The patient was admitted to the ICU due to acute hypoxic respiratory failure on May 9, 2021; brain death in a vaccinated, immunocompromised patient who presented with COVID-19 pneumonia; brain death in a vaccinated, immunocompromised patient who presented with COVID-19 pneumonia; brain death in a vaccinated, immunocompromised patient who presented with COVID-19 pneumonia; This is a literature report from the Clinical Imaging, Brain death in a vaccinated patient with COVID-19 infection.  In this report, author detail the clinical course and neuroimaging findings of a critically ill COVID-19 pneumonia patient, who ultimately suffered catastrophic intracranial events and imaging and clinical findings compatible with brain death. A 60-year-old woman with medical history notable for type II diabetes, hypertension, atrial fibrillation on apixaban, and systemic lupus erythematosus, treated with a combination of steroids, rituximab, and methotrexate (25 mg per week, held upon hospital admission), presented on 02May2021 with a one-week history of fever (Tmax 104 F) and productive cough. Notably, the patient had been vaccinated with an mRNA vaccine (Pfizer) receiving the second dose on 18Feb2021. She underwent routine COVID testing in anticipation of screening colonoscopy procedure and tested positive on 01Apr2021; she was asymptomatic at that time. She subsequently developed the aforementioned symptoms on 24Apr2021 prompting hospital presentation. PCR testing for COVID-19 on day of hospital presentation returned positive. The patient was negative for SARS-CoV-2 antibodies upon hospital admission on 03May2021. Blood cultures taken at admission and on hospital day 6, 9, 14, 18, 21, 23, 25, 27, 29 were all negative. The patient was admitted to the ICU due to acute hypoxic respiratory failure on 09May2021. She had a complex course which included treatment with broad spectrum antibiotics given her immunocompromised state, high dose steroids for concern for lupus flair, and remdesivir. Of note, the patient received her home dose of apixaban during the initial 5 days of hospitalization; this was subsequently stopped given development of disseminated intravascular coagulopathy (DIC) with platelet count dropping to a nadir of 20 x 103/uL (platelet count on presentation 164 x 103/uL) on hospital day 8. On hospital day 13, the patient reported headache, and altered mental status was observed. She was intubated at this time for airway protection. Subsequent head CT demonstrated a new acute to subacute infarct involving the right frontal operculum and insular region, new parenchymal hemorrhages versus hemorrhagic infarcts involving the left parietal lobe and left cerebellar hemisphere, and multifocal acute subarachnoid hemorrhage (Fig. 1 A, B: Axial non contrast head CT demonstrates an acute to subacute infarct involving the right frontal operculum and insular region (A, arrow) and new parenchymal hemorrhages versus hemorrhagic infarcts involving the left parietal lobe (A, arrowhead) and multifocal acute subarachnoid hemorrhage (B, arrows).). CT angiogram of the head and neck performed later the same day demonstrated no definite evidence of an acute large vessel intracranial arterial occlusion or substantial arterial stenosis, however did demonstrate multifocal irregularity within the superior sagittal sinus, with differential notable for prominent arachnoid granulations and/or sinus venous thrombosis (Fig. 1C: CT angiogram demonstrates multifocal irregularity within the superior sagittal sinus, with differential notable for prominent arachnoid granulations and/or sinus venous thrombosis (C, arrows).). MRI of the brain performed the following day revealed acute left middle cerebral artery territory infarct, evolving right MCA territory infarcts, and redemonstration of previously seen parenchymal and subarachnoid blood products (Fig. 2: Axial non contrast brain MRI demonstrates acute left middle cerebral artery territory infarct (A and B, arrowhead) and evolution of right frontal lobe infarcts on diffusion weight imaging (A and B, arrow) with apparent diffusion weight imaging correlates. Representative gradient-echo image redemonstrates parenchymal blood products in area of known hemorrhage (C, arrow).). Contrast-enhanced MR venogram demonstrated non-occlusive superior sagittal sinus thrombosis (Fig. 3: Sagittal view from a contrast enhanced MR venogram of the head demonstrates multiple, non-occlusive, superior sagittal sinus thrombi. The transverse and sigmoid sinuses are patent bilaterally.). After interdisciplinary discussion with hematology, neurosurgery and neurology a heparin drip was initiated following MR venogram confirmation of venous sinus thrombosis. On hospital day 19, head CT demonstrated continued expected evolution of infarcts with sulcal effacement surrounding the dominant left sided infarcts and trace rightward midline shift. Final head CT, performed on hospital day 35, demonstrated cessation of contrast opacification of the anterior and posterior intracranial arterial circulation as well as new cerebral edema with effacement of the gray-white matter borders, sulci, ventricles and cisterns, new hemorrhage in the right frontal and left frontoparietal lobes at the site of previous infarctions, and new hyperdensity in the sylvian fissures consistent with pseudo-subarachnoid hemorrhage (Fig. 4, Final axial head CT images demonstrate cerebral edema with effacement of the gray-white matter borders, sulci, ventricles and cisterns with new areas of hemorrhage and hemorrhage at site of prior infarctions (A, arrows). New hyperdensity is seen in the sylvian fissures consistent with pseudosubarachnoid hemorrhage (B, arrow). Coronal MIP CTA of the head and neck reveals opacification of the carotids (black arrows) in the neck but not in the intracranial circulation.). Discussion: In this unfortunate case, despite vaccination, this patient who notably was on immunosuppression for systemic lupus erythematosus, succumbed to SARS-CoV-2 infection. Hypoxic respiratory failure, complicated by DIC and acute CVD including ischemic, hemorrhagic and venous thrombotic events were contributory to this patient's death. This case not only is illustrative of classic imaging findings of brain death, but also highlights the vulnerably of immunocompromised patients despite vaccination.; Sender's Comments: Based on known drug safety profile, there is reasonable possibility of causal association between the events drug ineffective (Fatal), covid-19 pneumonia (fatal), acute respiratory failure (fatal), and brain death (fatal) and BNT162B2.  The impact of this report on the benefit/risk profile of the Pfizer product is evaluated as part of Pfizer procedures for safety evaluation, including the review and analysis of aggregate data for adverse events. Any safety concern identified as part of this review, as well as any appropriate action in response, will be promptly notified to regulatory authorities, Ethics Committees, and Investigators, as appropriate. ; Reported Cause(s) of Death: brain death; brain death in a vaccinated, immunocompromised patient who presented with COVID-19 pneumonia; brain death in a vaccinated, immunocompromised patient who presented with COVID-19 pneumonia; The patient was admitted to the ICU due to acute