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Pulmonary embolism and seizures

Massive Pulmonary Embolism Presenting as Seizures

Chien-Kan Chen1, Ding-Kuo Chien1,2,3, Wei-De Tsai1, Yu-Jang Su1,2, Wen-Han Chang1
1

Department of Emergency Medicine, Mackay Memorial Hospital, Taipei, Taiwan

Mackay Medicine, Nursing and Management College

Graduate Institute of Injury Prevention and Control, Taipei Medical University

J Taiwan Emerg Med 2008;10:127-130

ABSTRACT
Massive pulmonary embolism (MPE) should be kept in mind in patients who present with new-onset generalized seizures and
hemodynamic instability, as a delayed the diagnosis may contribute to cardiac arrest. In this situation, emergency thrombolysis is an
effective rescue therapy. We report on a 50-year-old man with MPE who presented with new-onset generalized seizures and shock.
In the emergency department, the patient had another 4 generalized seizures accompanied by shock and cardiac arrest after the last
seizure. The patient was successfully treated with emergency thrombolysis (within 3 minutes of the cardiac arrest). The patient was
discharged uneventfully and neurologically intact, and treated with oral warfarin after a twenty-six-day hospitalization.
Keywords: massive pulmonary embolism, seizure, cardiac arrest, emergent thrombolysis

INTRODUCTION
Massive pulmonary embolism (MPE) is an emergency
that may deteriorate rapidly and contribute to death.1 Patients with MPE usually present with dyspnea, syncope
or cyanosis.2 New-onset generalized seizures are rarely
reported as a presentation of MPE,3 so the diagnosis may
be delayed. Emergency thrombolysis may be the most
effective therapy for treatment of MPE, especially in
cardiac arrest.4 We report a patient with MPE who presented with repeated generalized seizures following dyspnea and shock. Cardiac arrest subsequently occurred,
and the patient was successfully resuscitated with emergency thrombolysis.

CASE REPORT
A 50-year-old man presented to our emergency department (ED) with a new-onset generalized seizure which
lasted 1 minute and was witnessed by his family. The
patient had been an alcoholic for a long time without
any significant medical history. On arrival, he was alert
and oriented and his temperature was 36C, pulse rate

99 beats per minute, respiratory rate 20 breaths per

minutes, and blood pressure 86/62 mmHg. He had jugular vein engorgement and mild edematous changes in
both legs without decreased pulsation. Arterial blood
gases (ABG) with a mask at 100% (FiO2 about 0.6) oxygen were pH 7.29, PaCO2 16.6 mmHg, PaO2 147.6
mmHg, and base excess -18.8 mmol/L. The alveolararterial oxygen gradient was high[(760-47)0.6-16.6/
0.8-147.6= 259.4]. Electrocardiography (ECG) showed
sinus tachycardia and non-specific ST-T changes. Chest
radiography (CXR) showed non-specific findings. An
anticonvulsant (phenytoin 15 mg/kg) was prescribed immediately for prevention and control of seizures.
During observation in the ED, the patient had episodic shortness of breath with remarkable hypotension
(systolic blood pressure around 60 mmHg) and tachycardia (heart beat around 150/min). Each episode of
shortness of breath was followed by a generalized tonic
seizure. The duration of the seizures was less than one
minute, and there was no urinary incontinence. After
the seizures, the patient regained complete consciousness within one minute. A computed tomography (CT)
of the brain showed no organic problems. A central line
was inserted via the internal jugular vein and the central
venous pressure (CVP) was 34 cm of water. An inotro-

Received: August 18, 2008

Accepted: October 8, 2008
Address for requests and correspondence to: Ding-Kuo Chien, Department of Emergency Medicine, Mackay Memorial
Hospital, 92, Section 2, Chungshan North Road, Taipei, Taiwan
TEL: 886-2-25433535 FAX: 886-2-25433642 E-mail: anderson@ms1.mmh.org.tw
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C. K. Chen et al

Figure 1. Chest CT with enhancement shows some filling

deficits over both pulmonary arteries (arrow) and
a small right-side pleural effusion.

pic agent (dopamine at 20 ug/kg/min) was given, but it

was ineffective. The unusual type of seizure, unstable
hemodynamic status and high CVP level, in addition to
the poor response to conventional seizure medication
raised concerns of MPE. The D-dimer level was 2326
ng/mL DDU (automated latex enhanced immunoassay,
reference level < 278 ng/mL). Enoxaparin (1 mg/kg) was
given empirically and emergency chest CT with contrast revealed large emboli over both pulmonary arteries and a small right-side pleural effusion (Figure). Dyspnea and hemodynamic instability accompanied by a
generalized tonic seizure recurred, followed by pulseless
electronic activity. Standard cardiopulmonary resuscitation was initiated, and 100 mg recombinant tissue plasminogen activator (rt-PA) was given by intravenous
bolus through the central line within three minutes after
a brief discussion with family. The patient's spontaneous circulation returned eight minutes after CPR.
On the 3rd day of hospitalization, CT of the abdomen was performed because of lower back pain, revealing a retroperitoneal hematoma. His clinical condition
stabilized with supportive care and blood transfusion.
On the 8th hospital day, the ventilator was discontinued
and echocardiography showed no right ventricle enlargement or elevated pulmonary artery pressure. Duplex
venous ultrasound revealed partial occlusion of the right
popliteal and left femoro-popliteal veins. A neurological workup revealed no abnormalities. He was discharged uneventfully, with oral warfarin therapy after a
26-day hospitalization.

