Acute encephalitis

Abstract

Acute encephalitis remains one of the contemporary challenges of critical care medicine. The diagnosis is difficult and sometimes unconfirmed, and encephalitis remains without clear evidence-based therapies or even therapeutic goals for the prevention of high neurologic sequelae. This article provides a framework for pediatric intensivists to guide the diagnosis and management of patients with suspected encephalitis. It provides an in-depth review of the most common causes of encephalitis in children. The article promotes early recognition, appropriate testing and empiric treatment, and management of the expected complications of acute encephalitis.

Fig. 1

Adolescent with altered level of consciousness and suspected viral encephalitis found to have bacterial meningitis. (A) Axial computed tomography image after lumbar puncture showing decreased extra-axial space and slitlike lateral ventricles. (B) Sagittal MRI after lumbar puncture showing effacement of fourth ventricle and quadrigeminal cistern and tonsillar herniation.

Fig. 2

(A) A 12-year-old patient with HSV encephalitis; coronal fluid-attenuated inversion recovery (FLAIR) image (left) shows extensive infection-related edema involving the right temporal lobe, right insular lobe, and right temporofrontal junction (arrows) with uncal herniation noted (double arrowheads). There is also involvement of the left temporal lobe (arrowhead). Mild shift to the left of the midline structures is identified (dashed arrow). Postcontrast coronal T1-weighted image (right) shows enhancement consistent with leptomeningitis over the right frontal temporal region (arrows). (B) A 12-month-old patient with H1N1 influenza A infection and seizures. A focus of increased signal identified in the left posterior putamen on diffusion-weighted image (left, arrow) is consistent with restricted diffusion (cytotoxic edema), as shown on the apparent diffusion coefficient map (right, arrow). This lesion may result from direct brain viral entry as well as from H1N1-related vasculitides in the territory supplied by the perforating arteries. (C) A 16-year-old patient affected by ADEM. Sagittal (left) and coronal (right) FLAIR images show confluent T2-FLAIR hyperintense lesions in the subcortical white matter of the cerebral hemispheres bilaterally (arrows). A tumorlike ADEM lesion of the left middle cerebellar peduncle extending to the cerebellar white matter is also identified (arrowheads). (D) A 26-year-old patient with NMDAR encephalitis and ovarian teratoma. Axial FLAIR images show hyperintensity of the vermis of the cerebellum (left, arrow), and bilateral alterations in the hippocampus (right, arrows) and right temporal uncus (right, arrrowhead).