|
 
 |
| CASE REPORT |
|
| Year : 2023 | Volume
: 2
| Issue : 1 | Page : 59-61 |
|
Amitraz poisoning – A rare and uncommon case of poisoning and its management
Vikash Bansal1, Ridhima Sharma2, Ripon Choudhary2
1 Department of Anaesthesiology and Intensive Care, AIIMS, Deoghar, Jharkhand, India
2 Department of Anaesthesiology and Intensive Care, Lok Nayak Hospital and Maulana Azad Medical College, New Delhi, India
| Date of Submission | 04-Nov-2022 |
| Date of Decision | 15-Apr-2023 |
| Date of Acceptance | 24-Apr-2023 |
| Date of Web Publication | 25-May-2023 |
Correspondence Address:
Dr. Vikash Bansal
Department of Anaesthesiology and Intensive Care, AIIMS, Deoghar, Jharkhand
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/jica.jica_33_22
A 25-year-old male presented to the peripheral hospital with an alleged history of ingestion of amitraz toxin 12.5% (approximately 150 mL), and presented with complaints of nausea, vomiting, abdominal pain, and weakness. On examination, he was conscious but disoriented and agitated, oxygen saturation (SpO2) was 89%–90% on room air, pulse rate was 40/min, blood pressure (BP) was 110/70 mmHg, and bilateral (B/L) crepitations were present on auscultation. Emergency treatment included – intravenous(IV) fluid, atropine 0.6 mg IV, and gastric lavage. Oxygen was given through an oxygen mask with a reservoir bag at 10 L/min. After some time, the patient's Glasgow Coma Scale (GCS) started deteriorating, and arterial blood gas (ABG) analysis revealed severe acidosis with pH of 7.109, pCO2 – 73, and HCO3 – 23.1, and immediately, the patient was transferred to a higher center given falling GCS, decreased saturation, and ABG finding. On presentation in the emergency department in our tertiary care center, the patient was unconscious, SpO2 was 69% on oxygen nonrebreathing mask – NRBM Mask at 15 L, BP was 128/78 mmHg, pulse rate was 104/min, and B/L crepitations were present on auscultation. The patient was immediately intubated in casualty and shifted to the intensive care unit for further management. Amitraz is a triazapentadiene, 1,5 di (2,4 dimethylphenyl) 3 methyl 1,3,5 triaza penta 1,4 diene, a formamidine pesticide, α2 adrenergic agonist in the central nervous system belongs to the amidine chemical family. The systemic effect of amitraz toxin is due to the activation of the pure α2-adrenergic agonist. It is a rare kind of poisoning in humans, and there exists a paucity of literature on the management of the aforementioned poisoning. Only a limited number of case reports of human intoxication have been published and most of them are of accidental ingestion by children. Due to insubstantial data on its management, this case report will be advantageous for practitioners working in emergency and intensive care departments.
Keywords: Amitraz poisoning, bradycardia, α2-adrenergic agonist
How to cite this article:
Bansal V, Sharma R, Choudhary R. Amitraz poisoning – A rare and uncommon case of poisoning and its management. J Ind Coll Anesth 2023;2:59-61 |
| Introduction | |  |
Amitraz is a triazapentadiene compound member of formamidine pesticides used as an insecticide/acaricide for the treatment of ectoparasites in animals.[1],[2] There are limited case reports published in humans and most of them are of accidental ingestion in the pediatric age groups. Amitraz stimulates the α2-adrenergic receptor sites in the central nervous system (CNS) and α1 adrenergic and α2-adrenergic receptors in the periphery.[3] It also inhibits the synthesis of prostaglandin E2 and inhibits the activity monoamine oxidase enzyme.[1],[2],[3] Amitraz is available as a 12.5%–20% formulation as a pesticide in organic solvents, especially xylene, which is also used as a solvent in paints, cleaners, and glues.[4] The potential route for amitraz poisoning is oral or dermal routes and inhalation.[5] The signs and symptoms of acute amitraz intoxication appear rapidly and become well established within hours. The major clinical findings are somnolence, coma, miosis, mydriasis, bradycardia, respiratory failure requiring mechanical ventilation, and hypo- and hyperthermia.[6] However, altered consciousness, nausea, vomiting, and dizziness are nonspecific symptoms.
