In response to COVID-19, many states revised, developed, or attempted to develop plans to allocate scarce critical care resources in the event that crisis standards of care were triggered. To our knowledge, no prior analysis has assessed this plan development process, including whether plans were successfully adopted.

Complex pleural space infections often require treatment with multiple doses of intrapleural tissue plasminogen activator (tPA) and deoxyribonuclease, with treatment failure frequently necessitating surgery. Pleural infections are rich in neutrophils, and neutrophil elastase degrades plasminogen, the target substrate of tPA, that is required to generate fibrinolysis. We hypothesized that pleural fluid from patients with pleural space infection would show high elastase activity, evidence of inflammatory plasminogen degradation, and low fibrinolytic potential in response to tPA that could be rescued with plasminogen supplementation.

A 52-year-old woman with no significant medical history was referred to our hospital for expedited workup of progressive dysarthria and ataxia over the past year. Prior CT angiography of the head and neck showed no relevant neurologic findings but did reveal miliary lesions in the lung apices, which was later confirmed via dedicated CT chest scan (Fig 1). Review of systems was negative for any respiratory, constitutional, or rheumatologic symptoms, except for new xanthelasma-like lesions over her forehead. She previously had smoked with 20 pack-years and had no TB risk factors. MRI of the face showed a 21-mm mass within the left external temporal fascia. MRI of the head showed diffuse leptomeningeal enhancement, right frontal lobe enhancement, and cerebellar and brainstem T2/fluid-attenuated inversion recovery hyperintensity, which prompted her admission to hospital.

Living donor (LD) lung transplantation (LT) represents an exceptional procedure in Western countries. However, in selected situations, it could be a source of unique advantages, besides addressing organ shortage. We report a successful case of father-to-child single-lobe LT, because of the complications of hematopoietic stem cell transplantation from the same donor, with initial low-dose immunosuppressive therapy and subsequent early discontinuation. Full donor chimerism was hypothesized to be a mechanism of transplant tolerance, and this postulated immunological benefit was deemed to outweigh the risks of living donation and the possible drawbacks of single compared with bilateral LT. Favorable size matching and donor's anatomy, accurate surgical planning, and specific expertise in pediatric transplantation also contributed to the optimal recipient and donor outcomes. Ten months after LD LT, the patient's steadily good lung function after withdrawal of immunosuppressive therapy seems to confirm the original hypothesis.

An 88-year-old woman was admitted to our hospital with the sudden onset of dyspnea after eating. The patient had undergone nephrectomy for a left renal tumor 24 years previously. The patient had been prescribed ferrous citrate for iron-deficiency anemia. She complained of appetite loss a few days before admission but had no abdominal pain. CT scan showed no abnormalities in the lungs but a mass in the liver.

A 38-year-old previously healthy woman was referred to our sleep center for recurrent witnessed breathing arrest during sleep. She had been brought to the ED 3 months earlier because of sudden onset of dizziness with nausea and vomiting, numbness and weakness of the left limb, less clear speech, double vision, dysphagia, and choking cough while drinking water. Brain MRI showed an acute cerebral infarction in the left medulla oblongata (Fig 1). High-resolution MRI showed vertebral artery dissection (Fig 2). Antiplatelet aggregation, lipid reduction, plaque stabilization, and trophic nerve treatments were administered, and the left limb strength, speech, and swallowing function improved. She complained of poor sleep and difficulties with memory.

Technical and clinical developments have raised challenging questions about the concept and practice of brain death, culminating in recent calls for revision of the Uniform Determination of Death Act (UDDA), which established a whole brain standard for neurologic death. Proposed changes range from abandoning the concept of brain death altogether to suggesting that current clinical practice simply should be codified as the legal standard for determining death by neurologic criteria (even while acknowledging that significant functions of the whole brain might persist). We propose a middle ground, clarifying why whole brain death is a conceptually sound standard for declaring death, and offering procedural suggestions for increasing certainty that this standard has been met. Our approach recognizes that whole brain death is a functional, not merely anatomic, determination, and incorporates an understanding of the difficulties inherent in making empirical judgments in medicine. We conclude that whole brain death is the most defensible standard for determining neurologic death-philosophically, biologically, and socially-and ought to be maintained.