Emergency (****); * (*): *-*
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46 Emergency (2014); 2 (1): 46-47
CASE REPORT
Atypical Presentation of Massive Pulmonary Embolism, a Case Report
Alireza Majidi1, Sadrollah Mahmoodi2, Alireza Baratloo1, Sahar Mirbaha1*
1. Department of Emergency Medicine, Shohadaye Tajrish Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
2. Department of Emergency Medicine, Baghiatollah Hospital, Imam Hossein University, Tehran, Iran
Abstract
The lack of pathognomonic signs and symptoms makes the diagnosis of pulmonary embolism (PE) difficult. Here,
we report a case of a 42-year-old man presented to the emergency department with worsening epigastric pain,
hypotension, frank bradycardia, and final diagnosis of PE. Although previous studies have indicated that ab-
dominal pain was observed in 6.7% of patients with PE, the exact reason for abdominal pain in PE still remains
unknown. Tension on the sensory nerve endings, hepatic congestion, and distention of Gilson’s capsule are some
of the possible mechanisms of abdominal pain in PE. We conclude that emergency physicians should pay more
attention to PE, which is an important differential diagnosis of shock state. In this context, rapid ultrasound in
shock (RUSH) should be considered as a vital sign that needs to be evaluated when recording the history of pa-
tients presented to the emergency department with signs and symptoms of shock.
Key words: Pulmonary embolism; ultrasonography; shock; abdominal pain; bradycardia
Cite this article as: Majidi A, Mahmoodi S, Baratloo A, Mirbaha S. Atypical presentation of massive pulmonary embolism, a case
report. Emergency. 2014;2(1):46-7.
Introduction:1
he lack of pathognomonic signs and symptoms
makes the diagnosis of pulmonary embolism
(PE) difficult. A well-timed diagnosis and man-
agement of PE are necessary to decrease mortality. It
has been reported that, annually, 50,000–200,000
deaths occur as a result of PE, with a mortality rate of
30% without treatment (1). Postmortem studies have
revealed that up to 70% of PEs have been misdiag-
nosed. Moreover, 40% of the dying patients had visited
a clinician for ambiguous symptoms in the weeks prior
to their death (1, 2). This significant amount of misdi-
agnosis highlights the importance of reviewing the dif-
ferent possible presentations of this fatal medical condi-
tion. Here, we report a case of a patient presented to the
emergency department (ED) with worsening epigastric
pain, hypotension, frank bradycardia, and final diagno-
sis of PE.
Case report:
The patient was a 42 year-old man, admitted to the ED
with chief complaint of severe abdominal pain begun
from the morning. The pain was sensed prominently in
epigastric area with acceleration/deceleration pattern,
and also crusher/vague quality that increased after eat-
ing. The pain was not positional and had neither transi-
tion nor shifting. He had no significant past medical his-
tory or previous surgery. But should mention that was
*Corresponding Author: Sahar Mirbaha, Resident, Department of Emergency
Medicine, Shohadaye Tajrish Hospital, Tajrish square, Tehran, Iran. Postal code:
1989934148, Phone/Fax: 009822721155, Email: mirsa317@yahoo.com
Received: 1 December 2013; Accepted: 17 January 2014
addicted to methadone and was a heavy smoker (30
pack cigarettes per year) for many years. On admission
to ED, he was so agitated with 28/min respiratory rate,
68/min pulse rate, 85/65 mmHg blood pressure, 88%
oxygen saturation in room air, and 37°C axillary tem-
perature. Electrocardiogram (ECG) showed frank brad-
ycardia that not matches with other vital signs
(Figure1).
