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CASE REPORT
Year : 2019  |  Volume : 22  |  Issue : 3  |  Page : 442-444

Pyrethroid intoxication: A rare case report and literature review


1 Department of Anesthesiology, University of Health Sciences, Gazi Yaşargil Diyarbakır Training and Research Hospital, Diyarbakır, Turkey
2 Department of Anesthesiology, University of Health Sciences, Ümraniye Training and Research Hospital, Istanbul, Turkey
3 Department Anesthesiology, Silvan Yusuf Azizoğlu State Hospital, Diyarbakır, Turkey

Date of Acceptance08-Sep-2018
Date of Web Publication6-Mar-2019

Correspondence Address:
Dr. E T Kilic
Department of Anesthesiology, University of Health Sciences, Ümraniye Training and Research Hospital, Istanbul
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/njcp.njcp_241_18

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   Abstract 


Synthetic pyrethroid cypermethrin is commonly used in agriculture, veterinary, and household insects management. It has been found to be a newer insectiside poisoning reported in Turkey. Acute severe poisoning of cypermethrin is a rare event. Here we report a case of a 25-year-old woman presented with features of cypermethrin poisoning in intensive care unit. Management of acute rare poisoning is discussed in this case with literature review.

Keywords: Cypermetrin, intensive care unit, poisoning, pyrethroids


How to cite this article:
Akelma H, Kilic E T, Salik F, Bicak E A, Yektas A. Pyrethroid intoxication: A rare case report and literature review. Niger J Clin Pract 2019;22:442-4

How to cite this URL:
Akelma H, Kilic E T, Salik F, Bicak E A, Yektas A. Pyrethroid intoxication: A rare case report and literature review. Niger J Clin Pract [serial online] 2019 [cited 2019 May 21];22:442-4. Available from: http://www.njcponline.com/text.asp?2019/22/3/442/253445




   Introduction Top


Main insecticide compounds widely used for agriculture are pyrethrins and their synthetic derivates. The development of synthetic pesticides called pyrethroids is based on pyretrins, which derived from the flowers of chrysanthemums.[1] They are natural enviromental products with low toxicity to mammals degrading in daylight rapidly due to photolabile properties. They have been synthesized to be similar to pyrethrins, but are more resistant in the environment. Pyrethroids are simply divided into two types. Type I has a cyclopropane carboxylic acid structure, whereas type II has a alpha cyano group with benzylic carbon.[2] Type II pyrethroids have more toxic abilities such as salivation, hyperexcitability, and seizures. Local effects such as skin contamination producing paresthesia and gastrointestinal irritation are also seen. Pyrethroids may lead to poisoning in human beings through accidental, occupational exposure, or intentional events.[3],[4],[5]

Cypermethrin is a synthetic pyrethroid pesticide (type II) widely used in crops against pest and insect. Cypermethrin is primarily absorbed from gastrointestinal tract and may also be absorbed by inhalation of spray mist and only simply through contact with skin. The abundance and variety of pyrethroid use contribute to the risk of exposure and adverse effects in the general population.[6]

The insecticidal actions of pyrethroids depend on their ability to bind to and disrupt voltage-gated sodium channels. And they are important targets for neurotoxic effects of pyrethroids in mammals.[5],[6]


   Case Presentation Top


After using a pesticide named “Blottic” containing cypermetrin, a 25-year-old woman was found semi-conscious in barn. Her family did not take her to any hospital and decided to observe her for a while at home. Twelve hours later due to epigastric pain, nausea, and vomiting, the patient was admitted to the emergency department. She did not have any systemic, mental pscyhiatric illness or history of suicide. There was no sign of ingestion. The poison control center advised gastric lavage, activated charcoal treatment, and admision to the intensive care unit (ICU) following acute poisoning.

She was transferred to the ICU and fully monitorized. On examination, her blood pressure was 122/58, heart rate 110, regular respiratory rate 18/min, and oxygen saturation 90% on room air. She was drowsy and did not fully cooperate. She had seizures and tremors. She had conjuctival congestion but reactive to light. Cardiac examination was normal. Initially, blood cell line, and renal and liver function tests were within normal limits with arterial blood gas analysis. Electrocardiogram showed sinus tachycardia. On oscultation, bilateral rhonci were present.

