No abstract

There is a need to discriminate which COVID-19 inpatients are at higher risk for venous thromboembolism (VTE) to inform prophylaxis strategies. The IMPROVE-DD VTE risk assessment model (RAM) has previously demonstrated good discrimination in non-COVID populations. We aimed to externally validate the IMPROVE-DD VTE RAM in medical patients hospitalized with COVID-19. This retrospective cohort study evaluated the IMPROVE-DD VTE RAM in adult patients with COVID-19 admitted to one of thirteen Northwell Health hospitals in the New York metropolitan area between March 1, 2020 and April 27, 2020. VTE was defined as new-onset symptomatic deep venous thrombosis or pulmonary embolism. To assess the predictive value of the RAM, the receiver operating characteristic (ROC) curve was plotted and the area under the curve (AUC) was calculated. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were calculated. Of 9407 patients who met study criteria, 274 patients developed VTE with a prevalence of 2.91%. The VTE rate was 0.41% for IMPROVE-DD score 0–1 (low risk), 1.21% for score 2–3 (moderate risk), and 5.30% for score ≥ 4 (high risk). Approximately 45.7% of patients were classified as high VTE risk, 33.3% moderate risk, and 21.0% low risk. Discrimination of low versus moderate-high VTE risk demonstrated sensitivity 0.971, specificity 0.215, PPV 0.036, and NPV 0.996. ROC AUC was 0.703. In this external validation study, the IMPROVE-DD VTE RAM demonstrated very good discrimination to identify hospitalized COVID-19 patients at low, moderate, and high VTE risk.

Catamenial pneumothorax (CP) is an extremely rare pulmonary pathology seen in women of reproductive age, typically occurring within 72 hours from the onset of menstrual bleeding. Multiple theories have been proposed to explain the etiopathogenesis of CP; however, the exact underlying mechanism remains elusive. More than 90% of reported cases in the literature describe a right-sided presentation of pneumothorax. In this case report, we describe a rare left-sided presentation of CP and discuss the current literature on underlying etiopathogenesis, diagnostics, and available therapeutic modalities for managing this rare clinical entity.

A previously healthy, 59-year-old female presented with respiratory distress and dry cough for one week. Outpatient radiographic findings were suspicious for basilar pneumonia. Empiric broad-spectrum antibiotics were started; however, she continued to deteriorate rapidly over the next 48 hours, with chest X-ray showing diffuse bilateral multifocal airspace opacities consistent with acute respiratory distress syndrome. The ratio of partial pressure arterial oxygen to fraction of inspired oxygen was 225. She required a high-flow nasal cannula with a subsequent upgrade to the intensive care unit (ICU) for increasing respiratory compromise. Polymerase chain reaction (PCR) of the nasopharyngeal aspirate confirmed human rhinovirus (hRV). High-dose intravenous steroids were started as adjuvant therapy due to the rapid decline, presumably due to a dysregulated host immune response. After 10 days in the ICU, she was discharged with tiotropium and steroid taper. Historically thought to be limited to pandemic viruses, improved detection of hRV has led to its implication in serious respiratory disorders extending beyond the oropharynx in immunocompetent hosts. We report a rare case of hRV-induced severe acute respiratory distress syndrome (ARDS) in an immunocompetent host. This case highlights the need for the early identification of viral culprits, which can minimize the use of invasive diagnostic testing and antibiotic usage.

Coronavirus disease 2019 (COVID-19) causes acute microvascular thrombosis in both venous and arterial structures which is highly associated with increased mortality. The mechanisms leading to thromboembolism are still under investigation. Current evidence suggests that excessive complement activation with severe amplification of the inflammatory response (cytokine storm) hastens disease progression and initiates complement-dependent cytotoxic tissue damage with resultant prothrombotic complications. The concept of thromboinflammation, involving overt inflammation and activation of the coagulation cascade causing thrombotic microangiopathy and end-organ damage, has emerged as one of the core components of COVID-19 pathogenesis. The complement system is a major mediator of the innate immune response and inflammation and thus an appealing treatment target. In this review, we discuss the role of complement in the development of thrombotic microangiopathy and summarize the current data on complement inhibitors as COVID-19 therapeutics.