How Does the Brain Die After a Massive Posterior Fossa Lesion?
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How Does the Brain Die After a Massive Posterior Fossa Lesion? Chris Marcellino1,2 , Sherri A. Braksick1 and Eelco F. M. Wijdicks1* © 2020 Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society
A devastating neurological complication occurred [1–4] as a result of the hypercoagulability of COVID-19 pneumonia [5]. An ischemic stroke (or perhaps venous sinus thrombosis) involved the posterior inferior cerebellar artery (PICA) territory with hemorrhagic conversion, severe mass effect, and subsequent brain death despite maximal medical therapy. Rarely [6, 7] seen sequential imaging shows the radiographic development of supratentorial destruction from a posterior fossa hemorrhagic infarction.
Description of the Case A 61-year-old woman with a pertinent history of metabolic syndrome was hospitalized due to severe hypoxemia from COVID-19 pneumonia, diagnosed by positive nasal swab for SARS-CoV-2 and typical ground glass opacities on chest computed tomography (CT) imaging. She was transferred to the ICU on the 3rd day of hospitalization and was found to have a D-Dimer serum level above the upper limit of detection (> 42,000 ng/mL Fibrinogen Equivalent Units) despite having received subcutaneous prophylactic dose heparin since the time of admission. Imaging confirmed the absence of deep venous thrombosis and pulmonary emboli. She was intubated on the 5th hospital day after failing noninvasive oxygen therapy. Despite deep sedation and paralysis, she required prone positioning for refractory hypoxemia by the 6th day of hospitalization. Management of her respiratory and renal failure necessitated nearly continuous deep sedation, neuromuscular blockade, and renal replacement therapy. On the evening of the 11th day of hospitalization, sedation was weaned at which point she *Correspondence: [email protected] 1 Division of Neurocritical Care and Hospital Neurology, Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA Full list of author information is available at the end of the article
resumed some spontaneous movements as she had during prior sedation holidays. However, early in the morning of the 12th day, movement ceased and she became unresponsive. CT of the head was performed, which showed a large right cerebellar intraparenchymal hemorrhage with extensive mass effect resulting in basilar cistern effacement and upward transtentorial herniation (Fig. 1a). There was marked hydrocephalus and early loss of posterior fossa gray–white differentiation (Fig. 1b–d). The edema surrounding the hemorrhage was confined to the PICA territory, raising suspicion that a PICA or venous sinus thrombosis underwent hemorrhagic conversion. On exam, only cough and gag reflexes as well as the right corneal reflex were preserved, without central or peripheral motor response to pain. A ventriculostomy was placed as the patient was not a surgical candidate (due to neurological condition, coagulopathy, and multiorgan failure). There was brisk drainage of the ventriculo
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