Amitraz poisoning: an unusual cause of respiratory and peripheral circulatory failure

Introduction

Amitraz is a formamidine pesticide widely used in agriculture and veterinary medicine as an insecticide and acaricide for controlling the ectoparasites in animals. ¹ Amitraz may be toxic in animals and humans when ingested, inhaled or after skin exposure. ² Amitraz ingestion in humans causes myriad effects on the body, the major effects being observed in the nervous, respiratory and gastrointestinal systems. Amitraz is not a popular suicidal poison in our part of the world and, hence, clinician experience is limited. We report the first case from India of a person who ingested Amitraz with suicidal intent.

Case report

A 42-year-old healthy married man from Rishikesh, Uttarakhand was admitted with a history of pesticide ingestion (revealed later as Amitraz) along with alcohol 2 h previously. Thereafter, he developed progressive respiratory difficulty and within 30 min became unconscious. He had no seizure activity, headache, focal deficit, trauma or vomiting. He was deeply comatosed (Glasgow coma scale 3) with 3 mm sized pupils sluggishly reacting to light. His heart rate was 120 bpm, blood pressure was unrecordable and oxygen saturation was 76% on room air and 98% with 6 L/min oxygen by face mask. Systemic examination was unremarkable though there was a characteristic body odour of kerosene. Arterial blood gas analysis suggested mixed (metabolic and respiratory) acidosis.

He was intubated and ventilated mechanically, resuscitated vigorously with an intravenous bolus of 1.5 L normal saline followed by inotropic support with noradrenaline and dopamine. Two hours later, a blood pressure of 100/60 mmHg was recorded. In the next 7 h, his sensorium gradually improved, after which he was weaned off from ventilatory and inotropic support and later extubated. Results of the investigations are mentioned in Table 1.

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Table 1.

Laboratory parameters of the case with Amitraz poisoning at presentation.

Parameters	Value
Haemoglobin (g/L)	134
Total leucocyte count (×106/mm3)	10.0
Differential leucocyte count	Polymorphs: 79 Lymphocytes:16 Monocytes: 5
Platelet count (×103/cumm)	126.1
Alanine transaminase (IU/L)	32
Aspartate transaminase (IU/L)	29
Alkaline phosphatase (IU/L)	68
Albumin (g/dl)	3.3
Total bilirubin (mg/dl)	0.7
Blood urea nitrogen (mg/dl)	14.4
Serum creatinine (mg/dl)	1.0
Serum amylase (U/L)	507
Serum lipase (U/L)	26
Serum sodium (mmol/L)	143.2
Serum potassium (mmol/L)	3.73

After psychiatric counselling, he was discharged in a healthy condition after two days. At follow-up one week later, there were no residual sequelae.

Discussion

The clinical picture of Amitraz poisoning may be confused with other similar effects of organophosphates, opioids and centrally acting α2-agonist agents (e.g. clonidine).^2–4 In our case, owing to the presence of small pupils and the smell of kerosene, we suspected organophosphate ingestion; however, because of the absence of sweating and of crepitations on chest examination (observed in most of the patients presenting with organophosphate poisoning), we made particular efforts to confirm the container of the poison ingested. The overlapping clinical picture, the agricultural use of the drug and lack of information about Amitraz poisoning accounted for our diagnostic delay. The clinical effects of Amitraz poisoning include central nervous system (CNS) depression, convulsions, respiratory depression, bradycardia, hypotension, miosis (rarely mydriasis), decreased or absent deep tendon reflexes, polyuria, vomiting, hypothermia, decreased intestinal motility, intestinal distention, and hyperglycaemia; many of these effects may be due to its commonly used solvent, xylene.^2,3,5

Amitraz affects α2-adrenoreceptor sites in the CNS and both α1- and α2-peripheral adrenoreceptor sites besides inhibiting prostaglandin synthesis and monoamine oxidase enzyme activity. ⁶

Our patient also presented with mild hyperglycaemia, miosis and absent deep tendon reflexes. We did not perform a gastric lavage as the available literature suggests that the procedure is devoid of any clinical benefit. ⁷ Since our patient had consumed Amitraz with alcohol instead of its usual emetogenic solvent, xylene, vomiting was not seen. ⁷ Elevation of transaminases and non-specific ST-T changes have also been reported; however, these were not present in our case. However, we observed hyper-amylasemia which settled within the next ten days; this was attributed to alcohol intake. Our patient required a short duration of mechanical ventilation.^3,8 The usual duration of recovery is 2–48 h and our patient recovered within 9 h of ingestion. ⁸ Treatment was supportive; atropine may be used in haemodynamically unstable bradycardia. There is no known antidote though yohimbine and atimepazole have been used successfully in animal studies.

Reports on Amitraz poisoning in humans are not as common as those in animals. As there is considerable overlap in clinical features, Amitraz should be ruled out in cases where suspected organophosphorus poisoning is devoid of classical clinical features.