, Mullin LS, Piccirillo VJ, Sargent D, et al. Mechanisms of pyrethroid neurotoxicity: Implications for cumulative risk assessment. Toxicology 2002;171:3-59. |
6. | Ray DE, Forshaw PJ. Pyrethroid insecticides: Poisoning syndromes, synergies, and therapy. J Toxicol Clin Toxicol 2000;38:95-101. |
7. | Bradberry SM, Cage SA, Proudfoot AT, Vale JA. Poisoning due to pyrethroids. Toxicol Rev 2005;24:93-106. |
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