Biochemistry and Pharmacokinetics …………….. 1 Pathophysiology ………………………………… 2 Central Nervous System Depression ….. [620472]

Isopropyl Alcohol
Heath A. Jolliff
Contents
Biochemistry and Pharmacokinetics …………….. 1
Pathophysiology ………………………………… 2
Central Nervous System Depression .. …………….. 2
Gastrointestinal Effects …………………………… 2Metabolic Effects ………………………………… 3
Other Manifestations … … ……………………….. 3
Clinical Presentation and Life-Threatening
Complications ……………………………….. 3
Diagnosis ……………………………………….. 3
Treatment ………………………………………. 4
Special Populations ……………………………… 6
Pediatric Patients … ……………………………… 6
Pregnant Patients ………………………………… 6
References ………………………………………. 6Isopropyl alcohol (isopropanol, 2-propanol,
propan-2-ol, IPA) is a clear, colorless, and volatile
liquid that has a bitter taste and fruity odor similar
to that of acetone [ 1–3]. Most commonly,
isopropanol is found in rubbing alcohol as a
70 % volume/volume solution in water. It is
important to note that not all rubbing alcohol ismade with IPA, as ethanol is also used. IPA also is
found in solvents, inks, drug preparations, beauty
products, de-icing agents, and hand sanitizers [ 4,
5]. Toxic effects of IPA are seen most commonly
in alcoholics, who abuse it as a cheap, readily
available substitute for ethanol [ 5–9]. However,
most exposures occur in small children who
develop toxicity through ingestion of IPA or who
had long or repeated contact to IPA through der-mal or inhalational exposure. Occupational expo-
sure may occur by the dermal and inhalational
routes [ 10–12]. The primary effects of IPA toxic-
ity are central nervous system (CNS) depression,
gastrointestinal irritation, and ketosis. Treatment
is symptomatic and supportive.
Biochemistry and Pharmacokinetics
IPA is a volatile secondary alcohol. It has a vol-ume of distribution of 0.45 to 0.7 L/kg [ 13–15]
and is metabolized to acetone via hepatic alcohol
dehydrogenase (ADH) (Fig. 1). In contrast to
primary alcohols such as ethanol or methanol,
the secondary alcohol, IPA, is metabolized to aH.A. Jolliff ( *)
Wexner Medical Center, Ohio State University, Columbus,OH, USA
e-mail: [anonimizat]
#Springer International Publishing Switzerland 2016
J. Brent et al. (eds.), Critical Care Toxicology ,
DOI 10.1007/978-3-319-20790-2_53-11

ketone (acetone) but not to a carboxylic acid (see
Fig.1).
Pharmacokinetics of Isopropyl Alcohol
Volume of distribution: 0.45 –0.7 L/kg
Protein binding: negligible
Mechanism of clearance: hepatic alcohol
dehydrogenase metabolism, first-order
kinetics
Half-life: isopropyl alcohol, 2 –8 h; acetone,
7.7–27.7 h
Solubility: miscible in water
Vapor pressure: 33 mmHg
Data from references: [ 13,14,16,17]
Pathophysiology
Central Nervous System Depression
Central nervous system depression may occur
rapidly after ingestion of IPA [ 8,13,
18–20]. Peak serum concentrations of IPA occur
30–60 min after ingestion due to its rapid absorp-
tion from the gastrointestinal tract [ 17,21,22]. In
contrast to other toxic alcohols in which toxicity islargely dictated by metabolite production, IPA
seems to be the primary chemical responsible for
CNS depression because the onset of these man-ifestations clinically correlates with the time to
peak serum IPA levels [ 5,23,24]. Patients also
tend to clinically improve with declining serumIPA levels [ 8,14,20,22,23,25]. However, they
can also have prolonged CNS depression, despite
declining serum IPA levels [ 7,16]. Most of these
cases show rising serum acetone levels, which has
led to the theory that acetone may be responsiblefor CNS depression. Acetone is known to cause
CNS depression [ 26–30]. The literature also
reports cases of patients with initial CNS depres-
sion whose mental status improved despite
increasing acetone levels [ 8,31]. Therefore it
seems likely that both compounds are responsible
for the CNS depression seen with IPA toxicity.
