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Journal of Acute Medicine 5 (2015) 109e111
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Case Report

A rare but serious case of toluene-induced sudden sniffing death

Ting-Jang Guo
Department of Emergency Medicine, Kaohsiung Medical University Hospital, Kaohsiung City, Taiwan
Received 30 July 2015; accepted 18 September 2015
Available online 22 November 2015

Abstract

Sudden sniffing death is rare but serious during volatile substance sniffing or in the subsequent hours, especially in patients with toluene
(super-glues) sniffing. We present the case of a 38-year-old female who sustained out-of-hospital cardiac arrest temporally related to toluene
sniffing. Resuscitation of sudden sniffing death is seldom successful in the previous published reports. Our patient initially survived after
aggressive resuscitation. Toluene abuse is associated with major toxicities including severe metabolic acidosis with lactate accumulation, CNS
depression, ventricular arrhythmias, rhabdomyolysis, and liver toxicity. A possible mechanism of sudden sniffing death related to toluene abuse
is ventricular arrhythmias, yet the true mechanism is still unknown. Severe metabolic acidosis may be another possible and important cause of
sudden death in our patient. Sudden sniffing death should be considered in evaluating out-ofehospital cardiac arrest related to toluene sniffing,
especially in the severe metabolic acidosis condition.
Copyright © 2015, Taiwan Society of Emergency Medicine. Published by Elsevier Taiwan LLC. All rights reserved.

Keywords: sudden sniffing death; toluene; metabolic acidosis; hyperlactemia; rhabdomyolysis; liver toxicity

1. Introduction toluene intoxication. In the evening of April 7th, she sniffed 20

Toluene, the major component of glues, is commonly used
as an organic solvent in many industrial processes and
household products. Toluene abuse is prevalent around the
world because toluene is inexpensive and legal to buy.1 We
report an unusual case of sudden sniffing death with severe
mixed acidosis, hyperlactemia, rhabdomyolysis, and liver
toxicity resulted from toluene (super-glue) abuse.
2. Case report
A 38-year-old female patient presented to our emergency
department for out-of-hospital cardiac arrest on 7th April in
2015. She received cardiopulmonary resuscitation (CPR) for
10 minutes at the emergency department and then return of
spontaneous circulation (ROSC) was noted. According to her
family's statements, she was a heavy toluene (super-glues)
sniffer and she had frequent history of admission due to
E-mail address: cushing449@yahoo.com.tw.
tubes of super- glue and then her family witnessed her sudden
death. Her family called the ambulance immediately and
performed CPR for 5 minutes on the scene. She was sent to
our emergency department 30 minutes later.
On physical examination post ROSC, her Glasgow coma
scale was E1VeM1. Breathing sound of coarse crepitation was
noted on right side chest auscultation. The auscultation of the
sound on her left side chest was unremarkable. There was no
trauma mark on the physical examination. We noted that her
oral cavity was clear during intubation. The “super-glue” odor
was also noted during resuscitation. She was hemodynami-
cally unstable post ROSC (pulse rate: around 130 beats per
minute) and profound shock was noted (blood pressure post
ROSC: 49/27 mmHg).
Arterial blood gas interpretations showed severe mixed
acidosis with pH 6.74 (7.35-7.45). White blood cell count was
44.4 x1000/uL, hemoglobin was 11.9 g/dL and platelet count
was 395 x1000/uL. Cardiac enzymes were normal. Other
laboratory studies showed the following: serum creatinine,
1.66 mg/dL; blood urea nitrogen, 3.3 mg/dL; sodium,

