T H E AMERICAN JOURNAL OF CLINICAL PATHOLOGY
Vol. 38, No. 2, pp. 144-151
August, 1962
Copyright © 1962 by The Williams & Wilkins Co.
Printed in U.S.A.
FATAL INTOXICATION WITH ISOPROPYL ALCOHOL (RUBBING ALCOHOL)
Laboratory
L E S T E R A D E L S O N , M.D.
of the Cuyahoga County Coroner's Office, and the Institute of Pathology,
University School of Medicine, Cleveland, Ohio
Isopropyl alcohol (isopropanol, CH 3 CHOH
CH 3 ) has important uses in industry, where
it has been substituted for ethyl alcohol in
many processes.11 In 70 per cent solution
it is readily and cheaply available to the
public as "rubbing alcohol," sold in all
drug stores and most grocery stores. Found
in many homes, it is surprising that it is
not more often responsible for fatal accidental and suicidal incidents. The chronic
alcoholic who is "desperate when sober and
fearless when drunk" 1 is apparently less
apt to indulge in this substitute for ethyl
alcohol than in wood (methyl) alcohol.
Fatal methanol intoxication is much more
common than fatal isopropanol poisoning.
Nonfatal intoxication by isopropyl alcohol has been described with the severity
of the clinical syndrome varying from comparatively trivial to life-threatening;2' 4> 6>
"• 14 published studies of fatal human poisoning by this substance are rare. Standard
pharmacologic texts scarcely mention or
ignore entirely the lethal potentialities of this
common household compound.15, 16 The bulk
of the available data that deal with the
physiologic actions of isopropyl alcohol is
based on study of experimental fatal and
nonfatal intoxication in a variety of animals
and a few limited observations of human
volunteers who drank relatively small quantities. 3, 5.8,9,12
Investigation and study at the Cuyahoga
County Coroner's Office of a recent fatality
after ingestion of isopropanol prompted a
search of our files for other deaths caused by
this nonpotable liquid, and 4 additional
examples were found, all of which had occurred during the past 7 years. This paper
Received, J a n u a r y 25, 1962; accepted for p u b lication April 30.
D r . Adelson is Pathologist and Chief D e p u t y
Coroner, Cuyahoga County Coroner's Office, and
Associate Professor of Forensic Pathology, D e p a r t m e n t of Pathology, Western Reserve University School of Medicine.
144
Western
Reserve
deals with the clinical and antemortem
and postmortem laboratory aspects of these
5 deaths. Autopsies were performed on all
of the patients.
R E P O R T OF CASES
Case 1
A 37-year-old man was found unconscious
at approximately 9:00 P.M., after having
drunk a pint of rubbing alcohol earlier in
the evening. After repeated efforts to arouse
him failed, he was rushed to a nearby hospital
where he was pronounced dead on arrival,
at 12:15 A.M. A history of mental illness and
previous suicide attempts was obtained.
Gross and microscopic autopsy examinations were negative other than for the
presence of pulmonary congestion and moderate hemorrhagic edema. Postmortem levels
of isopropyl alcohol in the blood and urine
were, respectively, 150 mg. and 180 mg.
per 100 ml. Tests for ethanol and methanol
in the blood and urine were negative.
Comment. An acute course (4 to 6 hr.)
in a healthy young man. The deep coma is
characteristic. Absence of specific anatomic
changes is noteworthy.
Case 2
A 70-year-old man who had been despondent over ill health was brought to the
hospital by the police within 1 hr. after
having drunk a pint of rubbing alcohol.
At the time of admission to the hospital, he
was comatose and in shock, with a blood
pressure of 80/40 and a pulse of 100 per
min. The skin was cold and clammy, and the
respirations were shallow, rapid, and irregular. The lungs were clear, and the heart
sounds faint. Painful stimuli elicited no
response.
Treatment consisted of immediate gastric
lavage, shock position, oxygen under positive pressure via an endotracheal tube, and
1000 ml. of 5 per cent glucose in distilled
Aug. 1962
I S O P R O P Y L ALCOHOL
water with Aramine intravenously. Shortly
thereafter the vital signs were: rectal temperature 35.6 C , pulse 115 per min., respirations 27 per min., and blood pressure
100/80. Two hours later his breathing became deeply stertorous and irregular, and
he died 3 hr. after admission, without having
regained consciousness.
