Novel Use of Home Pulse Oximetry Monitoring in COVID-19 Patients Discharged From the Emergency Department Identifies Need for Hospitalization.

OBJECTIVES: Our objective was to evaluate patient-reported oxygen saturation (SpO2 ) using pulse oximetry as a home monitoring tool for patients with initially nonsevere COVID-19 to identify need for hospitalization. METHODS: Patients were enrolled at the emergency department (ED) and outpatient testing centers. Each patient was given a home pulse oximeter and instructed to record their SpO2 every 8 hours. Patients were instructed to return to the ED for sustained home SpO2  < 92% or if they felt they needed emergent medical attention. Relative risk was used to assess the relation between hospitalization and home SpO2  < 92% in COVID-19-positive patients. RESULTS: We enrolled 209 patients with suspected COVID-19, of whom 77 patients tested positive for COVID-19 and were included. Subsequent hospitalization occurred in 22 of 77 (29%) patients. Resting home SpO2  < 92% was associated with an increased likelihood of hospitalization compared to SpO2  ≥ 92% (relative risk = 7.0, 95% confidence interval = 3.4 to 14.5, p < 0.0001). Home SpO2  < 92% was also associated with increased risk of intensive care unit admission, acute respiratory distress syndrome, and septic shock. In our cohort, 50% of patients who ended up hospitalized only returned to the ED for incidental finding of low home SpO2 without worsening of symptoms. One-third (33%) of nonhospitalized patients stated that they would have returned to the ED if they did not have a pulse oximeter to reassure them at home. CONCLUSIONS: This study found that home pulse oximetry monitoring identifies need for hospitalization in initially nonsevere COVID-19 patients when a cutoff of SpO2 92% is used. Half of patients who ended up hospitalized had SpO2  < 92% without worsening symptoms. Home SpO2 monitoring also reduces unnecessary ED revisits.

Carbon monoxide toxicity after lighting coals at a hookah bar.

INTRODUCTION: Unintentional non-fire-related (UNFR) carbon monoxide (CO) poisonings continue to account for a significant health and economic burden in the United States. While most of these poisonings are related to faulty central heating or water heaters in private dwellings, less common sources should also be considered when a patient presents with any signs or symptoms suggestive of CO toxicity. CASE REPORT: The authors present a case where a patient was found to have severe CO poisoning, a COHgb level of 33.8 %, after lighting coals for a water pipe called a hookah. The patient was initially unconscious and was found to have electrocardiogram (ECG) changes consistent with cardiac ischemia that resolved following treatment with hyperbaric oxygen therapy. DISCUSSION: In recent years, hookah bars have gained in popularity, especially in urban areas and around college campuses. This was the first case to identify the potential occupational exposure of employees working at hookah bars to CO. Furthermore, the patient's COHb level of 33.8 % was higher than any previously reported in the literature with exposure via hookah pipe. The practitioner should consider CO poisoning in patients who smoke tobacco via a hookah and consider early hyperbaric oxygen therapy in those experiencing significant symptoms.

Interleukin-1beta and anaphylatoxins exert a synergistic effect on NGF expression by astrocytes.

C3a and C5a anaphylatoxins are proinflammatory polypeptides released during complement activation. They exert their biological activities through interaction with two G protein-coupled receptors named C3aR and C5aR, respectively. In the brain, these receptors are expressed on glial cells, and some recent data have suggested that anaphylatoxins could mediate neuroprotection. In this study, we used RT-PCR and ribonuclease protection assays (RPA) to investigate the role of anaphylatoxins on neurotrophin expression by the human glioblastoma cell line T98G and by rat astrocytes. Our data show that for both cell types, anaphylatoxins upregulate expression of NGF mRNA. This response depended on a G protein-coupled pathway since pre-treatment of cells with pertussis toxin (PTX) completely blocked NGF mRNA increases. This effect was anaphylatoxin-specific since pre-incubation with anti-C3a or anti-C5aR antibodies abolished the effects of C3a and C5a, respectively. The regulation of NGF mRNA by anaphylatoxins was not accompanied by translation into protein expression, but there was a significant synergic effect of anaphylatoxins/IL-1b costimulation. Our demonstration of involvement of anaphylatoxins in the NGF release process by astrocytes suggests that C3a and C5a could modulate neuronal survival in the CNS.