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{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T1","span":{"begin":287,"end":300},"obj":"http://purl.obolibrary.org/obo/GO_0003968"},{"id":"T2","span":{"begin":287,"end":300},"obj":"http://purl.obolibrary.org/obo/GO_0003899"},{"id":"T3","span":{"begin":1127,"end":1133},"obj":"http://purl.obolibrary.org/obo/GO_0060004"}],"text":"On March 25, a 68-year-old man with previous history of hypertension and diabetes mellitus presented to the emergency department with dyspnea, fever, fatigue, and productive cough. Diagnosis of coronavirus 2 (SARS-CoV-2) pneumonia was confirmed by nasopharyngeal swab specimen using the transcriptase-polymerase chain reaction assay. Following the development of severe acute respiratory syndrome and acute kidney failure, the patient was admitted to our intensive care unit (ICU) and intubated; mechanical ventilation and continuous veno-venous hemodialysis (CVVHD) were started. Table 1 reports the main mechanical ventilation settings, data on respiratory function, and laboratory results. He was started on steroids, hydroxychloroquine, and ceftaroline. A prophylactic dose of enoxaparin (6000 u once/day) was subsequently switched to 6000 u/bd, due to increase of D-dimer values. Respiratory function improved over days, and he was switched to assisted mechanical ventilation, while CVVHD was continued for persistent anuria. On day 9, on sedation hold, his Glasgow Coma Score was 3 (Eyes 1,Verbal 1, Motor 1). Photomotor reflex was present, and brainstem reflexes (including cough) were preserved. After 2 days from sedation hold, an electroencephalography (EEG) revealed a severe voltage attenuation (signal diffusely \u003c 20 μV), with background activity substituted by irregular theta and delta activities widely distributed, without antero-posterior gradient. No focal or generalized interictal/ictal epileptiform discharges nor periodic discharges were observed. Two days later, a second EEG showed no significant changes. At brain MRI (Fig. 1), DWI shows multiple small supratentorial areas of restricted diffusion, consistent with acute ischemic foci, involving the bilateral fronto-parietal deep and subcortical white matter and the genu and body of the corpus callosum. SWI revealed several hypointense foci throughout the brain, both infratentorial and supratentorial, mostly bithalamic. On T1-weighted images obtained after intravenous gadolinium injection, there was no evidence of parenchymal or meningeal enhancement. Cerebrospinal fluid (CSF) analysis showed 0.492 g/L [0.130–0.520 g/L] proteins, 88 mg/dL [44–74 mg/L] glucose, no leukocytes and red blood cells, CSF/serum albumin ratio 7.74 [1.92–7.30], and CSF/serum immunoglobulin G (IgG) ratio 4.48 [0.82–3.26]. SARS-CoV-2 RNA was detected in the CSF. Over the following days, the patient developed a systemic candida and gram-negative bacteria infection. His respiratory function significantly worsened, and he developed a septic shock with multiorgan failure. He died on day 21.\nTable 1 Laboratory data, respiratory function, and mechanical ventilation†\nVariable Reference range, adults On admission ICU day 3 ICU day 7 ICU day 14\nWhite blood cell (109/L) 4.50–9.80 9.58 13.99 24.14 23.58\nC-reactive protein (mg/L) 0.0–5.0 137 77.7 138 121\nProcalcitonin (mcg/L) 0.00–0.25 1.37 2.09 1.67 2.07\nIL (interleukin)-6 (ng/L) \u003c 3.4 491 32.7 NA NA\nFerritin (mcg/L) 30–400 605 378 NA NA\nD-Dimer (mcg/L) 0.00–500.0 1605 810 3497 6941\nFibrinogen (g/L) 2.00–4.00 6.10 3.84 6.06 8.47\nActivated partial-thromboplastin time (sec) 28.0–40.0 39 27.3 33.6 32.2\nCreatinine (mg/dL) 0.51–0.95 2.4 5 2.9 2.6\nUrea nitrogen (mg/dL) 21–54 90 172 135 167\nLactate dehydrogenase (U/L) 135–214 425 282 357 265\nArterial pH 7.35–7.45 7.36 7.35 7.23 7.34\nArterial partial pressure of oxygen (mmHg) 83–108 71.8 73.3 80.8 56.1\nArterial partial pressure of carbon dioxide (mmHg) 32–45 42.4 48.1 54.1 55.4\nLactate (mmol/L) 0.5–1.6 1.1 1.1 1.6 0.8\nNasopharyngeal swab Positive-quite positive-negative Positive Positive Positive Quite positive\nVentilation mode Controlled Controlled Controlled Assisted\nFraction of inspired oxygen 0.8 0.6 0.6 0.6\nPositive end-expiratory pressure (cmH2O) 15 15 13 12\nContinuous renal replacement therapy NO YES YES YES\n†To convert the values for urea nitrogen to millimoles per liter, multiply by 0.357. To convert values for creatinine to micromoles per liter, multiply by 88.4. NA denotes not available\nFig. 1 Diffusion-weighted imaging (DWI) b1000 (a) and apparent diffusion coefficient map (b) show multiple areas of restricted diffusion, involving the bilateral fronto-parietal white matter and the genu of the corpus callosum, compatible with acute ischemic foci. Susceptibility-weighted imaging (SWI) (c) shows several millimetric hypointense areas, predominantly distributed in the thalami bilaterally, but also in the genu of the corpus callosum and in the parietal iuxtacortical white matter, consistent with microhemorrhages or alternatively microthrombi. T1-weighted post-contrast image (d) demonstrates the lack of parenchymal or meningeal enhancement at the level of these lesions (lack of enhancement was also observed in the rest of the brain, not shown)"}

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