selected reports
Pulmonary Embolism
Presenting as Seizures*
Joseph E. Marine, MD; and Samuel Z. Goldhaber, MD, FCCP

Two patients with massive pulmonary embolism (PE)
presented with generalized seizures. Pathophysiologic abnormalities that explain this clinical syndrome include respiratory acidosis, hypoxemia, and
cerebral hypoperfusion due to decreased cardiac
output. PE should he considered in the differential
diagnosis of new-onset and otherwise unexplained
seizures.
(CHEST 1997; 112:840-42)

nous administration of pressor agents. An echocardiogram
showed a normal left ventricle and a dilated and hypokinetic right
ventricle \vith preserved apical systolic function (McConnell's
sign 3 ). Pulmonary artery catheterization revealed a pulmonary
artery pressure of 52/30 mm Hg and multiple large bilateral
pulmonaty emboli. In preparation for thrombolysis, aCT scan of
the head was normal. He then received 100 mg of tissue
plasminogen activator over a 3-h period followed by continuous
intravenous administration of heparin sodium. Ultrasound of the
lower extremities revealed a deep venous thrombosis of the calf.
The follov.ing day, an inferior vena cava filter was placed.
Gradual improvement was noted, the patient was extubated, and
therapy with warfarin sodium was started. An EEG on the 4th
postoperative day showed no significant abnormality. He was
discharged home uneventfully on the lOth postoperative day.
MRI of the head performed after discharge was normal.

Key words: diagnosis; pulmonary e mbolism; seizures

Case 2
Abbreviations: PE=pulmonary embolism

A!though pulmonary embolism (PE) can present with

syncope, 1 generalized seizure activity has not been
reported.2 We, therefore, describe two patients with massive PEs in which the principal presenting features were
generalized seizures (Table 1).
REPORT OF CASES

Case 1
A previously healthy 33-year-old man presented with acute
appendicitis and under.vent an uncomplicated appendectomy on
the night of admission. He did not receive prophylactic therapy
for venous thromboembolism. On the second postoperative day,
while ambulating, he suddenly felt nauseated, fe ll to the ground,
and had approximately 30 s of generalized tonic-clonic seizure
activity with urinary and fecal incontinence . Postictally, he complained only of incisional abdominal pain, and he denied chest
pain or dyspnea. On initial examination after the seizure, he was
confused, tachycardic, tachypneic, and normotensive; he had a
pulse oximetry value of 88% while receiving 100% oxygen by face
mask. Examination by a neurologist l h after th e seizure disclosed
no abnormalities except for mild hyperreflexia in the left arm and
leg. A chest radiograph showed low lung volumes and vague
opacities in the lower lobes of both lungs. Initially, the diagnosis
was a seizure due to general anesthesia followed by aspiration .
In the ensuing 4 h ,the patient became progressively confused,
hypoxic, and hypotensive and required intubation and intrave*From the Cardiovascular Division, Depattment of Medicine,
Brigham and Women's Hospital, Harvard Medical School, Boston.
Dr. Matine was supported, in part, by the Sandra Bakalar Fund.
Manuscript received December 26, 1996; revision accepted
March 2, 1997.
Rep rint requests: Samuel Z. Goldhaber, MD, Cardiovascular
Division, Brigham and Women's Hospital, 75 Francis St, Boston
MA 02115

840

A 34-year-old woman previously in excellent health had several
days of upper respiratory tract symptoms followed by l day of
mild dyspnea on exertion, which she ascribed to a"cold." At
home, her husband \vih1essed her having sudden nausea, followed by a 10-s spell characterized by tonic bilateral upgaze and
extensor posturing of all four extremities associated \vith fecal
incontinence. She regained consciousness but had four successive
similar spells inte rrupted by brief periods of an awake confusional
state.
A CT study of the head and a lumbar puncture both revealed
no abnormalities. She then had two episodes of transient hypotension, which prompted transfer to the ICU of a regional
medical center. Upon arrival, she was in cardiogenic shock and
hypercapneic respiratory failure. She was intubated and treated
with pressors. An ECG and echocardiography revealed strain on
the right side of the heart. A pulmonary angiogram showed an
obstructing thrombus in the left main pulmonary trunk and
multiple smaller PEs in the lower lobe of the right lung. The
thrombus in the le ft pulmonary artery was mechanically fragmented with the pulmonary artery catheter, and the more distal
branches were then visualized on angiography.
She was subsequently treated with bolus urokinase (2,000
units/kg over a period of l h)followed by continuous intravenous
administration of heparin, which resulted in clinical and electrocardiographic improvement. Ultrasound of the lower extremities
revealed a right popliteal deep venous thrombosis. A follow-up
lung scan showed only minimal nonsegmental perfusion defects.
She was discharged on hospital day 18, neurologically intact, on a
regimen of aspirin and acenocoumarol. On a follow-up visit 1
month after discharge, she remained well and had no further
seizures or neurologic sequelae.
DISCUSSION

