Resolving delayed sleep-wake phase disorder with a pandemic: two case reports.

Two patients with delayed sleep-wake phase disorder (DSWPD) demonstrated improvement in sleep quality and duration, reduction in symptoms, and elimination of the need for hypnotic or stimulant medications after changing their sleep schedules in response to the coronavirus disease 2019 (COVID-19) pandemic lockdown work schedule changes. These cases highlight the impact of work schedules on patient health and raise questions about approaches to workplace schedule requirements postpandemic. CITATION: Epstein LJ, Cai A, Klerman EB, Czeisler CA. Resolving delayed sleep-wake phase disorder with a pandemic: two case reports. J Clin Sleep Med. 2022;18(1):315-318.

Approach to critical illness myopathy and polyneuropathy in the older SARS-CoV-2 patients.

One of the major concerns of the health care community and the public surrounding the SARS-CoV-2 pandemic is the availability and use of ventilators. Unprecedented surges of patients presented to intensive care units across the country, with older adults making up a large proportion of the patient population. This paper illustrates contemporary approaches to critical illness myopathy (CIM), critical illness polyneuropathy (CIP), and critical illness polyneuromyopathy (CIPNM) in older patients, including incidence, risk factors, mechanisms for pathology, diagnosis, contemporary treatment approaches, and outcomes. We hope that the following analysis may help educate clinicians and ultimately decrease the duration of the mechanical ventilation required by these patients, resulting in improved clinical outcomes and an increase in ventilator availability for other patients in need.

COVID-19: Catastrophic Cause of Acute Lung Injury

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak that began in 2019 and spread rapidly across the globe has been observed to cause acute lung injury and multiorgan system failure. While common symptoms are flu-like, this population has been observed to decompensate at an alarmingly rapid rate to severe hypoxia. SARS-CoV-2 infects host cells by targeting the angiotensin-converting enzyme 2 (ACE2) receptor, which is present on endothelial cells in the lung, heart, kidney, and gastrointestinal tissue. The pathophysiology of acute respiratory distress syndrome (ARDS) in SARS-CoV-2 infection has a component of lung perfusion dysregulation and is described as a "cytokine storm" that causes increased vascular permeability and disease severity. Older adults and those with comorbid conditions, particularly hypertension, diabetes, and history of ischemic heart disease, are especially vulnerable. These high-risk populations are often on angiotensin-modulating therapies, which are theorized to increase ACE2 expressivity, but current evidence for or against discontinuation is equivocal. The standard for SARS-CoV-2 testing is through reverse transcription polymerase chain reaction, which has presented problems due to low sensitivity and possible co-infection with other pathogens. Treatment for ARDS in the setting of SARS-CoV-2 should follow pre-established goals of care and the wishes of the patient and family members or caregivers and consider the high risk for polypharmacy, cognitive decline, malnutrition, and depression, particularly in older adults. Treatment recommendations have outlined ventilation goals to minimize further lung injury. Compassionate use of pharmacologic therapies such as remdesivir has shown promise, and further clinical trials of anticytokine agents are underway.