 |
 |
 |
|
| home | CME | help | feedback | subscriptions | archive |
|
© 1999 The Journal of Bone and Joint Surgery, Inc. Paradoxical Cerebral Embolism Complicating a Major Orthopaedic Operation. A Report of Two Cases* , NEW YORK, N.Y.Investigation performed at the Department of Orthopaedic Surgery, New York University-Hospital for Joint Diseases Orthopaedic Institute, New York City
Thromboembolism is a frequent complication following major orthopaedic procedures. Cerebrovascular accidents, however, are less commonly seen postoperatively; their prevalence, as reported in the surgical literature, has been between 0.08 percent (twenty of 24,641 operations) and 1.1 percent (four of 354 operations in a series of patients older than sixty years of age)9,16. Paradoxical embolism, the systemic embolization of a venous thrombus through a right-to-left shunt (such as a patent foramen ovale), is an even rarer entity. We report the cases of two patients who had a paradoxical cerebral embolism and a concomitant pulmonary embolism following a major orthopaedic procedure.
CASE 1. A sixty-two-year-old woman had a right hybrid total hip arthroplasty (meaning that the femoral component was inserted with cement and the acetabular component was inserted without cement) under spinal anesthesia for the treatment of osteoarthritis. Her medical history included hypertension, non-insulin-dependent diabetes mellitus, and hypercholesterolemia. She had no history of thromboembolism, cerebrovascular disease, or myocardial ischemia. A preoperative echocardiogram and a stress thallium scan revealed mild anteroseptal ischemia and septal hypokinesis. Postoperatively, the patient was neurologically intact and was managed with low-molecular-weight heparin as routine prophylaxis against thromboembolism; the first dose was administered twelve hours postoperatively, and subsequent doses were given every twelve hours thereafter. On the first postoperative day, the patient reported a loss of vision in the right visual field and was noted to have an expressive aphasia. The patient did not have shortness of breath or chest pain. Neurological examination revealed a right-sided homonymous hemianopsia and a facial droop. The remainder of the neurological and general physical examination was normal. An emergent computed tomographic scan of the brain showed an acute, nonhemorrhagic left parietal infarct. An electrocardiogram showed no interval change, and a radiograph of the chest showed that the lungs were clear. Serial measurements of cardiac isoenzymes were negative for myocardial infarction. A duplex scan of the carotid artery and Holter monitoring revealed normal findings. A transesophageal echocardiogram revealed a patent foramen ovale. No intracardiac thrombus or vegetations were identified, and there was no evidence of atherosclerosis in the aortic arch. On the basis of these findings, paradoxical cerebral embolization was suspected. An arterial blood-gas analysis done with the patient breathing room air revealed severe hypoxia, with an oxygen partial pressure of forty-three millimeters of mercury (5.73 kilopascals) (normal, eighty to 100 millimeters of mercury [10.66 to 13.33 kilopascals]) and an alveolar-arterial oxygen gradient of thirty-six (normal, less than eighteen). A ventilation-perfusion scan showed a high probability of pulmonary embolism, with two mismatched defects in the right upper lobe. The presence of a pulmonary embolism was confirmed with pulmonary angiography, and a filter was placed in the inferior vena cava. The decision to proceed with placement of the filter was made as the angiography showed a large saddle pulmonary embolus (and thus additional emboli may have been life-threatening) and anticoagulation was deemed contraindicated as the patient had had the arthroplasty less than twenty-four hours previously. At the follow-up examination three months later, the patient had no residual deficit in neurological function. CASE 2. A forty-six-year-old woman who had idiopathic scoliosis was seen because of a one-year history of atraumatic, progressively worsening low-back pain that radiated to the left thigh and interfered with the activities of daily living. Radiographs of the spine revealed a right thoracic curve of 113 degrees and a compensatory lumbar curve of 50 degrees. The medical history was notable for restrictive lung disease secondary to scoliosis. There was no history of thromboembolism, cerebrovascular disease, or myocardial infarction. Motor and sensory examinations revealed normal findings. Staged anterior and posterior spinal arthrodesis was indicated for correction of the scoliotic deformity. The patient had an anterior spinal arthrodesis from the sixth thoracic to the first lumbar vertebra with discectomy and thoracoplasty. Postoperatively, the patient was managed with bed rest. Sequential compression devices were applied to both lower extremities preoperatively