Fatal Large-Volume Mouthwash Ingestion
in an Adult: A Review and the Possible
Role of Phenolic Compound Toxicity
Guy W. Soo Hoo, MD*
Robert L. Hinds, DO*
Eugene Dinovo, PhD†
Stephen W. Renner, MD†
Objective: To describe a case of fatal mouthwash ingestion
and review possible sources of toxicity. Design: Case
report. Setting: Veterans Administration Medical Center.
Patient: Single patient with massive mouthwash ingestion.
Main results: This patient was a 45-year-old man who
developed cardiovascular collapse and multiorgan system
failure following a massive ingestion of mouthwash
(almost 3 liters). His presentation was remarkable for a
profound anion-gap metabolic acidosis and a significant
osmolar gap. No other co-ingestants were identified, and
he expired despite full supportive care including dialysis
and mechanical ventilation. An autopsy failed to identify
any other cause of death. Nonalcoholic ingredients of this
mouthwash are phenolic compounds (eucalyptol, menthol, and thymol), and large-volume mouthwash ingestion
will produce exposure in the reported toxic range of these
ingredients. Conclusions: When ingested in large quantities, the phenolic compounds in mouthwash may contribute to a severe anion-gap metabolic acidosis and osmolar gap, multiorgan system failure, and death. These compounds, in addition to alcohol, may account for the adverse
effects associated with massive mouthwash ingestion.
Key words: mouthwash, poisoning, phenolic compounds,
anion-gap metabolic acidosis, osmolar gap
Toxicity associated with mouthwash ingestion is
usually attributed to its ethanol content and may
result in death, especially in young children [1-3].
The ethanol content can be as high as 26.9% (54
From the *Pulmonary and Critical Care Section and †Laboratory
Medicine Service, West Los Angeles Healthcare Center; VA
Greater Los Angeles Healthcare System, UCLA School of Medicine.
Received Oct 28, 2002, and in revised form Dec 3, 2002.
Accepted for publication Dec 11, 2002.
Address correspondence to Guy W. Soo Hoo, MD, Pulmonary and
Critical Care Section (111Q), West Los Angeles VAMC, 11301 Wilshire
Blvd, Los Angeles, CA 90073; e-mail: guy.soohoo@med. va.gov.
Soo Hoo GW, Hinds RL, Dinovo E, Renner, SW. Fatal LargeVolume Mouthwash Ingestion in an Adult: A Review and the
Possible Role of Phenolic Compound Toxicity. J Intensive Care
Med. 2003;18:150-155
DOI: 10.1177/0885066602250783
proof) in some preparations. Fatal mouthwash
ingestion in adults has been reported but is a rare
occurrence [4]. We recently encountered a patient
who died after ingestion of a large quantity of
mouthwash. The following provides details of his
presentation and a review of the literature, and
raises the possibility that other mouthwash ingredients also contributed to his death.
Case Presentation
The patient was a 45-year-old resident of a Veterans
Administration domicilliary facility. He had a history of hypertension, hyperlipidemia, coronary artery
disease, coronary artery bypass graft surgery 7
months previously, hypothyroidism, and heavy
alcohol use. He had lived in the domicilliary facility for the past 2 months prior to his presentation
and had been confined in his room for 2 days prior
to his admission. He was brought to the emergency
room by facility staff when noted to be more lethargic and hyperventilating. His main complaint was
nausea and emesis for the past 2 days with some
epigastric discomfort. He admitted to drinking a
large bottle of Listerine® as a substitute for alcohol.
Of note, previous records documented the ingestion of Listerine to the point of intoxication (alcohol level = 268 mg/dl) 6 months prior to this
episode. He denied ingestion of any other substance including alcohol, rubbing alcohol,
antifreeze, or any other illicit substance. His medication list included levothyroxine, metoprolol,
simvastatin, fosinopril, aspirin, and thiamine.
On initial exam, several medical personnel noted
a strong odor of alcohol. One interviewer commented on the odor of Listerine. Initial vital signs
were BP 115/72, HR 91, Temp 92.7°F, RR 29, and a
room air pulse oximetry reading of 98%. There
were no orthostatic changes. The physical exam
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Fatal Large-Volume Mouthwash Ingestion
was unremarkable except for accessory muscle use
and dysmetria on neurologic exam. He appeared
intoxicated but arousable, able to answer questions
and provide a brief history.