The patient was pale, had dry mucosa, presented
marked epigastric tenderness on deep palpation, and
had neither rebound tenderness nor guarding. The
pulses in the extremities were filiform, lung examina-
tion was normal, and there were multiple red rushes
(red macules) on the chest and extremity skin. Focused
assessment with sonography for trauma (FAST) re-
vealed mild, free fluid in Morison’s pouch. With the im-
pression of perforated hollow viscous organs, the
emergency surgical consultant performed an upright
chest X-ray (CXR) examination after primary resuscita-
tion, but noted no specific finding. This examination
was repeated after pushing 500 mL of air via nasogas-
tric (NG) tube, but no specific observation could be
found. Double contrast abdominal and pelvic spiral
computed tomography (CT) scan revealed intraperito-
neal infiltration with increased intestinal wall diameter
and ascites. The white blood cell count was
16200/mm3, arterial blood pH was 7.3, PCO2 was 18.6
mmHg, HCO3 was 11.2 mEq/L, and BE was −10.7. All
other laboratory data, including serum amylase and
lipase, urine analysis, hepatic and renal function tests,
and coagulation profile were normal. During admission
T
mailto:mirsa317@yahoo.com
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Majidi et al 47
to ED, the patient’s blood pressure was low and did not
get better with fluid therapy. Hence, rapid ultrasound in
shock (RUSH) examination was performed. RUSH exam-
ination showed weak heart ventricles contractibility,
right ventricular (RV) strain, and a clot in the apex of
RV; hence, pulmonary CT angiography of the chest was
immediately performed (Figure 2). Spiral pulmonary CT
angiography showed massive emboli in the distal right
pulmonary artery, hypodense clot in the right atrium
with increased diameter, and also a hypodense clot in
the RV apex. With the diagnosis of massive pulmonary
emboli, high dose of heparin was initiated and cardiac
surgery intervention was accomplished. The patient
was transferred to the intensive care unit (ICU), but
unfortunately died.
Discussion:
A well-timed diagnosis and management of PE are nec-
essary with the aim of decreasing mortality. Because of
the lack of pathognomonic signs or symptoms, the diag-
nosis of PE remains vague. The classic symptoms of
dyspnea, tachypnea, and decreased oxygen saturation
may occur in up to 92% of cases. However, because of
numerous atypical presentations, physicians must focus
on other clinical features to include or exclude them as
possible diagnosis. Although previous studies have
demonstrated that abdominal pain was observed in
6.7% of patients with PE (1, 3). The exact reason for
abdominal pain in PE still remains unknown. Tension
on sensory nerve endings, infarctions within the micro-
vasculature of the mesentery, hepatic congestion, dis-
tention of Gilson’s capsule, or diaphragmatic pleurisy
resulting from pulmonary infarction are some of the
possible reasons for abdominal pain in PE, which have
neither been proved nor refuted (1, 4). In contrast, syn-
cope and bradyarrhythmia may cause parasympathetic
reflex, because simultaneous slowing of the sinus rate
with concomitant arteriovenous block is a common
presentation of increased vagal tone. Such reflex may be
a mechanism for syncope in patients with PE (5). In ad-
dition, bradycardia is also a side effect of methadone
hydrochloride (6). Therefore, addiction to methadone,
pump failure owing to massive emboli, and activation of
vagal tone may explain the absence of tachycardia that
we expected in our case. Bedside ultrasound allows di-
rect visualization of pathology or abnormal physiologi-
cal states, and thus has become an essential and useful
component in the evaluation of hypotensive patients via
RUSH protocol, which was clearly the key point in the
diagnosis of our patient (7).
Conclusion:
PE is an important differential diagnosis of shock state,
and hence, emergency physicians should pay more at-
tention to it. In this context, RUSH should be considered
as one of the vital signs (such as blood pressure or tem-
perature), which needs to be evaluated when recording
the history of patients presented to ED with signs and
symptoms of shock.
Acknowledgments:
The authors would like to thank the emergency ward
staff for their invaluable help.
Conflict of interest:
None
Funding support:
None
Authors’ contributions:
All authors passed four criteria for authorship contribu-
tion based on recommendations of the International
Committee of Medical Journal Editors.
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Figure 1: Electrocardiogram of patient at the time of admis-
sion.
Figure 2: Pulmonary computed tomography angiography of
the patient.