In ICU, gastric lavage was repeated and charcoal was given. Supportive treatment and i.v. fluid were administered. Nebulization with albuterol, ranitidine, chlorpheniramine maleate, and prednisolone were administered as symptomatic treatment. The patient became unstable on the second day with features of respiratory failure and dysphagia and her Glasgow Coma Scale was 6/15. Due to severe hypoxia, intubation was performed. Arterial blood gas showed pH 7.32, PCO2 25, PO2 65, HCO3 23, and SPO2 90. Blood investigations were normal except coagulation parameters. Sedation was started to control the seizures.

She required ventilator support for 3 days, improved over the next 24 h, and after a week she recovered completely and was discharged from the hospital after psychiatric consultation.


   Discussion Top


Cypermethrin, a pyrethroid compound, is reported to be less toxic for human use due to poor dermal absorption and rapid metabolism. Cypermethrin in its commertial form alters the normal activity of the nervous system. It behaves a fast-acting neurotoxin.

Cypermethrins cause neurotoxicity in mammals by causing a long-lasting prolongation of the normally transient increase in sodium permeability of nerve membrane channels during excitation. These long-lasting trains cause thousands of repetative nerve impulses which induce oxidative stress. Brain, which is a vital part of the organism's functioning and coordinating system for the body parts, is highly vulnerable to oxidative stress than any other organs of the body consuming high amount of oxygen.[7],[8],[9] Sharma et al. showed the neurotoxic effect of cypermethrin in Wistar rats. It was reported to cross blood–brain barrier in animal models.[10]

Aggarwal et al. reported a 30-year-old male who presented to the emergency department with complaints of recurrent vomiting, epigastric pain, increased salivation, lacrimation, anxiety, cough, and dyspnea. He gave a history of 300 mL of liquid ingestion. He improved after symptomatic treatment over the next 24 h.[11]

Das and Parajuli reported cypermethrin poisoning in a 30-year-old male patient with normal liver, renal function tests, and normal glucose levels. The patient recovered uneventful.[12]

Luty et al. assessed the immunotoxic effects of dermally applied alpha cypermethrin in rats' internal organs. Doses of 50 and 250 mg/kg were dermally applied for 4 h daily for 28 days. Lung, liver, kidney, and heart were examined at the end of the study. Pathological changes were observed in the heart. Dermal application of the preparation resulted in slight histological changes.[13]

In animal studies, type I and type II pyrethroids showed generally different patterns of systemic toxicity in case of parenteral administration. In rats, cymethrins produce tremor syndrome.[13] Type II pyrethroids produce repetitive behaviors in animals at lower doses. Progressive development of chewing, jaw openings, coreiform movements, salivation, and tremors can be seen when parenterally used.[5]

Typically developed symptoms following poisonings are dizziness, increase in salivation, headache, seizures, nausea, vomiting, and abdominal pain. Respiratory failure, pulmonary edema, coma, sinus tachycardia, and ventricular premature beats can also be seen.

Dermal exposure causes paraesthesiae. Most commonly, the face is affected. Symptoms start 2 h after exposure and recovery is complete within 24 h. For the treatment of scabies, the doses rarely cause irritant effects. Pruritus, burning, and blisters are the most common complaints.[14]

In another study, a child after playing with her dog that had been recently treated with pyrethrin developed unilateral miosis. Eye irritation may also occur.[15]

Pyrethroids are not volatile. In another report, 12 workers who used lambda-cyhalothrin in doors complained of nasal and throat irritation. A 47-year-old pesticide applicator developed asthma after working 7 years in this profession.[16]

A 45-year-old man died 3 h after eating beans and cheese prepared with cypermethrin. He developed symptoms within a few minutes and died.[17]

Peter et al. reported fatality due to aspiration pneumonia within 10 h after ingesting 30 mL of cypermethrin.[18] In another case, a farmer was found unconcious in a room after using spray of permethrin. Within 2 weeks he developed neurological symptoms and died in 18 months. He made a complete recovery, but 2 weeks later he developed neurological symptoms. Autopsy findings were compatible with diagnosis of motor neurone disease.[16]

Systemic toxicity of pyrethroids is rare and most of the patients recover with symptomatic and supportive treatments. Due to similarities between organophosphorus poisonings, it is difficult to diagnose. Active charcoal may be considered in case the amount is considered toxic.[11]

Cypermethrin-induced neurotoxicity can be a result of free radical formation, reduced antioxidant defence mechanism, and inhibition of AChE activity. Management of pyrethroids is supportive. Convulsions and seizures can be controlled with diazepam. Ventilation is rarely needed in case of paralysis. Hypersalivation is seen in most cases. Atropine administration is useful. There are still limited data about the mechanism of severe toxicity of pyrethroids. More studies are needed to optimize the management of severe poisonings.


