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Departments of *Anesthesiology and
Orthopedic Surgery, University Hospital of Bern, Switzerland; and
Institute for Legal Medicine and
Department of Intensive Care Medicine, University of Bern, Switzerland
Address correspondence to Kay Stricker, MD, DEAA, Department of Anesthesiology, University Hospital, CH-3010 Bern, Switzerland. Address e-mail to Kay.Stricker{at}insel.ch Reprints will not be available from the authors.
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Abstract |
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IMPLICATIONS: Osteoporotic spine fractures are increasingly treated by injection of bone cement into the vertebral body. Polymethylmethacrylate embolism is a rare but potentially fatal complication. We report on a case of polymethylmethacrylate embolism that was at first unrecognized because of uncharacteristic signs and symptoms.
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Introduction |
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Case Report |
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On arrival in the operating room, the patient, who had not received any premedication, was monitored and turned to the prone position. During the entire 55-min procedure, she was given oxygen 6 L/min and repeated IV doses of alfentanil (250 µg). During insertion of the injection needles, arterial blood pressure was approximately 140/50 mm Hg, heart rate was 75–90 bpm, respiratory rate was 12 to 16 breaths/min, oxygen saturation was 100%, and the patient was arousable and responsive. PMMA injection was started approximately 30 min after the beginning of surgery. During the last injection of PMMA (all performed under continuous lateral fluoroscopic control), the patient became restless and moaned but remained responsive, and the anesthesiologist observed increased spontaneous respiration. This was interpreted as pain and was treated with another 250 µg of alfentanil. A gradual decrease of transcutaneous oxygen saturation to 92% and an arterial blood pressure increase to 160/65 mm Hg were observed. After termination of the PMMA injection, the patient was no longer responsive to verbal and painful stimuli; the respiratory rate was approximately 12 breaths/min, and transcutaneous oxygen saturation was still 92%. Loss of consciousness was related to alfentanil, and because the procedure was shortly before completion, it was decided to await skin closure before turning the patient to the supine position. Besides sinus tachycardia, there were no electrocardiographic changes at this time. Another 10 min later, she was turned to the supine position, and arterial blood pressure further increased to 190/90 mm Hg and heart rate to 120 bpm, whereas oxygen saturation further decreased to 80%. Assisted bag/mask ventilation was started to support spontaneous ventilation, which was approximately 7 L/min as measured with the breathing circuit and a tight-fitting face mask; this was higher than the expected minute ventilation for a patient of this weight (3.5–5 L/min). After 20 min of assisted mask ventilation with 100% oxygen (approximately 10 L/min), the patient remained unresponsive, and an arterial blood gas analysis showed a pH of 7.11, a PaO2 of 71 mm Hg, a PaCO2 of 96 mm Hg, a base excess of -3.9 mEq/L, and a bicarbonate level of 28.2 mmol/L. Although the total dose of alfentanil administered during the procedure was only 1.5 mg and although the respiratory rate and pattern were not typical for opioid-induced respiratory depression, incremental IV doses of naloxone were administered (120 µg in total). This indeed increased assisted spontaneous ventilation to 12 L/min. However, neither hypercapnia nor level of consciousness improved, and the trachea was intubated after the administration of etomidate and atracurium. The change from assisted spontaneous ventilation to positive-pressure ventilation induced a decrease in systolic arterial blood pressure from 150 to 70 mm Hg, and distended neck veins were recognized. With repeated IV boluses of noradrenaline (5–10 µg each) and adrenaline (10 and 100 µg), hemodynamic variables improved. During hypotension, an ST segment depression was noted.
A transthoracic echocardiogram demonstrated a massively dilated right ventricle. A high-resolution computed tomographic (CT) scan performed 6 h later revealed several pieces of high-contrast material (PMMA) in the pulmonary arteries of the right upper, middle, and lower lobes. At the same time, a string of PMMA could be seen that reached from the fourth lumbar vertebra to the inferior vena cava at the level of the left renal vein. During the CT scan, the patient developed pulseless electrical activity but could be successfully resuscitated within 10 min. Cardiopulmonary variables normalized within 48 h; however, the patient did not regain consciousness over the following 9 days. Several bilateral occipitotemporal infarctions were found on a cranial CT scan. Therefore, therapy was withdrawn, and the patient died within a few hours thereafter. At autopsy, the findings of the thoracoabdominal CT scan were confirmed; PMMA strings were found in the right pulmonary artery (Fig. 1), and a PMMA string exited the lumbar venous plexus and continued through the inferior vena cava (Fig. 2).
