J Anesth
DOI 10.1007/s00540-017-2396-1

CLINICAL REPORT

Pre‑eclampsia and acute pulmonary embolism—the importance
of making a differential diagnosis: a case report
R. Suthar1 · S. Abdelfattah1 · H. Goldman1 · G. Garcia1 · D. Romero‑Fischmann1 ·
M. Escobar2 · V. Behrens1

Received: 9 March 2017 / Accepted: 26 July 2017
© Japanese Society of Anesthesiologists 2017

Abstract We describe the case of a 41-year-old pregnant
patient who presented at 38 weeks of gestation for an urgent
cesarean section, with new onset of pre-eclampsia as the
initial diagnosis. The intraoperative course was complicated
by seizures and hemodynamic collapse. Initially, the presentation of seizure pointed to pre-eclampsia/eclampsia; however, with careful consideration of each event as it occurred,
the correct diagnosis was later determined to be pulmonary
embolism and stroke. This case illustrates the importance of
considering multiple possible etiologies, even when a particular diagnosis seems obvious.
Keywords Pre-eclampsia · Pulmonary embolism ·
Stroke
* R. Suthar
rekhasutharmd@gmail.com
S. Abdelfattah
Sarah.r.abdelfattah@gmail.com
H. Goldman
howardg264@aol.com
G. Garcia
bgarcia28@aol.com

Introduction
Pre-eclampsia is the third leading cause of peripartum
maternal morbidity and mortality in the USA [1]. It is a
multi-organ disease process that occurs in up to 5–8% of
pregnancies after 20 weeks gestation [2], and it has a broad
spectrum of associated signs and symptoms. The clinical dilemma is that there are a plethora of conditions with
similar presentations. Patients presenting with seizure and
a known history of pre-eclampsia still require a differential
diagnosis, especially if other complications occur, such as
hemodynamic collapse. As perioperative physicians, anesthesiologists need to take a leading role and develop preoperative, intraoperative, and postoperative treatment plans,
keeping an open mind to all applicable differential diagnoses. Our case presentation will outline the sequence of
events, laboratory work, and imaging that led to the correct
diagnosis and treatment.
Consent for publication
Written consent for publication was obtained from the
patient.

D. Romero‑Fischmann
Darofi72@gmail.com

Case description

M. Escobar
Mauricioe@sanjuanbautista.edu

A 41-year-old female, 38 weeks of gestation (gravida 2,
para 1), with a past medical history of migraines and anemia, presented to her obstetrician’s office complaining of a
headache. She was found to be hypertensive [blood pressure
(BP): 167/83 mmHg] and subsequently was booked for an
urgent cesarean section with the diagnosis of pre-eclampsia .
As there were no contraindications to neuraxial anesthesia,
we decided to perform a spinal anesthetic. Standard ASA
monitors were used throughout the procedure. Vitals signs

V. Behrens
vbehrens@fiu.edu
1

Department of Anesthesiology, Mount Sinai Medical Center,
Miami Beach Anesthesiology Associates, Inc., 4300 Alton
Road, Miami Beach, FL 33140, USA

2

San Juan Bautista School of Medicine, San Juan,
Puerto Rico

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before the spinal anesthesia were: BP 140/79 mmHg, heart
rate 78 bpm, oxygen saturation 99% on room air. The L4–L5
interspace was identified and, using a midline approach with
the patient in sitting position, a 25-gauge 10-cm Whitacre
needle was advanced until clear free flow of cerebrospinal
fluid was seen. Hyperbaric bupivacaine 0.75% (10.5 mg), 15
µg of fentanyl and 0.3 mg of morphine were injected into
the subarachnoid space. After obtaining and confirming an
adequate anesthetic level up to T4, the patient underwent a
cesarean section.
Immediately after successful delivery of the baby, the
patient suddenly developed a tonic–clonic seizure, requiring immediate intubation for airway protection and ventilation. Concomitantly, the patient developed unstable ventricular tachycardia (up to 160 bpm) demanding initiation
of Advanced Cardiovascular Life Support (ACLS) protocol,
including shock, chest compressions and epinephrine. A
left radial arterial line and a right femoral central line were
placed. An infusion of magnesium sulfate ­(MgSO4) was
also started. She subsequently went into pulseless electrical
activity for 1 min, which was treated with chest compressions and epinephrine before sinus rhythm and normal blood
pressure were re-established. The patient was transferred to
the intensive care unit (ICU).
In the ICU, the patient responded well to resuscitation
efforts, which included crystalloids, colloids, and vasopressors. Empiric antibiotics were started for possible sepsis.

