Hospital Practice

ISSN: 2154-8331 (Print) 2377-1003 (Online) Journal homepage: http://www.tandfonline.com/loi/ihop20

An Unresponsive Patient with a History of Stroke
Chad Hood, Joe L. Lezama, Rajani P. Shah, Harold M. Adelman , Edward P.
Cutolo , Bryan A. Bognar & Charlotte A. Truitt
To cite this article: Chad Hood, Joe L. Lezama, Rajani P. Shah, Harold M. Adelman , Edward P.
Cutolo , Bryan A. Bognar & Charlotte A. Truitt (1999) An Unresponsive Patient with a History of
Stroke, Hospital Practice, 34:11, 21-22, DOI: 10.1080/21548331.1999.11443922
To link to this article: http://dx.doi.org/10.1080/21548331.1999.11443922

Published online: 24 Jun 2015.

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Date: 25 March 2016, At: 19:04

MORN

NG

REPORT

Downloaded by [Laurentian University] at 19:04 25 March 2016

An Unresponsive Patient
with a History of Stroke

CHAD HOOD
JOE L. LEZAMA
RAJANI P. SHAH
HAROLD M. ADELMAN
University of South Florida,
James A. Haley Veterans Hospital, Tampa

HAROLD M. ADELMAN

75-yea,...old woman
was brought by her
family for evaluation
of her mental status,
which had begun to deteriorate
several weeks earlier. For the last
two days, she had been unresponsive and had had a low-grade
fever (~37.8°C).

A

Editor

EDWARD P. CUTOLO
Associate Editor

BRYAN A. BOGNAR
Associate Editor

CHARLOTTE A. TRUITT
Assistant Editor

Dr. Adelman is Professor, and Drs. Cutolo, Bognar,
and Shah are Assistant Professors, Department of
Internal Medicine, University of South Florida College of Medicine, Tampa. Dr. Adelman is also Assistant Chief, Drs. Cutolo and Shah are Hospitalists,
Medical Service, and Ms. Truitt is Clinical Medical
Librarian, James A. Haley Veterans Hospital, Tampa.
In addition, Dr. Bognar is Codirector of Medical
Clerkship at the university and Attending Physician,
Tampa General Hospital. This case was presented by
Dr. Hood, Medical Resident. and moderated by Dr.
Lezama, Chief Medical Resident, Veterans Hospital.

MEDICAL HISTORY. Seizures and

dementia, beginning after a stroke
four years ago; parkinsonism; chronic obstructive pulmonary disease;
coronary artery disease with angina pectoris; hypertension; allergy to
levofloxacin.
MEDICATIONS. Phenytoin, carbidodopa/levodopa, paroxetine,
albuterol, atenolol, aspirin. (The
family was unaware of any recent
change in regimen.)
FAMILY HISTORY. Noncontributory.
SOCJAL. HISTORY. Married; lives at
home with her husband; smokes
and drinks socially.
PHYSICAL EXAMINATION. Well developed, well nourished; minimally responsive. Vital signs: blood pressure, 125/72 mm Hg; pulse, 88 bpm;
temperature, 36.5°C; respirations,
22/min; Sp02 on room air, 92%.
Eyes: pupils dilated, unresp:-msive

OCTOBER

15.

to light; extraocular muscles could
not be tested. Neck: supple. Breasts:
unremarkable. Heart: regular rate
and rhythm; no murmur or gallop.
Lungs: clear to percussion and auscultation. Abdomen: normal bowel sounds; soft, nontender; no masses or hepatosplenomegaly. Pelvis:
unremarkable. Rectum: no masses; hard guaiac-negative stool.
Extremities: normal. Neurologic
responses: cogwheel rigidity bilaterally; 2+ deep tendon reflexes bilaterally; Babinski sign bilaterally.
LABORATORY FINDINGS. Hemoglobin, 8.4 gm/dL (normal, 14-17);
mean corpuscular volume, 109
1-1m3 (80-100); white blood cell
count, 4,200/mm3; platelet count,
75,000/mm 3 (150,000-410,000);
Serum: sodium, 131 mEq/L (136145); potassium, 4.4 mEq/L; chloride, 99 mEq/L; C02 , 21 mEq/L;
blood urea nitrogen, 25 mg/dL; creatinine, 0.9 mg/dL; glucose, 220
mg/dL (65-110); total protein, 6.1
gm/dL (6.3-8.2), albumin, 2.7
gm/dL (3.8-4.8), liver enzymes,
within normal limits; calcium, 8.2
mg/dL. Urine: average of 35 white
and 24 red blood cells per high
powered field; ketones, present;
few bacteria.

