American Journal of Emergency Medicine 34 (2016) 681.e3–681.
e5
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Case Report
Thrombolysis during continuous chest compression in a patient with
cardiac arrest due to pulmonary embolism: prolonged CPR–induced
spinal cord injury
Pulmonary embolism (PE) is a life-threatening condition, and
cardiac arrest is the most serious clinical circumstance. Clinical practice
guidelines recommend systemic thrombolysis for high-risk or massive
PE patients as the primary treatment. However, there are insufficient
data to argue for or against the routine use of thrombolytic therapy
during cardiac arrest. We report a 47-year-old man with acute PE com-
plicated by cardiac arrest with pulseless electrical activity. Intravenous
thrombolytic therapy with 1.5 million U of urokinase was performed
by a constant infusion pump within 30 minutes during continuous me-
chanical chest compression with LUCAS (Jolife AB, Lund, Sweden). After
46 minutes of cardiopulmonary resuscitation, return of spontaneous cir-
culation was achieved, and the patient eventually survived to discharge.
Unfortunately, he had an irreversible spinal cord injury due to
prolonged cardiopulmonary resuscitation and traumatic injury.
Pulmonary embolism (PE) is a common disorder and associated
with significant morbidity and mortality. Pulmonary emboli usually
arise from thrombi originating in the deep venous system, and most pa-
tients present with worsening respiratory insufficiency and tachycardia.
Although the most common symptom is dyspnea, the clinical presenta-
tion of PE can be variable, ranging from nonspecific symptoms to hemo-
dynamic instability with systemic hypotension, persistent profound
bradycardia, and cardiogenic shock [1]. In the worst clinical scenario, it
can lead to cardiac arrest and sudden death. The mortality attributable
to cardiac arrest in the event of PE is extremely high [2]. Recently, clin-
ical practice guidelines recommend thrombolysis for high-risk or mas-
sive PE patients as the primary treatment [3,4]. However, in the
setting of cardiac arrest due to PE, the use of the fibrinolytic therapy dur-
ing cardiopulmonary resuscitation (CPR) has very limited evidence
from randomized clinical trials. Here, we report a case with acute PE
complicated by cardiac arrest who survived after administration of uro-
kinase during continuous mechanical chest compression.
A 47-year-old man was admitted to our emergency department
(ED) with dyspnea and syncope. His initial vital signs included temper-
ature, 37.0°C; heart rate, 128 beats per minute; blood pressure, 84/
52 mm Hg; and respiratory rate, 24 breaths per minute. The initial elec-
trocardiogram (ECG) revealed sinus tachycardia. Bedside transthoracic
echocardiography showed an enlarged right ventricular with severe tri-
cuspid regurgitation and pulmonary artery hypertension (right ventric-
ular systolic pressure, 75 mm Hg). The blood tests revealed a leukocyte
level of 16.61 × 109/L; a platelet count, 78×10 9/L; the serum levels of
troponin I of 3.24 ng/mL (reference range 0-0.04 ng/mL); and the D-
dimers level of 10.86 g/mL (reference range, 0.0-0.5 g/mL). Arterial
blood gases showed PaO2, 55 mm Hg/PaCO2, 26 mm Hg, with a
0735-6757/© 2015 Elsevier Inc. All rights reserved.
peripheral saturation of oxygen 84%. Based on these findings, he was
presumptively diagnosed with acute PE.
While the patient was transferred from the ED to the cardiac care
unit, he had a witnessed cardiac arrest with pulseless electrical activity
(Fig. 1A). Continuous chest compression was preformed immediately,
and a single dose of epinephrine 1 mg was administered intravenously.
The ECG monitor demonstrates wide QRS complex pulseless electrical
activity, and there was still no cardiac output (Fig. 1B). He was intubated
with ventilation support, and 1.5 million U of urokinase was given by a
constant infusion pump within 30 minutes while continuous mechani-
cal chest compression with LUCAS (Jolife AB, Lund, Sweden) device sup-
port. After another 16 minutes of CPR, return of spontaneous circulation
was achieved for the first time, and the heart's rhythm was also restored
to sinus rhythm with blood pressure increasing to 130/84 mm Hg.
Bedside echocardiographic examination was performed again, which
revealed right ventricular volume overload improvement with mild
tricuspid regurgitation, and right ventricular systolic pressure decreased
to 38 mm Hg. The patient recovered consciousness approximately 2
hours after resuscitation and was extubated on the second day. Unfortu-
nately, the patient appeared with double lower limb paralysis and a
massive lower gastrointestinal bleeding requiring blood transfusion.
Multidetector computed tomography pulmonary angiography revealed
PE with a large thrombus burden in the main segmental branches
(Fig. 2). Computed tomography showed a sternal body fracture and
the seventh and eighth thoracic spine fractures (Fig. 3A and B). Magnet-
ic resonance imaging examination was performed on seventh day after
admission, which also revealed the seventh and eighth thoracic
compression fractures with edema surrounding thoracic and lumbar
spinal muscles (Fig. 3C and D). Although the patient finally survived to
discharge from the hospital 45 days after admission, he had an
