nication, February 1984). 2. Gerace RV: Near-fatal intoxication by 1,1,1 12.

Pointer J: Typewriter correction fluid

In our experience, the inhalation
abuse of gasoline and spray paint,
especially metallic gold or silver prod¬
ucts, is a widespread problem, partic¬
ularly among economically disadvan-
taged youth groups. This is consistent
with previously reported findings."
Despite this extensive use, no sudden
deaths resulting from the inhalation
abuse of spray paint or gasoline alone
were identified in New Mexico during
the six-year period covered by this
report. The four deaths attributed to
TCF suggest toxicity unique to this
type of product. At the present time,
TCF appears to be gaining popularity
as an agent of abuse within our
school-aged population.
References
TR, Maykoski RT: A fatal methyl
1. Hatfield
chloroform (trichloroethane) poisoning. Arch
Environ Health 1970;20:279-281.
trichloroethane. Ann Emerg Med 1981;10:533\x=req-\
534.
3. Kleinfield M, Tabershaw IR: Trichloro-
ethylene toxicity. Arch Ind Hyg Occup Med
1954;10:134-141.
4. Bass M: Sudden sniffing death. JAMA 1970;
212-2075-2079.
5. Harenko A: Two peculiar instances of psy-
chotic disturbance in trichloroethylene poison-
ing. Acta Neurol Scand 1967;43(suppl 31):139\x=req-\
140.
6. Hall FB, Hine CH: Trichloroethane intoxi-
cation: A report of two cases. J Forensic Sci
1966;11:404-413.
7. Musclow CE, Awen CF: Glue sniffing:
Report of a fatal case. Can Med Assoc J 1971;
104:315-319.
8. Travers H: Death from 1,1,1 trichloro-
ethane abuse: Case report. Milit Med 1974;
139:889-890.
9. Guberan E, Fryc O, Robert M: Mort subite
par fibrillation ventriculaire, apr\l=e`\sinhalation
volontaire de chlorothene, chez un apprenti
m\l=e'\canicien.Schweiz Med Wochenschr 1976;
106:119-121.
10. Garriott J, Petty CS: Death from inhalant
abuse: Toxicological and pathological evaluation
of 34 cases. Clin Toxicol 1980;16:305-315.
11. Banathy LJ, Chan LTF: Fatality caused by
inhalation of 'Liquid Paper' correction fluid.
Med J Aust 1983;2:606.
inhalation: A new substance of abuse. J Toxicol
Clin Toxicol 1982;19:493-499.
13. Greer JE: Adolescent inhalation abuse of
typewriter correction fluid. South Med J 1984;
77:297-301.
14. Sniffing typewriter correction fluid. Dawn
Briefings 1984;1(May):1-2.
15. Hudson P: 'Huffing.' NCME News 1984;
5(Nov 1):8-9.
16. Rumack BH (ed): Poisindex. Denver,
Micromedex, 1984.
17. Carroll E: Notes on the epidemiology of
inhalants, in Sharp CW, Brehm ML (eds):
Review of Inhalants: Euphoria to Dysfunction,
NIDA Research Monograph 15. US Dept of
Health, Education, and Welfare, 1977.
18. White J, Carlson G: Epinephrine-induced
cardiac arrhythmias in rabbits exposed to tri-
chloroethylene: Role of trichloroethylene metab-
olites. Toxicol Appl Pharmacol 1981;60:458-465.
19. White J, Carlson G: Epinephrine-induced
cardiac arrhythmias in rabbits exposed to tri-
chloroethylene: Potentiation by ethanol. Toxicol
Appl Pharmacol 1981;60:466-471.
20. Clayton BD, Clayton FE (eds): Patty's
Industrial Hygiene and Toxicology, ed 3. New
York, John Wiley & Sons Inc, 1981, vol 2B.
21. Material Safety Data Sheet: Thinner for
Liquid Paper Correction Fluid. Rockville, Md,
Gillette Medical Evaluation Laboratories, 1982.