| Case Report | | |
A 25-year-old male presented to the peripheral hospital with an alleged history of ingestion of amitraz toxin 12.5%, approximately 150 mL around 2 pm, followed by nausea, vomiting, abdominal pain, and weakness. On examination, he was conscious but disoriented and agitated, oxygen saturation (SpO2) was 89%–90% on room air, pulse rate was 40/min, blood pressure (BP) was 110/70 mmHg, and bilateral (B/L) crepitations were present on auscultation. Immediately, supportive management was started including intravenous (IV) fluid, gastric lavage, and atropine 0.6 mg iv. and the patient was given oxygen through an oxygen mask. After some time, the patient's Glasgow Coma Scale (GCS) started falling and became more agitated. Immediately, arterial blood gas (ABG) was done, which revealed severe acidosis with pH of 7.109, pCO2 – 73 mmHg, HCO3 – 23.1, and SpO2 – 64 mmHg on an oxygen mask. The patient was transferred to a higher center because of falling GCS, decreased saturation, and ABG findings. On presentation in the emergency department, the patient was unconscious, SpO2 was 69% on oxygen NRBM Mask at 15/L, BP and pulse rate were 128/78 mmHg and 104/min, respectively, and B/L crepitations on auscultation were present. The patient was immediately intubated in casualty and shifted to the intensive care unit (ICU) for further management. In the ICU, the patient was put on synchronized intermittent mandatory ventilation mode of ventilation, and FiO2 was titrated to maintain SpO2 around 92%. On FiO2 of 50%, the patient started maintaining saturation around 95%. Other symptomatic management was done as per ICU protocol, and atropine 0.6 mg was advised on an SOS basis when HR drops below 60/min. After around 4 h of intubation, BP started falling, and noradrenaline infusion was started and titrated to maintain mean arterial pressure >65 mmHg. On the morning of day 2, the patient started improving clinically, and inotropes were tapered slowly. All the vitals were within the normal limits. ABG revealed pH of 7.40, pCO2 – 31, HCO3 – 19.7, pO2 – 173 mmHg on FiO2 of 50%, and lactate – 2.1. Sedation was stopped, and GCS was assessed. The patient was fully conscious and oriented and was extubated successfully. The rest of the course of recovery was uneventful, and the patient was discharged successfully.
| Discussion | | |
Globally, amitraz is used as a pharmaceutical, veterinary, and agricultural product. Poisoning can occur in animals and humans due to accidental ingestion, inhalation, or after skin exposure.[2] In our case, it occurred due to the ingestion of a 12.5% formulation in a suicide attempt. The common initial symptoms are altered consciousness, nausea, vomiting, and dizziness. The major clinical findings in the ICU were somnolence, coma, miosis, mydriasis, bradycardia, respiratory failure requiring mechanical ventilation, and hypo- and hyperthermia.[6] The CNS depression was the predominant sign in our case which was also observed in another case report, constant with the effect of amitraz on α2-adrenergic receptors.[7] A direct inhibitory effect of the agent on the respiratory center may lead to respiratory depression concomitant with CNS depression.[6] Some poisoning, such as organophosphate or opioids, may mimic the clinical picture of amitraz poisoning. The co-existence of bradycardia and miosis can lead to dubiety in diagnosis and management. A careful and detailed history and examination should be done to exclude the possibility of other poisonings.[8] An atropine bolus dose was already given in the peripheral hospital as HR was 40/min and one more bolus was given in the ICU. In one case report, it was also given in the peripheral hospital as emergency management before transferring the patient to a higher center.[7] Although, the role of atropine in the treatment of bradycardia associated with amitraz poisoning is controversial.[2],[5],[7],[9],[10] However, most studies reported that using atropine for those with both miosis and bradycardia resolved the problem.[9],[11] Atropine is considered the drug of choice in the treatment of bradycardia that results from vagal stimulation and atrioventricular blocks, but not for those related to other mechanisms.[12] The cause of bradycardia is the stimulation of α2-adrenergic in the CNS.[13] Hsu et al. claimed that atropine increased heart rate and prevented amitraz-induced bradycardia in animals.[14] Eizadi-Mood et al. concluded that in amitraz poisoning, atropine is effective when there is bradycardia. In parallel to our case report, slight hyponatremia was also observed in other reports.[7],[10] The levels of blood urea nitrogen, creatinine and serum sodium, and potassium usually do not exhibit variation in amitraz poisoning[5] and the same picture was found in our case as all the blood investigations were within normal limits. The ABG showed respiratory acidosis; in our case, Eizadi-Mood et al. also showed an acidotic picture;[7] and Kalyoncu et al. reported respiratory alkalosis in two cases, respiratory acidosis in three cases, and metabolic acidosis in five cases.[10] We did not observe any changes in the electrocardiogram (ECG), similar to the case reported by Eizadi Mood et al. as they also didn't see any changes in ECG.[7] Aydin et al. reported nonspecific ST changes in the ECGs of seven children with no history of cardiac disease.[9] The time to resolve CNS depression was reported to be 2–48 h in the previous reports, and the length of stay was between 2 and 5 days.[6],[7] Our patient gained consciousness after 21 h and was extubated successfully. Blood glucose levels might increase significantly in some cases, but in our case, no significant alterations in glucose levels were observed. Hepatic, renal, and cardiac profiles were also found to be within the normal limits in our case.