DISCUSSION
New-onset generalized seizures are usually managed as
a neurological problem. Most generalized tonic-clonic
seizures, which are caused by an abnormal electrical
discharge from brain neurons, start with abrupt loss of
consciousness and a warning or aura is rare. After the
seizure, consciousness usually returns gradually, and
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postictal confusion may last for hours.5 However, the

neurological presentation of this patient was different
from that of true epilepsy, because he had repeated generalized seizures following dyspnea and shock. He recovered consciousness very rapidly and there was little
postictal confusion. In addition, the seizures responded
poorly to anticonvulsant therapy and the neurological
examination was normal. We feel these seizures were
caused by transient hypoperfusion caused by a massive
pulmonary embolism, because he recovered consciousness rapidly after his hemodynamic status stabilized.
Pulmonary embolism (PE) is difficult to detect, because patients present with diverse symptoms and
signs.6 Patients with MPE usually present with dyspnea,
syncope or cyanosis.2 Marine et al. first reported two
patients with MPE who had sudden nausea followed by
generalized seizures. They suggested that transient cerebral ischemia, acidosis and hypoxia might be the contributing factors.3 Courtney et al. reported unexplained
seizures as part of a clinical decision rule to detect MPE,
and found that patients with fatal MPE commonly manifested components of a triad including dyspnea, altered
mental status and shock prior to death.7
ABG, CXR, and ECG are the initial diagnostic tools
for PE, although they have limited value. The alveolararterial oxygen gradient of an MPE is always greater
than 20,8 and its value reflects the severity.9 ECG and
CXR may exclude alternative diagnoses such as acute
myocardial infarction, pulmonary edema, pneumohemothorax and pneumonia. The D-dimer measurement
is useful because of its high sensitivity and negative predictive value,10 and it is valuable particularly in atypical
presentations of pulmonary embolism. With advances
in technology and clinical convenience, spiral CT is being used increasingly as a diagnostic modality.11
Our reported patient had repeated generalized seizures following dyspnea and hemodynamic instability.
The new-onset generalized seizure led to an initial diagnosis of a neurological problem, but hemodynamic
instability, engorgement of the jugular vein, a high alveolar-arterial oxygen gradient and an increased D-dimer
level, raised the possibility of MPE. Chest CT with contrast confirmed the diagnosis of MPE. However, a
patient's condition needs to be relatively stable to tolerate transportation to the CT department.
Cardiac tamponade is a critical condition with a presentation very similar to massive pulmonary embolism,
with restriction of right ventricular filling, hemodynamic
instability, and engorgement of the jugular vein.12 Cardiac tamponade should be treated immediately by
pericardiocentesis, and this fatal condition could be diagnosed or excluded by rapid bedside sonography. If
MPE is highly suspected and the patient's condition is
too unstable for chest CT, a bedside cardiac echo can
exclude cardiac tamponade and emergency thrombolysis can be done.
Systemic fibrinolytic therapy is recommended as the

Pulmonary embolism and seizures

standard, first-line treatment for patients with MPE, especially for those with shock or major disability.1,2,13 The
standard regimen for PE is 100 mg rt-PA over 2
hours,1,13 but the standard dosage and timing of rt-PA
for sudden cardiac arrest is still controversial.14 We used
a bolus injection of 100 mg rt-PA as recommended by
Kline15 and Moretii et al16 for a witnessed cardiac arrest
caused by MPE. The patient was successfully resuscitated and had full neurological recovery without major
bleeding complications.

CONCLUSION
A new-onset unexplained seizure with hemodynamic
instability may be a clue to MPE, and delaying the diagnosis may contribute to cardiac arrest. Chest CT is a
useful tool to confirm massive pulmonary embolism.
Emergency thrombolysis was efficacious and safe for
treatment cardiac arrest caused by MPE in this particular case. More clinical trials are necessary to establish
the safety, dosage and timing of thrombolytic agents in
these critical circumstances.

NOV

10. Ginsberg JS, Wells PS, Kearon C, et al. Sensitivity and

specificity of a rapid whole-blood assay for D-dimer in
the diagnosis of pulmonary embolism. Ann Intern Med
1998;129:1006-11.
11. Schoepf UJ, Goldhaber SZ, Costello P. Spiral computed
tomography for acute pulmonary embolism. Circulation
2004;109:2160-7.
12. James T. Niemann. The Cardiomyopathies, Myocarditis,
and Pericardial Disease. In: Tintinalli JE, Kelen GD,
Stapczynski JS, editors. Emergency medicine : A comprehensive study guide. 6 ed. New York, USA: The
McGraw-Hill companies, Inc.; 2004;378-85.
13. Kucher N, Goldhaber SZ. Management of massive pulmonary embolism. Circulation 2005;112:e28-32.
14. Kurkciyan I, Meron G, Sterz F, et al. Pulmonary embolism as a cause of cardiac arrest: presentation and
outcome. Arch Intern Med 2000;160:1529-35.
15. Kline JA. Pulmonary embolism. In: Tintinalli JE, Kelen
GD, Stapczynski JS, editors. Emergency medicine: A
comprehensive study guide. 6 ed. New York, USA: The
McGraw-Hill companies, Inc.; 2004;386-94.
16. Moretti C, De Felice F, Mazza A, Pinneri F. [Bolus injection of recombinant tissue-type plasminogen activator during cardiopulmonary resuscitation in massive
pulmonary embolism complicated with heart arrest.
Report of 2 cases and review of the literature]. Ital Heart
J Suppl 2003;4:420-23.

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J Taiwan Emerg Med
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