Background Baseline diaphragmatic dysfunction (DD) at the initiation of non-invasive ventilation (NIV) correlates positively with subsequent intubation. We investigated the utility of DD detected 2 hours after NIV initiation in estimating NIV failure in acute exacerbation of chronic obstructive pulmonary disease (AECOPD) patients. Methods: In a prospective-cohort design, we enrolled 60 consecutive patients with AECOPD initiated on NIV at intensive care unit admission, and NIV failure events were noted. The DD was assessed at baseline (T1 timepoint) and 2 hours after initiating NIV (T2 timepoint). We defined DD as ultrasound-assessed change in diaphragmatic thickness (ΔTDI) <20% (predefined criteria [PC]) or its cut-off that predicts NIV failure (calculated criteria [CC]) at both timepoints. A predictive-regression analysis was reported. Results: In total, 32 patients developed NIV failure, nine within 2 hours of NIV and remaining in next 6 days. The ∆TDI cut-off that predicted NIV failure (DD-CC) at T1 was ≤19.04% (area under the curve [AUC], 0.73; sensitivity, 50%; specificity, 85.71%; accuracy; 66.67%), while that at T2 was ≤35.3% (AUC, 0.75; sensitivity, 95.65%; specificity, 57.14%; accuracy, 74.51%; hazard ratio, 19.55). The NIV failure rate was 35.1% in those with normal diaphragmatic function by PC (T2) versus 5.9% by CC (T2). The odds ratio for NIV failure with DD criteria ≤35.3 and <20 at T2 was 29.33 and 4.61, while that for ≤19.04 and <20 at T1 was 6, respectively. Conclusions: The DD criterion of ≤35.3 (T2) had a better diagnostic profile compared to baseline and PC in prediction of NIV failure.
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Effective use of noninvasive ventilation in patients with chronic obstructive pulmonary disease is well-known. However, noninvasive ventilation in patients presenting with altered sensorium and severe acidosis (pH <7.1) has been rarely described. Invasive mechanical ventilation is associated with high mortality in coronavirus disease 2019 (COVID-19), and use of noninvasive ventilation over invasive ventilation is an area of investigation. We report a case of COVID-19-induced acute exacerbation of chronic obstructive pulmonary disease in a 66-year-old male. His past medical history included obstructive sleep apnea, hypertension, cor pulmonale, atrial fibrillation, and amiodarone-induced hypothyroidism. On presentation, he had acute hypercapnic respiratory failure, severe acidosis (partial pressure of carbon dioxide [PCO2], 147 mm Hg; pH, 7.06), and altered mentation. The patient was successfully managed with noninvasive ventilation, avoiding endotracheal intubation, invasive ventilation, and related complications. Although precarious, a trial of noninvasive ventilation can be considered in COVID-19-induced acute exacerbation of chronic obstructive pulmonary disease with hypercapnic respiratory failure, severe acidosis, and altered mentation.
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Stress-induced cardiomyopathy (SICM) is an acute cardiac condition that causes left ventricular apical ballooning which mimicks acute coronary syndrome. The risk of in-hospital mortality with SICM is generally low (1% to 3%) and supportive care is usually sufficient for resolution.
Swine-origin influenza A (H1N1, S-OIV) is a recently spreading pandemic and a serious public health problem.
Although most S-OIV infections have a mild, self-limited course, clinical cases resulting in fatalities and associated with variable co-morbidities remain as a serious concern in some individuals. Among such serious complications, there have been few reports of SICM caused by S-OIV infection. We herein report, for the first time in the literature, a case with fatal hemodynamic instability secondary to SICM caused by S-OIV infection with viral pneumonia.