The initial laboratory studies were hemoglobin
13.1 g/dL, WBC 11.3 × 1000/uL, differential of 64
segs, 2 bands, 30 lymphs, 4 monos, platelets
133,000, serum Na 138 mmol/L, K 4.5 mmol/L, Cl
95 mmol/L, bicarb < 5 mmol/L, BUN 21 mg/dl, Cr
2.0 mg/dl, Glu 135 mg/dl, Ca 8.5 mg/dl, PO4 8.1
mg/dl, Mg 2.8 mg/dl, ALT 151 U/L (7-45), AST 600
U/L (13-35), alkaline phosphatase 152 U/L (33-94),
lipase 203 IU/L (5-58), amylase 455 U/L (25-240),
albumin 4.5 g/dL, troponin-I < 0.03 ng/ml, creatinine kinase 89 U/L. Baseline laboratory studies
from a month previous were all within normal. An
arterial blood gas revealed a pH 6.95, PaCO2 12 mm
Hg, PaO2 97 mm Hg, and lactate 9.1 mmol/L (0.51.6 mmol/L). The ethanol level was 161.6 mg/dl
(legal limit 80 mg/dl). The measured osmolality
was 369 mOsm/kg H2O (275-295 mOsm/kg H2O)
and calculated osmolality including alcohol was
326 mOsm/kg H2O. The calculated osmolar gap
was 43 mOsm/kg H2O (expected < 10 mOsm/kg
H2O), and the calculated anion gap was 38 mmol/L.
Urinalysis revealed urinary ketones of 40 but was
otherwise unremarkable, with a Woods lamp exam
negative, and no oxalate crystals were noted. He
was given 2 ampules of NaHCO3 by rapid intravenous push and an additional 3 ampules by continuous infusion over 4 hours and admitted to the
intensive care unit. Results of the toxicology studies were not available at presentation, and he was
empirically treated for a possible co-ingestion of
methanol or ethylene glycol with alcohol and
emergent hemodialysis. He was also treated with
antibiotics (piperacillin/tazobactam and vancomycin). Other therapy included thiamine 100 mg
IV, multivitamins, and a warming blanket. His initial chest roentgenogram did not reveal any infiltrates or evidence of congestion. Subsequent films
were only notable for the interval development of
vascular congestion as a result of treatment with
large volumes of fluids. The EKG was notable for
sinus tachycardia, but without acute ischemic
changes and unchanged from previous tracings.
Toxicology results returned with methanol < 5
mg/dl, ethylene glycol < 5 mg/dl, salicylate level <
4 mg/dl, and acetaminophen level < 2.5 mcg/mL. A
urinary toxicology screen was negative for the following substances: amphetamine, barbiturate, benzodiazepine, cannabis, cocaine, opiates.
Despite initial correction of his electrolyte and
acid-base disturbances with hemodialysis, the
patient developed respiratory and cardiovascular
collapse within 12 hours of hospital admission,
requiring intubation, mechanical ventilation, and
maximal vasopressor support. He developed multiple organ system failure, becoming nearly anuric,
developing disseminated intravascular coagulation,
and was unable to be oxygenated despite high levels of positive end-expiratory pressure, pressure
control ventilation, and paralytics. Sputum cultures
grew methicillin sensitive Staph aureus, E. coli, and
Klebsiella pneumoniae. Blood and urine cultures
were negative. Ultrasound of his abdomen revealed
gallbladder sludge and a small, nonobstructing
stone, but no bilary dilatation. He was switched to
continuous veno-venous hemodialysis. He developed progressive acidosis, hepatic failure, and
hypoxemia despite full supportive care, and died
approximately 48 hours after hospital admission.
Postmortem examination was remarkable for evidence of a healing myocardial infarction of about 2
weeks in age, but there was no evidence of a more
recent cardiac injury. Other findings included pulmonary vascular congestion, focal pneumonia,
mild pancreatitis, and a fatty liver. There was no
evidence of pulmonary emboli.
A subsequent search of his room revealed two
1.5-liter bottles of Listerine underneath his bed.