Autopsy revealed no external or internal
abnormalities that could be attributed to
isopropyl alcohol, other than pulmonary
congestion and edema. The epiglottis and
aryepiglottic folds were conspicuously edematous. Pre-existing diseases included generalized arterio- and arteriolar sclerosis,
cardiomegaly (740 Gm.), bilateral pulmonary emphysema, and portal cirrhosis. Postmortem levels of isopropyl alcohol (in mg.
per 100 ml.) were blood, 150; spleen, 130;
brain, 100; and liver, 100. Ethyl alcohol
was absent.
Comment. Again an acute situation ( 3 ^
hr.), this time in an elderly person with
extensive pre-existing natural disease. Deep
coma, shock, hypotension, and hypothermia
indicate the severity of the insult. The
edema of the larynx is probably the result
of intubation rather than local damage from
isopropanol. There are no anatomic stigmata
that can be ascribed to the drug.
Case 8
A 31-year-old man was brought to the
hospital after he had been found unconscious with an empty isopropyl alcohol bottle
nearby. Initial examination revealed coarse
tremors of the extremities with generalized
convulsions. The skin was cold and clammy
with profuse diaphoresis. Respirations were
shallow, irregular, and rapid, with a fruity
odor on the breath. Painful stimuli elicited
no response. The pupils were dilated and
did not react to light. The knee jerks and
ankle jerks were hyperreactive. Crepitant
rales were audible over the entire chest.
Vital signs included a temperature of 36 C ;
pulse, 104 per min.; respirations, 40 per min.;
and a blood pressure of 164/78.
Significant laboratory data were 4-plus
acetonuria without glycosuria, CCVcombining power of 13.5 mEq. per 1. and BUN of
16 mg. per 100 ml. No ethyl or methyl
alcohol was detected in the blood or urine.
INTOXICATION
145
Treatment during his brief hospital stay
consisted of oxygen under positive, pressure,
sodium phenobarbital, 1000 ml. of glucose
in physiologic saline solution, M/6 sodium
lactate, Cedilanid, and digitoxin.
Study of an EKG made soon after admission revealed a sinus tachycardia of
150, and peaked and widened T waves.
Shortly thereafter the blood pressure fell
to 60/20, respirations decreased to 17 per
min., both lungs filled with coarse rales, and
intense cyanosis and opisthotonus developed.
The patient died 5 ^ hr. after admission
without regaining consciousness.
Autopsy disclosed bloody mucoid fluid
in both nostrils. The chest cavities contained
blood-tinged, watery fluid which had apparently entered through a large area of
esophagomalacia. Extensive bilateral hemorrhagic pulmonary edema and early bronchopneumonia were present. The liver revealed
diffuse fatty infiltration.
Postmortem chemical analyses revealed
no isopropyl or ethyl alcohol in the blood,
acetonemia (8 mg. per 100 ml.) and acetonuria (40 mg. per 100 ml.).
Comment. No information is available on
the duration of coma prior to finding the
patient. He is the only person in this series
who manifested tremors, convulsions, and
hyperactive reflexes. The probability that
he had been a chronic alcoholic (suggested
by the diffuse fatty liver) can not be excluded, and this may account for some of
the neurologic abnormalities. Deep coma is
once more the presenting clinical complaint.
Case 4
An 83-year-old woman was brought to
the hospital in coma, with a history of
having attempted suicide by drinking an
unknown quantity of rubbing alcohol some
2 hr. previously. Shortly thereafter she
complained of nausea and cramp-like abdominal pains and vomited several times.
Loss of consciousness followed rapidly.
At the time of admission to the hospital,
she was cyanotic, comatose, completely
areflexic, and without response to painful
stimuli. Profuse lacrimation was present,
and the mouth was filled with blood-tinged,
frothy fluid. Both lungs were filled with
bubbling rales. The rectal temperature was
146
Vol. 38
ADELSON
36.5 C , pulse 72 per min., respirations 32
per min., and blood pressure 130/74. Laboratory work revealed a trace of acetone in the
urine without glycosuria, a white blood
count of 18,200 per cu. mm., with 91 per
cent neutrophils, and 200 mg. of isopropanol
per 100 ml. of blood.
