CASE REPORT
A case of suicide by ingestion of caffeine
Alessandro Bonsignore
•
Sara Sblano
•
Fulvia Pozzi
•
Francesco Ventura
•
Alessandro Dell’Erba
•
Cristian Palmiere
Accepted: 9 April 2014 / Published online: 27 April 2014
Ó Springer Science+Business Media New York 2014
Abstract Intentional or unintentional caffeine abuse due
to excessive intake of beverages or energy drinks con-
taining caffeine is relatively frequent. However, death due
to caffeine intoxication is rare and case reports of fatalities
from caffeine toxicity are relatively infrequent. In this
report, we describe an autopsy case involving a 31 year-old
man who intentionally took a large amount of caffeine
tablets in the form of a weight loss supplement as part of a
suicide plan. Caffeine femoral blood concentration
(170 mg/l) was within the toxic and potentially lethal
ranges reported in the literature in similar cases. Post-
mortem biochemistry results suggested depressed glomer-
ular filtration rate and pre-renal failure at the time of death
but failed to reveal myoglobinuria, glycosuria, ketonuria or
ketonemia. Based on the absence of pathological findings
at autopsy and the high blood caffeine level, death was
attributed to acute caffeine toxicity. The case emphasizes
the usefulness of performing exhaustive toxicology and
searching for all potentially relevant information in order to
formulate appropriate hypotheses concerning the cause and
manner of death.
Keywords Caffeine Fatal intoxication Toxicology
GC–MS Postmortem biochemistry
Introduction
Caffeine (1,3,7-trimethylxanthine) is a natural xanthine
alkaloid that acts as a central nervous system stimulant.
Individuals may be exposed to caffeine via classical bev-
erages (coffee, tea, chocolate, and most colas), food, pre-
scription and over-the-counter medications, as well as
herbal and dietary supplements. The molecule is one of the
ingredients in health food products sold as appetite sup-
pressants. Caffeine consumption has increased in recent
years. This is especially true among young people, stu-
dents, and athletes who also consume it in a more con-
centrated form as energy drinks, ‘‘energy shots’’ (smaller in
volume as they lack the large amounts of sugars, carbo-
hydrates, and/or carbonated water of classical energy
drinks containing caffeine) or, of most concern, as 100 %
caffeine anhydrous, a high-dose self-administered drink
additive [1–15].
Intentional or unintentional caffeine abuse due to
excessive intake of beverages or energy drinks containing
caffeine is relatively frequent and responsible for classical
clinical manifestations of overstimulation. However, death
due to caffeine intoxication is rare and case reports of
fatalities from caffeine toxicity are relatively infrequent. In
recent years, the risk of intentionally or unintentionally
ingesting potentially lethal levels of caffeine has been
heightened by its easy availability. Indeed, energy drinks
and shots with high caffeine content are readily found in
A. Bonsignore S. Sblano A. Dell’Erba
DIM – Section of Legal Medicine, University of Bari, Bari, Italy
A. Bonsignore F. Ventura
Department of Legal Medicine, University of Genova, Genoa,
Italy
F. Pozzi
Department of Public Health, Neurosciences, Experimental and
Forensic Medicine, University of Pavia, Pavia, Italy
C. Palmiere (&)
Centre Universitaire Romand de Me
´
decine Le
´
gale, University
Center of Legal Medicine, Rue du Bugnon 21, 1011 Lausanne,
Switzerland
e-mail: cristian.palmiere@chuv.ch
123
Forensic Sci Med Pathol (2014) 10:448–451
DOI 10.1007/s12024-014-9571-6
shops and health stores and pure caffeine anhydrous and
anorecting tablets can be purchased online [16–22].
In this report, we described an autopsy case involving a
31 year-old-man who intentionally took a large amount of
caffeine tablets in the form of a weight loss supplement as
part of a suicide plan.