One bottle was empty, and the other was about
one quarter full. The contents of the remaining bottle were tested for methanol and ethylene glycol,
and neither were detected.
Discussion
This man died of complications related to massive
mouthwash ingestion. A conservative estimate would
place consumption of at least 2 liters and probably
closer to 3 liters. An extensive search for co-ingestants
including other alcohol substitutes (methanol, ethylene glycol) was not revealing. The likelihood of
consumption of any other substance other than
mouthwash is low, given his institutional setting
and his claim of only mouthwash ingestion to numerous interviewers. Documentation of mouthwash
use as a substitute for alcohol 6 months previous
also provides further support that he was capable
of consuming large quantities of mouthwash.
This case underscores the risk of major toxicity,
including death, associated with ingestion of large
amounts of mouthwash. Most reported cases of
fatal mouthwash ingestion have involved children
[1-3]. Children are especially vulnerable because of
their smaller size and toxic alcohol levels after as
little as 1 ounce (depending on product formulation) of mouthwash.
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Soo Hoo et al
Fatal mouthwash ingestion in adults has been
reported, but the magnitude of this problem is not
well recognized. Very few deaths have been reported in any detail and have occurred in the context
of restricted sales (Sunday), with mouthwash ingestion producing alcohol levels of 502 mg/dL and 565
mg/dL, respectively [4].
The magnitude of reported mouthwash ingestion
is better appreciated in review of data from the
American Association of Poison Control Centers [57]. Summary data since 1983 have been used to
generate an annual Toxic Exposure Surveillance
System (TESS) report. More than 12,000 cases of
alcohol-containing mouthwash ingestion are
reported annually. An additional 2000+ involve
non-alcohol-containing preparations. More than a
thousand required treatment in a health care facility. Major adverse effects (eg, repeated seizures,
intubation, cardiac or respiratory arrest) involve 20
to 40 patients, with 1 or 2 deaths annually.
Between 1998 and 2000, there were 39,892 cases of
alcohol-containing mouthwash ingestion, with 87
experiencing major adverse effects and 5 deaths.
Only 11,526 (28.9%) were reported in subjects less
than 6 years of age, with 19,388 (48.6%) reported
in those over 19 years of age. Despite the increased
potential toxicity to children, no fatalities were
reported in children. All of the fatalities were in
adults. Therefore, despite the increased potential
toxicity in children, mouthwash ingestion actually
occurs more frequently and with greater morbidity
and mortality in adults.
The frequent occurrence of toxic mouthwash
ingestion becomes less surprising when the magnitude of non-beverage alcohol consumption is recognized [8-9]. Fifteen to 20% of alcoholics hospitalized in VA alcoholism treatment units admit to consuming non-beverage alcohol as a substitute for
alcohol, with figures as high as 50% in a survey of
prisoners. The most common reasons are its easy
availability and low cost, especially during restricted access to alcohol (hospitalization) or “dry” periods (restricted liquor sales). The most common
alcohol substitutes are mouthwash (Listerine; alcohol content = 26.9%) and aftershave lotion
(Mennen’s®; alcohol content = 50%). These nonbeverage alcohol preparations with their other aromatic components facilitate surreptitious alcohol
use, especially in situations where alcohol consumption would not be acceptable or permitted as
in the case of this patient.
This case bears striking similarity to another
report of toxic mouthwash ingestion [10]. A patient
with schizoaffective disorder and alcohol abuse
ingested Listerine in a suicide attempt. She admit152
ted to drinking 5 bottles of unspecified size on the
day of presentation. She was found to be comatose
with only a withdrawal response. She was getting
an arterial blood gas drawn when she went into
asystolic arrest. She was profoundly acidemic with
a pH of 6.54, HCO3 of 2.5 mEq/L, lactate level of 29
mmol/L, serum alcohol level of 125 mg/dl, measured osmolality of 342 mOsm/L, and osmolality
gap of 30 and anion gap of 42 mEq/L. Her condition reversed with supportive care and dialysis, and
she was eventually discharged from the hospital.
Ethylene glycol and methanol levels were not
processed. The authors speculate on the causes of
her severe acidemia and conclude that it was likely multifactorial in etiology, attributable to starvation, alcohol, and lactic acidosis.