Hyperosmolality Induced by Propylene Glycol

A Complication of Silver Sulfadiazine Therapy
Corinne L. Fligner, MD; Rhona Jack, PhD; Gary A. Twiggs, MD; Vidmantas A. Raisys, PhD

An 8-month-old male infant was treated with topical silver sulfadiazine silver sulfadiazine (Silvadene) during
for a burn and complicating toxic epidermal necrolysis involving 78% of his topical therapy for a burn resulted in
total body surface area. Transdermal absorption of propylene glycol from the hyperosmolality and possibly contrib¬
silver sulfadiazine produced hyperosmolality with an increased osmolal gap. uted to cardiorespiratory arrest.
A peak propylene glycol concentration of 1,059 mg/dL was documented,
and its osmotic effect was that predicted from its concentration. Our data Report of a Case
support either zero-order elimination at a rate of 13.5 mg/dL/hr or first-order An 8-month-old male infant sustained a
elimination with a half-life of 16.9 hours. Elevated concentrations of
deep second- and third-degree burn of the
propylene glycol may have contributed to the patient's cardiorespiratory anterior part of the chest, involving 8% of
arrest. The osmolal gap may be used as a screen for suspected propylene his total body surface area. Initial therapy
glycol intoxication in selected clinical settings. included topical silver sulfadiazine for six
(JAMA 1985;253:1606-1609) days, saline dressings for three days, and a
five-day course of oral penicillin V potas¬
sium. On the tenth day after the burn,
PROPYLENE glycol is a polyalcohol used solvent for intravenous (IV)
as a erythema and desquamation of the skin
of reputedly low toxicity, commonly drugs and as a component of the over 70% of his total body surface area

From the Children'sOrthopedic Hospital and
Medical Center (Drs Fligner and Twiggs); and the
Departments of Laboratory Medicine (Drs Fligner,
Jack, and Raisys), Pediatrics (Dr Twiggs), and
Pathology (Dr Fligner), University of Washington,
Seattle.
to King County Medical Examin-
Reprint requests
er Office, 325 Ninth Ave, Seattle, WA 98104 (Dr
Fligner).
cream base of many topical pharma¬
ceutical and cosmetic preparations.'"3
There are few reports of adverse
effects of this substance in humans
and few data relating serum concen¬
trations of propylene glycol to clinical
effects. We report a case in which
absorption of propylene glycol from
occurred, including the trunk, perineum,
and extremities. The desquamation was
diagnosed as toxic epidermal necrolysis
and was considered equivalent to a super¬
ficial and deep second-degree burn. Treat¬
ment with topical silver sulfadiazine and
dicloxacillin was begun, and the patient
was transferred on day 11 to Children's
Orthopedic Hospital and Medical Center

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 1,300f 1,200-
1,200t 1,100
1,100+
A 1,000
1,000t / \
900
190° / \ 800
E. 80° / \ 700
8 700
^ /
/ t\\
T \ 600
U 600 f' V
o ; v\ 500
S 500+ ; v:^.
1400 y Nj 400
' 300 \. 300

200+ \\ ..,
'
200
100« A.S S S
S T \N. 100
I I II I I i \ I
0^-.*.*.N
10 20 30 40 50 60 70 80 90 100 110 120 130
0
10 20 30 40 50 60 70 80 90 100110 120 130140
Elapsed Time, hr Osmolal Gap, mOsm/kg
Fig 1.—Relationship between propylene glycol concentrations and Fig 2.—Relationship between propylene glycol concentration and
time after admission (zero hours). S indicates silver sulfadiazine osmolal discrepancy: y=84.6+7.8x; r=.99.
application; A, cardiorespiratory arrest; T, termination of silver sulfa¬
diazine therapy; dots, concentrations during therapy; squares, post-
absorptive concentrations. Solid linear regression line in postabsorp-
tive phase: y=1,704-13.5x; r=.97.

