Acute respiratory distress syndrome (ARDS) survivors experience a high prevalence of cognitive impairment with concomitantly impaired functional status and quality of life, often persisting months after hospital discharge. In this review, we explore the pathophysiological mechanisms underlying cognitive impairment following ARDS, the interrelations between mechanisms and risk factors, and interventions that may mitigate the risk of cognitive impairment. Risk factors for cognitive decline following ARDS include pre-existing cognitive impairment, neurological injury, delirium, mechanical ventilation, prolonged exposure to sedating medications, sepsis, systemic inflammation, and environmental factors in the intensive care unit, which can co-occur synergistically in various combinations. Detection and characterization of pre-existing cognitive impairment imparts challenges in clinical management and longitudinal outcome study enrollment. Patients with brain injury who experience ARDS constitute a distinct population with a particular combination of risk factors and pathophysiological mechanisms: considerations raised by brain injury include neurogenic pulmonary edema, differences in sympathetic activation and cholinergic transmission, effects of positive end-expiratory pressure on cerebral microcirculation and intracranial pressure, and sensitivity to vasopressor use and volume status. The blood-brain barrier represents a physiological interface at which multiple mechanisms of cognitive impairment interact, as acute blood-brain barrier weakening from mechanical ventilation and systemic inflammation can compound existing chronic blood-brain barrier dysfunction from Alzheimer’s-type pathophysiology, rendering the brain vulnerable to both amyloid-beta accumulation and cytokine-mediated hippocampal damage. Although some contributory elements, such as the presenting brain injury or pre-existing cognitive impairment, may be irreversible, interventions such as minimizing mechanical ventilation tidal volume, minimizing duration of exposure to sedating medications, maintaining hemodynamic stability, optimizing fluid balance, and implementing bundles to enhance patient care help dramatically to reduce duration of delirium and may help prevent acquisition of long-term cognitive impairment.

COVID-19 is a severe infectious disease that has claimed >150,000 lives and infected millions in the United States thus far, especially the elderly population. Emerging evidence has shown the virus to cause hemorrhagic and immunologic responses, which impact all organs, including lungs, kidneys, and the brain, as well as extremities. SARS-CoV-2 also affects patients’, families’, and society’s mental health at large. There is growing evidence of re-infection in some patients. The goal of this paper is to provide a comprehensive review of SARS-CoV-2-induced disease, its mechanism of infection, diagnostics, therapeutics, and treatment strategies, while also focusing on less attended aspects by previous studies, including nutritional support, psychological, and rehabilitation of the pandemic and its management. We performed a systematic review of >1,000 articles and included 425 references from online databases, including, PubMed, Google Scholar, and California Baptist University’s library. COVID-19 patients go through acute respiratory distress syndrome, cytokine storm, acute hypercoagulable state, and autonomic dysfunction, which must be managed by a multidisciplinary team including nursing, nutrition, and rehabilitation. The elderly population and those who are suffering from Alzheimer’s disease and dementia related illnesses seem to be at the higher risk. There are 28 vaccines under development, and new treatment strategies/protocols are being investigated. The future management for COVID-19 should include B-cell and T-cell immunotherapy in combination with emerging prophylaxis. The mental health and illness aspect of COVID-19 are among the most important side effects of this pandemic which requires a national plan for prevention, diagnosis and treatment.

FRESH is the first clinical tool to prognosticate long-term outcome after spontaneous SAH in a multidimensional manner. Ann Neurol 2016;80:46-58.

In this large population-based sample, over half of mechanically ventilated stroke patients died in the hospital despite the fact that younger patients were more likely to receive mechanical ventilation. Future studies are indicated to elucidate mechanical ventilation strategies to optimize long-term outcomes after severe stroke.

A gradual increase in the volume of the induced gas space follows artificial pneumoperitoneum in dogs and cats with sulphur hexafluoride (SF,).' The volume change occurs because the rate of diffusion of nitrogen from the blood in to the pneumoperitoneum exceeds the rate of loss of SF, from the pneumoperitoneum to blood. The volume increases in artificial pneumothoraces during nitrous oxide anaesthesia are well-known.2 In these cases the rate of diffusion of nitrous oxide inwards exceeds the rate of diffusion of nitrogen outwards. The effect of similar anaesthesia on a non-compliant gas space causes rapid increases in pressure in the air-filled cisternal spaces of dogs following N 2 0 admini~tration.~ Similar effects occur in the middle ear during N 2 0 anaesthesia in patients4 Measurements in middle ear gas pressure and composition in cats and in man have confirmed these finding^.^." The effect is independent of airway pressure, and temporary or permanent hearing loss has occurred in several patients following N 2 0 anaesthesia.'. * Tympanic membrane graft displacement is commonly seen in middle ear surgery under N20 anaesthesia, yet the agent is used almost universally in this work. The possible effects of N 2 0 excretion into the middle ear cavity suggest that the gas should be withdrawn some minutes before the middle ear is ~l o s e d .~*~-" It has also been suggested that N 2 0 anaesthesia may be hazardous for the hearing of patients with polyethylene struts or surgical reconstructions for chronic ear disease.8The present study was undertaken because of the occurrence of a marked hearing loss following N 2 0 anaesthesia in one such patient. Its purpose was to confirm the effects of the gas on the normal middle ear, to compare the effect with that of non-N20 anaesthesia and to explore the time course of the events observed. Case historyThe patient, a 43-year-old woman, had a left stapedectomy for otosclerosis about 10 years ago and a standard 4.5-mm Schucknecht gelfoam and stainless steel prosthesis was inserted. Figure l(a) shows her audiogram at postoperative review; the upper trace is her (normal) sensorineural level and the lower is her hearing level to air conduction. The functional result of surgery was good with complete closure of the conductive gap.A year later she had a hysterectomy under general anaesthesia and immediately after operation complained of severe deterioration in her hearing. Her complaint was confirmed by audiometry which showed a 20-25 dB conductive loss- Figure I(b)-which has persisted to the present. The anaesthetic sequence was thiopentone, alcuronium, intubation and ventilation with N 2 0 and O2 to which 0.5% halothane was added.