Anesth Analg 1999;89:300
© 1999 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
Early Postoperative Stroke in a Patient with an Atrial Septal Aneurysm
Masahiro Ide, MD,
Hiroyuki Ishida, MD, and
Hiroko Kato, MD
Department of Anesthesia, Kobe City General Hospital, Kobe, Japan
Address correspondence and reprint requests to Dr. Ide, Department of Anesthesia, Kobe City General Hospital, 4-6, Minatojima-nakamachi, Chuo-ku, 650-0046, Kobe, Japan.
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Introduction
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Perioperative stroke (POS) after general surgery is a rare but serious complication. Patients with previous cerebrovascular disease (1,2), advanced age (2,3), or cardioembolic sources (3,4) are at higher risk of POS. We report a case in which the patient, with no common risk factors for POS, had early postoperative stroke. During a search for the cause, transesophageal echocardiography revealed an atrial septal aneurysm (ASA).
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Case Report
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A 43-yr-old, 47-kg, 154-cm woman was admitted to our hospital for resection of a retroperitoneal tumor. She had been in good health until 2 wk before admission, when she developed lower abdominal pain. Her medical history excluded cardiac disease, hypertension, cerebrovascular symptoms, smoking, and regular use of oral contraceptives. Physical examination, including neurological evaluation, revealed no abnormalities. Her blood pressure was 100/60 mm Hg. Admission laboratory values and the electrocardiogram were within normal limits.
Induction and maintenance of general anesthesia with thiamylal, fentanyl, vecuronium, and sevoflurane were uneventful. The patient was placed in the left kidney position. During the course of anesthesia, there was a normal sinus rhythm, and blood pressure remained stable, with systolic pressure of 90–100 mm Hg and diastolic pressure of 50–60 mm Hg. Resection of the tumor (hemangiopericytoma), right nephrectomy, and right adrenalectomy were performed via a retroperitoneal right flank approach. There were no untoward events intraoperatively. During the 145-min procedure, 2000 mL of lactated Ringer’s solution was given, and blood loss was 340 mL. At the end of the procedure, the muscle relaxant effect was reversed with neostigmine and atropine. The patient awakened soon, was tracheally extubated in the operating room, and was transferred to the intensive care unit.
Vital signs continued to be stable, and hematocrit was 28%. The next morning, the patient developed a right facial droop, a mild right hemiparesis, and dysphasia. A computed tomographic (CT) scan was normal on this day, but a CT scan taken on the second postoperative day revealed a left putamen infarction. She was treated with heparin 5000 U subcutaneously twice daily, and neurological deficits resolved over the next 5 days. Magnetic resonance imaging performed on the 10th postoperative day showed a small, old infarction in the left cerebellum, as well as a left putamen hemorrhagic infarction in the same area identified on the previous CT scan. Magnetic resonance angiography revealed no apparent stenosis of cerebral vessels. Transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) were performed to identify potential cardiac sources of emboli. TEE, but not TTE, detected an ASA with a base width of 1.7 cm in the region of the fossa ovalis, protruding 1.8 cm into the right atrium with phasic left atrial excursion. Thrombus was not identified in the cardiac chambers. There was no evidence of shunting flow by transesophageal Doppler color flow mapping during the Valsalva maneuver and a cough test. Warfarin therapy was started after discharge from the hospital on the 14th postoperative day.
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Discussion
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POS occurs with an incidence of 0.07%–0.2% of general surgical cases, excluding cardiac and carotid surgery (2,3). The incidence is significantly increased in patients >65 yr old. It is not known how often hypotension, hypercoagulability, and dehydration contribute to POS (1,3). Most cases of POS after general surgery result from cardiogenic embolism (3,4), or, rarely, from paradoxical embolism through an intracardiac shunt (5).
Since the first report by Gallet et al. (6) in 1985, several echocardiographic studies have suggested that an ASA may behave as a possible cardioembolic source leading to ischemic stroke, particularly when it is associated with a patent foramen ovale (PFO) (7–11). We identified only one case report of POS in a patient with an ASA and a PFO (12). ASA is an uncommon lesion, with a prevalence of 0.22% in a large prospective study with TTE (7), 3%–8% in studies with TEE (9,11), and 1% in autopsies (13). ASA is often associated with other cardiac abnormalities, including PFO, mitral valve prolapse, and atrial septal defect (ASD) (10). Because an interatrial shunt, such as a small ASD or a PFO, has been noted in 54%–85% of patients with ASA (10,11,14), paradoxical embolism may be one potential mechanism related to stroke. Another possible mechanism is that an ASA itself may be thrombogenic because a thrombus within the ASA has occasionally been visualized by TEE (9,10,14). It has been questioned whether ASA per se could be a risk factor of cardiogenic embolism, despite the occurrence of embolic events in patients with no other potential cardiac sources of embolism (8,10). Our patient may have had a cerebral infarct, clinically silent and only demonstrated on magnetic resonance imaging. Because contrast TEE, which is more sensitive than TEE color Doppler alone in detecting a PFO and a small ASD (15), had not been performed, failure to demonstrate a right-to-left shunt would not conclusively rule out the diagnosis of paradoxical embolus.
In a patient with an ASA and a history of stroke, anticoagulant and/or antiplatelet therapy are generally recommended for prevention of recurrent stroke (6,8,11,16), but their efficacy has not been thoroughly evaluated (17). Atrial septal repair may be another approach to avoid long-term anticoagulant therapy and its complications. In a study of patients with a history of previous stroke, POS was more common in patients given preoperative heparin but not aspirin (18). Heparin therapy might have induced a delayed hemorrhagic transformation in our patient. Both preventive and acute treatment strategies for cardioembolic stroke need to be prospectively studied in a large series of patients. Considering the low incidence of POS, perioperative antithrombotic therapy remains unjustified in a patient with an ASA.
In summary, we treated a woman with early postoperative stroke possibly related to an ASA. TEE aided in identifying the potential etiology.
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References
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Accepted for publication March 29, 1999.
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Introduction
Case Report