Several cardiopulmonary conditions have been reported
to present with seizures. These include torsade de
pointes, 4 long QT inte1val syndrome, 5 severe bradycardia,6
asystole, 7 and systemic arterial hypertension.8 The two
cases described h erein are the first reported, as best as can
Selected Reports

Table !-Clinical Features of Cases*
Clinical Data

Case l

Case 2

Risk factors for
PE
Type of seizure
No. of seizures
Neurologic
studies
Clinical features
ofPE

Recent surgety

Oral contraception,
family history
Generalized tonic
Five
CT, lumbar
puncture
Tachycardia,
hypoxia,
hypotension

Confirmation of
PE
RV failure on
echocardiogram
Treatment

Neurologic
sequelae
Cardiopulmonary
sequelae

Generalized
One
CT, MRI, EEG
Tachycardia,
tachypnea,
hypoxia,
hypotension
Angiogram

Angiogram

Present

Present

TP A and filter
placement

None

Urokinase;
disruption of
embolus with
pulmonmy artery
catheter
None

None

None

*RV = right ventricular; TPA = tissue plasminogen activator

be determined, in which PEs presented wi.th seizure
activity. In each case, initial clinical attention focused upon
the neurologic condition of the patient and only later,
when hemodynamic compromise ensued, was the diagnosis of PE pursued. In both cases, electrocardiographic or
echocardiographic evidence of failure of the right side of
the heart played a key role in detecting PEs.
The first patient responded well to tissue plasminogen
activator alone. In the second case, a combination of
mechanical clot fragmentation and thrombolysis was utilized, as previously described by Essop et al. 9 Initial
disruption of thrombus \vith the catheter converted the
clot from totally obstructive to nonobstructive in this
patient, thereby permitting urokinase to lyse emboli in the
distal branches of the pulmonary arterial tree.
Seizures that are associated vvith PEs raise several
important clinical issues. First, clinical evaluation may be
compromised by the patient's postictal confusional state.
Second, well-established clinical signs of PE , such as
tachypnea, tachycardia, and hypoxia, may likewise be
attributed to a postictal state vvith or without aspiration
pneumonitis. In addition, new-onset seizure activity usually leads to a neurologic workup, which may distract the
clinician from consideration of cardiovascular causes of
seizure. Finally, treatment for massive PEs usually involves immediate systemic anticoagulation when the diagnosis is suspected, followed by thrombolysis when the
diagnosis is confirmed. In a patient presenting vvith seizures, however, such therapy must be delayed until intracranial hemorrhage is excluded. Furthermore, since embolic stroke and small tumors may present with seizure
and a normal CT scan, treatment of PEs in association

FIGURE 1. Proposed pathophysiologic features of seizure in PE.

V\i.th new seizures probably entails some increased risk of
intracranial bleeding. In each case described previously,
CT scanning was performed prior to thrombolysis; however, this test does not guarantee immunity from intracranial hemorrhage.l 0
While the exact cause of seizures in the two patients
described herein cannot be established definitively, the
most likely contributing factors include transient cerebral
ischemia, hypoxia, and acidosis (Fig 1). In each case, a
further workup and follow-up revealed no intrinsic neurologic pathologic findings , indicating that PE was the
plimary cause of seizure in each case.
In conclusion, clinicians should consider PEs in the differential diagnosis of new-onset unexplained seizures, particularly if tachycardia, tachypnea, and hypoxemia are present,
regardless of whether or not aspiration occurred. Furthermore, patients who have had both seizures and PEs require
careful and rapid neurologic evaluation for contraindications
to anticoagulant and thrombolytic therapy.

REFERENCES
1 Thames MD, Alpert JS, Dalen JE. Syncope in patients with
pulmonary embolism. JAMA 1977; 238:2509-ll
2 Stein PD, Te rrin ML, Hales CA, et a!. Clinical, laboratory,
roentgenographic, and electrocardiographic findings in patients without pre-existing cardiac or pulmonary disease.
Chest 1991; 100:598-603
3 McConnell MV, Solomon SD, Rayan ME , et a!. Regional
right ventricular dysfunction detected by echocardiography in
acute pulmonary embolism . Am J Cardiol 1996; 78:469-73
4 Sundaram MBM , McMeekin JD , Gulamhusein S. Cardiac
tachyarrhythmias in hereditary long QT syndromes presenting as a seizure disorder. Can J Neurol Sci 1986;
13:262-63
5 Herman LL, Stoshak M, Rittenbaum TJ. Long QT syndrome
presenting as a seizure. Am J Emerg Med 1992; 10:435-38
6 Mendes LA, Davidoff R. Cardiogenic seizure with bradyarrhythmia: documentation of the mechanism during asystole. Am Heart J 1993; 125:1786-88
7 Howell SJL, Blumhardt LD. Cardiac asystole associated with
epileptic seizures: a case report with simultaneous EEG and
CHEST/112/3/SEPTEMBER, 1997

