Background Secondary pulmonary infections (SPI) have not been well described in COVID-19 patients. Our study aims to examine the incidence and risk factors of SPI in hospitalized COVID-19 patients with pneumonia. Methods This was a retrospective, single-center study of adult COVID-19 patients with radiographic evidence of pneumonia admitted to a regional tertiary care hospital. SPI was defined as microorganisms identified on the respiratory tract with or without concurrent positive blood culture results for the same microorganism obtained at least 48 hours after admission. Results Thirteen out of 244 (5%) had developed SPI during hospitalization. The median of the nadir lymphocyte count during hospitalization was significantly lower in patients with SPI as compared to those without SPI [0.4 K/uL (IQR 0.3-0.5) versus 0.6 K/uL (IQR 0.3-0.9)]. Patients with lower nadir lymphocyte had an increased risk of developing SPI with odds ratio (OR) of 1.21 (95% CI: 1.00 to 1.47, p=0.04) per 0.1 K/uL decrement in nadir lymphocyte. The baseline median inflammatory markers of CRP [166.4 mg/L vs. 100.0 mg/L, p=0.01] and D-dimer (18.5 mg/L vs. 1.4 mg/L, p<0.01), and peak procalcitonin (1.4 ng/mL vs. 0.3 ng/mL, p<0.01) and CRP (273.5 mg/L vs. 153.7 mg/L, p<0.01) during hospitalization were significantly higher in SPI group. Conclusions The incidence of SPI in hospitalized COVID-19 patients was 5%. Lower nadir median lymphocyte count during hospitalization was associated with an increased OR of developing SPI. The CRP and D-dimer levels on admission, and peak procalcitonin and CRP levels during hospitalization were higher in patients with SPI.
Acute respiratory distress syndrome secondary to severe acute respiratory syndrome coronavirus-2 pneumonia or coronavirus disease 2019-related acute respiratory distress syndrome is the primary cause of mortality in coronavirus disease 2019. Some studies have described the concept of “high and low” elastance coronavirus disease 2019-related acute respiratory distress syndrome and proposed individualized management for the acute respiratory distress syndrome, deviating from low tidal volume ventilation. We report simultaneously measured respiratory parameters (static lung compliance, alveolar dead space ventilation, and shunt fraction) in 14 patients with advanced coronavirus disease 2019-related acute respiratory distress syndrome. The results were consistent with typical acute respiratory distress syndrome and did not support the concept of high-type coronavirus disease 2019-related acute respiratory distress syndrome and low-type coronavirus disease 2019-related acute respiratory distress syndrome.
A 19-year-old woman presented to pulmonary clinic with recurrent episodes of fevers and productive cough over the last 2 years. She was diagnosed with several episodes of respiratory infection that required antibiotic therapy. Her symptoms improved transiently after antibiotic therapy. However, symptoms continued to recur every 1 to 2 months. She denied any close TB contacts or travel outside the United States. She was a nonsmoker and had no history of immunodeficiency. There was no history of cystic fibrosis or any foreign body aspiration.
INTRODUCTION: Atypical Hemolytic Uremic Syndrome (aHUS) is a severe form of thrombotic microangiopathy that presents with nonimmune hemolytic anemia, thrombocytopenia, and renal failure. Diffuse alveolar hemorrhage (DAH) due to disruption of alveolar-capillary basement membrane is an exceedingly rare presentation of aHUS. CASE PRESENTATION:A 19-year-old-male presented with acute respiratory distress, hemoptysis, tachypnea, tachycardia, elevated blood pressure, and oliguria. One month prior the patient was diagnosed with infectious mononucleosis associated with thrombocytopenia and splenomegaly. Initial labs demonstrated hemolytic anemia, thrombocytopenia, and acute renal failure. CT chest showed diffuse bilateral central alveolar opacities concerning for alveolar hemorrhage. Patient was stabilized with supplemental oxygen and urgent hemodialysis was initiated. Further studies revealed schistocytes on peripheral blood smear, hypocomplementemia, borderline low activity of ADAMTS-13, positive IgM/IgG to EBV nuclear antigen and a renal biopsy consistent with acute thrombotic microangiopathy affecting nearly all blood vessels and glomeruli. Serologies were negative for ANA, anti-dsDNA, ANCA, Anti-GBM ab, rheumatoid factor, HIV, HBV, and HCV. Patient was diagnosed with EBV infection associated Atypical Hemolytic Uremic Syndrome (aHUS) and received treatment with plasmapheresis and eculizumab. With this treatment, patients' respiratory distress, hemoptysis, and renal function improved, following which he was discharged with outpatient hemodialysis. He continues follow up with hematology and nephrology. DISCUSSION: aHUS is much less frequent than Shiga-toxin mediated hemolytic uremic syndrome. Endothelial injury and thrombotic microangiopathy are hallmarks of this complement mediated process. It is associated with high risk of ESRD. Recent advances in therapeutics targeted at complement regulatory proteins including Eculizumab, have offered better outcomes. DAH is a life-threatening complication that has rarely been reported with aHUS. Treatment of diffuse alveolar hemorrhage depends on etiology. In our patient, diagnosis and targeted management of aHUS helped improve hemoptysis and respiratory distress from DAH.CONCLUSIONS: Atypical HUS can present with acute onset renal failure and diffuse alveolar hemorrhage in some instances. Association with EBV infection is extremely rare.
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