Based on animal studies, IPA is estimated to
have twice the intoxicating effect of ethanol at
similar serum concentrations [ 32]. This effect
may be due to the higher molecular weight ofIPA compared with ethanol [ 13] or perhaps the
additive toxicodynamic effect of the acetone
metabolite.
Respiratory depression and hypotension may
accompany coma resulting from IPA intoxication
[13,17,23–25,33,34]. These effects are most
likely the result of peripheral vasodilation and
depression of the brain stem [ 8,13,14,17,
20,
23,25,35]. Tachycardia is common and may be a
compensatory response to hypotension [ 36].
Common CNS effects of ethanol ingestion,
such as ataxia, nystagmus, and dysarthria, occurbut are not as common in IPA toxicity [ 36,
37]. Diminished re flexes are commonly seen in
comatose patients with IPA toxicity [ 17,31,
36]. Seizures are rare but have been reported in
infants [ 35].
Gastrointestinal Effects
IPA may cause gastritis, mucosal irritation, and, in
severe cases, hemorrhagic gastritis. Patients who
ingested IPA may present with nausea, vomiting,and abdominal pain. It often is reported that hem-
orrhagic gastritis is caused by IPA [ 37,38]. How-
ever, it is not clear that hemorrhagic gastritis isany more common than the upper gastrointestinal
bleeding seen with ethanol abuse. Most abusers of
IPA are alcoholics, and there is considerable over-lap between these two groups. Systemic toxicity
has been reported after rectal administration of
IPA [ 39–41]. In these cases, serum IPA levels
were comparable to serum levels attained after
oral ingestion. Elevation of serum transaminases
has been reported after IPA ingestion [ 42].OH
Isopropanol AcetoneCH H3C CH3O
Alcohol
DehydrogenaseNAD+NADH
C H3CC H3
Fig. 1 Conversion of isopropanol to its primary metabo-
lite acetone. Small amounts of isopropanol are excretedunchanged in the urine and expired air2 H.A. Jolliff

Metabolic Effects
Acetone is the major end product of IPA metabo-
lism (see Fig. 1). Because no acidic product is
generated, the metabolic acidosis associated with
other toxic alcohols, like methanol or ethylene
glycol, does not occur with IPA toxicity. Ketonesor, more speci fically, acetone can be measured in
the serum and urine of patients with IPA toxicity.
Acetone can be measured in the serum within30–60 min of IPA ingestion but may not be mea-
surable in the urine until 180 min after IPA inges-
tion [ 8,21]. Patients poisoned with IPA often have
a ketotic or sweet smell to their breath secondary
to the presence of exhaled acetone [ 8,20,43,44].
Other Manifestations
Hypothermia has been reported after IPA inges-
tion and is thought to be secondary to the CNS
depression and peripheral vasodilation that canaccompany IPA toxicity [ 14,34,45]. Hypothermia
should be ruled out in all patients with decreased
mental status, especially if they are found out-
doors. Hypothermia may be secondary to the
toxic effects of IPA, the environment itself, or acombination of the two.
Miosis and mydriasis have been reported in
patients poisoned with IPA [ 13,31,34–36,
46]. Nystagmus has also been reported but is not
a speci ficfinding with IPA toxicity [ 31].
Mild hyperglycemia has occurred in patients
who ingested IPA. Hypoglycemia should be
suspected and ruled out in all patients with CNS
depression.
Renal insuf ficiency and renal failure have
occurred secondary to hypotension and rhabdo-
myolysis in IPA-toxic patients [ 34,42,47,
48]. Rhabdomyolysis should be ruled out in all
patients who are found comatose, especially when
the duration of the coma is unknown.Coingestants should be considered in all patients
presenting with altered mental status.
