CLINICAL COMMUNICATION TO THE EDITOR

Seizure with Acute Pulmonary Infiltrates

To the Editor:
Neurogenic pulmonary edema is a rare form of pulmo-
nary edema that can occur after almost any kind of acute
central nervous system insult. The entity, which was de-
scribed as early as 1908,1 continues to be underdiagnosed.
Because of the considerable morbidity and mortality asso-
ciated with neurogenic pulmonary edema,2 it is important
that there is an increased awareness of this life-threatening
complication.

CASE PRESENTATION
A 42-year-old man with seizure disorder and hypertension
presented to the emergency department with multiple epi-
sodes of generalized seizure that began 2 days previously.
He had a cough with blood-streaked sputum. There were no
other associated symptoms. Physical examination showed a
blood pressure of 140/90 mm Hg, pulse rate of 110 beats/
min, respiratory rate of 19 breaths/min, temperature of
101°F, and room air oxygen saturation of 88%. Examination
further revealed mild respiratory distress without any jugu-
lar distension and diminished breath sounds with fine crack-
les in both lung bases. The rest of the examination results,
including the cardiac examination, were normal. Laboratory
results showed increased A-a gradient and leukocytosis
17,000/cmm (segments 92%). Electrocardiogram showed a
normal sinus rhythm of 93 beats/min without left ventricular
hypertrophy or ischemic changes. Other laboratory results,
including cardiac enzymes and urine toxicology, were nor-
mal. Chest x-ray showed encephalization and bilateral opac-
ities (Figure 1). Echocardiogram revealed an ejection frac-
tion of 64%, normal chamber size, and no wall motion or
diastolic abnormality.
Therapy was initiated with antiepileptics and empiric
antibiotics. Within 24 hours, the patient’s vital signs nor-
malized, including temperature, and all symptoms resolved.
Repeat chest x-ray showed resolution of the opacities (Fig-
ure 2), and the white blood cell count had returned to
Funding: None.
Conflict of Interest: None of the authors have any conflicts of interest
associated with the work presented in this manuscript.
Authorship: All authors had access to the data and played a role in
writing this manuscript.
Requests for reprints should be addressed to Rajat Nog, MD, Division
of Infectious Diseases, Department of Medicine, Hartford Hospital, 80
Seymour Street, Hartford, CT 06102.
E-mail address: rnog@harthosp.org.
Figure 1 Chest x-ray showing bilateral airspace opacities.
baseline. The presumed diagnosis was neurogenic pulmo-
nary edema; the patient was discharged without complica-
tions on antiepileptic and antihypertensive medications.
DISCUSSION
Neurogenic pulmonary edema is a rare form of pulmonary
edema characterized by an increase in pulmonary interstitial
and alveolar fluid due to and usually after an acute central
nervous system insult.2 Epileptic seizures, head injury, and
cerebral hemorrhage are the most common precipitants, but
neurogenic pulmonary edema may follow any acute central
nervous system injury. It frequently manifests within min-
utes to hours after the injury. The clinical presentation of
neurogenic pulmonary edema varies from an asymptomatic
incidental finding to florid pulmonary edema requiring in-
terventional management to sudden death. It is a diagnosis
of exclusion with a broad range of differentials: aspiration
or infective pneumonia, pulmonary hemorrhage, and con-
gestive cardiac failure. Its prevalence is not well known
largely because of underrecognition of the disease entity.
Terrence et al3 reported neurogenic pulmonary edema in
more than 80% of epileptic patients who die unexpectedly,
and Muroi et al4 reported an incidence of 8% in patients
with subarachnoid hemorrhage.
Although the underlying pathophysiologic mechanisms
remain incompletely understood, elevated intravascular
pressure and pulmonary capillary leakage are both impli-
cated in the development of injury. Edema develops sec-

0002-9343/$ -see front matter © 2011 Elsevier Inc. All rights reserved.
e2
Figure 2 Chest x-ray (24 hours later): significantly improved
bilateral airspace opacities.
ondary to changes in pulmonary and systemic vasoconstric-
tion resulting from increased sympathetic stimulation
accompanying increased intracranial pressure. Pulmonary
microvascular injury with subsequently increased permea-
bility from sudden medullary or hypothalamic sympathetic
outflow surges (the Blast theory)5 or a systemic inflamma-
tory response may play an integral role in the development
of pulmonary dysfunction associated with brain injury
(Double Hit model).6 Some authors suggest that the devel-
opment of these symptoms may be the result of “cardiac
stunning.”7
Treatment of neurogenic pulmonary edema focuses on
the underlying disorder and supportive care. Alpha- and
beta-adrenergic antagonists, chlorpromazine and dobut-
amine, have been shown to be helpful in its management.
Experimental studies suggest that nursing in the prone ven-
tilatory position aids in resolution of neurogenic pulmonary
edema.8
The American Journal of Medicine, Vol 124, No 11, November 2011
CONCLUSIONS
Diagnosis and appropriate management of neurogenic
pulmonary edema require a high index of clinical suspi-
cion. Given that this disease entity is infrequently seen
but has a high mortality rate, it is important that it be
included in the list of differential diagnoses for postictal
patients with respiratory signs and symptoms.
Rajat Nog, MDa
Korshie Dumor, MDb
Cyrus Badshah, MD, PhDc
a
Division of Infectious Diseases, Department of Medicine,
Hartford Hospital, Hartford, Conn
b
St John’s Clinic, Rolla, Mo
c
Division of Infectious Diseases, Department of Medicine,
Columbia University Medical Center, the Affiliation at Harlem
Hospital,
New York, NY
doi:10.1016/j.amjmed.2011.03.023
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