841

ECG. J Neurol Neurosurg Psychiatry 1989; 52:795-98
8 Ng SKC, Hauser WA, Brust JCM , eta!. Hypertension and the
risk of new-onset unprovoked seizures. Neurology 1993;
43:425-28
9 Essop MR, Middlemost S, Skoularigis J, et al. Simultaneous
mechanic;al clot fragmentation and pharmacologic thrombolysis in acute massive pulmonary embolism. Am J Cardiol
1992; 69:427-30
10 Kanter DS , Mikkola KM , Patel SR, et al. Thrombolytic
therapy for pulmonary embolism: frequency of intracranial
hemorrhage and associated risk factors. Chest 1997; 111:
1241-45

Left Main Coronary Artery
Compression During Primary
Pulmonary Hypertension*
Jean-Fnideric Patrat, MD;
Guillaume Jondeatt, MD, PhD, FCCP;
Olivier Dubourg , MD, FCCP; Pascal Lacombe, MD;
Michel Rigaud, MD; Jean-Pierre Bourdarias, MD; and
lracij Gandjbakhch, MD

ular ischemia or pulmonary artery (PA) dilation. We
herein describe a patient in whom compression of the
left main coronary artery (LMCA) by the severely
dilated pulm onary trunk produced severe left ventricular (LV) myocardial ischemia.
CASE REPORT

A 37-year-old woman with severe PPH complain ed of anginal
pain both at rest and exercise. According to New York Heart
Association classification, her functional status was class IV and
she was referred to be investigated before heart-lung transplantation. ECG showed right bundle-branch block, right ventricular
hypertrophy, and during chest pain episodes, ST segment and T
wave c hanges in the left precordial leads. Right atrial pressure
was 27 mm Hg, PA pressure was 132/60 mm Hg (mean , 90 mrn
Hg), wedge pressure was 12 mm Hg, and cardiac index was 1.50
Urninlrn 2 . Pulmonary angiography ruled out postembolic disease. On 201 thallium scintigraphy, an anterior perfusion defect
was noted at rest, which was reversible after 4 h. Coronmy
angiography showed severe stenosis of the LMCA (Fig 1) with
distal filling of the left anterior descending mte1y (LAD ) by
collaterals from the right coronary artery (RCA), and a competitive flow was visuali zed during le ft coronary arte ry opacification (Fig 2). Th e LV ante rior wall was slightly hypokin etic and
LV ejection fraction was 0.58 . Th e pati ent underwent success-

Primary pulmonary hypertension (PPH) is often associated with angina-like chest pain, the mechanism
of which is controversial. A 37 -year-old woman with
severe PPH and angina had transient ischemic ECG
changes and reversible anterior perfusion defect on
2 01
thallium scintigraphy. Coronary angiography revealed severe stenosis of the left main coronary
artery (LMCA) and otherwise normal vessels. After
heart-lung transplantation, examination of the explanted heart showed normal coronary arteries.
Compression of the LMCA by the dilated pulmonary
artery trunk was responsible for myocardial ischemia. This mechanism should be considered in patients with PPH and angina and might contribute to
the high sudden death rate.
(CHEST 1997; 112:842-43)
Key words: angina; chest pain; heart-lung transplantation; left
coronary artery; primary pulmonary hypertension
Abbreviations: LAD= left anterior descending artery;
LMCA=left main coronary artery; LV=left ventricle;
PA = pulmonary artery; PPH = primary pulmonary hypertension;
RCA=right coronary arte1y

About
50% of patients with severe primary pulmonary
artery hypertension (PPH) complain of precordial
pain, 1 which has been ascribed either to right ventric*From the Departments of Cardiology (Drs. Patrat, Jondeau,
Dubourg, Rigaud, and Bourdarias) and Radiology (Dr. Lacombe), Hopi tal Ambroise Pare, and the Department of Cardiac
Surgery (Dr. Gandjbakhch), Hopital de la Pitie, Boulogne,
France.
Manusc1ipt received Janumy 22, 1997; accepted March 2.
842

FIGURE 1. Top: Left coronary artery angiography (left anterior
oblique view) shows severe stenosis of the LMCA. The left
circum flex artery is completely opacifled wh ile only the proximal
part of the LAD is visuali zed. Bottom: On RCA angiography
(right anterior oblique view), the LAD is well opacified by
collaterals from the RCA.
Selected Reports