Gastric lavage was performed immediately, with the removal of large quantities
of muddy brown fluid with a strong odor
of isopropanol. Analysis of the gastric contents yielded a 4-plus test for isopropanol.
Treatment consisted of oxygen under
positive pressure and stimulants, without
lightening of the coma. Nine hours after
admission her blood pressure decreased to
70/0. Norepinephrine was administered, with
excellent pressor response; however, she
did not regain consciousness during her
entire hospital stay. On her second hospital
day her temperature rose to 39.2 C , accompanied by hypotension which did not
respond to norepinephrine. Blood urea nitrogen (BUN) at this time was 36 mg. per 100
ml. She died approximately 47 hr. after
admission to the hospital.
Noteworthy gross abnormalities at autopsy were thick, tenacious, yellow-green
purulent exudate filling the bronchi, and
mottled yellow and red discoloration of the
magenstrasse. Microscopic studies revealed
acute necrotizing bronchitis, acute focal
ulcerative tracheitis, and acute focal hemorrhagic necrotizing gastritis. The liver, kidneys, heart, and brain manifested no specific
changes that could be attributed to isopropanol. Generalized arterio- and arteriolar
sclerosis, with nephrosclerosis, bronchiectasis, and myocardial fibrosis was noted. The
urine acetone was 2 plus, and levels of
acetone in the tissues (in mg. per 100 ml.)
were reported as follows: brain, 11.5; liver,
4.0; kidney, 7.4; spleen, 5.3; and blood,
13.2.
Comment. Two-day survival after ingestion of isopropanol in an elderly woman,
with extensive chronic natural disease. Persistent coma and hypothermia were prominent, with subsequent hypotension. The
necrotizing tracheobronchial inflammatory
process is probably the result of aspiration
of vomitus. Gastric damage is encountered
for the first time. There were no clinical or
postmortem indications of renal damage.
Case 5
A 41-year-old chronic alcoholic was
brought to the hospital from police headquarters, where he had been found unconscious in his cell. He had been arrested
21 hr. previously for what seemed to be
ordinary acute alcoholic intoxication. At
that time he was conscious, semirational,
and ambulatory, and walked into the police
station under his own power to be booked.
He was put into a cell to "sleep it off" and
failed to respond some 20 hr. later, when
attempts were made to rouse him. Subsequent investigation disclosed that he had
drunk \]/% pints (700 ml.) of rubbing alcohol
after writing 3 suicide notes.
At the time of arrival at the hospital, he
was flaccid and deeply comatose, with an
unobtainable blood pressure. The pupils
were fixed and dilated, and the eyes were
rotated upward and outward. Complete
areflexia was present, and painful stimuli
elicited no response.
Aramine was administered immediately,
with good pressor response. Shortly thereafter the vital signs were: temperature,
34.7 C.; pulse, 72; respirations, 16; and
blood pressure, 100/70.
Significant laboratory data at the time
of admission were: hematocrit reading, 49;
hemoglobin, 15.8 Gm. per 100 ml.; white
blood count, 8200 per cu. mm. (61 per cent
neutrophils); serum acetone, 160 mg. per
100 ml.; BUN, 14 mg. per 100 ml.; sodium,
130 mEq. per 1.; potassium, 3.2 mEq. per 1.;
and CCVcombining power, 11 mEq. per
1. The urine contained 4-plus acetone and
150 mg. of isopropyl alcohol per 100 ml.
The level of isopropanol was 20 mg. per
100 ml. of blood.
Immediate gastric aspiration yielded several ounces of coffee-ground material. Five
hours after admission, 300 mg. of Megimide
were administered, with reappearance of
the corneal reflex and some deep tendon
reflexes. The blood pressure was initially
well-maintained with intravenous Aramine.
After 24 hr., a satisfactory blood pressure
was sustained without the use of pressor
Aug. 1962
I S O P R O P Y L ALCOHOL
drugs. Response to pain returned, and the
sensorium cleared gradually. Seventy-two
hours after admission the patient was mentally clear, and the serum acetone had fallen
to zero.
