Fatal butane inhalation from gas cartridges: a case report and

Transcription

Fatal butane inhalation from gas cartridges: a case report and
Rom J Leg Med [23] 115-120 [2015]
DOI: 10.4323/rjlm.2015.115
© 2015 Romanian Society of Legal Medicine Fatal butane inhalation from gas cartridges: a case report and literature review
Kaori Kimura-Kataoka1,*, Junko Fujihara1, Toshihiro Yasuda2, Haruo Takeshita1
_________________________________________________________________________________________
Abstract: Volatile substances are commonly misused with easy-to-obtain commercial products, such as glue, shoe
polish, nail polish remover, butane lighter fluid, gasoline and computer duster spray. This report describes a case of sudden death
of a 29-year-old woman after presumably inhaling gas cartridge butane from a plastic bag. Autopsy, pathological and toxicological
analyses were performed in order to determine the cause of death. Pulmonary edema was observed pathologically, and the
toxicological study revealed 2.1μL/mL of butane from the blood. The causes of death from inhalation of volatile substances have
been explained by four mechanisms; cardiac arrhythmia, anoxia, respiratory depression, and vagal inhibition. In this case, the
cause of death was determined to be asphyxia from anoxia. Additionally, we have gathered fatal butane inhalation cases with
quantitative analyses of butane concentrations, and reviewed other reports describing volatile substance abuse worldwide.
Key Words: forensic science, butane, inhalation, volatile substance, autopsy, toxicology.
V
olatile substances are those that vaporize
at ambient temperatures, and they are
commonly misused with easy-to-obtain commercial
products, such as glue, shoe polish, nail polish remover,
butane lighter fluid, gasoline, and computer duster spray
[1]. There are several methods by which these volatile
substances can be inhaled: (1) bagging, whereby volatile
substances are placed into a plastic bag and inhaled; (2)
sniffing, whereby volatile substances are inhaled directly
from the container; (3) spraying directly into the oral or
nasal cavities; and (4) huffing, whereby volatile substances
are inhaled from a substance-soaked cloth placed over
the nose or mouth [1].
Butane, one of the most common volatile
substances, has the chemical formula C4H10, with a
molecular weight of 58.12. It is highly flammable,
colourless, and odourless. Butane and many other volatile
substances cross the blood–brain barrier rapidly due to
their nonpolar, hydrophobic, lipophilic characteristics,
where the concentration peaks are observed within 1 to 3
minutes after inhalation [2, 3].
The most common effects of volatile inhalant
use are euphoria, relaxation, vertigo, and headache [4].
According to Garland, 63.7% and 62.9% of adolescent
inhalant users experienced euphoria and relaxation,
respectively, and volatile substances are presumably
inhaled for these positive effects.
This report describes a case of sudden death,
presumably after inhaling gas-cartridge butane from a
plastic bag. An autopsy and pathological and toxicological
analyses were performed in order to determine the cause
of death. Furthermore, we have gathered fatal butane
inhalation cases with quantitative analyses of butane
concentrations and reviewed other reports describing
volatile substance abuse worldwide.
1) Department of Legal Medicine, Shimane University School of Medicine, Izumo, Shimane, Japan
* Corresponding author: MD, PhD, Department of Legal Medicine, Shimane University School of Medicine, 89-1 Enya,
Izumo, Shimane 693-8501, Japan, Tel: +81-853-20-2159, Fax: +81-853-20-2155, E-mail: [email protected]
2) Division of Medical Genetics and Biochemistry, Faculty of Medical Sciences, University of Fukui, Fukui, Japan
115
Kimura-Kataoka K. et al.
Fatal butane inhalation from gas cartridges: a case report and literature review
Case
The night before her 30th birthday, a 29-yearold woman was found dead, face down, with her lower
body under a kotatsu table (Fig. 1). She was found with a
plastic bag attached to her mouth. Butane gas cartridges
(liquefied butane; presumably greater than 70% butane)
were discovered inside the house: 1 on top of the kotatsu
table was almost full, 10 near the table were empty, 1
near the table was half full, and 9 in the kitchen were
full. Additionally, there were about 50 more empty gas
cartridges in the house (Fig. 2). She had learned how to
inhale gas from gas cartridges from her ex-boyfriend and
had continued the practice ever since.
Moreover, bliseter packages located on the table
had 2 empty spaces for Paxil® (paroxetine, antidepressant),
1 empty space for Desyrel® (trazodone, antidepressant),
1 empty space for Lendormin® (brotizolam, sedativehypnotic thienodiazepine), and 1 empty space for Seroquel®
(quetiapine, antipsychotic). The woman had been visiting
a hospital for mental instability on a regular basis.
