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Family engagement is a key component of high-quality critical care, with known benefits for patients, care teams, and family members themselves. The COVID-19 pandemic led to rapid enactment of prohibitions or restrictions on visitation that now persist, particularly for patients with COVID-19. Reevaluation of these policies in response to advances in knowledge and resources since the early pandemic is critical because COVID-19 will continue to be a public health threat for months to years, and future pandemics are likely. This article reviews rationales and evidence for restricting or permitting family members' physical presence and provides broad guidance for health care systems to develop and implement policies that maximize benefit and minimize risk of family visitation during COVID-19 and future similar public health crises.
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Survivors of community-acquired pneumonia (CAP) are at increased risk of cardiovascular disease, cognitive and functional decline, and death, but the mechanisms remain unknown. ⋯ An important proportion of CAP survivors have persistent pulmonary foci of increased inflammatory activity beyond resolution of their infection. As inflammation contributes to cardiovascular disease, cognitive decline, functional waning, and mortality risk in the general population, this finding provides a plausible mechanism for the increased morbidity and mortality that have been observed post-CAP.
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The COVID-19 pandemic placed considerable strain on critical care resources. How US hospitals responded to this crisis is unknown. ⋯ Responses of hospitals to the mass need for critical care services due to the COVID-19 pandemic were highly variable. Most hospitals canceled procedures to preserve ICU capacity and scaled up ICU capacity using existing clinical space and staffing. Future research linking hospital response to patient outcomes can inform planning for additional surges of this pandemic or other events in the future.
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Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) affects tens of millions worldwide; the causes of exertional intolerance are poorly understood. The ME/CFS label overlaps with postural orthostatic tachycardia (POTS) and fibromyalgia, and objective evidence of small fiber neuropathy (SFN) is reported in approximately 50% of POTS and fibromyalgia patients. ⋯ These results identify two types of peripheral neurovascular dysregulation that are biologically plausible contributors to ME/CFS exertional intolerance-depressed Qc from impaired venous return, and impaired peripheral oxygen extraction. In patients with small-fiber pathology, neuropathic dysregulation causing microvascular dilation may limit exertion by shunting oxygenated blood from capillary beds and reducing cardiac return.
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A 57-year-old man who had been intubated and placed on venovenous extracorporeal membrane oxygenation for hypoxemic respiratory failure due to COVID-19 pneumonia was transferred to our facility. He underwent anticoagulation with IV heparin titrated to an anti-Factor Xa goal of 0.1 to 0.3 international unit/mL. ⋯ He simultaneously experienced the development of fluid-refractory shock that required multiple vasopressors and received stress-dose hydrocortisone when his WBC was 30,000 cells/μL. He remained afebrile and was started on broad-spectrum antimicrobials that included antifungal and anthelminthic therapy.