An EKG made during the first hospital
day revealed premature atrial beats, peaked
T waves, and left ventricular predominance.
Repeat tracings on the second, fifth, tenth,
and twelfth hospital days revealed persistance of the peaked T waves, interpreted
as indicating hyperkalemia.
On the day after admission the left radial
pulse was absent, and the left forearm (the
site of Aramine injection) was cold and
clammy, with the fingers of the left hand
fixed in flexion deformity. Incision of the
forearm revealed ischemic muscular necrosis.
Urinary output during the 24 hr. after
admission was 360 ml., and thereafter the
urinary flow was never more than 125 ml.
in any 24-hr. period. By the third hospital
day the BUN had risen to 95. Peritoneal
dialysis was performed on 4 occasions, with
temporary decrease in the BUN; however,
the general level of the BUN continued
to climb, and shortly before death it had
reached 168. Serum creatinine levels rose
and fell parallel with the total BUN.
Approximately 8 days after admission
repeated episodes of brisk upper gastrointestinal bleeding occurred, which necessitated multiple whole blood transfusions.
The patient's general condition deteriorated
progressively, and he died on the fourteenth
hospital day, 15 days after his ingestion of
isopropanol.
Noteworthy observations at autopsy included 1600 ml. of clear, watery fluid in the
peritoneal cavity, and 100 ml. of similar
fluid in each pleural cavity, hemoglobinuric
nephrosis (lower nephron nephrosis), hemorrhagic gastritis with blood clot adherent to
the floors of multiple shallow mucosal ulcerations, focal and confluent areas of ischemic
splenic necrosis, and pulmonary congestion
and edema.
Comment. The longest survival in this
limited series, with death ultimately caused
by renal shutdown and gastric hemorrhage.
The initial clinical aspects are similar to
the preceding cases. This is the sole instance
147
INTOXICATION
of emergence from coma. The development
of hemoglobinuric nephrosis, with resultant
uremia, produced a complex clinical picture
in which gastric hemorrhage was an important factor.
CLINICOANATOMIC
CORRELATION
No specific organic lesions were found in
those who died within a few hours after
ingestion of isopropyl alcohol (cases 1, 2,
and 3). Death which occurs rapidly after
absorption is the result of profound central
nervous system depression, with ultimate
respiratory paralysis. In this respect, isopropanol acts in the same manner as other
respiratory depressants, e.g., ethyl alcohol,
anesthetics, barbiturates, and so on.
The hemorrhagic gastritis observed in
case 4 may be the result of the severe vomiting which followed the drinking of the
rubbing alcohol, together with the intragastric excretion of isopropanol (see below)
or some product of its metabolism. Azotemia
or uremia can be excluded from the pathogenesis of the gastric damage. The BUN
never rose above 36, and the brief duration
of the illness (2 days) is too short an interval
for the development of gastritis on this
basis.
Case 5 had an extremely complicated
clinical course, starting with oliguria and
progressing to classical hemoglobinuric nephrosis despite repeated (4) episodes of peritoneal dialysis. This type of renal damage
has been previously reported after ingestion
of isopropanol, with complete recovery.2
Severe gastritis with massive bleeding made
its appearance after approximately 8 days,
and required multiple transfusions. This
facet of his clinical picture may stem from
the isopropanol effects as previously noted,
the uremia, or a combination of both. The
kidney damage probably arose from the deep
shock which was a prominent feature of
his presenting initial syndrome, with the
superimposed insult of extensive muscle
damage in his left forearm. Ischemic necrosis
of muscle is a potent factor in causing
hemoglobinuric nephrosis, and was at one
time thought to be the prime basis for this
lesion ("crush syndrome").
1.48
ADELSON
DISCUSSION
Review of the preceding 5 cases and
comparison of their clinical courses and
laboratory data with those observed in
nonfatal intoxications with isopropanol point
up several significant aspects of poisoning
with this commonly occurring compound.
Clinically, the most prominent presenting
feature is deep coma with marked depression
to absence of all reflexes. All 5 patients in
the present study group were either found
in or admitted to the hospital in this state,
and only 1 (case 5) regained consciousness.
