Anesthesia & Analgesia:
CARDIOVASCULAR ANESTHESIA: Case Report
An Unusual Cause of Seizures After Cardiopulmonary Bypass
Wong, Alvin P. MD; Huss, Michael G. MD
Department of Anesthesia, Presbyterian Hospital of Dallas, Texas
December 5, 2002.
Address correspondence and reprint requests to Alvin P. Wong, MD, Pinnacle Anesthesia Consultants, 13601 Preston Rd. #900W, Dallas, TX 75240. Address e-mail to firstname.lastname@example.org.
Seizures after open-heart procedures can be life threatening and necessitate a rapid search for the cause. Neurocysticercosis (NCC) is an infection caused by the tapeworm Taenia solium, and seizure is a common clinical manifestation (1–5). Several forms of the infection can occur, and their treatments differ. We present a case of seizures in a patient who underwent cardiopulmonary bypass (CPB) for an atrial septal defect (ASD) repair.
A 34-yr-old Hispanic woman was scheduled for an ASD repair. After the birth of her second child, a murmur was detected, and an echocardiographic examination demonstrated a secundum ASD with a 3:1 left-to-right shunt. The patient had no medical history and no history of neurological disorders. She was born in Mexico but had lived in the United States for the last 17 yr. She last traveled to Mexico 2 mo before admission for cardiac surgery.
She was premedicated with 3 mg IV of midazolam and induced with midazolam (total, 5 mg), 150 μg of sufentanil, and 6 mg of pancuronium. Standard monitors were used along with arterial and central venous pressure catheters. A transesophageal echocardiographic examination confirmed the presence of a large secundum ASD. The anesthetic was maintained with oxygen and desflurane at an end-tidal concentration of 2%–4%. After establishment of CPB with full cardiac arrest, a pericardial patch closure of a 2- × 4-cm ASD was performed. The intraoperative course was uneventful, with a cross-clamp time of 22 min and CPB duration of 35 min. She was transferred to the intensive care unit in stable condition. During transfer, the patient was treated with propofol for sedation and nitroglycerine for hypertension.
Two hours after arriving in the intensive care unit, the patient had four seizures (three left-sided and one generalized tonic-clonic seizure). Vital signs, metabolic indices (Na+ 136 mM and glucose 116 mg/dL), and blood gas variables (pH value, 7.42; Pco2, 36.8 mm Hg) were normal. Phenytoin was successfully used to treat the seizures. Computed tomography (CT) of the brain was performed showing two densely calcified parenchymal lesions (Fig. 1, A and B) consistent with NCC. The magnetic resonance image (MRI) of the brain was negative; there were no active parasites. The patient experienced no further seizures, and her subsequent hospitalization was uneventful. She was discharged home on postoperative day 5 on phenytoin, celecoxib, and propoxyphene.
Cysticercosis is an infection caused by the encysted larval stage of the tapeworm Taenia solium. Involvement of the nervous system is a major public health problem for most of the developing world. Travel to endemic areas and immigration of people from these areas have resulted in cases in the United States. Cysticercosis is not acquired from ingesting pork but rather from a human tapeworm carrier. Our patient’s stay in Mexico led to her contact with a tapeworm carrier. Clinicians should be aware of the pathogenesis of NCC because the disease can occur in persons born in nonendemic countries and in those who have never traveled to endemic regions (6,7). Our patient was diagnosed based on presentation, head CT, MRI findings, and history of travel to Mexico.
The most common clinical manifestation of NCC is seizures (1–5). However, seizures do not distinguish between active and inactive disease because they are thought to result from the host response and not the parasitic infection. Patients may present with signs and symptoms of increased intracranial pressure and other neurological sequela such as learning disabilities, depression, and psychosis (7).
Neuroimaging studies in NCC are usually abnormal but often not pathognomonic (8). The most common form of inactive infection appears as 2- to 10-mm parenchymal calcifications on CT (9,10). MRI and CT provide complimentary diagnostic information in NCC. CT scanning is more sensitive than MRI at detecting intracerebral calcifications. MRI is performed to exclude active disease because it is more sensitive at detecting cysticerci in the cerebrospinal fluid.
Treatment of NCC depends on the form of the disease. Extraparenchymal NCC is treated with a combination of corticosteroids, antiparasitics, and surgery if hydrocephalus is present. The other active form of NCC is parenchymal NCC. Most patients present with seizures, and anticonvulsants are the mainstay of therapy. In prospective trials comparing antiparasitics with symptomatic treatment, meaning only anticonvulsants in the presence of seizures, results were similar (11–13). Even without antiparasitics, the cysticerci will complete degeneration or they will calcify, leading to inactive NCC (9). Therefore, there is currently no clear evidence that the use of antiparasitic drugs in active parenchymal NCC is beneficial. The most benign presentation of NCC is inactive parenchymal NCC where there is no evidence of viable or degenerating parasites. These patients are at high risk for seizures, and because they may recur years after the initial diagnosis, chronic anticonvulsants are required. As described for our patient, there is no role for antiparasitics in inactive NCC.
The true incidence of seizures is difficult to ascertain for cardiac operations (14). The most common causes are cerebral injury, drug toxicity, and metabolic abnormalities. All of our patient’s common metabolic indices were normal, and she was not receiving any medications known to cause seizures. The appearance of calcified parenchymal lesions on the brain CT and her association to an endemic region led to the diagnosis of NCC. Although it is difficult to prove that CPB contributed to her seizures, their temporal relationship and the fact that brain tissue edema is a documented sequela of CPB suggest a link between the two (15,16). Possible origins of brain edema are cytotoxic edema induced by microemboli, hypoperfusion, and hemodilution (15). We report a case of seizures in a patient after cardiac surgery whose overall presentation was consistent with NCC. Clinicians should be familiar with this disease to have the required level of suspicion in making the diagnosis and offering the appropriate treatment.
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