Risk factors of complications during noninvasive mechanical ventilation -assisted flexible bronchoscopy.

PURPOSE: Flexible bronchoscopy (FB) causes airway narrowing and may cause respiratory failure (RF). Noninvasive mechanical ventilation (NIV) is used to treat RF. Until recently, little was known about noninvasive mechanical ventilation assisted flexible bronchoscopy (NIV-FB) risk and complications. MATERIALS AND METHODS: A retrospective analysis of NIV-FB performed in 20 consecutive months (July 1, 2018-February 29, 2020) was performed. Indications for: FB and NIV, as well as impact of comorbidities, blood gas results, pulmonary function test results and sedation depth, were analyzed to reveal NIV-FB risk. Out of a total of 713 FBs, NIV-FB was performed in 50 patients with multiple comorbidities, acute or chronic RF, substantial tracheal narrowing, or after previously unsuccessful FB attempt. RESULTS: In three cases, reversible complications were observed. Additionally, due to the severity of underlining disease, two patients were transferred to the ICU where they passed away after >48h. In a single variable analysis, PaO2 69 â€‹± â€‹18.5 and 49 â€‹± â€‹9.0 [mmHg] (p â€‹< â€‹0.05) and white blood count (WBC) 10.0 â€‹± â€‹4.81 and 14.4 â€‹± â€‹3.10 (p â€‹< â€‹0.05) were found predictive for complications. Left heart disease indicated unfavorable NIV-FB outcome (p â€‹= â€‹0.046). CONCLUSIONS: NIV-FB is safe in severely ill patients, however procedure-related risk should be further defined and verified in prospective studies.

Chronic Obstructive Pulmonary Disease and Platelet Count.

Recently, it has been shown in the murine model that platelet maturation takes place, to some extent, in the lungs. The extrapolation of these findings to humans leads to the possibility that chronic lung diseases could affect platelet maturation and, consequently, the platelet count. The aim of this study was to investigate whether there are changes in the platelet count in patients with chronic obstructive disease (COPD). The study included 44 patients, aged 66.5 ± 5.5 years, in stage II-IV COPD. The control group consisted of 48 age- and gender-matched patients without any respiratory diseases. We failed to find a significant difference in the platelet count between the two groups: 231 ± 80 vs. 223 ± 63 x 103/µL, respectively (p = 0.61). However, the number of platelets in the COPD patients was inversely associated with hemoglobin content (r = -0.57; p < 0.001), hematocrit (r = -0.40; p = 0.006), and the red cell count (r = -0.51; p < 0.001); the blood morphology indices that are typically increased in severe COPD. Such associations were absent in the control non-COPD group. We conclude that COPD has no influence on the platelet count in humans.