| Conclusion | | |
The signs and symptoms of acute amitraz intoxication appear rapidly and become established within minutes to hours. Prompt recognition of symptoms and management of this rare poisoning under close supervision in the ICU is mandatory in these cases. An initial approach to the patient with amitraz poisoning includes initial stabilization to correct immediate life-threatening problems, measures to reduce absorption, and elimination of the toxin. There exists no specific antidote for amitraz poisoning, and the management is mainly symptomatic and supportive. The role of gastric lavage, activated charcoal, and cathartics is not well established, although they can be considered for treatment. Effects of α2-agonists are dose dependent; increased intake may lead to severe effects on the body systems causing coma and respiratory failure. Our case was a severe case of amitraz poisoning requiring intensive care. Initial supportive management is a timely intervention that includes monitoring and care, and the prognosis is usually good, thereby reducing mortality and morbidity.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Queiroz-Neto A, Zamur G, Gonçalves SC, Carregaro AB, Mataqueiro MI, Harkins JD, et al. Characterization of the antinociceptive and sedative effect of amitraz in horses. J Vet Pharmacol Ther 1998;21:400-5.  |
| 2. | Jorens PG, Zandijk E, Belmans L, Schepens PJ, Bossaert LL. An unusual poisoning with the unusual pesticide amitraz. Hum Exp Toxicol 1997;16:600-1. |
| 3. | Cullen LK, Reynoldson JA. Central and peripheral alpha-adrenoceptor actions of amitraz in the dog. J Vet Pharmacol Ther 1990;13:86-92. |
| 4. | Jones RD. Xylene/amitraz: A pharmacologic review and profile. Vet Hum Toxicol 1990;32:446-8. |
| 5. | Aydin K, Kurtoğlu S, Poyrazoğlu MH, Uzüm K, Ustünbaş HB, Hallaç IK. Amitraz poisoning in children: Clinical and laboratory findings of eight cases. Hum Exp Toxicol 1997;16:680-2. |
| 6. | Ulukaya S, Demirag K, Moral AR. Acute amitraz intoxication in human. Intensive Care Med 2001;27:930-3. |
| 7. | Eizadi-Mood N, Sabzghabaee AM, Gheshlaghi F, Yaraghi A. Amitraz poisoning treatment: Still supportive? Iran J Pharm Res 2011;10:155-8. |
| 8. | Balali-Mood M, Saber H. Recent advances in the treatment of organophosphorous poisonings. Iran J Med Sci 2012;37:74-91. |
| 9. | Aydin K, Per H, Kurtoglu S, Poyrazoglu MH, Narin N, Aslan D. Amitraz poisoning in children. Eur J Pediatr 2002;161:349-50. |
| 10. | Kalyoncu M, Dilber E, Okten A. Amitraz intoxication in children in the rural Black Sea region: Analysis of forty-three patients. Hum Exp Toxicol 2002;21:269-72. |
| 11. | Doganay Z, Aygun D, Altintop L, Guven H, Bildik F. Basic toxicological approach has been effective in two poisoned patients with amitraz ingestion: Case reports. Hum Exp Toxicol 2002;21:55-7. |
| 12. | Stancil SA. Case study: Atropine & the bradycardia patient. Questioning the need for medical interventions is Key to patient care. EMS Mag 2010;39:47-50, 57. |
| 13. | Sanders KH, Jurna I. Effects of urapidil, clonidine, prazosin and propranolol on autonomic nerve activity, blood pressure and heart rate in anaesthetized rats and cats. Eur J Pharmacol 1985;110:181-90. |
| 14. | Hsu WH, Lu ZX, Hembrough FB. Effect of amitraz on heart rate and aortic blood pressure in conscious dogs: Influence of atropine, prazosin, tolazoline, and yohimbine. Toxicol Appl Pharmacol 1986;84:418-22. |
|
Search Pubmed for