A 67-year-old male presented with severe mid-back pain of 3 months duration after a minor fall. His past medical history included well-controlled diabetes mellitus and hypertension, and his only medications were oral antihypertensive and antihyperglycemic drugs. He was treated conservatively with acetaminophen, ibuprofen, and hydrocodone for 3 months but with continued pain. On examination, he was acutely tender over the upper lumbar and lower thoracic vertebral spinous processes, and his neurological examination was grossly intact. A plain roentgenograph of his thoracic and lumbar spine showed L1 vertebral body compression fracture. Magnetic resonance imaging (MRI) of his thoracic and lumbar spine showed edema of the L1 vertebral body on short T1 inversion recovery (STIR) images, confirming the acute nature of the fracture, and there was absence of any retropulsed bone fragments. Due to the intense and persistent pain unrelieved with conservative measure and MR images confirming acute vertebral body fracture conducive to augmentation, decision was made to proceed with L1 vertebroplasty (VP).

The procedure was performed under monitored anesthesia care (MAC) in the pain medicine department procedure room. Transpedicular approach for VP using biplanar fluoroscopy was employed. After placing bipedicular trocars and confirming their adequate positioning on anteroposterior and lateral fluoroscopic images, a total of 4 cc of PMMA was injected with ease under live fluoroscopy. No venous, discal, or epidural extravasation of the cement was observed during the injection, and the patient remained hemodynamically stable throughout the procedure. After completion of the procedure, the MAC anesthesia was concluded, and the patient was transferred to the recovery area. Upon arrival in the recovery room, the patient complained of shortness of breath and chest tightness. He was tachycardic and tachypneic and his neurological examination was grossly intact. The patient was given supplemental oxygen and an urgent EKG was obtained. The latter showed ST segment depression and T wave inversion in precordial leads V1 to V3 and in leads II, III, and AVF. Due to the continued shortness of breath, unrelenting chest pain, tachycardia, tachypnea, and EKG pattern suggestive of right heart strain, a preliminary diagnosis of pulmonary cement embolism (PCE) was rendered, and the patient was transferred to the cardiovascular intensive care unit (CV-ICU). In CV-ICU, the laboratory studies showed elevated serum troponin and creatine kinase (CK), and a chest computed tomographic (CT) scan with contrast enhancement and three-dimensional image reconstruction showed PMMA in both major pulmonary arterial trunks. After a failed attempt at minimally invasive embolectomy by interventional radiology, pulmonary embolectomy using cardiopulmonary bypass was performed, and a PMMA embolus straddling bifurcation of the main pulmonary artery was extracted. Patient’s postoperative recovery was uneventful, and he was discharged home a week after the surgery.

VP and KP are routinely performed minimally invasive techniques for a variety of pathological or osteoporotic vertebral body compression fractures. The use of these procedures is widespread due likely to their minimally invasive nature, ease of performance, and a well-reputed efficacy. Even though the stated risk of VP and KP is minimal, a number of serious complications have been reported. These include pedicular fractures, segmental nerve and spinal cord injury, spinal canal and intra-discal extravasation of the bone cement, infection, and vascular PMMA uptake. Of the various complications cited, vascular PMMA uptake appears to be the most common. PMMA extravasation occurs into the perivertebral and azygos veins and can extend to the inferior vena cava (IVC) and ultimately into the pulmonary veins [1, 2]. A number of procedure-related factors may contribute to vascular PMMA uptake and include (1) injection of large cement volume, (2) PMMA injection under significant pressure, and (3) relatively liquescent cement injection. Host factors also may contribute to greater PMMA vascular uptake and include greater vertebral body vascularity such as from invasive vascular tumors and the presence of osteoporosis. The ensuing cement embolic phenomenon includes IVC thrombosis [3], cardiac tamponade from cement penetration of the right ventricle, renal artery cerebral and other peripheral arterial embolism, and PCE. Among the various cement embolic phenomena, PCE appears to be the most common. The majority of reported cases of PCE are asymptomatic. Two studies of routine imaging—plain X-rays and CT—after vertebroplasty showed PMMA in pulmonary vasculature in 3.5–23% of the patients, respectively [4, 5]. Symptoms of PCE range from mild to life-threatening and may occur days to weeks after the procedure [6].