(Seattle).
On admission, he appeared alert, with a
temperature of 38.4 °C; pulse rate, 132
beats per minute; respirations, 28/min;
and weight, 9.3 kg. Silver sulfadiazine
covered approximately 78% of his total
body surface area. Findings from the
remainder of the examination, including
neurological assessment, were unremark¬
able. Laboratory tests disclosed the fol¬
lowing values: WBCs, 7,700/cu mm with a
differential count shifted to the left (7%
segmented neutrophils and 47% band neu-
trophils); hematocrit, 36%; hemoglobin,
12.1 g/dL; normal RBC indices; Na, 136
mEq/L; Cl, 99 mEq/L; K, 5.8 mEq/L;
bicarbonate, 21 mEq/L; serum urea nitro¬
gen (BUN), 11 mg/dL; and serum creati-
nine, 0.7 mg/dL. Continued topical therapy
consisted of application twice daily
gauze impregnated with 600 to 800 g of
silver sulfadiazine.
On day 12, a cardiorespiratory arrest
occurred approximately one hour after a
dèbridement bath and a dressing change;
no medications had been administered
other than 15 mg of oral diphénhydramine
given four hours before the arrest. Results
of an initial arterial blood gas test showed
an acute respiratory acidosis (pH, 7.28;
Pco2, 50 mm Hg). No bacteria were
detected by blood culture. A definitive
cause for the arrest was not determined.
After resuscitation, results of a neurologi¬
cal examination reflected substantial hy-
poxic damage. Transient elevation of the
serum creatinine level (1.2 mg/dL) nor¬
malized in one day (0.7 mg/dL).
The next day, a measured serum osmo-
lality was 388 mOsm/kg H20, with a
simultaneously calculated serum osmolali-
ty of 314 mOsm/kg H;0 (Na, 145 mEq/L;
serum urea nitrogen, 33 mg/dL; and glu-
cose, 186 mg/dL). The osmolal gap (dis¬
crepancy between the measured and calcu¬
lated osmolalities) was 74 mOsm/kg H¡0.
During the course of the day, the mea¬
sured serum osmolality increased to a
peak of 420 mOsm/kg H¡0, with a peak
osmolal gap of 130 mOsm/kg H¡0. The
following day, a serum glycol screen dem¬
onstrated a large amount of propylene
glycol, later quantitated at 771 mg/dL.
Evaluation of all administered medica¬
tions revealed no source for the propylene
glycol other than silver sulfadiazine,
which contains 76.7 mg/g. Silver sulfadia¬
zine therapy was discontinued; during the
preceding 70 hours of hospitalization,
3,400 g had been applied, resulting in a
topical propylene glycol dose of 9 g/kg/24
hr.
of During the four days after discontinua¬
tion of therapy with silver sulfadiazine,
the serum osmolality gradually decreased
to 298 mOsm/kg H20, and the osmolal gap
normalized to less than 9 mOsm/H20. The
mild lactic acidosis (blood lactate concen¬
tration of 5.8 mmole/L; reference range,
2.0 mmole/L), thought to be due to propyl¬
ene glycol metabolism, resolved, and alkali
therapy was never required to maintain
the arterial pH in the range of 7.30 to 7.52.
Mechanical ventilation continued for three
weeks. The patient's later course was
marked by severe, persistent hypoxic
encephalopathy.
.Methods
Serum osmolality was measured by
freezing-point depression on an osmome-
ter (Advanced DigiMatic Osmometer Mod¬
el 3D II, Advanced Instruments Inc). The
following formulas were used to calculate
serum osmolality and osmolal gap (mil-
liosmols per kilogram of water)4:
Osm.=1.86(Na*)+(Serum Urea Nitrogen/
2.8)+(Glucose/18)
Osmolal Gap=Osm„,-(Osm,/0.93)
where Osmc is the calculated osmolality
and Osm„, is the measured osmolality. The
concentrations of serum urea nitrogen and
glucose were not consistently measured
simultaneously with sodium concentration
and osmolality. Because the serum urea
nitrogen and glucose levels were relatively
stable for the four days after discontinua¬
tion of silver sulfadiazine therapy, mean
values (serum urea nitrogen, 14.5 mg/dL;
glucose, 173 mg/dL) were used in the
osmolality calculations.
Propylene glycol was quantitated using
a gas Chromatograph equipped with a
flame ionization detector and a ô-ftx'/s-in
internal diameter glass column packed
with Porapack S 80/100 mesh (Hewlett-
Packard Model 5700A and Waters Asso¬
ciates, respectively). Oven and detector
temperatures were 190 °C and 200 °C,
respectively. The internal standard used
was w-propyl alcohol, and unknowns were
quantitated against a 104-mg/dL propyl¬
ene glycol standard using the peak-height
ratio method. Retention times were 1.8
minutes for w-propyl alcohol and nine
minutes for propylene glycol. A calibra¬
tion range was documented up to 1,040
mg/dL; within-run precision was approxi¬
mately 10% to 15% over the linear range.
Specimens were stored at 4 °C, and quan-
titation was performed 12 to 16 days after
sampling.
Elimination pharmacokinetics during
the postabsorptive phase were determined
by regression analysis using the propylene
glycol values obtained after termination of
silver sulfadiazine therapy at 70 hours.
The relationship between propylene glycol
and the osmolal gap was obtained by

