Amitraz is an acaricide and insecticide indicated for the treatment of dogs and for the control of ticks and mites in cattle and sheep. We report the clinical, laboratory and postmortem features of a suicide case by ingestion of amitraz. The major clinical findings were unconsciousness, respiratory failure requiring mechanical ventilation, miosis, hypothermia and bradycardia. The laboratory findings were hyperglycemia. The postmortem findings were pulmonary edema and congestion in the lungs and fatty changes in the liver.

In this case report, we concluded that xylene aspiration was responsible for pulmonary edema and congestion in the lungs, and the aspiration pneumonitis rapidly led to septicemia which was the probable cause of death. This case was reported because of the limited information in the literature on this subject.

Key Words: Amitraz, xylene, poisoning, fatality, forensic medicine.

Amitraz [1, 5 di-(dimethylphenyl)-3-methyl-1, 3, 5-triazapenta-1, 4-diene] is a formamidine pesticide widely used in agriculture and veterinary medicine. Amitraz inhibits monoamine oxidase and prostaglandin synthesis and is an alpha-2 adrenergic agonist. Xylene, a mixture of o-, m-, and p-dimethylbenzene, is widely used in industry (Bonsall and Turnbull 1983). In Turkey, amitraz is available commercially under the proprietary name Kenaz, in the form of an emulsion in xylene containing 12.5 % amitraz and 57.5 % xylene in water.

Amitraz is a potent a2-adrenegic agonist and many of the clinical effects observed in amitraz poisoning are related to a2-adrenegic agonistic activity. In addition, amitraz possesses other pharmacological properties, including monoamine oxidase inhibition and prostaglandin E2 synthesis inhibition (Bonsall and Turnbull 1983; Cullen and Reynoldson 1990). Reported effects of amitraz poisoning in humans include central nervous system (CNS) depression, bradycardia, hypotension, vomiting, hyperglycemia, and miosis (Jorens and Zandijk 1997; Aydin et al. 1997). Information about the biological actions of amitraz in humans is primarily based on theories from animal studies. Cases of human poisoning with amitraz are extremely rare in the literature. Mortality in humans due to amitraz poisoning has been reported in some research studies (Bonsall and Turnbull 1983; Abu-Al Ragheb et al. 1986). Sporadic fatal cases due to accidental industrial inhalation or ingestion of this product have also been reported (Abu-Al Ragheb et al. 1986). In the current case we present the clinical and laboratory features of a 46-year-old man who died from complications of amitraz ingestion for suicidal purposes.

A previously healthy 46-year-old man, 72 kg body weight ingested approximately 100 ml kenaz (amitraz 12.5% + xylene 57.5%) for purposes of intentional suicide. Approximately two hours later after drinking the poison the initial predominant initial symptoms, were nausea, vomiting, dizziness, and dysphagia. This was followed later by loss of consciousness and his family examined him more closely. That is when they found near him, a 100 ml bottle of kenaz, which they were certain had been full. During this time the individual was not conscious and he vomited twice while unconscious. Based on this information the family understood he had attempted to commit suicide and decided to take him to the hospital. About 6 hours after ingestion, the victim was brought to the emergency room of Cumhuriyet University Hospital. Upon arrival, the major clinical findings of the case were lethargy, hypothermia (350C), respiratory distress (moist crackles in his right lung), miosis (2 mm in diameter), heart rate 90 beats/min. Arterial blood pressure (120/80 mmHg), and ECG and brain stem reflexes were normal. Arterial blood gas results were pH 7.26, pO2 80 mmHg, pCO2 52.4 mmHg, HCO3 20.1 mmol/L, BE -4.1mmol/L, O2 saturation 92 %. The other laboratory findings can be seen in Table 1. The man was transferred to the intensive care unit for close monitoring.

After gastric lavage, activated charcoal (1 g/kg) was administered. He was hydrated intravenously and was given oxygen by mask. About one hour after admission, his blood pressure was 75/40 mmHg, and heart rate was 40 beats/min. Dopamine infusion was begun immediately and atropine was administered. Five hours after he was hospitalized, his respirations were inadequate and examination of the blood gases showed respiratory acidosis and hypoxia (pH 7.19, pO2 58.2 mmHg, pCO2 60.2 mmHg, HCO3 18.1 mmol/L, BE -5.9 mmol/L, O2 saturation 81 %). He was intubated immediately with an endo-tracheal tube and connected to a mechanical ventilator with CMV (Control Mechanic Ventilation) mode. There was a little clinical improvement in the level of consciousness, at 24 hours after amitraz ingestion. The post intubation arterial blood gas result were pH 7.35, pO2 109.4 mmHg, pCO2 48.8 mmHg, HCO3 21.3 mmol/L, BE -2.9 mmol/L, O2 saturation 98.6 %.