and were left in place postoperatively for prophylaxis against thromboembolism. Six days later, a posterior spinal arthrodesis with instrumentation was performed from the second thoracic to the fourth lumbar vertebra with use of autologous bone from the iliac crest. During closure of the wound, the patient became acutely hypoxic and monitoring of the somatosensory and motor evoked potentials revealed a sudden increase in conduction latency and a decrease in amplitude. The abnormal electrophysiological signals did not normalize despite a return to normal oxygen saturation when the concentration of inspired oxygen was increased. A wake-up test revealed movement of the upper but not the lower extremities. The spinal instrumentation and the bone graft were removed, the thoracic and lumbar vertebrae were decorticated, the bone graft was replaced, and the wound was closed. Postoperatively, the patient was managed with methylprednisolone (a bolus of thirty milligrams per kilogram followed by a continuous infusion of 5.4 milligrams per kilogram per hour for twenty-four hours). Physical examination in the recovery room revealed generalized muscular weakness on the right, normal muscular strength on the left, and persistent hypoxia. A computed tomographic scan of the brain demonstrated an acute left frontoparietal infarct. A ventilation-perfusion scan indicated a high probability of pulmonary embolism. A filter was placed in the inferior vena cava because anticoagulation with heparin therapy was deemed contraindicated given the proximity of these events to the spinal reconstruction as well as the patient's poor oxygenation despite mechanical ventilation. The presumptive diagnosis of paradoxical pulmonary embolism was confirmed with a transesophageal echocardiogram, which demonstrated a patent foramen ovale. No intracardiac thrombus or vegetations were identified, and there was no evidence of atherosclerosis in the aortic arch. The patient was extubated on the fifth postoperative day, and a regimen of heparin therapy was begun. Physical examination on the tenth postoperative day demonstrated improved muscular strength (grade 4 of 5) and a persistent footdrop (grade 1 of 5) on the right. A thoracolumbar brace was applied. When the patient was medically stable, the brace was removed and a Risser body cast was applied from the area of the greater trochanter to the upper thorax. Given the sequence of events that occurred, it is probable that the patient had a large intraoperative pulmonary embolism with resultant hypoxia during the second operation. The hypoxia predisposed the patient to ischemia of the spinal cord, which resolved with removal of the hardware. Concomitantly, systemic embolization of a venous thrombus to the cerebral vasculature (that is, a paradoxical embolism) occurred with resultant hemiplegia. At the follow-up examination one year later, radiographs demonstrated a successful spinal fusion with a thoracic curve of 85 degrees. Physical examination revealed persistent muscular weakness on the right (grade 4 of 5) and a decrease in the severity of the footdrop (grade 3 of 5).
The first description of paradoxical embolism of which we are aware was by Cohnheim4 in 1877; the medical literature now contains descriptions of more than 170 instances of this phenomenon10,19. Nevertheless, to our knowledge, paradoxical embolism combined with pulmonary embolism has not previously been reported as a postoperative complication in the orthopaedic literature. Most thrombi that cause embolic stroke originate in the heart or arise from atherothrombotic lesions in the aorta, the carotid artery, or the vertebrobasilar system. However, emboli may arise from the venous circulation and enter the arterial circulation through a right-to-left shunt (such as a patent foramen ovale) with resultant cerebral ischemia. This syndrome, known as paradoxical embolization, is a rare and potentially underdiagnosed cause of ischemic stroke11,19. In a report by Loscalzo12, seven of thirty patients who had a paradoxical embolism had had a recent operation. Given the prevalence of thromboembolic events after major orthopaedic operations, recognition of the potential for paradoxical embolization is important. Giachino et al.6 reported cerebral infarctions in association with 0.5 percent of 4721 total joint arthroplasties. Intraoperative cerebral infarctions as a result of paradoxical embolization of fat during total knee arthroplasty also have been described20. Massini and Stulberg15 reported the case of a patient who had paradoxical embolization to the brain through a large patent foramen ovale during a revision total hip arthroplasty; there was no evidence of a pulmonary embolus or deep venous thrombosis, and the emboli had arisen from the periprostatic venous plexus. In our report, both patients had a documented pulmonary embolism. A patent foramen ovale was documented in approximately 35 percent