In that case as well as in our case, the only identified agent ingested was Listerine. Both patients
were institutionalized at the time of their presentation, with limited access to other sources of alcohol. In our case, analysis for other ingested compounds at the time of presentation was negative.
Listerine remains the sole agent responsible for his
presentation. The question arises as to whether his
decompensation and death can be entirely attributable to the alcohol in his mouthwash. Our analysis
suggests that the ethanol in Listerine is insufficient
to explain all of his metabolic disturbances.
First, the alcohol level of 169 mg/dL is increased,
but not sufficient to account for the severity of his
presentation. This level is usually associated with
intoxication, but not multiorgan system failure or
death. This might have been a plausible explanation in a novel drinker, but not in a chronic alcoholic. It is possible that the level is somewhat
remote from his last drink, which would make his
severe metabolic disturbances even less likely to be
solely attributable to ethanol. He had a marked
anion-gap acidosis, was profoundly acidemic, with
a markedly increased osmolar gap. None of the
nonethanol alcohols usually associated with an
anion-gap acidosis (methanol and ethylene glycol)
were detected. Alcoholic ketoacidosis is commonly
encountered in this population, but never to the
degree noted in this patient. He did have a lactic
acidosis, but not severe enough to account for his
profound acidemia. He had some renal insufficiency, but again, not severe enough to account for his
severe metabolic acidosis. He also had pancreatitis,
and severe pancreatitis could account for his presentation. However, the extent of pancreatic injury
on postmortem examination was mild and not sufficient to account for the severity of his illness.
There was evidence of a recent (2 weeks previous)
myocardial infarction at autopsy, but none of his
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Fatal Large-Volume Mouthwash Ingestion
Table 1. Listerine: Nonalcohol Ingredients, Composition, and Amount Potentially Consumed
Listerine
Eucalyptol 0.092%
Menthol 0.042%
Thymol 0.064%
Total consumed:
phenolic compounds
Methyl Salicylate 0.060%
Total consumed
Gm/100 ml
In 2 Liters
In 3 Liters
Molecular
weight
Mmol/L
0.092
0.042
0.064
1.84 g
0.84 g
1.28 g
2.76 g
1.26 g
1.92 g
154.24
156.26
150.21
11.9
5.4
8.5
0.06
3.96 g
1.2 g
5.16 g
5.94 g
1.8 g
7.74 g
152.14
7.9
serum markers would corroborate more recent cardiac ischemia and there is no evidence on his chest
film of pneumonia or pulmonary edema. There
was pneumonia noted at autopsy, but this is more
likely a complication of his mouthwash ingestion
than the cause of his decompensation. None of the
findings at presentation or autopsy seem sufficient
to account for the severity of his illness. No other
causes of an anion-gap acidosis could be identified.
His presentation was clearly multifactorial in etiology, but none of the aforementioned processes
(alcohol intoxication, alcoholic ketoacidosis, lactic
acidosis, renal failure, pancreatitis), alone or even
in combination, can account for the severity of his
illness and progression of his multiorgan system
failure following presentation. By process of elimination, this leads to speculation about the toxicity
of the other ingredients in Listerine and their contribution to his illness.
Ethanol is the major constituent of Listerine, composing 26.9% of its content in a solution including
water, sorbitol, caramel color, flavor additives, and
other ingredients. Sorbitol is not subject to substantial absorption. The other ingredients are listed
in Table 1 and compose a very small percentage of
the solution. However, with ingestion of 2 to 3
liters of mouthwash as in this case, the amounts
reach more significant levels. These ingredients
(thymol, eucalyptol, and menthol) are all derivatives of phenol, and it is well known that phenols
and phenolic compounds can be toxic in large
quantities.
Phenol (or carbolic acid) and phenolic compounds have been constituents of medicinal compounds since the early 1900s. It is a disinfectant
and germicide, and acts by denaturing protein [11].
It is formulated for topical application in 1% to 2%
solutions because higher concentrations cause
severe irritation and necrosis. Phenol ingestion can
be fatal [12-14]. In 1909, of 3376 reported poisoning deaths in the United States, 1621 were attributed to phenol [14]. Deaths due to phenol have
dropped dramatically with the decline in medicinal
phenol-containing preparations. However, phenol
and phenolic compounds remain ingredients of
disinfectants and medicinal compounds (throat
lozenges, ear and nasal sprays, and mouthwash),
and there are still reports of fatal ingestion of phenol or its derivatives [7].
