Toxic intracerebral demyelination in a case of suicidal Cypermethrin poisoning


A 15 years old boy was admitted with history of suicidal pyrethroid compound ‘cypermethrin’ consumption. Subacute evolution of central nervous system manifestations and radiologically documented subcortical demyelination were observed. Gradual and partial recovery could be achieved with conservative treatment over few weeks. Although generally considered safe pyrethrin compounds can occasionally result in devastating neurological consequence as observed in this case.

Keywords: Cypermethrin, insecticide poisoning, neurotoxicity

How to cite this article:
Majumdar BB, Guha G, Ray AN, Bala B. Toxic intracerebral demyelination in a case of suicidal Cypermethrin poisoning. Ann Trop Med Public Health 2012;5:615-7
How to cite this URL:
Majumdar BB, Guha G, Ray AN, Bala B. Toxic intracerebral demyelination in a case of suicidal Cypermethrin poisoning. Ann Trop Med Public Health [serial online] 2012 [cited 2017 Nov 14];5:615-7. Available from:

In our country, lethal and potent poisonous insecticides are very easily available over-the-counter to the people without any safety norms and protocols. [1] In recent times, incidence of consumption of these commonly used household insecticides has increased dramatically for suicidal attempts. The synthetic pyrethroids such as cypermethrin and deltamethrin are being used increasingly in recent times, but serious human poisoning from these relatively safe agents is rarely reported. However, neurotoxicity in a case of cypermethrin poisoning, leading to subcortical demyelination is extremely rare, and to the best of our knowledge not yet been reported till date. Hereby, we elucidate this unusual entity in our case report, which abolishes the myth that the pyrethroids are relatively safe agents to man.

Case Report

A 17-year-old boy, resident of Alipurduar, was admitted in the General Medicine indoor with complains of vomiting and salivation due to suicidal intake of an unknown poison. Further interrogation revealed an ingestion of 50ml of “Ostad”, having a concentration of 10% of cypermethrin, which is equivalent to 5 gm of poison about 8 hrs ago. Initially, his parents noticed frothing from his mouth, and sought medical aid and shifted him into a local hospital from where he was treated with gastric lavage and intravenous medications, and referred to district hospital. As the condition deteriorated in the next few hours, he was referred to the present institute. There was no definite history of trauma, drug intake, fever, family history or psychiatric illness.

General examination revealed congested eyes with constricted pupils, but normal reaction to light.The lips and the buccal mucosa were slight red in colour with few mucosal ulcerations. The patient was afebrile with no signs of meningeal irritation. His detailed neurological examination was unremarkable. Blood pressure was 110/70mm of Hg and pulse was 88/min. There was no fasciculation or tremor.

A mixture of activated charcoal (initially 100gm and later 50gm) and water was given with the help of a nasogastric tube. We observed him and gave symptomatic treatment with low dose atropine and fluid support. The patient gradually recovered and became fully conscious and started enteral feeding by the 3 rd day. There was sudden neurological deterioration on the 4 th day, when the patient suddenly became unconscious with fever and hemodynamic collapse. Examination revealed diffuse crackles all over the chest. He also developed seizures, which occurred intermittently over the next few days [Figure 1] and [Figure 2].

Figure 1: Comatose patient after sudden neurological deterioration

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Figure 2: Patient was provided with supportive therapy

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Routine hematological and biochemical investigations were within normal limits.His liver function and renal function tests, Spo 2 , hemogram, serum electrolytes and glucose were normal. Dual antigen for malaria, CSF study was also done, which were within the normal limits.

We managed the patient with broad spectrum antibiotics, anticonvulsants, ionotropes, fluid support and Ryle’s tube feeding. Over the next 4 days, the patient gradually improved and regained hemodynamic stability, but his neurological symptoms lacked an improvement.

He was monitored closely for vitals and serum electrolytes and any progressive neurological deficit. We ordered for an MRI scan to evaluate for the sudden neurological impairment. MRI of brain revealed patchy areas of demyelination in subcortical part of the cerebrum [Figure 3] and [Figure 4]. He was provisionally diagnosed as having toxic demyelination and started on dexamethasone. In the next 1 week, he gradually improved and an oral feeding was started subsequently. The GCS score improved from 5/15 to 10/15. He could follow commands, but was not ambulatory on his own. On repeated requests by the patient’s relatives (due to financial reasons), we were forced to discharge the patient, however, he was counselled for regular follow-up in the OPD. He was discharged with all the supportive measures and was advised for good nursing care.