Case history
The body of a 31 year-old Caucasian man was found in his
ex-girlfriend’s apartment where he was staying although
they had broken up. She had left the man alone in her
apartment at 8:00 p.m. He did not indicate any problems to
her at that time. He called her at 11:00 p.m. from the
apartment, complaining of a sudden onset of bloody
vomiting. Since he had previously used illness and physical
symptoms as a pretext to gain her attention when she went
out alone, the woman did not take this complaint seriously.
When she returned at 4:00 a.m. she was unable to enter the
apartment. She called the police after trying to contact the
victim unsuccessfully by mobile phone several times. Upon
arrival, police and first-aid workers found the door locked
from the inside with the key still in the lock. The decedent
was discovered in a bedroom. No blood or vomit was
present around the body. A suicide note was found next
him in which he purportedly mentioned that he was ending
his life and wanted his ex-girlfriend to take care of his
parents. No cardiopulmonary resuscitation attempts were
performed and his death was pronounced at 5:25 a.m.
The body was found on the floor in a supine position, fully
clothed. No tools or weapons were identified in the immediate
vicinity of the body or in the other rooms of the apartment. No
electrical appliances were switched on. No signs of drug use
were discovered during the course of the inspection and no
pills or tablets were found elsewhere in the apartment.
The deceased was 175 cm tall and weighed 65 kg.
External examination did not reveal anything remarkable.
No bleeding wounds were observed at any site. The heart
weighed 315 g and did not reveal any hypertrophy or
dilatation. The myocardium did not exhibit fibrosis or
ischemic areas, and the coronary arteries did not present
morphological abnormalities. The lungs were relatively
edematous and congested (left 600 g, right 720 g). The
liver weighed 1,560 g and appeared yellowish brown, but
no nodular lesions were found. The urinary bladder con-
tained 50 ml of cloudy yellow urine. The spleen (120 g)
and kidneys (right 120 g, left 130 g) showed no significant
macroscopic changes. The brain weighed 1,400 g and
displayed edema with slight flattening of the gyri and mild
cerebellar tonsillar grooving. The esophagus and the
stomach contained an estimated 200 g of whitish-brownish
material with identifiable fragments of undigested tablets.
No other abnormalities were observed elsewhere in the
body. Histological examinations revealed areas of fatty
degeneration and focal fibrosis of the liver as well as slight
acute renal tubule necrosis and hyalinized glomeruli in the
kidneys. Acute generalized visceral congestion as well as
cerebral and pulmonary edema was also noted.
Peripheral blood from the femoral vein, bile, urine,
gastric content, and samples of certain tissues (brain, lung,
liver, spleen, and kidney) were recovered for toxicological
and biochemical analyses.
Biochemical investigations were performed in femoral
blood and urine (Table 1). These included measurements
of renal, hepatic, and cardiac function markers (in post-
mortem serum) as well as determination of beta-tryptase
(in postmortem serum), beta-hydroxybutyrate (in blood and
urine), glycated hemoglobin (in blood), myoglobin (in
urine), glucose (in urine), and carbohydrate-deficient
transferrin (CDT, in postmortem serum). The results were
consistent with the presence of depressed glomerular fil-
tration rate and pre-renal failure. Markers of cardiac
function (N-terminal pro-brain natriuretic peptide and tro-
ponin I) and CDT levels were increased. Urine myoglobin,
urine glucose, as well as beta-hydroxybutyrate in blood and
urine, were not increased.