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 linear regression analysis using available 7.6 mg/dL/mOsm (76/10), with an
data (subsequent to 57 hours). observed slope of 7.8 (Fig 2). These
data suggest that the increase in
Results
serum osmolality produced by propyl¬
Serum propylene glycol concentra¬ ene glycol is equivalent to the molal
tions increased during the period of concentration of propylene glycol.
application of silver sulfadiazine, This finding differs from that of
with a peak of 1,059 mg/dL (Fig 1). previous investigators, who found
Sampling was too erratic to allow only 16% of the osmotic activity
characterization of absorption pa¬ expected from propylene glycol."
rameters; it is possible that higher About 45% of absorbed propylene
peak values were achieved after each glycol is excreted by the kidneys, and
dressing change. the remainder is oxidized by hepatic
Analysis of the postabsorptive con¬ alcohol dehydrogenase to lactate, py-
centration data (Pig 1) by linear and ruvate, or acetate.7 Ethanol, metabo¬
log-linear regression produced lines lized by the same enzyme, has zero-
with similar goodness of fit (r=.97 order elimination kinetics (at all but
and r=.95, respectively). Thus, the the lowest concentrations), with an
data support either zero-order elimi¬ elimination rate of 15 mg/dL/hr.
nation, with a rate of 13.5 mg/dL/hr, These similarly metabolized com¬
or first-order elimination, with a
pounds might be expected to show
half-life of 16.9 hours (range, 13.1 to similar elimination kinetics. How¬
23.8 hours). ever, our kinetic data are compatible
The relationship between propylene with either zero- or first-order elimi¬
glycol concentration and osmolal gap nation and cannot discriminate be¬
(Fig 2) was as follows: tween the two. Pharmacokinetic data
Propylene Glycol (mg/dL) = for propylene glycol in humans are
84.6+(7.8xOsmolal Gap [mOsm/kg H20]) scanty, but the half-life we calculated
is consistent with the only previously
Thus, the osmotic effect of propylene
glycol was that predicted from its reported literature value of 19.3 hours
molecular weight (76 daltons) and (range, 10.8 to 30.5 hours).6 If zero-
order kinetics apply, the half-life of
concentration.
propylene glycol will vary, depending
Comment on the blood concentration.
Hyperosmolality associated with a Absorption of propylene glycol
discrepancy between measured and through intact skin is inconsequen¬
calculated osmolalities of greater tial3; however, previous studies have
than 10 mOsm/kg H20 (increased documented that loss of the epidermis
osmolal gap) occurs in two clinical can result in the absorption of sol¬
settings: (1) decreased serum water vents from topical pharmaceuticals.
content, as in hyperlipidemia or An early report implicated absorbed
hyperproteinemia, where the calcu¬ hexylene glycol as a cause of coma in
lated osmolality is underestimated burned children.8 Absorption of pro¬
because of a falsely low serum sodium pylene glycol from silver sulfadiazine
(78%) provided substantial absorp¬
tive area. Enhanced capillary perme¬
ability and vasodilation caused by
inflammatory mediators, warm dé-
bridement baths, and low-grade fever
may have contributed to increased
propylene glycol absorption. The topi¬
cal dose of propylene glycol was high;
the acceptable daily intake specified
by the World Health Organization for
oral propylene glycol is 25 mg/kg/24
hr,'2 while the topical dose applied to
our patient was 9 g/kg/24 hr.
Impaired hepatic metabolism or renal
excretion could have contributed to
the high concentrations, but there
was no laboratory evidence of serious
dysfunction of either organ.
In experimental animals, propylene
glycol has been shown to have tran-
quilizing effects, producing general¬
ized hypotonia, decreased respira¬
tions, and ataxia13; it acts as a CNS
depressant2 and is one third as intoxi¬
cating as ethanol on a weight-for-
weight basis.14 After IV injection,
both hemolysis and cardiac arrhyth¬
mias have been noted. In humans,
oral ingestion of vitamins dissolved in
propylene glycol has resulted in
intractable seizures and episodes of
unresponsiveness.1516 Additional toxic
effects are the production of lactic
acidosis" and cardiac arrhythmias,
the latter associated with the IV
administration of phenytoin dissolved
in a propylene glycol carrier.18 The
only report in the literature relating
neurological status and propylene
glycol concentrations describes a pa¬
tient with a serum propylene glycol
concentration of 760 mg/dL as "con¬
scious."' A recent report failed to find
a relationship between clinical status

