A Lethal Pulmonary Embolism During Percutaneous Vertebroplasty

Abstract

Percutaneous vertebroplasty is a therapeutic, interventional radiologic procedure that involves injection of bone cement into a vertebral body lesion for the relief of pain and the strengthening of bone. This procedure is used in the treatment for osteolytic lesions caused by bone metastases, aggressive hemangioma, multiple myeloma, and for patients who have medically intractable debilitating pain resulting from osteoporotic compression fractures. Complications are infrequent and consist of bleeding at the puncture site, local infection, cement leakage into the spinal canal, the paravertebral tissues, or the perivertebral venous system, and several instances of pulmonary embolism (1–3). The following report describes a case of lethal pulmonary embolism caused by bone cement injection during percutaneous vertebroplasty. Case Report A 75-yr-old woman suffering from persistent, severe low back pain because of osteoporosis with compression fractures of T12, L2, and L4 was admitted for L2 and L4 percutaneous vertebroplasty. She had a history of hypertension treated with antihypertensive drugs, and the electrocardiogram (ECG) revealed a slight inverted T wave in the V2–5 leads. The echocardiogram showed no evidence of myocardial ischemia or infarction, but minor diastolic dysfunction and pulmonary hypertension with a mean pulmonary artery pressure of 46 mm Hg were noted. All laboratory data were within normal limits. Before anesthesia, her baseline blood pressure (BP) was 130/80 mm Hg, heart rate was 67 bpm, and her respiratory rate was 18 breaths/min. General anesthesia was induced with IV fentanyl 100 μg, atracurium 5 mg, thiopental 200 mg, and lidocaine 70 mg. Tracheal intubation was facilitated with IV succinylcholine 70 mg. Anesthesia was maintained with desflurane in oxygen (300 mL/min) via a closed-circuit system, with the end-tidal desflurane concentration being maintained at approximately 6.0% ± 0.5%. Atracurium was used for muscle relaxation. Standard monitoring during the operation included pulse oximetry, ECG, direct radial arterial BP, body temperature, and capnography. After the induction of anesthesia, the patient was placed in the prone position, and percutaneous vertebroplasty (L2 and L4) was performed by the bilateral transpedicular approach with 2 10-gauge needles in each vertebral body. Methylmethacrylate cement was prepared at room temperature (20°C) and opacified with 1 g of tungsten powder, and 6 mL was then injected under lateral fluoroscopic guidance into each vertebral body. Multiple vertebral punctures and injections of several batches of cement were performed at the L4 vertebra. During the operation, the patient’s vital signs were stable. At the time of skin closure, sudden onset of bradycardia (heart rate = 36 bpm), hypotension (BP = 64/30mm Hg), desaturation (Spo2 = 70%), and hypocapnia (end-tidal CO2 = 8 mm Hg) were observed. The patient was turned from the prone to the supine position, and resuscitation was started immediately. Despite cardiac massage and several epinephrine injections (total, 10 mg IV), the ECG revealed pulseless electrical activity, and no arterial or end-tidal CO2 waveforms were obtained. One hour later, resuscitation was discontinued. A transesophageal echocardiogram (TEE) was performed immediately after the pulseless electrical activity was noted, and the four-chambers view showed that the right atrium and ventricle were almost completely filled with multiple small deposits of diffusely echogenic material (Fig. 1). Subsequently, a decrease in hemoglobin levels (from 13.2 mg/dL before operation to 9.2 mg/dL after resuscitation), thrombocytopenia (from 392,000 to 89,000/mm3), gross hematuria (occult blood = +++), and proteinuria (protein = +++) were found. However, negative findings for cardiac isoenzymes (creatine kinase = 134 U/L, creatine kinase-MB = 8.4 U/L, and troponin C = 0.11 ng/mL) excluded myocardial infarction.Figure 1: Four-chamber transesophageal echocardiographic (TEE) view showing multiple small deposits of diffusely echogenic material completely filling the right atrium and right ventricle (RV).Discussion The lethal pulmonary embolism in our patient may have been caused by the bone cement implantation. Although percutaneous vertebroplasty is considered a minimally invasive procedure, it may result in the severe complication of bone cement implantation syndrome, as in our patient. This syndrome is characterized by systemic hypotension, pulmonary hypertension, and oxygen desaturation at the time of applying the cement and prosthesis (4), and it is thought to be caused by pulmonary fat emboli, rather than by a toxic effect of methylmethacrylate (5–8). Bone cement may increase intramedullary pressure and thereby increase the volume of marrow contents forced into the venous circulation. During the operation, the contents of the bone cavity are pressurized, and contents, such as air, fat, and bone marrow, may enter the disrupted medullary vessels and embolize the pulmonary vasculature, resulting in increased pulmonary vascular resistance and hypoxemia and thus decreased cardiac output (9). In patients undergoing total hip replacement, most emboli occur during the reaming of the femur and insertion of the femoral prosthesis (10). In our patient, multiple vertebral punctures and the injection of several batches of cement (total, 6 mL) were attempted at the L4 vertebra. This may have increased the pressure of marrow contents causing extravasation of bone marrow debris and fat into the lumbar venous plexus. A significant showering of emboli was observed by TEE (Fig. 1), which resulted in complete right heart outlet obstruction and failure to observe end-tidal CO2 and arterial pressure waves during resuscitation. Clinical reports have suggested that bone cement implantation syndrome is caused by right ventricular (RV) failure secondary to increased pulmonary artery pressure, resulting in systemic hypotension and sudden cardiac arrest (11)1. Byrick (8) found important factors for cardiac arrest and death to be the degree of hemodynamic compromise and hypoxemia but not the amount of emboli formation. With an acute increase in pulmonary vascular resistance, the thin-walled, compliant RV rapidly dilates and shifts the interventricular septum to the left within the restricted pericardial cavity. These changes cause an immediate reduction in left ventricular compliance, left ventricular filling, and cardiac output. The coronary perfusion pressure is also decreased by the hypotension, and the right coronary flow is further decreased as the RV end-diastolic pressure is increased, resulting in myocardial ischemia. Minor unrecognized embolic events are common, and most patients tolerate this modest increase in RV afterload without any clinical consequence. Patients with a limited preoperative cardiopulmonary reserve because of preexisting pulmonary hypertension, RV dysfunction, or coronary artery disease, are susceptible to myocardial ischemia and infarction. In this report, the age of the patient together with severe osteoporosis, preexisting pulmonary hypertension, diastolic dysfunction, and the injection of several batches of cement made her a high risk for fatal pulmonary fat embolism. The bone cement implantation syndrome is a time-limited phenomenon (8). In human and animal studies, Byrick et al. (12,13) found that the pulmonary artery pressure may normalize within 24 hours. In healthy patients, the hemodynamic instability can recover within seconds to minutes, even from large embolic loads. Early and aggressive hemodynamic support is crucial for survival. Acute pulmonary hypertension and secondary RV failure are reversible. Treatment can result in the survival of even elderly and critically ill patients. This case report illustrates a fulminant form of pulmonary embolization caused by bone cement implantation. Autopsy was not performed in this case. But the presence of sudden desaturation, abruptly decreased end-tidal CO2, bradycardia, hypotension, the rapid development of anemia and thrombocytopenia, and the significant emboli observed on TEE are diagnostic of this condition. Surgical precautions, anesthetic monitoring, and intraoperative TEE are paramount in the avoidance, minimization, and early recognition of severe fat emboli formation during bone cement application, especially in high-risk patients.