A forensic autopsy was performed 3 days after
the discovery of her death in order to specify the cause of
death.
Figure 1. Picture taken at the scene (the body had been moved
by the discoverer from face-down to face-up position). Closed
arrow indicates a white plastic bag. Open arrows indicate gas
cartridges.
Figure 2. Gas cartridges found in the kitchen.
116
Autopsy findings
The body was 147.0 cm in height and weighed
52.0 kg. Bright red liver mortis was present on the
anterior surface of the body. Numerous petechiae were
observed on the palpebral conjunctiva, lungs, anterior
neck, upper chest, and axillary regions. There were several
subcutaneous haemorrhages on the lower extremities
ranging from 1.0 cm×1.0 cm to 3.0 cm×2.5 cm. There
were 6 circular scars of 1.0 cm to 1.5 cm in diameter,
which resemble scars from cigarette burns. No apparent
traumatic lesions related to the woman’s death were
discovered. The heart weighed 255 g, with no apparent
arteriosclerosis of coronary arteries. The colour of cardiac
blood was dark red and did not contain any coagulation.
Viscous fluid with fine foam was observed in the trachea
and bronchi. Organ weights were as follows: right lung
345 g, left lung 375 g, liver 1,260 g, spleen 94.1 g, pancreas
95 g, right adrenal gland 4.3 g, left adrenal gland 4.1 g,
right kidney 110.1 g, left kidney 105.0 g, and brain 1,330 g.
Pathological findings
Moderate to severe congestion was evident in
most of the organs. Severe fat deposition and mild to
moderate adipose infiltration in the heart, pulmonary
edema (Fig. 3), and sinusoidal dilation of the liver were
observed. No apparent inflammatory lesions or natural
diseases related to the woman’s death were found in any
organ.
Toxicology
The concentration of butane in blood samples
was determined in triplicate by gas chromatography (GC)
using a modified method of Fuke [5]. Blood samples
(0.5 mL) were placed into a sealed vial with an internal
standard solution containing 0.5 mL of 0.15% acetone.
The vial was heated at 60°C for 30 minutes and then
cooled down to room temperature. A 1.0 mL headspace
sample was injected into the GC. Controls were prepared
by adding standard gases (butane, GL sciences; balance
Figure 3. Pulmonary edema and congestion of the left lung
(HE staining, ×100).
Romanian Journal of Legal Medicine gas, nitrogen) after the fortification of 0.5 mL of distilled
water and an internal standard solution containing 0.5 mL
of 0.15% acetone. Controls were conditioned in the same
manner as previously described. The horizontal axis was
designated as the amount of standard gas added and the
longitudinal axis as the butane and internal standard area
ratio. An approximation formula was calculated from the
data, and the concentration of butane in the blood was
determined.
Samples were analysed by GC/MS using
an Agilent 6890N with a flame ionization detector.
Separation of components was achieved using a 30 m
GS-Q capillary column (J&W, 0.53 mm i.d.). The column
temperature was maintained at 120°C. The injector
and detector temperatures were set at 200 and 250°C,
respectively. Helium was used as a carrier gas at a flow
rate of 5.8 mL/min.
The blood alcohol concentrations were below
the detection limit. The qualitative toxicological analysis
revealed the presence of paroxetine and trazodone,
which are main ingredients of antidepressant drugs. The
concentration of butane in the blood was determined to
be 2.1 μL/mL.
Discussion
The causes of death from inhalation of volatile
substances have been determined to be cardiac
arrhythmia, anoxia, respiratory depression, and vagal
inhibition [6].
Cardiac arrhythmia is considered to be the
most probable cause of death by inhalation of volatile
substances. The association between inhalation of volatile
anesthetics and cardiac arrhythmias has been well
documented within the long history of anaesthesiology
[7–9]. Adrenaline, also known as epinephrine, is a
hormone secreted in the medulla of adrenal glands and
also at the end of sympathetic nerves in response to fightor-flight situations, such as stress and fear. It is a powerful
vasoconstrictor and stimulates the heart [10]. Adrenaline
is used to treat cardiac arrest and cardiac dysrhythmia.
However, the higher the adrenaline level, the greater
the cardiovascular effect and the greater the likelihood
of triggering arrhythmias [6, 9]. Shepherd suggests that
hallucinations caused by inhalant intoxication provoke
disturbing fear and increase the level of adrenaline. Indeed,
auditory and visual hallucinations are experienced by
adolescent inhalant abusers [4].