Contact dermatitis, allergic dermatitis, and
defatting dermatitis have all been reported in
patients with prolonged contact to IPA[49–51]. This may be more common in the occu-
pational setting. Flushing and diaphoresis, though
uncommon, have been reported after ingesting
IPA [ 19,34,52,53].
Clinical Presentation and Life-
Threatening Complications
Patients most commonly develop CNS depres-
sion, ketosis, and a fruity breath odor but notmetabolic acidosis [ 5,7]. They also may present
with abdominal pain, emesis, or gastritis. Patients
with IPA toxicity should be monitored closely forrapid changes in their mental and cardiopulmo-
nary status. Hypotension and respiratory failure
have occurred after large ingestions of IPA [ 14,
17,23,34,35,45,48]. If not monitored closely
and treated, these conditions may lead to death.
IPA exposures occur primarily by ingestion;
however, dermal, inhalational, and rectal expo-
sures resulting in toxicity also have occurred
[13,18,24,33,41,45,46,54,55]. A common
exposure pathway in children is by bathing or
sponge bathing with IPA to lower a fever [ 18,
31,35,38,45,46,54,55]. Dermal and inhala-
tional exposures in adults may occur in the occu-
pational setting.
Diagnosis
Isopropyl alcohol toxicity should be considered inthe differential diagnosis of CNS depression. It
also should be considered in an intoxicated patientwho does not smell of ethanol, has a fruity breath
smell, or has an unexplained ketosis. Non-acidotic
ketosis should raise the possibility of IPA or ace-tone ingestion in the differential diagnosis. IPA
also should also be considered in patients with an
unexplained osmolar gap.
Serum IPA concentrations may not be readily
available in many hospitals [ 5]. If possible, how-
ever, they should be obtained in all patients whoare suspected to have been exposed to IPA. Serum
concentrations can be used to document IPA
exposure. The patient ’s overall clinical condition,Isopropyl Alcohol 3

not the IPA level, should be used to judge toxicity.
Levels should be drawn at least 30 –60 min after
the exposure to identify peak IPA levels [ 5,13,17,
22]. The best method for measuring serum IPA
levels is headspace gas chromatography withflame ionization or proton nuclear magnetic reso-
nance imaging [ 5]. If IPA levels are determined by
ADH-based enzymatic assays, the assay mayinterpret IPA as ethanol and give a falsely low
IPA level [ 5,44]. Although IPA may be detected
with breathalyzers used to measure ethanol, theselevels are unreliable [ 56]. A possible erroneous
diagnosis of IPA poisoning may occur in patients
with diabetic ketoacidosis. Cases of measurableIPA in these patients have been reported, although
no exposure to IPA was known [ 57]. It has been
theorized that the acetone produced with diabeticketoacidosis might be reduced to IPA via ADH [ 5,
58]. It is also possible that in these cases, there was
an unrecognized IPA exposure or that a laboratoryerror occurred.
Serum IPA levels greater than 120 mg/dL
(20 mmol/L) have been associated with deepcoma [ 14,19,48,54]. An ingestion of 90 mL
(3 oz) of 70 % IPA can theoretically produce a
serum IPA level of 100 mg/dL (16.7 mmol/L) in a70-kg patient. As with ethanol, chronic alcoholics
may tolerate higher IPA levels [ 7,59].
Serum ketone or acetone concentrations may
be helpful in the diagnosis of IPA toxicity. Ace-
tone is not usually detected in the serum until
30–60 min post-ingestion [ 8,13,43]. Detection
in the urine is usually delayed for at least 3 h post-
ingestion [ 13]. An initial non-detectable urine
acetone level should be repeated in patients ifthere is a high index of suspicion for IPA inges-
tion. Acetone levels increase as ADH metabolizes
IPA. Acetone should be measurable even after IPAlevels are undetectable.