Similar deep narcosis has been observed in
persons who suffered nonfatal intoxication
by isopropanol, and who went on to complete recovery. 2 ' 4 ' 6' "• 14
Acetonuria is an important and constant
laboratory finding. In combination with
coma, it could lead to an erroneous diagnosis
of diabetic coma, except that glycosuria is
absent. (A helpful clue in establishing the
correct diagnosis is offered by the environmental circumstances surrounding the incident. These point strongly to exogenous
intoxication, rather than an endogenous
metabolic derangement as the etiologic factor responsible for coma.) Although a portion of the acetone found in the urine of
some victims of intoxication with isopropanol
may be present as a result of the starvation
ketosis seen frequently in the severe chronic
alcoholic, the bulk of this abnormal urinary
constituent arises from the incomplete oxidation of isopropyl alcohol. It has been estimated that 12 to 15 per cent of the ingested
isopropanol is converted to acetone,5 which
is readily detected in the blood, breath,
and urine. As little as 0.1 Gm. of isopropyl
alcohol produces acetonuria in man, and a
single dose of 10 Gm. produces acetonuria
which lasts up to 48 hr. Similar observations
have been made in rabbits.12
A striking aspect of fatal and severe
nonfatal intoxication by isopropanol is the
relatively narrow range of the blood levels
found in the comatose patients. This holds
true whether the patient is a child, 4 ' 14
a healthy young adult (cases 1, 3, and 5),
or an elderly person with extensive and
widespread chronic degenerative disease
(cases 2 and 4). Although accurate figures
Vol. 88
are not available with regard to the amounts
actually inhaled 4 ' 14 or ingested in the uncontrolled situations surrounding intoxication with isopropanol (the commonly quoted
quantity is "1 pint"), the highest blood
levels observed in the comatose patients
range between 128 mg. per 100 ml.4 and
200 mg. per 100 ml. (case 4), with the majority not rising above 157 mg. per 100 ml.
This feature of acute intoxication with
isopropanol has previously not been commented upon. Two possible mechanisms
would reasonably explain this phenomenon.
One is an "absorption ceiling," a hypothetical
mechanism that limits the amount of isopropyl alcohol entering the blood stream.
A more likely possibility involves the prompt
excretion of isopropanol from the blood once
it reaches a "threshhold" value, together
with catabolic processes which destroy the
drug. Isopropanol is excreted by the kidneys,
salivary glands, and stomach. 9 This participation of the latter 2 excretory pathways
also helps to explain the prolonged coma so
characteristic of intoxication with isopropanol. Re-entry of the alcohol into the
stomach via swallowed saliva and intragastric secretion would set up a vicious
cycle, with opportunity for continued reabsorption. The therapeutic corollary of
this hypothesis is the advisability of repeated episodes or continuous gastric lavage
in the comatose patient, in order to remove
not only the isopropanol initially present in
the stomach, but also the fraction that may
find its way back into this organ via the
above excretory mechanisms.
The maximal levels of isopropyl alcohol
in the blood, as noted above, are far below
those that would be found were an equal
quantity of ethyl alcohol ingested. At maximal absorption in a 150-lb. man, an ounce
of 80 proof whiskey (40 per cent ethyl
alcohol) raises the blood alcohol level approximately 0.02 per cent. Rubbing alcohol
is a 70 per cent solution of isopropyl alcohol, and thus each ounce ingested contains almost twice as much alcohol as an
equal volume of whiskey. A pint of whiskey
(16 ounces—500 ml.) drunk fairly rapidly,
produces a level of 0.30 to 0.32 per cent
of alcohol in the blood. Were isopropyl
41
Case 5
c
w
30
Case 3
M
M
F
w
c
50
40
c
M
w
?
>
•>
"1 pint"
Inhaled
M
47
Inhaled
F
Yes
Yes
Yes
No data
150 mg. per 100 ml.
No data
Yes
Yes
Yes
Yes
No data
128 mg. per 100 ml.
Yes
20 mg. per 100 ml.
(appioximately 20
hr. after ingestion)
130 mg. per 100 ml.
pints"
200 mg. per 100 ml.
?