Table 1 Postmortem biochemical investigation results
Measured analyte Measured
concentration
Clinical reference
value
Postmortem serum urea 11.1 mmol/l
(31.09 mg/dl)
2.9–7.7 mmol/l
(8.1–21.6 mg/dl)
Postmortem serum
creatinine
126 lmol/l
(1.43 mg/dl)
62–106 lmol/l
(0.70–1.20 mg/dl)
Postmortem serum uric
acid
480 lmol/l
(8.07 mg/dl)
202–416 lmol/l
(3.40–7.00 mg/dl)
Postmortem serum beta-
tryptase
9 ng/ml 13 ng/ml
Blood beta-
hydroxybutyrate
126 lmol/l
(1.31 mg/dl)
50–170 lmol/l
(0.52–1.77 mg/dl)
Urine beta-
hydroxybutyrate
168 lmol/l
(1.75 mg/dl)
50–170 lmol/l
(0.52–1.77 mg/dl)
Blood glycated
hemoglobin
5.8 % 5.0–6.6 %
Urine myoglobin n.d. –
Urine glucose 0.2 mmol/l
(3.6 mg/dl)
0.8 mmol/l
(14 mg/dl)
Postmortem serum CDT 2.2 % 1.6 %
Postmortem serum
troponin I
0.16 lg/l 0.03 lg/l
Postmortem serum NT-
proBNP
308 ng/l 115 ng/l
CDT carbohydrate-deficient transferrin, NT-proBNP N-terminal pro-
brain natriuretic peptide, n.d. not detected
Forensic Sci Med Pathol (2014) 10:448–451 449
123
Toxicology included carbon monoxide, cyanide, etha-
nol, and other volatile compound determination as well as
general screening for nonvolatile drugs, poisons, and
metabolites by gas chromatography–mass spectrometry
(GC–MS) using commercial mass spectrum libraries, high-
performance liquid chromatography with ultraviolet/diode-
array detection (HPLC–UV–DAD) and headspace–gas
chromatography (HS–GC) for volatile compound analysis.
Toxicological investigations performed on the blood
samples revealed the presence of ethanol (0.24 g/l), caf-
feine (170 mg/l), and acetylsalicylic acid (169 mg/l). Eth-
anol was measured in the blood using HS–GC–FID.
Caffeine was quantified by HPLC–UV–DAD.
Analyses carried out in other samples and tissues to
measure caffeine concentrations provided the following
results: gastric content 10,204 mg/ml, urine 79 mg/l, bile
365 mg/l, brain 544 mg/l, lung 811 mg/l, liver 556 mg/l,
spleen 824 mg/l, kidney 1,755 mg/l.
The measured concentration of caffeine in the gastric
content (10,204 mg/ml) and the volume of the gastric
content at autopsy (200 g) enabled investigators to estimate
the amount of caffeine in the gastric content to be
approximately 2 g.
Based on the high blood caffeine level (in agreement
with those reported in the literature in fatal cases due to
caffeine poisoning) and the absence of pathological find-
ings at autopsy, death was attributed to acute caffeine
toxicity.
Other investigations
According to medical records that were obtained from
relatives of the decedent, local health services and general
practitioners, the man suffered from chronic alcohol abuse.
A year prior to his death he had been hospitalized for
attempted suicide using analgesic pills (ibuprofen).
After having received the toxicology results, pathologist
and police investigators tried to obtain information from
relatives and friends about the origin of the caffeine
responsible for his death. The decedent’s ex-girlfriend
declared that, some weeks after the man’s death, she found
an empty vial that once contained 100 concentrated caf-
feine tablets (100 mg pure caffeine/tablet) in his sport’s
bag. She had bought these pills 1 year prior to his death as
an over-the-counter weight-loss supplement. However, she
had rapidly stopped taking them as she had experienced
significant adverse cardiac effects from them. She had
completely forgotten about the tablets and was quite sur-
prised to find the empty vial in his bag. She did not give
any special meaning to this finding and did not announce it
to the police. Indeed, she thought that he had taken these
tablets over the months prior to his death to improve his
sport performance. She did not have any suspicion that the
drugs may have been involved in his death as she was
convinced that he had died from alcohol and illicit sub-
stance intake.
Discussion
Death from caffeine poisoning, although rare, does occur.
The direct cause of death is generally attributed to ven-
tricular dysrhythmia, though caffeine cardiovascular
effects are not limited to arrhythmogenesis [5, 11, 18].
