Treatment of a resistant Neurogenic fever after ischemic stroke: a report
Dr L. G. Giaccari at Department of Women, Child, General and Specialistic Surgery, University of Campania “L. Vanvitelli”, Naples, Italy and colleagues have reported a case of Neurogenic fever after ischemic stroke resistant to conventional therapy with Acetaminophen. The case has appeared in the Journal of Medical Case Reports.
Elevation in body temperature within the first 24 hours of ischemic stroke is fairly common and known to be associated with worse outcomes. Only after thoroughly ruling out infection and the noninfectious etiologies and in the appropriate clinical setting should the diagnosis of central fever be made. Acetaminophen and nonsteroidal anti-inflammatory drugs are typical therapeutic options. External cooling is frequently used when pharmacologic interventions are inadequate.
A 70-year-old Caucasian woman arrived at the emergency department of a local hospital a few hours after a sudden loss of consciousness. Her medical history included type 2 diabetes mellitus being treated with oral hypoglycemic agents and insulin, untreated chronic atrial fibrillation, and transient ischemic attack about 10 years earlier.
On the basis of suspicion of stroke, computed tomographic angiography was performed, which revealed evidence of right middle cerebral artery (MCA) occlusion. Being within 6 hours of stroke onset, intra-arterial thrombectomy was performed, which did not resolve the occlusion. After 7 days of apparent clinical improvement, the patient had a rapid deterioration of the state of consciousness with acute respiratory failure, for which she was intubated, mechanically ventilated, and transferred to our intensive care unit (ICU).
At the time of admission, the patient presented with a state of neurological deterioration (Glasgow Coma Scale [GCS] score, 3) and a body temperature of 39 °C. Blood and urine tests, infection investigations, and chest x-ray were performed. Blood tests showed the absence of leukocytosis and negative C-reactive protein (CRP), whereas procalcitonin was not available at the time of admission to the ICU. Tests for urinary, pulmonary, and bloodstream infections required 48 hours for results. No abnormalities were observed on the chest x-ray. Tailored antibiotic treatment was initiated on the basis of suspicion of late-onset hospital-acquired pneumonia with piperacillin/tazobactam 4.5 g intravenously every 6 hours and linezolid 600 mg intravenously every 12 hours. The patient’s fever was treated with acetaminophen 1000 mg up to four times per day, which produced a nonsignificant reduction in body temperature. Brain computed tomography (CT) was performed, which confirmed the presence of an ischemic lesion of the right MCA with involvement of the structures of the right cerebral hemisphere.
The results of blood, urine, and infection investigations, including bronchial aspirate, were negative, as was the procalcitonin test. Chest x-ray and lung CT did not show signs of infection.
Antimicrobial therapy was stopped. Despite the administration of acetaminophen and external cooling, there was no reduction in body temperature (maximum body temperature [TCmax], 40.5 °C) during the first 4 days after ICU admission. After thoroughly ruling out infections and the other noninfectious etiologies, the diagnosis of central fever was made. After informing family members and having received written informed consent, a continuous infusion of diclofenac sodium (DFC) was decided. After an initial bolus of DCF (0.2 mg/kg in 100 ml of saline solution in 30 minutes), a continuous infusion (75 mg in 50 ml of saline solution) was started. The dosage of DCF (0.004–0.08 mg/kg/hour) was managed on the basis of the response of body temperature. The DCF infusion was discontinued if the patient’s body temperature was less than 37.5 °C for more than 12 hours with a dose of 0.004 mg/kg/hour.
During the infusion, the patient’s complete blood count, blood pressure, and liver and kidney function were strictly monitored. Continuous monitoring of temperature using an oesophagal probe was adopted.
A reduction in body temperature was recorded from the first day of treatment (TCmax, 38.5 °C), and after 5 days of treatment, the patient’s body temperature was constantly below 37.5 °C, and the DCF infusion was stopped.
During treatment with DCF, complete blood count, blood pressure, and urinary output were within the normal range. Transient increases in glutamic oxaloacetic transaminaseglutamic (GOT) or aspartate aminotransferase (AST), serum glutamate-pyruvate transaminase (GPT) or alanine transaminase (ALT), and gamma-glutamyl transferase (GGT) were recorded, with immediate normalization after the suspension. Renal function was preserved (creatinine, 0.83 mg/dl; glomerular filtration rate, 72 ml/minute/1.73m2).
The patient showed clinical improvement with increased neurological status (GCS score, 9) and hemodynamic stability. Neurological examination revealed evidence of left hemiparesis. During hospitalization, the patient’s neurological status showed no improvement. She died of infectious complications 40 days after admission. The patient’s family members were informed prior to the publication of this article, and they provided written informed consent regarding both the case and the images used.
Journal of Medical Case Reports
For more details click on the link: https://doi.org/10.1186/s13256-019-2281-7