Pulmonary edema following tonic–clonic seizure

نویسندگان

  • Hiroaki Izumida
  • Koichiro Homma
  • Junichi Sasaki
  • Shingo Hori
چکیده

Dear Editor, We report a case of pulmonary edema following tonic–clonic seizure not associated with congestive heart failure. A 68-year-old man was transferred to our department with self-limited tonic–clonic seizure continuing for 3 min. The patient’s medical history was notable for epilepsy treated with carbamazepine (400 mg/day). The last seizure had occurred more than 25 years previously. The emergency medical service reported the patient’s vital signs as follows: consciousness, Glasgow Coma Scale 6; blood pressure, 178/80 mmHg; heart rate, 108 b.p.m.; respirations, 18 per min; and oxygen saturation, 99% on 6 L of supplemental oxygen. When he arrived at our hospital, his vital signs were: consciousness, clear; blood pressure, 167/86 mmHg; heart rate, 84 b.p.m.; respirations, 23 per min; and oxygen saturation, 99% on 6 L of supplemental oxygen. Laboratory data and head computed tomography (CT) showed no abnormality. After the head CT scan, as oxygen saturation was adequate, we discontinued oxygen supplementation. Hypoxemia was then found unexpectedly (oxygen saturation, 87% on room air). Blood-gas analysis showed hypoxemia (PaO2, 85 mmHg on 6 L supplemental oxygen). We thus performed more radiographic tests after restarting the supply of oxygen. Chest radiography and chest CT showed bilateral pulmonary edema. After the chest CT examination, oxygen saturation was 89% on room air. As echocardiography showed no sign of heart failure, postictal pulmonary edema (PPE) was the best-fitting diagnosis. The patient was treated with supplemental oxygen and sulbactam/ampicillin, as it was difficult to differentiate his condition from aspiration pneumonia. His hypoxemia improved promptly, and he did not require supplemental oxygen next day. The dose of carbamazepine was controlled to 600 mg/day, and he was discharged on hospital day 9. Postictal pulmonary edema is a type of neurogenic pulmonary edema that was first reported by Shanahan in 1908. It typically presents within minutes to hours after a seizure and resolves within a few days. The pathophysiology of neurogenic pulmonary edema is likely related to sympathetic activation, but it remains incompletely understood. Postictal pulmonary edema may have an association with sudden unexpected death in epilepsy. In an autopsy study, 52 of 74 cases of sudden unexpected death in epilepsy underwent microscopic examinations of the lungs, and in all 52 cases, moderate to marked pulmonary congestion and edema were detected. Diagnosis of PPE is clinical and difficult because of a lack of specific signs and diagnostic tests. Differential diagnoses include aspiration pneumonia, congestive heart failure, and acute respiratory distress syndrome; aspiration pneumonia is particularly challenging to differentiate from PPE. While prolonged antimicrobial treatment is required for aspiration pneumonia, only respiratory support is needed for PPE, and recovery is usually rapid and spontaneous. Kennedy et al. reported that 11 of 24 post-seizure patients in their study had radiographically revealed chest abnormalities, including PPE in seven patients (of which two also had focal infiltrates) and focal infiltrates without PPE in four patients. That report showed that a long duration of seizure was associated with the presence of radiographically revealed chest abnormalities. In particular, seizures lasting >200 s were strongly associated with chest abnormalities. Given that PPE is considered a rare condition, it is possible to overlook mild PPE. To clarify how often a pulmonary evaluation is performed for patients following seizure, we undertook an investigation and found that 61 patients were transferred to our emergency department with seizure over a 4-month period. In some of these patients, blood-gas analysis showed mild hypoxemia overlooked by pulse oximetry (approximately 70–80 mmHg on room air), but radiographic tests were not always carried out for these patients, suggesting the possibility of misdiagnosis. Clinicians should have a high level of suspicion for this potentially fatal condition in any patient with a history of seizure with or without suddenly developed respiratory distress as an autopsy study showed.

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عنوان ژورنال:

دوره 4  شماره 

صفحات  -

تاریخ انتشار 2017