Case report
The Profile of Cypermethrin Intoxication as Differential Diagnosis of Organophosphate Poisoning: A Case Report
Correspondence Address :
Sneha Gang,
GNRC Hospitals, Super Market, Dispur, Guwahati-781006, Assam, India.
E-mail: drsneha.gang@gnrchospitals.com
Cypermethrin, a type II pyrethroid, is easily available over the counter, increasing the possibility of accidental and intentional exposures. Severe Cypermethrin exposure is rare but may lead to an organophosphate-like toxidrome, posing a diagnostic quandary to the critical care personnel. The authors present a case of a 25-year-old lady patient, who intentionally ingested a toxin or poison. On repeated investigation by medical personnel and family members, it eventually turned out to be cyperhit. On, immediate shifting to the Intensive Care Unit (ICU) following acute poisoning, her vital signs were more or less stable, but with mouth filled with copious mouth secretions and mild bronchorrhoea. An intravenous dose of 1.2 mg of atropine sulfate was administered because of bronchorrhoea, which led to satisfactory improvement, except for hypoglycaemia {(Random Blood Sugar (RBS): 67 mg/dL}. To address hypoglycaemia, an initial bolus of 25% dextrose (IV)/100 mL was injected followed by an infusion of 25% dextrose at a rate of 10 ml/hr. At the end of three days of close monitoring and psychiatric counseling sessions, she was fully alert, oriented, afebrile, and had stable vital signs. The present case suggests that Cypermethrin poisoning should be considered a differential diagnosis of patients presenting with classical features of organophosphorus poisoning. Inadvertent administration of pralidoxime and atropine can be avoided if emergency physicians are aware of this entity. Optimum Atropine administration is useful when the dose is adjusted as per the patient’s response.
Hypoglycaemia, Pyrethroid, Toxin
A 25-year-old married female presented to our Emergency Department (ED) with an alleged history of intentionally ingesting some illicit/non-illicit substance of unknown nature. In rural areas of Asian countries, most suicides by consuming poison involve the use of pesticides, such as organophosphates and carbamates. With this mindset the initial urgent treatment was initiated. On subsequent interrogation, it gradually evolved that the patient ingested cyperhit 10% EC (cypermethrin) solution in a concentration that could not be quantified by her relatives. Initially, her family did not to take her to the hospital and decided to observe her at home. Two hours later, she was hurried to the ED of our hospital’s ED after several episodes of vomiting and slow rise in abdominal pain at her residence. The patient and her relatives denied any history of other co-morbidities. Upon arrival at the ED, her soiled clothing was removed, and she underwent superficial decontamination by cleaning her skin thoroughly with soap and water. After initial assessment, she was advised admission to the Intensive Care Unit (ICU) following acute poisoning. In rural areas of Asian countries, most suicides by consuming poison consumption typically involve the use of pesticides, such as organophosphates and carbamates. Therefore, urgent treatment was initiated On subsequent interrogation, it gradually evolved that the patient had ingested a concentration of cypermethrin (Cyperhit 10% EC solution) that could not be quantified by her relatives.
During the general physical examination in the ICU, her Glasgow Coma Scale (GCS) score was 11 out of 15 (E4V3M4), indicating slight muscle weakness in the limbs. Her right pupil was slightly constricted for the right eye but the left eye was mildly dilated. She was otherwise a healthy mother to a kid with no previous history of suicidal ideations. in the past. Her mouth was filled with copious mouth secretions and mild bronchorrhea. There were no complaints of chest pain, palpitations, seizures, bowel or bladder incontinence, or shortness of breath at the time of admission to the hospital. Her vital signs were stable, with a blood pressure of 100/60 mmHg, oxygen saturation of 96% on room air, a Respiration Rate (RR) of 22 breaths per minute, and an axillary temperature of 98 degrees Fahrenheit. Her random blood sugar level was 98 mg/dL. Neurological and overall physical examinations revealed fairly unremarkable findings. Chest radiography showed clear lung fields. Initial tests, including liver and renal function, serum sodium, potassium, calcium, coagulation profile, arterial blood gas analysis, haemogram, and serum cholinesterase level, were within normal ranges. A 12-lead electrocardiogram done at the time of arrival showed normal results. Urine output was satisfactory and monitored regularly along with other vital signs. She was finally diagnosed with acute Cypermethrin poisoning (suicidal) and an adjustment disorder.
Treatment
After the patient was shifted to the ICU for further treatment, her condition, treatment options, cost issues, risks/benefits, the necessity of ICU care, and prognosis were disclosed and discussed in detail with her family members. Based on the detailed history and clinical evaluation, a working diagnosis of ‘Acute Cypermethrin poisoning (suicidal)’ was made and accordingly, the treatment was started.
Due to delayed hospital presentation and to prevent aspiration, the medical team refrained from administering activated charcoal therapy as well as gastric lavage. An intravenous dose of 1.2 mg of atropine sulfate was administered in view of bronchorrhoea, which eventually resulted in satisfactory improvement. Following this, her heart rate increased to 86 beats per minute however, it gradually decreased to 70 beats per minute within half an hour. After two hours, one more dose of intravenous 0.6 mg of atropine sulfate was administered two encounter bronchorrhoea. During 48 hours of close monitoring, she was treated with i.v. hydration, prophylactic broad-spectrum antibiotics (Amoxicillin and Potassium Clavulanate), Injection Proton Pump Inhibitor (Inj. PPI) (Pantoprazole), intravenous anti-emetics (Ondansetron), multivitamins, aerosol therapy (Ipratropium bromide and Levosulbutanol Respules), anti-psychotic drugs (Escitalopram Oxalate, Clonazepam, and Tofisopam), along with chest physiotherapy, and bowel and bladder care as supportive care. These interventions helped maintain stable vital signs, except for hypoglycaemia (RBS: 67 mg/dL). An initial bolus by an intravenous 25% Dextrose in 100 mL was given. The random blood sugar level was rechecked using a glucometer after 10 minutes and was found to be 72 mg/dL.
