[Application of acute physiology and chronic health evaluation II score in the timing of noninvasive ventilation in patients with acute exacerbation of chronic obstructive pulmonary disease].

OBJECTIVE: To explore the application of acute physiology and chronic health evaluation II (APACHE II) score in the timing and nursing of noninvasive ventilation for patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). METHODS: 106 AECOPD patients admitted to Haikou People's Hospital from January 2018 to October 2019 were selected as the study objects. According to the method of random number table, the patients were divided into observation group and control group, with 53 patients in each group. The control group selected the timing of noninvasive ventilation treatment according to the standards of Mechanical ventilation (second edition), weaned according to Clinical practice of mechanical ventilation, and received routine nursing in intensive care unit (ICU), including creating comfortable indoor environment, reasonable diet, condition monitoring, psychological nursing and complications nursing. On the basis of the control group, the patients in the observation group were given noninvasive ventilation when APACHE II score was more than 10, and were weaned when APACHE II score was less than or equal to 10. According to APACHE II score < 10, 10-14, 15-19 and ≥ 20, the patients were given level-3 care, level-2 care, level-1 care and intensive care. The pulmonary function before and 3 days after the noninvasive ventilation treatment was monitored, and the duration of mechanical ventilation, the length of ICU stay, endotracheal intubation rate, incidence of complication [ventilator associated pneumonia (VAP)] and ICU mortality were recorded. The self-designed questionnaire of nursing satisfaction was used to evaluate the patients' nursing satisfaction. RESULTS: There was no significant difference in general data such as gender or age between the two groups. After 3 days of noninvasive ventilation, the forced expiratory volume in one second (FEV1), forced vital capacity (FVC) and FEV1/FVC ratio of the two groups were increased significantly as compared with those before treatment, especially in the observation group, with statistical significances as compared with the control group [FEV1 (L): 3.02±0.22 vs. 2.54±0.19, FVC (L): 3.01±0.32 vs. 2.13±0.28, FEV1/FVC ratio: 0.89±0.08 vs. 0.79±0.08, all P < 0.05]. Compared with the control group, the duration of mechanical ventilation and length of ICU stay in the observation group were significantly shortened [duration of mechanical ventilation (days): 4.32±0.73 vs. 8.42±1.94, length of ICU stay (hours): 32.23±10.22 vs. 38.52±9.85, both P < 0.01]. The intubation rate, incidence of VAP and ICU mortality in the observation group were significantly lower than those in the control group [intubation rate: 1.9% (1/53) vs. 13.2% (7/53), incidence of VAP: 1.9% (1/53) vs. 15.1% (8/53), ICU mortality: 1.9% (1/53) vs. 13.2% (7/53), all P < 0.05]. The nursing satisfaction of patients in the observation group was significantly higher than that in the control group [96.2% (51/53) vs. 75.5% (40/53), P < 0.01]. CONCLUSIONS: APACHE II score can be used to guide the choice of noninvasive ventilation treatment opportunity and nursing intervention measures for AECOPD patients. It can significantly improve the pulmonary function of patients, improve the treatment effect, reduce the incidence of complications, and improve the satisfaction of patients with nursing, which is effective in clinical application.

Dkk1-mediated inhibition of Wnt signaling in bone results in osteopenia.

Mutations affecting the activity of the Wnt co-receptors LRP5 and LRP6 that cause alterations in skeletal biology confirmed the involvement of Wnt signaling in bone formation. We evaluated the potential role of Dkk1, an inhibitor of LRP5/6 activity, in bone formation by examining the normal expression pattern of Dkk1 in normal young mice and by assessing the consequences of osteoblast overexpression of Dkk1 in transgenic mice. Endogenous Dkk1 expression was detected primarily in osteoblasts and osteocytes. Transgenic over-expression of Dkk1 using two different rat collagen 1A1 promoters resulted in distinct bone phenotypes. More widespread Dkk1 expression (driven by the Col1A1 3.6 kb promoter) yielded osteopenia with forelimb deformities and hairlessness, while expression restricted to osteoblasts (driven by the Col1A1 2.3 kb promoter) induced severe osteopenia without limb defects or alopecia. The decrease in bone mass in vivo resulted from a significant 49% reduction in osteoblast numbers and was reflected in a 45% reduction in serum osteocalcin concentration; an in vitro study revealed that Dkk1 caused a dose-dependent suppression of osteoblast matrix mineralization. These data indicate that Dkk1 may directly influence bone formation and suggest that osteopenia develops in mice over-expressing Dkk1 at least in part due to diminished bone formation resulting from reduced osteoblast numbers.