H1N1 encephalitis with malignant edema and review of neurologic complications from influenza

Abstract

Background: Influenza virus infection of the respiratory tract is associated with a range of neurologic complications. The emergence of 2009 pandemic influenza A (H1N1) virus has been linked to neurological complications, including encephalopathy and encephalitis.

Methods: Case report and literature review.

Results: We reviewed case management of a 20-year old Hispanic male who developed febrile upper respiratory tract signs and symptoms followed by a confusional state. He had rapid neurologic decline and his clinical course was complicated by refractory seizures and malignant brain edema. He was managed with oseltamavir and peramavir, corticosteroids, intravenous gamma globulin treatment, anticonvulsants, intracranial pressure management with external ventricular drain placement, hyperosmolar therapy, sedation, and mechanical ventilation. Reverse transcriptase polymerase chain reaction analysis of nasal secretions confirmed 2009 H1N1 virus infection; cerebrospinal fluid (CSF) was negative for 2009 H1N1 viral RNA. Follow-up imaging demonstrated improvement in brain edema but restricted diffusion in the basal ganglia. We provide a review of the clinical spectrum of neurologic complications of seasonal influenza and 2009 H1N1, and current approaches towards managing these complications.

Conclusions: 2009 H1N1-associated acute encephalitis and encephalopathy appear to be variable in severity, including a subset of patients with a malignant clinical course complicated by high morbidity and mortality. Since the H1N1 influenza virus has not been detected in the CSF or brain tissue in patients with this diagnosis, the emerging view is that the host immune response plays a key role in pathogenesis.

Fig. 1

CT brain imaging demonstrates rapid development of brain edema. The top row displays CT images from admission and the bottom row displays CT images 2 days later. The arrow on the top row (left) illustrates open basal cisterns. On the bottom row, the small arrow points to effacement of basal cisterns (left) and subcortical brain edema (larger arrows, bottom row, left and right). This subcortical edema is confirmed on MR imaging (Fig. 2)

Fig. 2

Magnetic resonance imaging was done at the time of patient transfer a, c to the neuro-intensive care center and at 1 month of treatment b, d with influenza-specific antiviral therapy, corticosteroids, and intravenous gamma globulin therapy. a Coronal FLAIR image shows diffuse brain edema with sulcal effacement and symmetric hyperintensities selectively affecting the white matter and sparing cortex and subcortical nuclei such as basal ganglia and thalami. b Coronal FLAIR image at 1 month shows resolution of sulcal effacement, marked reduction in white matter hyperintensity, and relative brain atrophy (20 year old patient). c Diffusion-weighted imaging on admission showed some increased signal in the periventricular zones that were also bright on T2 and FLAIR sequences consistent with T2 shine-through. d Diffusion-weighted imaging at 1 month revealed hyperintensity in the caudate and putamen with corresponding decreased signal in ADC map and lack of hyperintensities on T2 and FLAIR sequences (see Fig 1b)

Fig. 3

Neurologic complications of influenza