concentration, and (2) increased se¬
rum concentration of unmeasured,
osmotically active, low-molecular
weight compounds (<150 daltons),
such as mannitol, ethanol, methanol,
isopropyl alcohol, ethylene glycol,
propylene glycol, ethyl ether, paralde-
hyde, and acetone.5 The concentration
of the unmeasured substance (milli¬
grams per deciliter) should be equal
to the product of the osmolal gap
(milliosmols per kilogram of water)
and the molecular weight, divided by
10." We found this relationship to
hold true for propylene glycol, within
the error ofour methods: the
expected slope of the line relating
propylene glycol and osmolal gap was
has been well documented in only two
patients, both with large burns (70%
and 90%)."° In that study, an addi¬
tional nine patients had hyperosmo¬
lality with increased osmolal gap,
which was presumed, but not proved,
to be caused by propylene glycol; all
had burns involving greater than 35%
of their body surface area. Hyperos¬
molality caused by absorption of glyc¬
erin from a povidone-iodine-glycerin
ointment has been described."
Although silver sulfadiazine has
been widely used for 15 years, few
reports of propylene glycol absorption
or high serum propylene glycol con¬
centrations have appeared. In the
present case, the large surface area
and serum propylene glycol concen¬
trations of up to 1,000 mg/dL in ten
infants receiving parenteral nutrition
containing multivitamins dissolved in
propylene glycol.6
In our patient, an elevated serum
propylene glycol concentration (369
mg/dL) was temporally related to the
cardiorespiratory arrest and may
have been causally related, through
production of cardiac arrhythmia,
CNS depression, or synergism with a
second CNS depressant (diphenhy-
dramine). Definite correlation be¬
tween propylene glycol concentra¬
tions and clinical effects was not
possible because of the subsequent
hypoxic encephalopathy.