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Discussion |
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The main cause of hypercapnia was a massive increase in dead space ventilation. An increase of pulmonary arterial pressure may have led to the recruitment of previously nonperfused pulmonary vessels and thebesian veins, resulting in shunting of blood and hypoxemia. Opioid-induced hypoventilation, in contrast, had little effect, because spontaneous minute ventilation was 7 L/min and mechanical ventilation did not improve hypercapnia. Lung function and blood gas analysis at rest were not evaluated before surgery in this patient with severe chronic obstructive pulmonary disease; thus, preexisting hypercapnia cannot be differentiated from changes due to the embolism.
Current medical textbooks typically relate decreases in end-tidal CO2 during pulmonary embolism to a decrease in cardiac output and an increase of physiologic dead space (9,10). A decrease in arterial PCO2 may also occur due to hyperventilation caused by hypoxic ventilatory drive or stimulation of airway irritant receptors (10). However, not only hypocapnia, but also hypercapnia, has previously been described in clinical and experimental cases of overwhelming pulmonary thromboembolism (11,12). Detection of hypercapnia was delayed in this case, because hypertension and loss of consciousness were the only signs of embolism, whereas respiratory distress may have been attenuated by the opioids. An insufficient increase in end-tidal CO2 has been noted even after prolonged periods of severe pulmonary embolism (12). Thus, monitoring of end-expiratory CO2 with a nasal cannula would not have shortened this delay.
Clinical cases of massive pulmonary embolism with hypercarbia were associated with severe hemodynamic instability (11). However, hypertension was noted initially in our patient. Cardiac output was not measured during the procedure; however, it must have decreased after this major embolism. Thus, arterial hypertension can be explained only by a massive increase in systemic vascular resistance, possibly because of adrenergic stimulation caused by hypercapnia. After tracheal intubation and positive-pressure ventilation, venous return to the right ventricle may have decreased and pulmonary vascular resistance may have increased. Both decreased right ventricular preload and increased afterload have attenuated right heart function. Hemodynamic collapse occurred only six hours later in the CT suite, when progressive right heart failure developed. Cardiac ischemia as the main cause is unlikely, because troponin levels were only slightly increased, with a maximum of 9.7 U/L 24 hours later (normal limit <0.6 U/L), and after resolution of a temporary right bundle branch block, there were no major ST segment changes in the electrocardiogram. Additionally, at autopsy, there were diffuse atherosclerotic changes in the coronary arteries, but no infarction was found. Furthermore, the foramen ovale was closed, and there were diffuse and massive hypoxemic insults in both hemispheres of the brain, most likely dating from the resuscitation in the CT suite.
Although the procedure was performed under continuous lateral fluoroscopic control, no signs of the impending catastrophe were noted. In fact, the string of PMMA was only 2 mm thick and was invisible during fluoroscopy because of the overlying vertebral body that was already partially filled with PMMA and lying parallel to the radiograph beam. Surgical removal of PMMA from the pulmonary artery under cardiopulmonary bypass, as reported by Tozzi et al. (5), was considered in this case. However, because the cardiopulmonary situation stabilized within hours after resuscitation, and considering the age and comorbidities of the patient, the risk/benefit ratio of this intervention did not seem favorable.
In conclusion, increasing numbers of elderly patients with osteoporotic spine fractures will undergo percutaneous vertebroplasty, which is generally a fast and effective procedure. Hypertension and hypercapnia, along with loss of responsiveness, may be symptoms of severe pulmonary embolism of PMMA during this intervention. Consequently, anesthesiologists may be confronted with similar cases of atypical presentation of cement embolism. Further, in case of suspected leakage of cement, fluoroscopic projection in two levels must be performed.
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