   Conclusion Top


Cypermethrin intoxication must be considered as a differential diagnosis in patients showing clinical features of organophosphorous poisoning. Cypermethrin poisoning can be life-threatening as presented in our case.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil

Conflict of interest

There are no conflicts of interest.



 
   References Top

1.
Majumdar BB, Guha G, Ray AN, Bala B. Toxic intracerebral demyelination in a case of suicidal cypermethrin poisoning. Ann Trop Med Public Health. 2012;6:615-17.  Back to cited text no. 1
    
2.
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.  Back to cited text no. 2
    
3.
Forshaw PJ, Ray DE. A voltage-dependent chloride channel in NIE115 neuroblastoma cells is activated by protein-kinase-c and also by the pyrethroid pyrethrin and piperonyl butoxide. Food Chem Toxicol 1994;32:51-3.  Back to cited text no. 3
    
4.
Kamienski FX, Casida JE. Importance of demethylenation in the metabolism in deltamethrin [abstract]. J Physiol 1993;467:252.  Back to cited text no. 4
    
5.
Forshaw PJ, Lister T, Ray DE. The role of voltage-gated chloride channels in type II pyrethroid insecticide poisoning. Toxicol Appl Pharmacol 2000;163:1-8.  Back to cited text no. 5
    
6.
Miyamoto J, Kaneko H, Tsuji R, Okuno Y. Pyrethroids, nerve poisons: How their risks to human health should be assessed. Toxicol Lett 1995;82-83:933-40.  Back to cited text no. 6
    
7.
Sayim F, Yavasoglu NU, Uyanikgil Y, Aktug H, Yavasoglu A, Turgut M. Neurotoxic effect of cypermethrin in Wistar rats: A haematological, biochemical and histopathological study. J Health Sci 2005;51:300-7.  Back to cited text no. 7
    
8.
Walters JK, Boswell LE, Green MK, Heumann MA, Karam LE, Morrissey BF, et al. Pyrethrin and pyrethroid illnesses in the Pacific Northwest: A five-year review. Public Health Rep 2009;124:149-59.  Back to cited text no. 8
    
9.
Giray B, Gurbay A, Hincal F. Cypermethrin-induced oxidative stress in rat brain and liver is prevented by Vitamin E or allopurinol. Toxicol Lett 2001;118:139-46.  Back to cited text no. 9
    
10.
Sharma P, Firdous S, Singh R. Neurotoxic effect of cypermethrin and protective role of resveratol in Wistar rats. Int J Nutr Pharmacol Neurol Dis 2014;4:104-11.  Back to cited text no. 10
  [Full text]  
11.
Aggarwal P, Jamshed N, Ekka M, İmran A. Suicidal poisoning with cypermethrin: A Clinical dilemma in the emergency department. J Emerg Trauma Shock 2015;8:123-5.  Back to cited text no. 11
    
12.
Das RN, Parajuli S. Cypermethrin poisoning and anti-cholinergic medication – A case report. Internet J Med Update 2006;1:42-4.  Back to cited text no. 12
    
13.
Luty S, Latuszynska J, Obuchowska-Przebirowska D, Tokarska M, Haratym-Maj A. Subacute toxicity of orally applied alpha-cypermethrin in Swiss mice. Ann Agric Environ Med 2007;7:33-41  Back to cited text no. 13
    
14.
Tucker SB, Flannigan SA, Smolesky MH. Comparison of therapeutic agents for synthetic pyrethroid exposure. Contact Dermatitis 1983;9:316.  Back to cited text no. 14
    
15.
Burns JD, Muller LT, Jenkins PF, Gunderson CA. Unilateral mydriasis associated with exposure to flea spray. Arch Ophthalmol 2002;120:665.  Back to cited text no. 15
    
16.
Pall HS, Williams AC, Waring R, Elias E. Motor neurone disease as manifestation of pesticide toxicity. Lancet 1987;2:685.  Back to cited text no. 16
    
17.
Poulos L, Athenaselis S, Coutselinis A. Acute intoxication with cypermethrin (NRDC 149). J Toxicol Clin Toxicol 1982;19:919-20.  Back to cited text no. 17
    
18.
Peter JV, John G, Cherian AM. Pyrethroid poisoning. J Assoc Physician India 1996;44:343-4.  Back to cited text no. 18
    




 

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