http://dx.doi.org/10.1016/j.jacme.2015.09.006
2211-5587/Copyright © 2015, Taiwan Society of Emergency Medicine. Published by Elsevier Taiwan LLC. All rights reserved.
110 T.-J. Guo / Journal of Acute Medicine 5 (2015) 109e111
141 mmol/L; potassium, 4.4 mmol/L; blood glucose, 152 mg/
dL; phosphate, 4.5 mg/dL; ionized calcium, 4.6 mg/dL; uric
acid, 9.5 mg/dL; C-reactive protein, 0.87 mg/L; lactate,
3.6 mmol/L; and ammonia, 549 ug/dL. She had elevated liver
enzymes, with aspartate transaminase (AST) 1158 unit/L,
alanine transaminase (ALT) 1328 (unit/L). Toxicology screens
were negative for alcohol, PCP, BZD, amphetamine, cocaine,
or cannabis.
Serial chest radiographs were obtained which showed
increased infiltrates on the right side. Computed tomography
(CT) of the brain showed brain edema. ECG showed sinus
tachycardia, without prolonged QTc, heart rate: 130 beats per
minute.
Patient received vasopressors, mechanical ventilation,
empiric antibiotics, and cooling therapy based on status post
successful cardiopulmonary resuscitation. Cooling therapy
was started immediately after admission in the intensive care
unit (ICU). We used empiric antibiotics for her aspirated
pneumonia. On the 2nd day, her acidosis was improved with
arterial blood gas pH 7.20, but she started to develop rhab-
domyolysis. Her creatine kinase (CK) increased from 300 to
25011 unit/L. On the 3rd day, her acidosis was further
improved with arterial blood gas pH 7.25. Her ammonia level
dropped to 90 ug/dL and CK decreased to 13927 unit/L. Her
WBC decreased to 29.2 x1000/uL. However, she was hemo-
dynamically unstable with shock status and still received va-
sopressors and mechanical ventilation. On the 4th day her
family refused further resuscitation because her consciousness
did not recover (Glasgow coma scale: E1VeM1). Her family
signed “Do Not Resuscitation” consent and finally she was
discharged from the ICU on the 4th day in a critical condition.
3. Discussion
Death related to volatile substance abuse mostly results
from asphyxia, suffocation, choking, and trauma due to
dangerous behavior during exposure to volatile substance or in
the subsequent hours after sniffing volatile substance. “Sudden
sniffing death” refers to a patient with cardiovascular collapse
during exposure to volatile substance or in the subsequent
hours after sniffing volatile substance. “Sniffing” refers to the
direct nasal inhalation from containers. Reported cases of
sudden sniffing death related to volatile substance abuse is
few, and most of these patients are associated with haloge-
nated hydrocarbons abuse.2e4 Halogenated hydrocarbon abuse
can cause a fatal arrhythmia.3 Reported cases of sudden
sniffing death with aromatic hydrocarbon abuse have been
even fewer, especially with toluene abuse which, at the same
time, is extremely fatal. Toluene, the major component of
super-glue, is a kind of aromatic hydrocarbons (C7H8). Cases
of toluene abuse therefore have been reported extremely
rarely; however, toluene abuse is prevalent around the world.
Unfortunately, resuscitation of sudden sniffing death is seldom
successful in the previous published reports.5 Our patient got
ROSC after the initial aggressive resuscitation. Favorable
prognosis could be expected with early diagnosis and proper
interventions.
Toluene is toxic to many body systems. The most important
toxicities are central nervous system (CNS) depression, ven-
tricular arrhythmia, and metabolic acidosis.3 A well-described
complication of toluene abuse is renal tubular acidosis6 and
liver toxicity may also occur.7 Acute respiratory distress
syndrome has been reported in the previous published
reports.8e10 CNS depression rarely causes respiratory arrest
and death.5 Toluene intoxication can result in cerebellar
dysfunction and cranial neuropathies.1,11 Brain CT may
demonstrate loss of brain mass.12e15 Fatal arrhythmias or
myocardial infarction may rarely occur.3,16 Ventricular dys-
rhythmias may result from an increase in QT duration and QT
dispersion.17 Yet there was no evidence of prolonged QT in-
terval noted in our patient's ECG. Besides, our patient's ECG
and cardiac enzymes were not consistent with an acute cor-
onary syndrome event. Heavy toluene abuse can cause severe
metabolic acidosis with lactate accumulation and few patients
with a pH less than 6.8 survived.18e20 Toluene is metabolized
to hippuric acid. Because of an excess of hippuric acid,
toluene abuse can result in metabolic acidosis. Potassium is
combined with hippurate anions, so the resulting is hypoka-
lemia and weakness, especially in patients with chronic
toluene abuse.21,22 Severe metabolic acidosis may be one of
the possible causes of her sudden death. Our patient initially
survived after aggressive resuscitation and perhaps favorable
outcome could be achieved. Her CK was significantly elevated
on the 2nd day and this consequence was probably owing to
rhabdomyolysis. It was regrettable that her family refused
further resuscitation.
Although exposure to toluene may be confirmed by
detection of hippuric acid in urine or direct measurement in
the blood, these laboratory data are not quickly available and
don't change management priorities. Thus, these laboratory
studies were not performed in our patient and exposure to
toluene was confirmed by detection of the “super-glue” odor
and her medical history. Management of toluene intoxication
is supportive treatment. There is no specific antidote to treat
toluene intoxication. Patients who have ventricular arrhyth-
mias after toluene abuse should receive amiodarone rather
than epinephrine because epinephrine can theoretically worsen
arrhythmias in the irritable myocardium.14,23
Sudden sniffing death has been documented since the
1970s.24,25 The probable mechanism of sudden sniffing death
after toluene abuse may be cardiac arrhythmias, but the true
mechanism is still unknown.5,26 The previous experimental
evidence suggested cardiac arrhythmias be resulted from
toluene abuse.5 Human researches are limited due to ethical
concerns. Specific post-mortem features of toluene abuse have
not yet been identified. Consequently, in all unnatural deaths
of toluene abuse, toxicological examination is strongly rec-
ommended.5 Chronic heavy toluene abuse was reported to
result in increases in QT interval, QTc duration, and QT
dispersion, good predictors for sudden cardiac death.27 How-
ever, QT interval, QTc duration, and QT dispersion did not
increase in our patient's ECG. Unfortunately, death from car-
diac arrhythmia after toluene abuse has been unpredictable so
far and thus resuscitation is rarely successful.5
 T.-J. Guo / Journal of Acute Medicine 5 (2015) 109e111
In conclusion, toluene abuse is associated with major tox-
icities including metabolic acidosis with lactate accumulation,
CNS depression, ventricular arrhythmias, rhabdomyolysis, and
liver toxicity. Sudden sniffing death should be considered in
evaluating out-ofehospital cardiac arrest related to toluene
sniffing, especially in the severe metabolic acidosis condition.
Aggressive resuscitation should be carried out because
favorable outcome is expected with early diagnosis and proper
interventions.
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