Keywords
pulmonary embolism - prone position - cervical vertebral fusion - vertebral artery
insufficiency - posterior circulation brain infarction
Introduction
Pulmonary embolism (PE) is the third most prevalent cardiovascular condition following
myocardial infarction and stroke.[1] The outcome of a massive intraoperative PE is often fatal, and its diagnosis and
management, especially in the perioperative period, can be extremely challenging.[2] A high degree of clinical suspicion, presence of risk factors, thorough evaluation,
and point-of-care imaging are essential in diagnosing and managing PE. We present
a case of sudden cardiac arrest caused by a massive PE after turning a patient from
prone to supine following cervical spine surgery. The patient was later found to have
multiple embolic infarcts in the posterior circulation, affecting the occipital lobes
and cerebellar hemispheres.
Case Report
A 46-year-old male, American Society Anesthesiologist (ASA) physical class III with
hypertension and obesity (BMI 40 kg/m2), was admitted for cervical spine surgery due to progressive myelopathy secondary
to ossified posterior longitudinal ligament (C2–D3 vertebral levels). The patient
could walk with support and perform daily activities. The patient had obstructive
sleep apnea (OSA) with a STOP-BANG score of 5, and was advised to use continuous positive
airway pressure (CPAP) during the night. Preoperative assessments, including routine
blood investigations, 2D echocardiography, and pulmonary function tests were normal
with no history of deep vein thrombosis (DVT) or clotting disorders.
The patient underwent posterior decompression and fusion of the C2–D3 vertebrae with
motor evoked potential (MEP) monitoring. Anesthesia was induced, and the trachea was
intubated with an 8.0-mm flexometallic endotracheal tube. Anesthesia was maintained
with propofol (3–5 mg/kg/h) targeted to keep a bispectral index (BIS) of 45 to 55,
fentanyl (0.5 µg/kg/h), and dexmedetomidine (0.2–0.5 µg/kg/h) to facilitate MEP monitoring.
Intermittent pneumatic pumps were applied to both legs as per the institutional protocol.
During the 10-hours surgery, intraoperative vitals were stable except for reduced
urine output (total intraoperative urine output = 350 mL). Urine output did not improve
despite ruling out mechanical obstruction and administering fluid challenges and diuretics.
Blood loss was 1,200 mL, replaced with 2 units of packed red blood cells.
Due to OSA and prolonged prone surgery, elective postoperative ventilation was planned.
The patient was turned supine, and the flexometallic tube was exchanged for a polyvinyl
chloride endotracheal tube in one attempt. In next few minutes, the patient developed
nonspecific arrhythmias, followed by bradycardia, hypotension, and asystole.
Cardiopulmonary resuscitation (CPR) was initiated, and return of spontaneous circulation
was achieved after three cycles of CPR. A central line was placed, and inotropes (noradrenaline
and adrenaline) were started.
A cardiology consultation and focused cardiac ultrasound (FOCUS) revealed normal right
atrium (RA) and right ventricle (RV) size, hypercontractility of the left heart, and
no thrombus. The patient had the end-tidal CO2 (EtCO2) of 20 to 24 mm Hg, while ABG revealed a pH of 6.86, PaCO2 of 85.4 mm Hg, PaO2 of 124 mm Hg, lactate of 9.6 mmol/L, and HCO3
− of 9.7 mmol/L. The patient was transferred to the intensive care unit (ICU). Despite
improvement in oxygen saturation and blood pressure, his EtCO2 remained low (∼18–24 mm Hg). In the ICU, PaCO2 increased to even higher values of approximately 110 to 120 mm Hg, while EtCO2 remained in the range of 18 to 24 mm Hg. A persistently high PaCO2–EtCO2 gradient (∼90 mm Hg) raised a strong suspicion for PE.
A repeat FOCUS in the ICU showed dilated RA/RV and paradoxical septal motion, suggesting
PE. A computed tomography pulmonary angiogram (CTPA) confirmed a saddle embolism in
the main pulmonary artery extending into the right and left pulmonary arteries ([Fig. 1]). The risk-to-benefit ratio of administering unfractionated heparin was discussed
with the surgical team. Given the life-threatening nature of the condition, intravenous
unfractionated heparin 5,000 IU was administered, followed by embolectomy in the interventional
suite (∼6 h later).
Fig. 1 CT pulmonary angiogram showing massive thromboembolism.
Postembolectomy, the patient's urine output improved, and hemodynamics stabilized.
However, the patient's consciousness remained impaired (Glasgow coma scale [GCS] of
E1VTM1) with sluggish reaction in bilateral pupils. Brain MRI revealed multiple embolic
infarcts in the occipital and cerebellar hemispheres (left > right), as well as left
vertebral artery thrombosis ([Fig. 2]). Doppler ultrasound of the lower limbs showed no evidence of DVT.
Fig. 2 MRI of the brain showing multiple areas of embolic infarcts (Yellow arrows indicate
infarct on right and left cerebellar hemispheres).
The patient remained in the ICU for 10 days, during which his GCS improved to E4VTM3
(tracheostomy). After 40 days, the patient was discharged with a GCS of E4VTM3 on
oral anticoagulant. At present (6 months after surgery), the patient has improved
to E4VTM6 with 2/5 power in all four limbs.
Discussion
This case underscores the diagnostic challenges of massive PE during cervical spine
surgery in the prone position, with risk factors including obesity, OSA, reduced mobility,
prolonged prone positioning, and blood transfusion.
Obesity is associated with venous stasis, chronic inflammation, and hypercoagulability,
increasing PE risk.[3] OSA predisposes patients to higher risk of DVT and PE (3.50- to 3.97-fold higher).[4] Blood transfusion can disrupt coagulation, enhance inflammatory cascades, and alter
red cell properties, further increasing thrombotic risk.[5]
The prone position exacerbates venous stasis by hindering lower extremity venous return
and compressing iliac vessels, promoting thrombus formation.[6] We hypothesize that the clot formed in this position and migrated upon supine repositioning
as vessel compression was relieved.
Diagnosing PE intraoperatively or immediate in postoperative period is particularly
challenging due to overlapping clinical features with other conditions, such as myocardial
infarction or hypovolemia. In this case, the sudden bradycardia, hypotension, and
asystole after repositioning suggested a cardiovascular event.
Despite hemodynamic stabilization, the patient developed significant neurological
complications, with brain MRI showing embolic infarcts in the occipital and cerebellar
hemispheres. A thrombus located in the V4 segment of the left vertebral artery can
contribute to quadriparesis due to lateral cord infarction (involving the posterior
inferior cerebellar artery).[7] Vertebral artery injuries (0.8–1.4%) are rare but recognized complications of cervical
spine surgery, especially during vertebral drilling and instrumentation.[7] These injuries can lead to arterial rupture, dissection, pseudoaneurysm, or thrombosis,
resulting in bleeding, hypotension, or posterior circulation infarction.[8]
This case highlights the critical need for thorough preoperative risk assessment,
prehabilitation (such as weight reduction and CPAP therapy),[9] and early thromboprophylaxis in high-risk patients. Strategies like minimizing operative
time, staging procedures, and optimizing positioning to minimize venous stasis can
reduce thrombotic risk. Vigilant perioperative monitoring, along with prompt point-of-care
imaging, ensures early detection and management of complications. Additionally, vertebral
artery injury led to adverse neurological outcomes, highlighting the importance of
vigilant monitoring, meticulous surgical technique, and prompt intervention to improve
patient outcomes.
