Background and Purpose: A variety of neurological manifestations have been attributed to COVID-19, but there is currently limited evidence regarding risk factors and outcomes for delirium in critically ill patients with COVID-19. The purpose of this study was to identify delirium in a large cohort of ICU patients with COVID-19, and to identify associated features and clinical outcomes at the time of hospital discharge. Methods: This is an observational cohort study of 213 consecutive patients admitted to an ICU for COVID-19 respiratory illness. Delirium was diagnosed by trained abstractors using the CHART-DEL instrument. The associations between key clinical features, sedation and delirium were examined, as were the impacts of delirium on clinical outcomes. Results: Delirium was identified in 57.3% of subjects. Delirious patients were more likely to receive mechanical ventilation, had lower P: F ratios, higher rates of renal replacement therapy and ECMO, and were more likely to receive enteral benzodiazepines. Only mechanical ventilation remained a significant predictor of delirium in a logistic regression model. Mortality was not significantly different, but delirious patients experienced greater mechanical ventilation duration, ICU/hospital lengths of stay, worse functional outcomes at discharge, and were less likely to be discharged home. Conclusions: Delirium is common in critically ill patients with COVID-19 and appears to be associated with greater disease severity. When present, delirium is associated with worse functional status at discharge, but not increased mortality. Additional studies are necessary to determine the generalizability of these results and the impact of delirium on longer-term cognitive and functional outcomes.

Background: Sodium chloride (NaCl) 23.4% solution has been shown to reduce intracranial pressure (ICP) and reverse transtentorial herniation. A limitation of 23.4% NaCl is its high osmolarity (8008 mOsm/l) and the concern for tissue injury or necrosis following extravasation when administered via peripheral venous access. The use of this agent is therefore often limited to central venous or intraosseous routes of administration. Our objective was to evaluate the safety and efficacy of administration of 23.4% NaCl via peripheral venous access compared with administration via central venous access. Methods:We reviewed pharmacy records to identify all administrations of 23.4% NaCl at our institution between December 2017 and February 2020. Medical records were then reviewed to identify complications, such as extravasation, soft tissue injury or necrosis, hypotension (mean arterial pressure less than 65 mm Hg), pulmonary edema, hemolysis, and osmotic demyelination. We also compared the change in physiological variables, such as ICP, mean arterial pressure, cerebral perfusion pressure, and heart rate, as well as laboratory values, such as sodium, chloride, bicarbonate, creatinine, and hemoglobin, following administration of 23.4% NaCl via the peripheral and central venous routes. Results:We identified 299 administrations of 23.4% NaCl (242 central and 57 peripheral) in 141 patients during the study period. There was no documented occurrence of soft tissue injury or necrosis in any patient. One patient developed hypotension following central administration. Among the 38 patients with ICP monitoring at the time of drug administration, there was no significant difference in median ICP reduction (− 13 mm Hg [central] vs. − 24 mm Hg [peripheral], p = 0.21) or cerebral perfusion pressure augmentation (16 mm Hg [central] vs. 15 mm Hg [peripheral], p = 0.87) based on route of administration.Conclusions: Peripheral venous administration of 23.4% NaCl is safe and achieves a reduction in ICP equivalent to that achieved by administration via central venous access.

This article describes the clinical course, radiological findings, and outcome of two patients with the novel 2019 coronavirus disease (COVID-19) who remained comatose for a prolonged duration following discontinuation of all sedation. These two male patients, one aged 59-years and another aged 53-years, both with a history of hypertension and neurologically intact on admission, developed worsening COVID-19 associated acute respiratory distress syndrome (ARDS). Both required benzodiazepine, opioid, neuromuscular blockade, therapeutic anticoagulation, and vasopressor infusions in addition to renal replacement therapy. Echocardiography demonstrated normal chamber size and systolic function in both cases. Each patient demonstrated only trace flexion to pain 7-10 days following discontinuation of all sedation. Magnetic Resonance Imaging on both patients demonstrated multifocal lesions on diffusion weighted imaging with apparent diffusion coefficient correlate in bilateral middle/anterior cerebral artery borderzones, and no large-vessel occlusion or severe stenosis. In both patients, continuous electroencephalography demonstrated no seizures. Neither patient had any documented period of sustained hypotension (mean arterial pressure <60 mmHg) or hypoxia (SpO 2 < 90%). Ninety days following initial presentation, the 59-years-old man was oriented, with fluent speech and able to ambulate with assistance, while the other 53-years-old man was at home and independent, undertaking the basic activities required by daily living. We conclude that critically-ill COVID-19 patients with prolonged coma following sedation discontinuation may demonstrate imaging features of ischemic injury in borderzone regions despite the absence of documented sustained hypotension or hypoxia. However, substantial neurological recovery is possible despite these findings.

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