Laboratory tests useful in the management of
IPA-poisoned patients include serum electro-lytes, creatinine, glucose, and creatine phospho-
kinase. If a signi ficant metabolic acidosis is
present, other causes must be considered (seechapter on “Acid –Base Disorders ”). Acetone
interferes with certain colorimetric assays used
to determine serum creatinine levels; this has ledto reports of falsely elevated serum creatininelevels in patients with acetone in their serum [ 5,
31,60–63]. Serum osmolality and an osmolar
gap may be determined. Caution must be used,
however, because not only are acetone and IPA
osmotically active compounds, but other sub-stances, such as methanol and ethylene glycol,
are as well [
64,65]. The absence of an elevated
osmolar gap does not rule out the presence ofeither compound and, in clinical practice, is not
useful [ 66,67].
Treatment
As with all toxic ingestions, treatment should
focus on the overall clinical condition of the
patient. The primary treatment centers on support-ive care. Because IPA is a CNS depressant, the
clinician must be vigilant with respect to the abil-
ity of a patient to maintain his/her airway. If thepatient is unable to maintain a patent airway,
endotracheal intubation should be performed and
mechanical ventilation maintained. These patientswarrant continuous cardiac monitoring and pulse
oximetry. In patients who are initially able to
maintain a patent airway, close monitoring forrespiratory compromise is advised.
Any patient with altered mental status should
have a rapid bedside assessment of the serum glu-cose to rule out hypoglycemia. Hypoglycemia can
be treated with intravenous dextrose. Intravenous
access allows for normal saline administration tomaintain blood pressure and ensure adequate
hydration and urine output. At least 100 mg of
thiamine should be administered intravenously orintramuscularly to any patient in whom nutritional
status is uncertain and who may be at risk for the
development of Wernicke –Korsakoff syndrome
(grade III recommendation).
Hypotension can be treated initially with intra-
venous fluids. In adults, normal saline can be
bolused in doses of 250 –500 mL each. When the
total amount of intravenous fluids has reached
approximately 2000 mL, one should be cautiousnot to fluid overload the patient. If the hypoten-
sion does not respond to intravenous normal
saline, an intravenous pressor is the logical nextstep. Adequacy of cardiac pump function can be4 H.A. Jolliff

ascertained by bedside echocardiography. No one
pressor agent has been shown to be more ef fica-
cious than others in toxicant-induced hypoten-
sion. (See chapter on “▶Hypotension and Shock
in the Poisoned Patient .”) Dopamine was tradi-
tionally the pressor of first choice because of its
relative ease of use and its availability as a
premixed intravenous preparation. However,incontemporary practice norepinephrine is often
used. There have, however, been no comparative
studies between pressors in cases of IPA toxicity.The dose administered should be based on clinical
response. Hypotension that does not respond to
the initial pressor of choice should be reassessedand may require higher doses or additional
pressors [ 68].
Gastrointestinal decontamination is not likely
to be of bene fit in IPA ingestions because IPA is
absorbed from the gastrointestinal tract within
30–60 min [ 24]. Gastric lavage is not likely to
influence this absorption and should not be done.
I nap a t i e n tw h op r e s e n t sw i t h i n3 0m i no fal a r g e
IPA ingestion, nasogastric emptying with a stan-dard nasogastric tube may decrease the total
amount of IPA absorbed. Nasogastric emptying
is theoretical and has not been tested [ 5,69,
70]. However, if it is done, attention to protect
the airway from aspiration is recommended
[5]. Activated charcoal also is of questionable
benefit, especially when used in the standard
dose of 1 g/kg. An in vitro model showed that a
20:1 ratio of charcoal to IPA was needed toadsorb 87 –92 % of the IPA [ 71]. It would require
a large amount of charcoal to adsorb even small
amounts of IPA. Using such large amounts ofcharcoal becomes impractical for the treating
physician and dangerous for the patient. It also
is of questionable ef ficacy considering how rap-
idly IPA is absorbed from the gastrointestinal
tract.
