and sterilisation of milk pumps and tubes). However, whether New born 2 was infected by breastfeeding or other modes of transmission remains unclear. Fur ther studies of milk samples from lactating women and possible virus transmission via breastfeeding are needed to develop recommendations on whether mothers with COVID19 should breastfeed.We declare no competing interests. RG, CC, and JAM contributed equally.

Background Recent data suggests an association between blood hyperviscosity and both propensity for thrombosis and disease severity in patients with COVID‐19. This raises the possibility that increased viscosity may contribute to endothelial damage and multiorgan failure in COVID‐19, and that therapeutic plasma exchange (TPE) to decrease viscosity may improve patient outcomes. Here we sought to share our experience using TPE in the first 6 patients treated for COVID‐19‐associated hyperviscosity. Study Design and Methods Six critically ill COVID‐19 patients with plasma viscosity levels ranging from 2.6 to 4.2 centipoise (cP; normal range, 1.4‐1.8 cP) underwent daily TPE for 2‐3 treatments. Results TPE decreased plasma viscosity in all six patients (Pre‐TPE median 3.75 cP, range 2.6‐4.2 cP; Post‐TPE median 1.6 cP, range 1.5‐1.9 cP). TPE also decreased fibrinogen levels in all five patients for whom results were available (Pre‐TPE median 739 mg/dL, range 601‐1188 mg/dL; Post‐TPE median 359 mg/dL, range 235‐461 mg/dL); D‐dimer levels in all six patients (Pre‐TPE median 5921 ng/mL, range 1134‐60 000 ng/mL; Post‐TPE median 4893 ng/mL, range 620‐7518 ng/mL); and CRP levels in five of six patients (Pre‐TPE median 292 mg/L, range 136‐329 mg/L; Post‐TPE median 84 mg/L, range 31‐211 mg/L). While the two sickest patients died, significant improvement in clinical status was observed in four of six patients shortly after TPE. Conclusions This series demonstrates the utility of TPE to rapidly correct increased blood viscosity in patients with COVID‐19‐associated hyperviscosity. Large randomized trials are needed to determine whether TPE may improve clinical outcomes for patients with COVID‐19.

H eart failure is a chronic disease state with substantial morbidity and mortality rates.1 End-stage heart failure is characterized by worsening symptoms despite optimal medical management, and heart transplantation is the definitive treatment. However, rates of heart failure are increasing, whereas the number of organs available for transplantation is static.2 Therefore, mechanical support for the failing heart, especially ventricular assist devices (VADs), has attracted strong interest. Left VAD (LVAD) implantation imparts higher survival rates in end-stage heart failure than does optimal medical management.3-6 Although LVADs are potentially life-saving, implantation sequelae include right ventricular failure, thromboembolism, bleeding, and infection. Investigators have reported infection rates of 18% to 59% in patients with LVADs, and mortality rates estimated at 70% for infections such as VAD-related mediastinitis and endocarditis.3,7-9 Depending on the site of the infection, treatment can range from simple wound care to device explantation.7,10 Multidrug-resistant organisms (MDROs) are increasingly prevalent and are associated with substantial morbidity and mortality rates. 11-13Patients with LVADs are at greater risk for MDRO infection because of their exposure during medical procedures and their generally longer lifespans after implantation. To our knowledge, no data have been published about the incidence of MDRO infections in patients who have LVADs. Our primary objective in this study was to determine that incidence, and our secondary objective was to evaluate outcomes and risk factors in MDRO infection. Patients and MethodsOur retrospective cohort study included patients whose permanent LVADs had been implanted at

We report 2 fatal exacerbations of systemic capillary leak syndrome (SCLS), also known as Clarkson disease, associated with coronavirus disease (COVID-19) in the United States. One patient carried an established diagnosis of SCLS and the other sought treatment for new-onset hypotensive shock, hemoconcentration, and anasarca, classic symptoms indicative of an SCLS flare. Both patients had only mild-to-moderate symptoms of COVID-19. This clinical picture suggests that these patients succumbed to complications of SCLS induced by infection with severe acute respiratory syndrome coronavirus 2. Persons with known or suspected SCLS may be at increased risk for developing a disease flare in the setting of mild-to-moderate COVID-19 infection.

Severe hypertension is a frequent condition among patients presenting to emergency departments. Historically, this has been referred to as a hypertensive crisis. In addition, these hypertensive crises have been further divided into either hypertensive emergencies or urgencies depending on the presence or absence of target organ damage, respectively. The management differs between these crises in both the rapidity of blood pressure correction and the medications used. Hypertensive emergencies must be treated immediately with intravenous antihypertensive medications. However, hypertensive urgencies may be treated with oral antihypertensive agents to reduce the blood pressure to baseline or normal over a period of 24-48 hr. Appropriate identification, evaluation, and treatment of these conditions are of great importance in the emergency department to prevent progression of organ damage and death. The purpose of this article is to provide an overview of the hypertensive crises and their management.