F
M
Yes
0 (postmortem)
>
M
Yes
"1 pint"
Yes
Coma
M
150 nig. per 1C0 ml.
(postmortem)
150 mg. per 100 ml.
(postmortem)
Maximal Blood Level
of Isopropanol
"1 pint"
Amount
of
Isopropanol
Ingested
M
Sex
Chapin 2
McCord and
associates11
Case 1
Case 2
w
82
Case 4
W
2
31
Case 3
W
w
70
Case 2
W
Race
2>S
37
Adelson
Case 1
Senz and
Goldfarb"
Garrison4
Age
Author
TABLE 1
Survival
Period
After
Ingestion
Yes
No
Yes
Yes
No data
Yes
Yes
Yes
Yes
No
No
No
Yes
No
No
Yes
Yes
Yes
No
Yes
Yes
No data
No data
Yes
Yes
Yes
Yes
Survived
Survived
Survived
Survived
Survived
Survived
15 days
49 hr.
?
No data No data No data 4 to 6 hr.
(DOA)
(DOA)
Yes
Yes
No data 3H hr.
AcetoHypoor
Hypo- tension or nuria
Acetothermia Shock, or nemia,
or
Both
Both
Metabolic acidosis
Depression of central nervous
system only
Depression of central nervous
system only
Hemorrhagic pulmonary
edema
Hemorrhagic gastritis,
necrotizing tracheobronchitis (probably aspiration)
Hemorrhagic gastritis, lower
nephron nephrosis, focal
ischemic splenic necrosis
Depression of central nervous
system only
Depression of central nervous
system only
Lower nephron nephrosis
Hemorrhagic pulmonary
edema
Pulmonary congestion and
edema
Anatomic Lesions or Clinical
Syndromes Resulting from
Isopropanol
SUMMARY OF CLINICAL AND ANATOMIC DATA IN FATAL AND NONFATAL ISOPROPANOL INTOXICATION
None
CD
I—»
55
Chronic alcoholism
Chronic alcoholism
None
>
3
Z
H
O
t"1
a
o
a
o
o
o
None
None
Generalized arterio- and arteriolar
sclerosis, cardiomegaly, portal
cirrhosis, pulmonary emphysema
Diffuse fatty metamorphosis of
liver. ? chronic alcoholism
Generalized arterio- and arteriolar
sclerosis, myocardial fibrosis,
bronchiectasis
Coronary atherosclerosis
None
Other Significant Abnormalities
to
s
150
Vol. 38
ADELSON
alcohol handled in the same manner by the
organism, blood levels almost twice this
figure would be found after the ingestion
of the classical quantity of 1 pint; however,
the concentrations of isopropanol are usually
half the figure for ethanol. This aspect of
isopropanol metabolism indicates a great
difference in biologic behavior of these 2
closely related substances. The major similarities between ethanol and isopropanol
are that both are readily absorbed from
the upper gastrointestinal tract, quickly
distributed throughout the entire organism,
and ultimately produce a central nervous
system depression and paralysis; however,
once absorbed, each follows its own metabolic
pathways. Unlike ethanol, the concentration of isopropanol in the blood bears no
fixed relation to its concentration in the
urine. The blood urine ratio for ethanol is a
fairly constant figure (1:1.35) and depends
upon the difference in the water content of
the 2 fluids. The same ratio for isopropanol
varies from 1:0.6 to 1:3.39, regardless of
the time of sojourn of this alcohol in the
body or the volume of urine excreted. Also
unlike ethanol, isopropyl alcohol has no
diuretic action.8
Discussions of the "relative toxicity" of
ethyl and isopropyl alcohol are quite common in the literature, and it is stated
categorically that isopropanol is twice as
toxic and twice as potent as ethanol in
producing narcosis. 5,7 ' u In this respect,
isopVopyl alcohol is said to obey Richardson's law, first enunciated in 1869, which
generalizes on the toxicity of alcohols. Richardson concluded that "weight caeteris
paribus intensifies the action (of alcohols)
and makes it more prolonged."13 Morris
and Lightbody, however, state that such
numerical expressions of relative toxicity
are not justifiable because of the differences
between the pharmacologic actions of the
2 alcohols.12
Comparison of the clinical courses and
laboratory data in those who survived acute
isopropanol intoxication and those who died
discloses that the most important single
prognostic factor is the presence or absence
of shock with hypotension. All who died
were in shock at the time of admission to
the hospital, whereas 5 of the 6 who survived
had no significant blood pressure depression.