On the second day after the ingestion of amitraz, the patient began to have respiratory effort. Respiratory support was changed to SMIV (Synchronized Intermittent Mandatory Ventilation) mode. But his respiratory effort continued to be inadequate, and dopamine infusion was started . And then, his condition deteriorated rapidly, pO2 decreased and his respiratory effort stopped, and the ventilator was changed to CMV mode from SMIV mode. Cultures of trans-tracheal aspiration material and blood samples were taken due to the symptoms of moist crackles with auscultation and hyperthermia (380C). On the second day after the ingestion of amitraz, his clinical condition improved hemodynamically (the blood pressure 120/80 mmHg), and the dopamine infusion was stopped. The bottle of amitraz was empty when the family brought it to the hospital for analysis but the quantity consumed by the patient was not known. In addition, he was known to consume large quantities of alcohol and had been in emotional and financial crises. No amitraz toxicology laboratory studies are available in our hospital or region. Blood alcohol level was not measured in the patient.

On the third day after the ingestion of amitraz, Pseudomonas auroginosa was isolated from blood and trans-tracheal cultures and antibiotic therapy was started according to the antibiogram results. On the fourth day the patient again became hypotensive and dopamine infusion was re-started. In spite of dopamine, the blood pressure ranged from 50/30 mmHg to 80/45 mmHg. In addition he again became bradycardic. Atropin is useful hemodynamically in the treatment of bradycardia. However the clinical findings deteriorated. The level of consciousness decreased and the blood gases worsened (pH 7.21, pO2 61.5 mmHg, pCO2 54.8 mmHg, HCO3 17.2 mmol/L, BE -8.1 mmol/L, O2 saturation 86 %). In spite of having a normal ECG, the patient went into sudden cardiac and respiratory arrest. Cardiopulmonary resuscitation was attempted, but the resuscitation efforts were unsuccessful and he was pronounced dead.


Postmortem Evaluation
On gross examination; no evidence of violence or trauma was noted. About 250 ml of the bloody fluid was obtained from his lung. The lungs were grossly firm in consistency. Tissue samples were taken for histopathologic examination. On microscopy; the lungs showed areas of pulmonary edema and congestion. The heart was free of infarcts and the coronary arteries were unremarkable. The liver showed fatty changes. The other viscera examined were essentially unremarkable. No superficial erosions or deep ulcerations could be identified on the gastric mucous.

The major findings of amitraz poisoning in humans are loss of consciousness, respiratory failure, miosis, hypothermia, bradycardia, and hyperglycemia (Jorens et al. 1997; Aydin et al. 1997; Doganay et al. 2002; Yaramis et al. 2000; Ertekin et al. 2002). The principal acute effects of xylene are its action on the CNS and respiratory depression (Abu-Al Ragheb et al. 1986). Similar findings were present in our case.

There is no specific therapy or antidote for the subsequent possible pharmacological effects of amitraz. Amitraz poisoning is generally benign and only requires supportive measures because amitraz metabolizes rapidly and the effects of the product last for a short of period of time (Jorens et al. 1997; Turnbull 1983). Yaramis et al. (2000) presented clinical and laboratory features of poisoning by oral route with amitraz in 11 children. They concluded that CNS depression resolved within 8-14 hours. Ertekin et al. (2002) concluded that the signs of CNS depression in 21 children of oral amitraz poisoning resolved within 6-28 hours. Respiratory depression from human poisoning has also been reported (Aydin et al. 1997; Doganay et al. 2002; Yaramis et al. 2000; Ertekin et al. 2002). Respiratory depression usually lasts less than 24 hours (Doganay et al. 2002; Aydin et al. 2002). Abu Al Ragheb et al. (1986) reported a case of a 27-year-old male of suicide by ingestion of a large quantity of xylene. They reported acute pulmonary edema end severe congestion in the lungs. Sevcik et al. (1992) emphasized that intravenous xylene leads to progressive pulmonary failure that develops in the course of a few minutes following the injection.

This case of poisoning did not progress benignly and the symptoms did not resolve rapidly. His CNS depression, which is the most important sign, never resolved completely. The respiratory depression seen after his arrival didn't recover completely. We concluded that pulmonary edema and congestion due to aspiration pneumonitis had been responsible for his respiration depression. In contrast to Elinav et al. (2005) and Gursoy et al. (2005), our case was dead. We concluded that the probable cause of death in this case was rapidly evolving septicemia due to pulmonary infection. Pulmonary aspiration probably caused the moist crackles observed in his right lung on first examination. He was seen to vomit while unconsciousness on the day of admission. Aspiration pneumonitis was not controlled and continued to progress. We concluded that the aspiration of xylene/amitraz in the gastric content was responsible for non-controlled aspiration pneumonitis because this product is an irritant to the skin and mucous membranes (Bonsall and Turnbull 1983; Abu-Al Ragheb et al. 1986). The postmortem changes observed in the lungs of the victim such as acute pulmonary edema and congestion, bloody fluid, pointed to non-controlled aspiration pneumonitis.

In the presented study, we concluded that xylene aspiration was responsible for pulmonary edema and congestion in the lungs, and that aspiration pneumonitis rapidly evolved, and that the cause of death could be due to septicemia. Also, we would like to emphasize that an increase in poisoning with amitraz has been seen since its usage has increased. Although amitraz poisoning causes serious CNS depression and respiratory failure, all cases can recover completely in a short period of time with close observation and supportive medical treatment.

Table 1. Laboratory data.

Back to text