of 1100 hearts of normal individuals in two autopsy studies7,18. Despite the apparently high frequency of intracardiac defects, cerebral infarction due to paradoxical embolism is uncommon. Normally, the foramen ovale is closed by the pressure gradient between the left and right atria. As circulatory pressures on the right side of the heart increase, however, flow from the right to the left atrium can occur. A presumptive clinical diagnosis of paradoxical cerebral embolism should be considered in the presence of venous thromboembolism, an abnormal right-to-left shunt (such as a patent foramen ovale), and arterial embolism without evidence of a left-sided source. Pulmonary embolism is the most common cause of acute elevation of right atrial pressure, which is secondary to the loss of at least 40 percent of the pulmonary vascular bed. Resulting elevations in pulmonary vascular resistance and secondary pulmonary hypertension are predisposing factors to paradoxical embolism. Paradoxical emboli can lodge in the cerebral, peripheral, and mesenteric vasculature as well as in the coronary arteries; patients often have embolization at multiple sites10,12. Patients who have signs and symptoms of cerebral infarction should be evaluated with a computed tomographic scan of the brain in order to confirm the presence of the suspected lesion and to differentiate between a hemorrhagic and an ischemic stroke. Patients who are determined to have had an embolic stroke must be evaluated to identify the source of the embolus; the evaluation should include serial measurements of cardiac isoenzymes and electrocardiography (to determine the presence or absence of a myocardial infarction), cardiac echocardiography (to search for an intramural thrombus or vegetation and to evaluate the aorta), Holter monitoring (to rule out cardiac arrhythmia), and duplex scanning of the carotid artery (to search for stenosis or atheromatous plaques with associated thrombi). Transesophageal echocardiography with use of contrast medium should be performed if paradoxical embolism is suspected, as this test has been shown to be superior to other techniques for the detection of a patent foramen ovale and other right-to-left shunts5,13,17. Given the prevalence of occult right-to-left cardiac shunts, patients who have had a postoperative thromboembolism, particularly a massive pulmonary embolism, should be monitored clinically for the possibility of cerebral and systemic embolization. Similarly, patients who have had a postoperative cerebral infarction must be evaluated for thromboembolism because the former may be a potentially fatal source of embolization. Treatment should be initiated with the assistance of a medical intensivist and a neurologist and should include anticoagulation with heparin followed by warfarin (if not contraindicated) for three to six months in order to prevent further extension of the thrombi. A vena cava filter can be used if anticoagulation therapy is contraindicated; such a device is also recommended for patients who have a large intracardiac defect. Short-term follow-up of two groups consisting of 140 and 132 patients who had a paradoxical embolism showed a 1.9 to 3.4 percent annual rate of recurrence of stroke or transient ischemic attack1,14. Recurrence of these events has been associated with larger septal defects and with the presence of an atrial septal aneurysm9. Lifelong anticoagulation or antiplatelet therapy has been recommended by some authors8,14, particularly for patients who have chronic risk factors (such as a hypercoagulable state) for venous thrombosis. Operative closure of a patent foramen ovale is recommended for patients who have a large cardiac defect or who have chronic elevation of right atrial pressure1,3; it is not indicated, however, if the elevation of right-sided pressure is related to an acute event such as a pulmonary embolus. A less invasive alternative may be transcatheter closure with use of a double-umbrella device2. Avoidance of paradoxical embolization relies on postoperative prophylaxis against thromboembolism, although intraoperative events may be unavoidable. Routine preoperative screening for a defect in the atrial septum that could lead to paradoxical embolization is indicated only for patients who have a known history of unexplained systemic embolization. Recognition of the potential for this rare complication is important for orthopaedic surgeons and for those involved with the postoperative management of patients.
*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.
  CiteULike  Connotea  Del.icio.us  Facebook  Technorati  Twitter What's this?
This article has been cited by other articles:
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Top
Introduction
Case Reports
| home | CME | help | feedback | subscriptions | archive | site index |
|
Stanford University Libraries' HighWire Press (TM) assists in the publication of JBJS Online. |