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 We have demonstrated that propyl¬
ene glycol predictably increases se¬
rum osmolality. In appropriate clini¬
cal settings, the osmolal gap may be
used to estimate the concentration of
propylene glycol and may be used as a
screen for suspected propylene glycol
intoxication. At this time, it seems
advisable to monitor the osmolal gap
in patients treated with topical silver
sulfadiazine who are at risk for
increased absorption or decreased
elimination of propylene glycol; this
group would include infants and
young children, patients with large
burns or large areas of abnormal
epidermis (such as epidermolysis
bullosa or toxic epidermal necrolysis),
and patients with hepatic or renal
dysfunction. Additional studies are
necessary to delineate the prevalence
and the causes of enhanced absorp¬
tion of propylene glycol, to describe
the mechanisms of toxicity, and to
establish the clinical correlates of
Pseudopheochromocytoma and Cardiac Arrest
THE SYMPATHOMIMETIC com-
pound phenylpropanolamine hydro-
chloride is found in a variety of easily
accessible medications including de-
congestants, anorectics, and stimu-
lants. Serious complications associ-
ated with the use of phenylpropanol-
amine have been described, including
hypertension,1-4 headaches,1-4 psycho-
sis,5,6 seizures,1,2 and fatal cerebrovas-
From the Departments of Pediatrics (Drs Hyams
and
Leichtner) and Pathology (Drs Breiner and
McComb), Hartford Hospital, Hartford, Conn; the
College of Agriculture and Natural Resources, Uni-
versity of Connecticut, Storrs (Dr Hill); and the
Department of Medicine, New York University, New
York (Dr Manger).
Reprint requests to Department of Pediatrics,
Hartford Hospital, Hartford, CT 06115-0729 (Dr
Hyams).
Downloaded From: http://jama.jamanetwork.com/ by a University of Iowa User on 05/24/2015
elevated propylene glycol concentra¬
tions.
Kent Opheim, PhD, provided suggestions and
encouragement.
References
1. Seidenfeld MA, Hanzlik PJ: The general
properties, actions, and toxicity of propylene
glycol. J Pharmacol Exp Ther 1932;44:109-121.
2. Hanzlik PJ, Newman HW, Van Winkle W
Jr, et al: Toxicity, fate and excretion of propyl-
ene glycol and some other glycols. J Pharmacol
Exp Ther 1939;67:101-113.
3. Rowe VK, Wolf MA: Glycols, in Clayton
GD, Clayton FE (eds): Patty's Industrial
Hygiene and Toxicology, ed 3. New York; John
Wiley & Sons Inc, 1982, vol 2C, pp 3852-3861.
4. Glasser L, Sternglanz PD, Combie J, et al:
Serum osmolality and its applicability to drug
overdose. Am J Clin Pathol 1973;60:695-699.
5. Gennari FJ: Serum osmolality: Uses and
limitations. N Engl J Med 1984;310:102-105.
6. Glasgow AM, Boeckx RL, Miller MK, et al:
Hyperosmolality in small infants due to propyl-
ene glycol. Pediatrics 1983;72:353-355.
7. Ruddick JA: Toxicology, metabolism, and
biochemistry of 1,2-propanediol. Toxicol Appl
Pharmacol 1972;21:102-111.
8. Procter DSC: Coma in burns\p=m-\thecause
traced to dressings. S Afr Med J 1966;40:1116\x=req-\
1120.
9. Kulick MI, Lewis NS, Bansal V, et al:
Hyperosmolality in the burn patient: Analysis of
Associated With Phenylpropanolamine
Jeffrey S. Hyams, MD; Alan M. Leichtner,
Robert B.
cular accidents.3 We recently cared
for a 16-year-old girl with a history of
recurrent episodes of paroxysmal hy-
pertension and seizures in whom two
episodes of cardiac arrest occurred.
Her clinical constellation prompted a
lengthy and expensive evaluation for
pheochromocytoma before surrepti-
tious ingestion of phenylpropanol-
amine was discovered. Increasing use
of phenylpropanolamine-containing
medications may make these compli-
cations more frequent.
Report of a Case
A 16-year-old girl was hospitalized for
evaluation of paroxysmal hypertension.
Four months prior to admission she noted
the onset of intermittent episodes of head-
an osmolal discrepancy. J Trauma 1980;20:223\x=req-\
228.
10. Bekeris L, Baker C, Fenton J, et al:
Propylene glycol as a cause of an elevated serum
osmolality. Am J Clin Pathol 1979;72:633-636.
11. Hershey SD, Gursel E: Hyperosmolality
caused by percutaneously absorbed glycerin in a
burned patient. J Trauma 1982;22:250-252.
12. Toxicological Evaluation of Certain Food
Additives With a Review of General Principles
and of Specifications: 17th Report of the Joint
FAO/WHO Expert Committee on Food Addi-
tives, Technical Report Series, No. 539. Geneva,
World Health Organization, 1974.
13. Singh PP, Junnarkar AY, Seshagirirao C,
et al: A pharmacological study of propane-
1,2-diol. Arzneimittelforsch 1982;32:1443-1446.
14. Lehman AJ, Newman HW: Propylene gly-
col: Rate of metabolism, absorption, and excre-
tion, with a method for estimation in body
fluids. J Pharmacol Exp Ther 1937;60:312-322.
15. Arulanantham K, Genel M: Central ner-
vous system toxicity associated with ingestion of
propylene glycol. J Pediatr 1978;93:515-516.
16. Martin G, Finberg L: Propylene glycol: A
potentially toxic vehicle in liquid dosing form. J
Pediatr 1970;77:877-878.
17. Cate JC IV, Hedrick R: Propylene glycol
intoxication and lactic acidosis. N Engl J Med
1980;303:1237.
18. Tozer TN, Winter ME: Phenytoin, in
Evans WE, Schentag JJ, Jusko WJ (eds): Applied
Pharmacokinetics: Principles of Therapeutic
Drug Monitoring. San Francisco, Applied Thera-
peutics Inc, 1980, p 294.
MD; Robert G. Breiner, PhD; Dennis W. Hill, PhD;
McComb, PhD; William M. Manger, PhD
ache, diaphoresis, nausea, pallor, abdomi-
nal pain, nervousness, and fatigue. These
episodes continued until the day of admis-
sion, when she was witnessed having a
brief grand mal seizure. Her blood pres¬
sure was noted to be 180/120 mm Hg, and
she was brought to the hospital. Examina¬
tion revealed an agitated and fearful ado¬
lescent whose blood pressure was 170/110
mm Hg; pulse rate, 60 beats per minute,
and respirations, 36/min. No other specific
abnormalities were noted. She denied tak¬
ing any prescription drugs, over-the-
counter medications, or illicit prepara¬
tions. Following treatment with several
doses of intravenous hydralazine, she
became normotensive.
On the second hospital day, she sudden¬
ly became hypertensive (160/110 mm Hg)
and following a generalized seizure be¬
came apneic and asystolic. Cardiopulmo-
nary resuscitation was instituted, and she