Aspiration and Death from Amitraz-Xylene
FATMA YÜCEL BEYAZTAS, SINAN GURSOY1,
YELTEKIN DEMIREL2, KENAN KAYGUSUZ1,
Department of Forensic
Medicine, Cumhuriyet University School
1Department of Anesthesiology, Cumhuriyet
University School of Medicine
2Department of Family Medicine, Cumhuriyet
University School of Medicine, Sivas
Prof.Dr. Fatma Yücel Beyaztas
Department of Forensic Medicine,
Cumhuriyet University School of Medicine,
58140 - Sivas Turkey.
Fax: 90 346 21912 84
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
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
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
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
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
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.
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