Cardiac workup showed elevated serum troponin I level
(6.6 ng/ml). The electrocardiogram (EKG) showed a right
bundle branch block (RBBB) and right ventricular strain pattern, without ST elevations (Fig. 1). Two-dimensional transthoracic echocardiogram (TTE) revealed a mild increase in
right ventricle size, normal ejection fraction 65–70%, and a
small thin thrombus attached to the ventricular side of the
tricuspid valve. Lower extremity ultrasound was negative
for any deep venous thrombosis. This could be due to complete dislodgement of thrombus because of the sequential
compression device for mechanical deep vein thrombosis
prophylaxis which was used intraoperatively, or false-negative venous duplex. The patient was started on intravenous
heparin, and a computed tomography angiogram (CTA) of
the chest was obtained. The CTA report described a saddle
pulmonary embolus, with extensive bilateral emboli extending throughout the left and right main pulmonary arteries
into lobar and proximal segmental branches (Fig. 2a–d).
There were also signs of right heart strain and bulging of
the fossa ovalis into the left atrium.
Interventional radiology administered an intrapulmonary artery thrombolytic (Alteplase) infusion. Because of
the patient’s extreme agitation and difficulty in appropriately comprehending verbal commands, we began to suspect cerebrovascular pathology. CT scan of the brain confirmed our suspicions, which revealed a 1.7-cm left middle
cerebral artery territory infarct. No thrombus was found in

Fig. 1  EKG showing sinus tachycardia and RBBB-prolonged QRS in right-sided and septal leads

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Fig. 2  Computed tomographic angiogram of the chest: a saddle embolism, b emboli extending to lobar arteries, c right ventricle strain, right
ventricle measuring 47.18 mm, d left ventricle measuring 30.33 mm

the inferior vena cava (IVC) and an IVC filter was inserted.
Finally, transesophageal echocardiography (TEE) showed
a small patent foramen ovale (PFO), which may have been
the risk factor which caused the cerebrovascular accident
(CVA). Hypercoagulability (Factor V Leiden mutation,
lupus anticoagulant, protein C and S activity, prothrombinII mutation) workup was negative. Over the next 2 weeks,
the patient’s status improved with aggressive critical and
rehabilitation care. She was discharged home without any
residual defects on postoperative day 32.

Discussion
In clinical practice, the classic textbook presentations of preeclampsia (hypertension, with concomittant proteinuria or
headache/visual disturbance/right upper quadrant pain, etc.)
are not always the case. Multiple clinical conditions share
similar symptoms, often making it hard to form a single
conclusion, which demands a multidisciplinary approach to
the care of critically ill patients.