Indications for ICU Admission in Isopropyl
Alcohol Poisoning
Coma
HypotensionRespiratory failure
Patients needing hemodialysisCriteria for ICU Discharge in Isopropyl Alcohol
Poisoning
Mental status returned to baseline
Normotensive without pressorsPatient maintains own airway
Oxygenation maintained without supple-
mental oxygen
No further need for hemodialysis
Isopropyl alcohol can be absorbed through the
skin with resulting toxicity [ 13,18,35,46]. If
dermal contact is suspected, washing the skin
with a mild soap and water solution is appropriate
for dermal decontamination.
Because of its small volume of distribution and
negligible protein binding, IPA is easily dialyz-
able [ 13]. The clearance of IPA with hemodialysis
has been reported as 137 mL/min [ 20,23]. The
acetone metabolite of IPA also is amenable to
dialysis. Hemodialysis is rarely indicated inthese patients, however. It has been suggested
that patients who are hypotensive due to IPA
toxicity may bene fit from dialysis [ 72]. Another
suggested indication for dialysis is for patients
who have serum IPA concentrations greater than
400 mg/dL (66.6 mmol/L) [ 13,72]. However,
most patients do well with supportive care alone,
even if the patient presents with hypotension or an
initially high serum IPA concentration [ 5,8,19,
34]. There are risks associated with hemodialysis,
and the overall clinical picture of the patient
should be considered [ 73]. Peritoneal dialysis
has been attempted in several reported cases, but
the clearance of IPA with this method was only
slightly better than the patients ’endogenous clear-
ance [ 74]. For patients who do not respond to
aggressive supportive care or who are unstable
due to high levels of IPA, hemodialysis shouldbe considered in consultation with a medical tox-
icologist or poison control center.
There are no antidotes for IPA toxicity.
Inhibiting ADH with ethanol or fomepizole
would only prolong the time for the metabolism
of IPA. Because acetone itself neither is life threat-ening nor causes signi ficant end-organ damage,
treatment with ADH inhibition is unnecessary
[75,76].Isopropyl Alcohol 5

Special Populations
Pediatric Patients
Children may have a different susceptibility to
dermal IPA absorption than adults owing totheir larger body surface ratio and thin dermis.
IPA has been applied dermally to reduce fever
in children, with resultant signi ficant toxicity
[45,46,54,55]. It is unclear if the toxicity is
due solely to the dermal absorption or possibly
to a combination of dermal and inhalationalabsorption. Infants have become toxic when
IPA was applied chronically to the umbilicus
for cleaning [ 35]. Coma, hypotension, and sei-
zures all have been reported in children with
IPA toxicity [ 33,35]. Children also have been
noted to experience dermal irritation and chem-
ical burns when IPA was applied to the skin
[77]. Unlike ethanol, hypoglycemia has not
been reported to occur in children intoxicated
with IPA [ 78–80]. A rare case of hemorrhagic
gastritis has been reported in a pediatric patientwith IPA toxicity [ 81].
Pregnant Patients
Based on the size of the molecule, its solubility,
and its similarity to ethanol, IPA is expected to
cross the placenta. Hypotension in the mother is aconcern for the overall status of the fetus. Sup-
portive care for the mother is paramount for
protecting the fetus. IPA is not considered ahuman carcinogen, and its teratogenicity to
humans is unknown [ 82].
Common Errors in Isopropyl Alcohol Poisoning
Not considering isopropyl alcohol as a poten-
tial cause in an intoxicated patient
Ruling out the diagnosis of isopropyl alco-
hol intoxication based on a normal osmolality
and osmolar gap
Attributing an anion gap metabolic acidosis
to isopropyl alcohol
Using hemodialysis instead of good sup-
portive care as a cornerstone of treatmentKey Points in Isopropyl Alcohol Poisoning
1. Toxicity may occur after oral, inhalational,
rectal, or dermal exposure.
2. Isopropyl alcohol can be a potent central
nervous system depressant.
3. The hallmark of IPA toxicity is ketosis
without metabolic acidosis.
4. Isopropyl alcohol toxicity may cause gas-
tritis as with other alcohols.
5. Treatment should focus on supportive care.
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