Anoxia is a total depletion of oxygen. There must
be occlusion of the airways or a decrease in the oxygen
concentration of the inhaled air in order to induce anoxia.
Anoxia is predominantly associated with inhalation of
volatile substances from a plastic bag. As an individual
inhales the volatile substance, the consciousness gradually
declines, and it becomes difficult for that individual to
remove the bag. This situation would result in anoxia and
Vol. XXIII, No 2(2015)
thus causes death [6].
Volatile substances easily migrate to the central
nervous system (CNS). Inhalation of high concentrations
of volatile substances would cause respiratory depression
and, ultimately, respiratory arrest [3, 6]. Clark exhibited
experimentally that exposures to either a CNS depressant
or a CNS stimulant resulted in narcosis, shallow
respiration, and eventually death from respiratory
depression [11]. Although it is often thought that the
major causes of death from inhaling volatile substances
are cardiac arrhythmia and anoxia, Cronk et al. reported
a case of a patient admitted to a hospital due to inhaling
a volatile substance [12]. His electrocardiogram only
exhibited sinus tachycardia, while he repeatedly suffered
respiratory arrest after numerous resuscitation attempts.
This case report illustrated that respiratory arrest alone
could be a significant cause of sudden death in volatile
substance inhalation.
Vagal inhibition of the heart is the over activity
of the parasympathetic nervous system from stimulation
of the laryngeal or pharyngeal mucosa. Such inhibition
may occur when swallowing a bolus of food or upon
sudden entry of cold water into the pharynx and larynx
[13], which resembles the rapid cooling of the mouth or
airways by spraying volatile substance gases into those
orifices [14].
As previously mentioned, volatile substances
can be found in commercial products, such as glue, shoe
polish, nail polish remover, lighter fluid, gasoline, and
computer duster spray. Depending on the product, gas
components could be 100% butane or mixtures of butane,
isobutane, propane, and other gases. Table 1 shows 15
fatal butane inhalation case reports, including this case,
displaying the blood butane concentration, cause of death,
and age and gender of the deceased. All but one case are
reports from Japan. This might be because commercially
available volatile substances consist mainly of butane in
Japan, and the major contents of gas products in other
countries may be different.
According to Table 1 [15-26], the blood butane
concentrations range from 0.11 to 15.3 μL/mL. The
most common cause of death was arrhythmia (6 cases),
followed by asphyxia due to anoxia (5 cases). Two cases
involved a combination of multiple causes. The causes of
death for the other 2 cases were determined to be butane
poisoning and asphyxia by inhalation of gastric contents.
In cases where it was evident that inhalation of gastric
contents or vomit caused asphyxia, these were concluded
to be the cause of death, regardless of the blood butane
concentration. If it was evident that the deceased was
using a plastic bag immediately before death to inhale
butane, commonly called “bagging,” and the inhalation
of butane was proved by toxicological analysis, the cause
of death was determined to be asphyxia due to anoxia.
On the other hand, the cause of death was decided to be
arrhythmia in cases where bagging was denied or the
117
Kimura-Kataoka K. et al.
Fatal butane inhalation from gas cartridges: a case report and literature review
Table 1.
Butane
concentration
in blood (μL/mL)
0,11
Cause of death
14M
Suspected
Inhalation
Method
Bagging
Sugie et al. Forensic Sci Int 2004; 143: 211-214. (15)
13M
Bagging
Al-Alousi. Med Sci Law 1989; 29: 189-208. (16)
24M
16M
13M
Unknown
Bagging
Bagging
Sugie et al. Forensic Sci Int 2004; 143: 211-214. (15)
Aoki T et al. Acta Crim Jpn 1982; 48: 202-204. (17)
Nishi K et al. Jpn J Legal Med 1985; 39: 214-216. (18)
Age
Gender
0,52
0,65
0,94
Arrythmia
Asphyxia by
inhalation of gastric
contents
Arrythmia
Asphyxia
Arrythmia/lung edema
1,22
Arrythmia
M in late
teens
Bagging
Tanaka N et al. Rom J Leg Med 2012; 20: 195-196. (19)
2,1
Asphyxia
29F
Bagging
This report
2,4
Arrythmia
14M
Bagging or
sniffing
Fuke C et al. Legal Med 2002; 4; 134-138. (5)
2,85
4,6
6,8
Asphyxia
Asphyxia
Arrythmia
Butane poisoning
Asphyxia by inhalation of
vomit
16M
31M
23F
Bagging
Bagging
No bagging
Nagata T et al. Jpn J Legal Med 1977; 31: 161-163. (20)
Zhu et al. Jpn J Clin Toxicol 2005; 18: 77-81. (21)
Tanaka N et al. Soud Lek 2010; 4: 44-45. (22)
13M
Unknown
Terada M et al. Jpn J Legal Med 1983; 37: 696.