irreversible spinal cord injury and double lower limbs paraplegia.
The present case report describes utilization of thrombolysis during
ongoing CPR in a patient with PE-induced cardiac arrest and has been
shown that continuous mechanical chest compression simultaneous
thrombolytic therapy could be effective treatment in the setting of
cardiovascular collapse secondary to acute PE.
Pulmonary embolism is a life-threatening condition, and cardiac arrest
is the most serious clinical circumstance. Hemodynamic collapse from PE
is due to suddenly increased pulmonary vascular resistance leading to di-
minished stroke volume and cardiac output. Multiple large thrombi are
generally responsible for the circulatory collapse. In this case, the patient
presented with dyspnea and syncope. Echocardiography showed right
heart enlargement, severe tricuspid regurgitation, and pulmonary artery
hypertension. Laboratory tests, such as the peripheral saturation of
681.e4 Z.-P. Zhang et al. / American Journal of Emergency Medicine 34 (2016) 681.e3–681.e5
Fig. 1. The patient had cardiac arrest in the cardiac care unit. A, The ECG monitor showing pulseless electrical activity. B, Continuous mechanical chest compression and thormbolytic
therapy were performed during continuous mechanical chest compression with LUCAS.
oxygen and PaO2, were significantly decreased, whereas the D-dimer
levels were elevated. According to the clinical symptoms, signs, and aux-
iliary examination, the patient was highly suspected of acute PE.
Hemodynamically unstable PE, such as persistent hypotension or
shock, is the only widely accepted indication for systemic thrombolysis,
with a class 1 level of evidence A [3,4]. However, there are insufficient
data to support for the routine use of thrombolytic therapy during car-
diac arrest caused by PE. Recently, case reports and series have reported
some success from systemic thrombolytic therapy during CPR when the
cardiac arrest is due to suspected or confirmed acute PE [5]. Kürkciyan
et al [6] reported a 5% incidence of PE in 1246 cardiac arrest victims,
and subgroup analysis suggested that thrombolysis was associated
with a greater rate of return of spontaneous circulation compared
with those who did not receive thrombolysis. Yin et al [7] reported ad-
ministration of thrombolytic therapy after initially unsuccessful CPR in 7
patients with presumed PE. Of these patients,5 achieved return of
spontaneous circulation after CPR and thrombolytic therapy, and 3
were discharged alive through successive treatments. Because more
than 70% of nontraumatic cardiac arrest is due to massive PE and
acute myocardial infarction, empirical utilization of thrombolysis in
the setting has also been shown to improve the return of spontaneous
circulation and neurologic outcome [7-9].
As a potentially lifesaving maneuver, systemic thrombolysis seems
to be effective for PE-induced cardiac arrest. However, thrombolysis
under ongoing CPR is associated with increased the risk of lethal bleed-
ing complications [10]. Recently, percutaneous catheter-directed treat-
ment is investigational, and thrombolytic agents can be infused
directly into the pulmonary artery via a pulmonary arterial catheter
[11].The potential advantage of catheter-directed thrombolysis is that
lower doses of thrombolytic agent can be administered, thereby reduc-
ing the risk of bleeding when compared with systemic therapy [12].
Fig. 2. Multidetector computed tomography pulmonary angiography showing PE with a large thrombus burden in the main segmental branches. Left pulmonary artery segmental
thrombus was more than right pulmonary artery (arrows).
However, percutaneous interventional treatment in the setting of
cardiac arrest requiring continuous chest compression could be a
challenge, and it is inevitably delayed thrombolysis treatment.
In our case, the patient had a witnessed cardiac arrest in the cardiac
care unit and had been diagnosed with acute PE before this episode of
cardiac arrest. Therefore, when he presented with a hemodynamic
collapse, continuous mechanical chest compression and thrombolytic
therapy were simultaneously performed immediately. Approximately
46 minutes after CPR, return of spontaneous circulation was achieved.
Although the patient was discharged alive, unfortunately, prolonged
CPR and chest compression–induced traumatic injury had caused the
irreversible spinal cord injury and lower limbs paraplegia.
Zhi-Ping Zhang, MD
Xi Su, MD
Cheng-Wei Liu, MD
Dan Song, MD
Jian Peng, MD
Ming-Xiang Wu, MD
Yu-Chun Yang, MD
Bo Liu, MD
Cheng-Yi Xu, MD
Fang Wang, MD
Cardiac Care Unit, Wuhan Asia Heart Hospital, Wuhan 430022, China
⁎ Corresponding author.
E-mail: whyxnk@hotmail.com
http://dx.doi.org/10.1016/j.ajem.2015.06.062
 Z.-P. Zhang et al. / American Journal of Emergency Medicine 34 (2016) 681.e3–681.e5 681.e5

B C D

Fig. 3. A and B, Computed tomography showing a sternal body fracture and the seventh and eighth thoracic fractures (arrows). C and D, Magnetic resonance imaging also revealing the
seventh and eighth thoracic compression fractures with edema surrounding thoracic and lumbar spinal muscles (arrows). The patient had an irreversible spinal cord injury due to prolong
CPR.

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