Figure 3: MRI revealed Subcortical demyelinations

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Figure 4: MRI Showing demyelinating plaques

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Insecticides like organophosphorus and organochlorine compounds are commonly used conventional poisons owing to an easy availability with serious consequences, and are classified under WHO hazard classification as class IA (extremely hazardous). Cypermethrin is 1 of the 18 synthetic pyrethroids available as insecticides and pediculocides. Besides the main ingredient pyrethroids, these insecticides also contain a surfactant, triton-x and an additive, piperonyl butoxide, which prolong its action by inhibiting the oxidizing enzymes. [2] This pyrethroid kills the insects by paralyzing the nervous system, blocks the inhibitory pathway and disrupts the voltage gated chloride channels on the cell membrane. [3] Mammals are protected by metabolizing and excreting it rapidly. And hence, pyrethroids were considered relatively safe to humans and classified by WHO hazard class 2 (moderately hazardous). Due to this reason, they began to be widely used in the underdeveloped countries like India. Our case contradicts the WHO hazard classification and elucidates that these agents are much more hazardous than the WHO hazard class suggest, and therefore, needs more strict vigilance to prevent liberal use of these agents.

The toxic oral dose is greater than 100-1000mg/kg body weight and the lethal dose is 1-10g. [4] Our patient consumed around 5 g, which is in the lethal range. Toxicity to humans are type I hypersensitivity reaction like anaphylaxis or irritant action to the exposed mouth, lips, eyes or skin as manifested by our case showing congested eyes and buccal mucosa. Cardiotoxicities has been reported viz ST-T changes, sinus tachycardia, and ventricular premature beats, [5] however, our case lacked any cardiac dysfunction except hemodynamic shock, probably due to aspitation pneumonia. Neurotoxicities like, tremor, fasciculation, convulsion, coma and even respiratory failure has been reported with lethal poisonings. Our case had predominant neurological manifestations; however, tremor and fasciculations were not documented. Moreover, to the best of our knowledge, no reported case of demyelinating plaques has been reported till date following this poison. It also causes an increased salivation, upper gastrointestinal bleeding, and rarely renal failure. WHO guidelines recommend no specific antidotes, but symptomatic and supportive measures for this type of poison. [6] Fortunately, our patient survived with supportive and symptomatic management and was discharged on the phase of ongoing recovery.

In our country, like ours usage of insecticides in agricultural, domestic and industrial fields is prolific. Suicidal and accidental ingestion is extremely common. Clinical manifestations being usually non-specific. An absence of specific biochemical markers, lack of toxicological assays, and the fact that the specific antidotes are available only for a few poisons, makes management extremely challenging. Although non-specific, our case demonstrated a neuro radiological manifestation of a systemic poison. An active search for specific markers and antidote for this common poison is urgently required for this country.

1. Peter VJ, John G, Cherrian AM. Pyrethroid poisoning. J Assoc Physians India 1996;44:343-4.
2. Nasuti C, Cantalamessa F, Falcioni G, Gabbianelli R. Different effects of Type I and Type II Pyrethroids on erythrocyte plasma membrane properties and enzymatic activity in rats. Toxicology 2003;191:233-44.
3. Burra SA, Ray DE. Structure activity and interaction effects of 14 ­different pyrethroids on voltage gated chloride ion channels. Toxicol Sci 2004;77:341-6.
4. Olsen KR. Poisoning and drug overdose. 2 nd ed. East Norwalk, CT: Appleton and Lange; 1994.
5. He F, Wang S, Liu L, Chen S, Zhang Z, Sun J. Clinical manifestations and diagnosis of acute pyrethroid poisoning. Arch Toxicol 1989;63:54-8.
6. World Health Organisation World health report 2002 reducing risk, promoting healthy life. Geneva: WHO; 2002.

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.109330


[Figure 1], [Figure 2], [Figure 3], [Figure 4]

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