(23)
9,2
Asphyxia
25M
Unknown
Kawata F et al. Jpn J Forensic Toxicol 1990; 18:
68-69. (24)
10,5
Butane poisoning
F in 30’s
Bagging
Tanaka N et al. Curr Study Environ Med Sci 2010; 3:
15-16. (25)
15,3
Arrythmia
15M
Unknown
Ago M et al. Legal Med 2002; 4: 133-118. (26)
0,24
7,0
deceased was able to move for a short time after bagging.
It seems there is congestion of internal organs and lung
edema to some degree [27–29]; however, there are no
pathological findings specific to butane inhalation. When
relatively high butane concentrations were observed and
no other possible causes of death were present, the cause
of death was determined to be butane poisoning [25, 26].
In the present case, the woman was found with a plastic
bag attached to her mouth, suggesting that she was
inhaling gas-cartridge butane from this plastic bag.
Autopsy findings, such as multiple petechiae, congestion
of internal organs, and the absence of coagulated blood
in the heart, indicated that the woman had an acute
course from the beginning of the inhalation to the time
of death. Pathological analysis also confirmed moderate
to severe congestion of most organs. Pulmonary
edema was observed microscopically; nevertheless,
this finding was not specific to butane inhalation. The
qualitative toxicological analysis revealed the presence
of paroxetine and trazodone, which are main ingredients
of antidepressant drugs. Trazodone is an antidepressant,
known to depress the central nervous system. Although
a quantitative analysis was not performed, trazodone
might have had some competitive impact along with the
respiratory depression effect of butane itself, similar to the
case reported by Tanaka et al. [25]. The concentration of
118
References
butane in the blood was determined to be 2.1 μL/mL, yet
this value was not high compared to other cases (Table 1).
Since the woman was supposedly inhaling butane from
a plastic bag, the cause of death was determined to be
asphyxia due to anoxia.
By comparing cases of fatal butane inhalation,
it could be stated that butane abusers consist mainly of
teenagers (Table 1). It is plausible that this is because
butane is commercially available in the form of lighter
fluid, aerosol spray, and gas cartridges, which could easily
be purchased by teenagers [30]. According to Johnston
et al., the lifetime prevalence of inhalants for 8th graders,
10th graders, 12th graders, college students, and young
adults (ages 19 to 28) has been decreasing in the United
States in the 12 years of their study [31]. However, the
2011 ESPAD report by the European Monitoring Centre
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inhalants in their lifetime [33]. This report summarizes
that the percentage of students (ages 12 to 15) who had
used inhalants in their lifetime in 2011 was no different
from that in 2008 and 2005.
Romanian Journal of Legal Medicine Moreover, the male-to-female ratio in Table 1
was 4:1 (80% male). A reasonable explanation for this
phenomenon is uncertain, yet 74%, 84.6%, 92.3%, and
83.8% of inhalant users were male in other studies (34–
37, respectively). However, in Australia, slightly greater
percentages of female students (ages 12 to 15) who used
inhalants over their lifetime were observed [33]. Some
reports not included in Table 1 have illustrated fatal
butane inhalation by male teenagers [28, 38]. Table 1
shows the cases of only 3 females, which were all reported
after 2010. The inhalant abusers consist not only of male
teenagers, the possibility an increase in the number of
female abusers should be considered. More effective
warnings should be given about the dangers and fatalities
of inhaling volatile substances, including butane.
The present case described fatal butane
inhalation, in which we concluded that the cause of death
was asphyxia due to anoxia. Many studies over several
Vol. XXIII, No 2(2015)
years have reported on volatile substances and their
fatal outcomes; yet there seem to be no specific remarks
concluding that the cause of death is cardiac arrhythmia,
anoxia, respiratory depression, or vagal inhibition.
Forensic pathologists need to consider the possibility of
volatile substance inhalation when sudden deaths are
reported, especially in teenagers and young adults.
Acknowledgment. The authors are grateful to
Dr. Masanori Hasegawa (International Research Institute
of Police Science, Department of Forensic Science) for
his toxicological analyses. We would also like to thank
Prof. Hiroshi Kinoshita (Kagawa University, Faculty of
Medicine, Department of Forensic Medicine) for his
helpful comments and critical review.
Conflict of interest. There was no conflict of
interest.
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