The effects of large-volume phenol ingestion
range from nausea, vomiting, and diarrhea, to
seizures, stupor, respiratory failure, cardiovascular
collapse, renal failure, severe acidosis, multiorgan
system failure, and death [15-17]. Most toxicity data
are from animals, with lethal phenol doses in
humans estimated to range between 1 and 32
grams.
Toxicity related to the specific phenolic compounds in Listerine has been reported. An infant
developed respiratory failure after inhalation of a
thymol-containing cold remedy [18]. A child developed lethargy, confusion, and weakness after
inhaling a preparation containing menthol and
methyl salicylate, with an estimated maximum
menthol dose of 200 mg [19]. The most intriguing
report involves a woman with surreptitious ingestion of mouthwash and repeated exacerbations of
acute intermittent porphyria [20]. The mouthwash
preparation was not identified but was either
Listerine or a similar generic preparation and resulted in repeated hospitalizations. Testing of the individual ingredients identified eucalyptol as the agent
with the greatest effect in inducing hepatic ∆aminolevulinic acid synthetase activity. This provides additional evidence that these compounds
can have a clinical effect despite the small amount
in mouthwash formulations. It follows that severe,
life-threatening toxicity could develop with largevolume ingestion.
Phenolic compounds can cause severe injury if
sufficient quantities are ingested. The lethal human
dose for menthol, thymol, and eucalyptol is estimated at 50-500 mg/kg (3.5-35 g in a 70 kg person)
[21,22]. The question arises whether the amount of
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Soo Hoo et al
phenolic compounds ingested with 2 to 3 liters of
Listerine falls within the lethal range. As seen in
Table 1, the amount of phenolic compounds in 2 to
3 liters of Listerine is within the toxic range for phenols (1-32 g) and, as a group, within the range of
the individual compounds. It should be noted that
toxicity data refer to a single ingestion and toxicity
of ingesting the agents over time is unknown.
There are few specific details regarding the treatment of phenolic compound ingestion other than
decontamination and supportive care. Recommendations for phenol ingestion focus on decontamination, limiting its systemic absorption, and supportive
care. Emesis is not recommended because phenol
is corrosive and may induce seizures. Gastric
lavage can be performed for large-volume ingestions with a nonabsorbable oil such as olive oil,
because enhanced binding of phenol by the oil
limits its absorption [13,23]. Castor oil is also used
because of its cathartic effects in addition to its high
affinity for phenol. Others recommend treatment
with charcoal and a cathartic [17]. Otherwise, management focuses on supportive care to allow the
patient to recover from the systemic effects of
ingestion.
In summary, phenolic compound toxicity (eucalyptol, menthol, and thymol) likely contributed to
this patient’s presentation and constellation of
symptoms. The observed presentation and course
is strikingly similar to that described with phenol
toxicity. These agents are well known to produce
significant toxicity in higher doses, and the amount
ingested certainly falls within the known toxic
range. The increased osmolality due to the phenolic compounds could account for the increased
osmolar gap. Phenolic compounds (carbolic acid)
could also contribute to the previously unexplained
anion-gap metabolic acidosis. Previous reported
cases of mouthwash intoxication were also noted
to have an anion-gap acidosis that was not
explained or seemed out of proportion to the
amount of ingested alcohol. In retrospect, the abnormalities in our case may have been due to these
phenolic compounds. Unfortunately, the possibility
of phenolic toxicity did not arise until his specimens had been exhausted from clinical testing.
We feel this case represents a previously unrecognized syndrome associated with massive mouthwash ingestion, specifically Listerine. The impact of
the alcohol component has long been recognized,
but the toxic effects of the other ingredients
become more evident with massive ingestion. The
major features of ingestion are a profound metabolic acidosis, with increased anion and osmolar
gap, not attributable to more commonly recognized
154
causes of these disturbances, subsequent multiorgan system failure, and death. The product labeling
for Listerine clearly warns that its contents are not
to be swallowed. This warning acknowledges the
potential toxicity of swallowing a few mouthfuls.
However, no one could ever envision the ingestion
of almost 3 liters as in this case.
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