Pre-eclampsia is a leading cause of peripartum morbidity and mortality due to intracranial hemorrhage, cerebral
infarction, acute pulmonary edema, respiratory failure,
hepatic failure and rupture, etc. [2, 3]. The underlying
lesion is uteroplacental insufficiency and systemic disruption of the endothelium [2]. Early recognition and intervention are essential to prevent the development of eclampsia. In our patient, the diagnosis of pre-eclampsia was
made using The American College of Obstetricians and
Gynecologists (ACOG) criteria 2013 with systolic blood
pressure ≥160 mmHg associated with headaches, a form
of cerebral disturbance [3]. However, it was the subsequent
clinical course that led to the discovery of entities other than
eclampsia.
All complications, no matter how straightforward,
deserve some thought to the differential diagnosis. For
example, the presentation of seizures in our patient
“labeled” her as eclamptic and led us to focus on the management of that entity. Although eclampsia is one of the
most frequent causes of seizures during pregnancy, other
causes of seizures must be excluded. In non-epileptic

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pregnant patients, causes of seizures include structural
and metabolic changes. Structural causes include CVA
(intracranial hemorrhage or infarction) and eclampsia.
Metabolic causes include but are not limited to hyperemesis
gravidarum, acute hepatitis, metabolic diseases or infection [4]. There was a cascade of different events suggesting
the possibilities of other diagnoses beyond pre-eclampsia/
eclampsia. Seizure was followed by hemodynamic collapse
which was managed by ACLS protocol. The patient’s intraoperative arterial blood gas showed respiratory acidosis (pH
7.21 and ­PCO2 83 mmHg, ­PO2 337 mmHg), which was
attributed to her seizure.
In retrospect, because the patient was adequately
mechanically ventilated, her hypercarbia deserved other
explanations. Her respiratory acidosis was most likely due
to the increased dead space associated with pulmonary
embolism. Similarly, her seizure was probably due to the
acute left frontal lobe infarction which was diagnosed on
post-operative day one. Indeed, the TEE finding of a PFO
was more than an incidental discovery: the small rightto-left shunt could have allowed microthrombi to cause
the CVA. Studies have shown an association between PFO
and cerebral embolism [5, 6]. An anatomically patent, nonfunctioning foramen ovale occurs in 5–10% of the general population, and in patients with cerebral infarction,
fifty percent have a PFO [7]. Pregnancy itself is associated
with hypercoagulability, a fivefold increased risk of venous
thromboembolism, and a 13-fold higher risk of stroke as
compared to non-pregnant women [8]. The hypercoagulable state is ascribed to several physiological alterations of
pregnancy, including changes in the hemostatic system,
mechanical obstruction by an enlarged uterus, hormonally
induced venous stasis, and vascular injury to pelvic vessels
during delivery [9].
Other cases have been reported in which seizures associated with pregnancy were initially misdiagnosed and
treated as eclamptic seizures. Farzi et al. [10] presented
a case of a 21-year-old primigravida with tonic–clonic
seizures several hours after undergoing an emergency
cesarean section. Brain magnetic resonance imaging
(MRI) later showed obstruction of the cerebral venous
plexus, confirming the diagnosis of cerebral venous sinus
thrombosis, probably due to the hypercoagulable state in
pregnancy. Aoki et al. [11] reported a 34-year-old patient
in her 35th week of gestation who presented to the hospital with tonic–clonic seizures. Although hematological exams, a urine protein exam, and an elevated blood
pressure of 170/90 mmHg all suggested eclamptic seizures, MRI scans revealed cerebral infarction and cerebral
edema, later found to be complicated by central nervous
system lupus.

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Conclusion
Physicians can become fixated on one diagnostic entity and
attribute all subsequent events to it. This case emphasizes
the importance of careful preoperative assessment and risk
stratification for each and every possible complication of a
particular clinical condition. Most importantly, a broad differential diagnosis is needed when faced with symptoms or
signs that do not fit the etiology that seems obvious. Modern
anesthesiologists should assume the role of a perioperative
physician, which includes the preoperative as well as the
postoperative period. The goal is to improve patient safety
and overall outcome and reduce perioperative morbidity and
mortality.
Author contribution statement Case review: RS, Vicente Behrens.
Literature review: RS. Manuscript preparation: RS, SA, VB, HG, ME,
GG, DR-F
Compliance with ethical standards
Source of funding

None.

Conflict of interest
conflict of interest.

All authors declared that they have no potential

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