Coma and hypothermia are almost universal
and offer no sound basis for prognosis.
Therapy in all instances was nonspecific
and included lavage, fluid replacement with
varying solutions (dextrose, lactate-Ringers),
and symptomatic treatment. Insulin, either
alone or in combination with dextrose, is
ineffective in reducing blood isopropanol
levels in dogs, and its use in human victims of isopropanol intoxication does not
seem to be indicated.8
SUMMARY
The deaths of 5 adults as a consequence of
drinking rubbing alcohol (isopropyl alcohol,
isopropanol) are reported. Survival periods
ranged from several hours to 15 days.
Autopsies were performed on all of the
victims.
Clinically, the victims were deeply and
stubbornly comatose, and manifested varying degrees of shock and hypothermia.
Acetonuria without glycosuria, and peaked
and widened T waves were important diagnostic clues.
Death, which occurs rapidly after exposure, results from central nervous system
paralysis without observable anatomic damage. When death was delayed for several
days or more, hemorrhagic gastritis and
hemoglobinuric nephrosis were present.
No specific therapy is available for the
patient with severe isopropanol intoxication.
Treatment should include immediate evacuation of the stomach with continuous gastric
suction until the victim emerges from coma,
antishock measures, oxygen via an endotracheal tube, maintenance of fluid balance,correction of electrolyte disturbances, and
symptomatic care generally.
Further clinical and laboratory observations are needed in cases of isopropanol
intoxication for a more complete understanding of the pharmacology and toxicology
of this compound. Especially valuable would
be additional laboratory studies of the bloodurine and blood-brain ratios.
SUMMARIO I N
1NTERLINGUA
Es reportate le mortes de 5 adultos causate
per le imbibition de alcohol de massage
Aug. 1962
I S O P R O P Y L ALCOHOL
(alcohol isopropylic, isopropanol). Le periodos de superviventia variava inter plure
horas e 15 dies. Necropsias esseva executate
in omne le victimas.
Le examine clinic monstrava que le victimas esseva profundemente e obstinatemente
comatose e que illes manifestava varie grados
de choc e de hypothermia. Acetonuria sin
glycosuria e piccate e allargate undas T
esseva importante indicios diagnostic.
Le morte, que occurre rapidemente post
le exposition, resulta ab paralyse del systema
nervose central sin observabile injuria anatomic. Quando le morte esseva retardate
durante plure dies, gastritis hemorrhagic e
nephrosis hemoglobinuric esseva presente.
Nulle therapia specific es disponibile pro
le patiente con sever intoxication per isopropanol. Le tractamento debe includer un
immediate vacuation del stomacho con
continue suction gastric (usque le victima
emerge ab le coma), mesuras anti choc,
oxygeno via un tubo endotracheal, mantenentia del balancia de liquido, correction del
disturbate stato de electrolytes, e sollicitude
symptomatic in general.
Plus observationes clinic e laboratorial in
casos de intoxication per isopropanol es
requirite pro le elucidation pharmacologic e
toxicologic de iste composite. De valor
special esserea nove studios laboratorial in re
le proportiones del concentration de alcohol
isopropylic in sanguine e urina e in sanguine
e cerebro.
Acknowledgments. The author acknowledges t h e
valuable advice a n d suggestions of D r . Alan R.
Moritz, Director of t h e I n s t i t u t e of Pathology,
and D r . Samuel R. Gerber, Coroner of Cuyahoga
County, in t h e preparation of this manuscript.
T h e chemical analyses were performed b y Irving
Sunshine, P h . D . , Toxicologist a t t h e Cuyahoga
County Coroner's Office.
INTOXICATION
151
REFERENCES
1. B E N N E T T , I . L., J R . : Poisoning due to substances commonly s u b s t i t u t e d for ethyl alcohol. V. A. Tech. Bull. T B 10-89, 6: 1-10,
1953.
2. C H A P I N , M . A . : Isopropyl alcohol poisoning
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