To address her persisting drowsiness, it was decided to initiate an infusion of 25% Dextrose @1 0 mL/Hr. Initially, every 30 mins the RBS was checked using Glucometer which continued on a two hours for the next 24 hours. Eventually, she reflected clinical signs of medical improvement and was transitioned to D5 saline. In the meantime, several episodes of neuro-psychiatric as well as clinical psychology counseling were conducted. At the end of three days of close monitoring, she was alert, oriented, afebrile, with stable vital signs. A cross-consultation was carried out with the neuro-psychiatry and clinical psychology department for further evaluation. Following their advice, she was discharged in improved condition and a list of medications included, Amoxicillin and Potassium Clavulanate; Ambroxol, Levosalbutamol, and Guaifenesin; Montelukast and Fexofenadine Hydrochloride; Sucral suspension; and Escitalopram oxalate. She was advised to have restful life for atleast seven days. During a follow-up appointment in the outpatient department the following week, she remained asymptomatic and was doing well.
According to the chemical structure and toxidromes, Pyrethroids are classified into two types: Type I (allethrin, permethrin) with a cyclopropane carboxylic acid structure, and Type II (cypermethrin, deltamethrin) which have an alpha-cyano group attached (1),(2). The World Health Organisation (WHO) has categorised cypermethrin as a moderately hazardous pesticide with a high toxic potential of LD50 250 mg/kg and an oral toxic dose range from 100-1000 mg/kg body weight (3). Cypermethrin is often used in the form of a miraculous chalk stick (locally known as Lakshman Rekha), liquid, or powder to rinse off kitchen insects. Cypermethrin shows a complex mechanism of action by modifying the voltage-gated sodium channels and thereby delaying their closure. Moreover, the toxic properties of cypermethrin are also attributed to the voltage-gated calcium channels and gamma-aminobutyric acid-mediated chloride channels (4). Though, mammals are less susceptible to it due to their large body size, poor dermal absorption, higher body temperature, and hence metabolising and excrete it more rapidly (5). The goals of immediate treatment for the poisoned patient can be divided into six phases: (a) stabilisation; (b) laboratory assessment; (c) decontamination of the gastrointestinal tract, skin, or eyes; (d) administration of an antidote; (e) enhancement of toxin elimination; and (f) observation and disposition (6). In this case, the systematic approach to treatment was achieved and the initial symptoms of vomiting and mild abdominal pain were resolved within a few hours.
Hypoglycaemia due to cypermethrin poisoning is a rare occurrence (7). In a study consisting of 104 patients with Type II pyrethroid poisoning, hyperglycemia has been reported as one of the prominent adverse outcome, which can be attributed to the increase in adrenergic activity (7). The rare condition of hypoglycemia in our case was beautifully taken care of by evaluating random blood sugar levels at a break of every 30 mins and accordingly IV infusion of Dextrose 25% in normal saline. While WHO recommends symptomatic and supportive measures with no specific antidotes for this type of poisoning (8), the UK National Poison Information Service suggested using atropine for managing increased salivation in deltamethrin poisoning (9). Atropine, an anticholinergic medication that functions as a muscarinic receptor-blocking agent and serves as a physiological antidote to cypermethrin poisoning, was administered in a dose-adjusted manner based on the patient’s response (10). Pralidoxime chloride (2-PAM) was used with atropine in the treatment to relieve nicotinic signs such as tremors and muscle weakness. The mechanism of action of 2-PAM is to reactivate the acetylcholinesterase enzyme (AChE) that has been deactivated by the poison. Intravenous supplementation of magnesium sulfate (MgSO4) i.v. supplementation was also given in association with atropine to address the patient’s serum hypomagnesemia, as it helps inhibit acetylcholine release from motor nerve terminals, antagonising the effects of the poisoning (11), hence reducing patient mortality and hospitalisation duration. days of the patients. A diagnosis is a medical diagnostic technique used in medicine that separates one disease or condition from others that have comparable clinical symptoms. Proficient healthcare professionals employ an evidence-based methodology, enhancing their clinical expertise with insights from clinical research when creating a differential diagnosis. The present case of self-poisoning could be dealt successfully with no major complications as cypermethrin poisoning was taken as the differential diagnosis of potential organophosphorus poisoning.
In summary, physicians working in the Emergency Department (ED) and Intensive Care Unit (ICU) should be attentive to Cypermethrin poisoning cases and consider it as a potential differential diagnosis in patients exhibiting classical features of Organophosphorus poisoning. The inadvertent administration of pralidoxime and atropine can be avoided if emergency physicians are aware of this entity. The authors found the administration useful when the dosage was adjusted as per the patient’s response. Though overall prospects of Cypermethrin poisoning, with its severe symptoms and lack of a specific antidote, show excellent results with conservative therapy, there is less availability of data detailing cypermethrin toxicity in humans. This makes it evident to report more cases which will eventually help in optimising the mechanisms and treatment therapies of severe poisoning.
DOI: 10.7860/JCDR/2024/70085.19786
Date of Submission: Feb 16, 2024
Date of Peer Review: Apr 06, 2024
Date of Acceptance: Jun 19, 2024
Date of Publishing: Aug 01, 2024
AUTHOR DECLARATION:
• Financial or Other Competing Interests: None
• Was informed consent obtained from the subjects involved in the study? Yes
• For any images presented appropriate consent has been obtained from the subjects. Yes
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ETYMOLOGY: Author Origin
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