Caffeine is absorbed rapidly and completely when it is
consumed orally. Clinical effects are identifiable within
15 min and peak plasma levels are attained within
15–45 min after ingestion. Caffeine undergoes hepatic
metabolism via N-demethylation, acetylation, and oxida-
tion. The CYP450 1A2 isoenzyme is largely responsible
for the N-demethylation of caffeine to paraxanthine, its
major metabolite. Chronic ingestion of alcohol and medi-
cations may prolong the half-life of caffeine by approxi-
mately 72 %, thus contributing to its toxic effects. Some
fatalities might result from heightened and prolonged caf-
feine levels attributable to multiple drugs metabolized
through the same metabolic pathway [3, 4, 8, 10, 13].
Blood caffeine concentrations within 80–100 mg/l are
generally considered lethal in humans, though correlations
between blood levels and clinical effects are difficult to
establish due to inter-individual variability, tolerance, and/
or pre-existing disease states. Fatalities among adults are
reported following ingested doses of 5–50 g, even though
recovery after ingestion of 30 g has been described.
Ingestion over a brief time of 3–10 g of caffeine might be
lethal [2–4, 8, 10, 13].
Cases of clinically significant toxicity in healthy adults
have been described following the intake of a large number
of energy drinks. However, to reach the dose of 3 g of
ingested caffeine, a person would need to drink a large
number of highly caffeinated beverages within a few hours
[4, 5,
8, 10, 13, 17, 20, 21].
Fatalities following ingestion of huge amounts of pure
anhydrous caffeine or caffeine pills have occasionally been
described in the literature. The lethal concentration of
80–100 mg/l in blood can theoretically be reached after
ingestion of 50–100 caffeine tablets containing 100 mg of
pure caffeine [3, 7].
In this case, the cause of death was attributed to fatal
caffeine intoxication, with the manner of death designated
as voluntary ingestion of several pure caffeine tablets. The
exact amount of the ingested tablets could not been
determined. Based on the decedent’s ex-girlfriend’s testi-
mony, the vial should have contained at least 90 tablets,
which, if they were all taken, would have resulted in
ingesting a total amount of about 9 g of pure caffeine. This
450 Forensic Sci Med Pathol (2014) 10:448–451
123
hypothesis is consistent with the aforementioned data
provided by the literature, which indicates that fatal blood
levels may be reached by ingesting 50–100 tablets of
100 mg pure caffeine [3, 13].
Toxicological analyses of the femoral blood, urine, bile,
and other tissue from the deceased confirmed that the
active ingredient in the ingested tablets was caffeine. The
femoral blood concentration (170 mg/l) was within the
toxic and potentially lethal ranges reported in the literature
in similar cases. Caffeine concentrations in the other bio-
logical samples tested were comparable to values found in
caffeine fatalities in which the molecule was analyzed in
numerous fluids and tissues collected during autopsy.
As acetylsalicylic acid is metabolized by uridine 5
0
-
diphospho-glucuronosyltransferase 1A6 and cytochrome
P450 2C9, its concomitant presence in the blood (169 mg/
l) does not seem to have played a role in modifying caf-
feine metabolism, prolonging its half-life or finally con-
tributing to the toxic effects. Postmortem biochemistry
results suggested that there was a depressed glomerular
filtration rate and pre-renal failure at the time of death,
likely following severe vomiting. Normal myoglobin,
glucose, and beta-hydroxybutyrate levels in blood and
urine suggested that the death occurred relatively rapidly
after the caffeine ingestion, thus not allowing metabolic
complications to take place.
Key points
1. Caffeine intoxications and suicides due to ingestion of
tablets with high caffeine contents, do occur, albeit
rarely.
2. The effects of caffeine after ingestion (or administra-
tion) are rapid and pharmacological interactions with
other drugs exist which can potentially raise blood
caffeine levels after concomitant intake.
3. High blood caffeine levels, though not lethal, should
be considered as potentially being involved in the
cause of death, especially in cases of pre-existing
diseases or when drugs sharing the same metabolic
pathway are concomitantly present.
4. The correlation of medical and social history, autopsy
observations, histology findings, toxicological data and
postmortem biochemical results are decisive in iden-
tifying the cause of death and characterizing the
pathophysiological mechanisms involved in the death
process.
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