Abusive head trauma (AHT) is a unique form of pediatric TBI with increased mortality and neurologic sequelae. Hemispheric hypodensity (HH) in association with subdural blood after AHT has been described. Though risk factors for HH are not understood, we hypothesized that risk factors could be identified. We retrospectively enrolled children under 5 years with TBI secondary to AHT (child advocacy diagnosis) who had undergone initial and interval brain imaging. Records were interrogated for prearrival and in-hospital physiologic and radiographic findings. HH was determined by a blinded observer. Twenty-four children were enrolled and 13 developed HH. HH was not significantly associated with age, initial Glascow Coma Scale, or mortality. Pediatric Intensity Level of Therapy (PILOT) scores ( p = 0.01) and daily maximal intracranial pressure (ICP max ; p = 0.037) were higher in HH. Hypoxia, hypotension, cardiopulmonary arrest, need for blood transfusion, and daily blood glucoses tended to be greater in HH. Whereas all children with HH had acute subdural hematoma (SBH), many children without HH also had subdural blood; the presence of skull fracture was more likely in the children who did not develop HH ( p = 0.04), but no other intracranial radiographic pattern of injury was associated with HH. Surgical intervention did not appear to protect against development of HH. A variety of insults associated with ischemia, including intracranial hypertension, ICP-directed therapies, hypoxia, hypotension, and cardiac arrest, occurred in the children who developed HH. Given the morbidity and mortality of this condition, larger studies to identify mechanisms leading to the development of HH and mitigating clinical approaches are warranted.

Background: Histoplasma capsulatum infection is largely seen in endemic regions; it results in symptomatic disease in <5% of those infected and is most often a self-limiting respiratory disease. Disseminated histoplasmosis is considered rare in the immunocompetent host. Central nervous system (CNS) dissemination can result in meningitis, encephalitis, and focal lesions in the brain and spinal cord, stroke, and hydrocephalus. An intramedullary spinal cord lesion as the only manifestation of CNS histoplasmosis has been rarely described. Case Description: We present an atypical case of a 44-year-old man from a nonendemic region, on adalimumab therapy for ulcerative colitis who developed an isolated intramedullary spinal cord lesion in the setting of disseminated histoplasmosis. His course was initially indolent with vague systemic symptoms that led to consideration of several other diagnoses including sarcoidosis and lymphoma. Biopsies of several positron emission tomography positive lymph nodes revealed granulomatous inflammation, but no firm diagnosis was achieved. He was ultimately diagnosed with histoplasmosis after an acute respiratory infection in the setting of anti-tumor necrosis factor therapy. With appropriate antifungal therapy, the spinal cord lesion regressed. The previous systemic biopsies were re-reviewed, and rare fungal elements consistent with H. capsulatum were identified. A presumptive diagnosis of CNS histoplasmosis was made in the absence of direct laboratory confirmation in the setting of rapid and complete resolution on antifungal therapy. Conclusion: Disseminated histoplasmosis should be considered in granulomatous disease, even if the patient resides in a nonendemic region. Furthermore, clinicians should be mindful that CNS histoplasmosis may present in an atypical fashion.

No abstract