1999

•

HOSPITAL

PRACTICE~

Downloaded by [Laurentian University] at 19:04 25 March 2016

MD/UNRESPONSIVE PATIENT WITH

DIAGNOSTIC IMAGING. Chest xray: normal. Electrocardiogram:
junctional rhythm, nonspecific ST
and T wave changes (same as earlier ECG). Computed tomography
of the head: cortical atrophy, ventricular prominence, right parietal
infarct.
DIFFERENTIAL DIAGNOSIS. Stroke;
bilateral subdural hematoma; decompensated parkinsonism, phenytoin toxicity; urinary tract infection
or constipation causing changes in
mental status.
HOSPITAL COURSE. Additional
laboratory tests revealed a plasma
phenytoin level of 102 !J.g/mL (adjusted for albumin binding). Once
the drug was withdrawn, the level
rapidly returned to the normal therapeutic level of less than 20 !J.g/mL,
and the patient's mental status improved. Her prescription for phenytoin was changed from 125 mg to
tid to 125 mg bid with careful monitoring. She was also started on an
antibiotic after urine cultures grew
enterococci. A problem with constipation was resolved by disimpaction,
and she was discharged on day 8.
RNAL DIAGNOSIS. Phenytoin toxicity, urinary tract infection, fecal
impaction.
OUTCOME. At the two-month
follow-up examination, the patient
appeared to be doing well. The reason for the apparent overdose was
not determined. She and her family were reshown how to administer
the medication properly.

HISTORY OF STROKE

C

ASE BREAKERS

Suspicion of phenytoin intoxication and subsequent confirmation by laboratory testing.

K

EY POINTS

1. The antiepileptic drug
phenytoin has a notoriously high
risk/benefit ratio. At serum levels
of 30 mg/mL, the drug is toxic in up
to 50% of patients.
2. The first sign of toxicity is
usually nystagmus, which manifests
at about 20 llg/mL. Cerebellar ataxia, tremor, and hyperreflexia occur
at about 30 llg/mL, and confusion,
lethargy, and coma at 40 llg/mL and
higher.
3. Many authorities advise
maintaining a serum level of 14 to
18llg/m1. Measurements must be
adjusted for albumin binding. The
adjusted value is calculated according to the following formula: phenytoin concentration/(0.2 X albumin
concentration)+ 0.1.
4. Drugs known to increase the
serum level of phenytoin include
amioderone, cimetidine, fluconazole, isoniazid, and certain sulfonamides. The effects of alcohol are
variable.
5. Hyperglycemia occasionally
occurs even with careful monitoring of phenytoin levels. The mechanism is believed to be postreceptor
inhibition of insulin action.
6. Other effects of phenytoin

~HOSPITAL PRACTICE • OCTOBER 15. 1999

include interference with folic acid
absorption and stimulation of folate
metabolism by enzyme induction,
which leads to megaloblastic anemia or pancytopenia in a small percentage of patients I< 1o/o). Either
condition can be corrected with 1
mg/day of folic acid, but the serum
level of phenytoin will be lowered.
7. A least 25% of patients taking phenytoin have mild macrocytosis without anemia.
8. Phenytoin overdose is generally treated by drug withdrawal
and gastrointestinal decontamination by gastric lavage and repeated
administration of an activated charcoal slurry. Hemodialysis and hemoperfusion are ineffective.
9. Deaths from phenytoin toxicity are rare. 0
SELECTED READING
ai-Rubeaan K. Ryan EA: Phenytoin-induced insulin
insensitivity. Diabetic Med 8:968. 199 I
Dukes MNG: Anticonvulsants./n Meyler's Side
Effects of Drugs. 13th ed. Dukes MNG (Ed). Elsevier, New York, 1996. pp 136-159
Rivey MR Schottelius DD. Berg Mj: Phenytoin-folic
acid: A review. Drug lntell Clin Pharm 18:292,
1984