Prognostic factors in elderly patients admitted to the intensive care unit with community-acquired pneumonia.
- 作者列表："Çelikhisar H","Daşdemir Ilkhan G","Arabaci Ç
:Objective: We aimed to determine the clinical, radiological and laboratory findings that may indicate poor prognosis in severe community acquired pneumonia (CAP) requiring intensified care to reduce the risk of death.Methods: The medical histories, demographic characteristics and laboratory values of over 65 years old patients admitted to the intensive care unit (ICU) and diagnosed with CAP were recorded.Results: Total of 86 patients were included in the study. Among those patients 39 were discharged from the ICU with health but 47 were expired. Diastolic blood pressure was significantly lower in expired patients (p = 0.044). In multivariate analysis, older age (>78 years) (p = 0.004), at admission elevated blood glucose (>108 mg/dL) levels (p = 0.048), decreased serum albumin (<3.5 g/dL) levels (p = 0.043), elevated serum procalcitonin levels (>0.63 μg/L) (p = 0.034) and in blood gas analysis decreased pH (<7.35) (p = 0.042)and increased lactate (>2mmol/L) (p = 0.001) were the significant risk factors for in-ICU mortality.Conclusions: At old age, blood glucose and procalcitonin levels increased at the time of admission, serum albumin levels decreased, pH decreased in blood gas analysis and lactate levels increased, and significant mortality determinants in CAP patients over 65 years of age who applied to the intensive care unit.
目的: 我们旨在确定需要加强护理以降低死亡风险的重症社区获得性肺炎 (CAP) 的临床、放射学和实验室检查结果可能表明预后不良。方法: 对入住重症监护病房 (ICU) 的 65 岁以上老年患者的病史、人口学特征和实验室检查值进行分析。确诊为社区获得性肺炎患者记录.结果: 86 例患者纳入研究.在这些患者中，39 例健康出院，但 47 例过期。过期患者舒张压显著降低 (p = 0.044)。在多变量分析中，年龄较大 (>78 岁) (p = 0.004)，入院时血糖水平升高 (>108 mg/dL) (p = 0.048),血清白蛋白水平降低 (<3.5g/dL) (p = 0.043)，血清降钙素原水平升高 (>0.63 μ g/L) (p = 0.034) 在血气分析中，ph值降低 (<7.35) (p = 0.042)，乳酸升高> 2mmol/L (p = 0.001) 是 ICU 病死率的显著危险因素。结论: 老年患者入院时血糖和降钙素原水平升高，血清白蛋白水平降低，血气分析 pH 降低，乳酸水平升高,65 岁以上申请重症监护室的 CAP 患者的显著死亡率决定因素。
METHODS:BACKGROUND AND PURPOSE:A critical role for sphingosine kinase/sphingosine-1-phosphate (S1P) pathway in the control of airway function has been demonstrated in respiratory diseases. Here, we address S1P contribution in a mouse model of mild chronic obstructive pulmonary disease (COPD). EXPERIMENTAL APPROACH:C57BL/6J mice have been exposed to room air or cigarette smoke up to 11 months and killed at different time points. Functional and molecular studies have been performed. KEY RESULTS:Cigarette smoke caused emphysematous changes throughout the lung parenchyma coupled to a progressive collagen deposition in both peribronchiolar and peribronchial areas. The high and low airways showed an increased reactivity to cholinergic stimulation and α-smooth muscle actin overexpression. Similarly, an increase in airway reactivity and lung resistances following S1P challenge occurred in smoking mice. A high expression of S1P, Sph-K2 , and S1P receptors (S1P2 and S1P3 ) has been detected in the lung of smoking mice. Sphingosine kinases inhibition reversed the increased cholinergic response in airways of smoking mice. CONCLUSIONS AND IMPLICATIONS:S1P signalling up-regulation follows the disease progression in smoking mice and is involved in the development of airway hyperresponsiveness. Our study defines a therapeutic potential for S1P inhibitors in management of airways hyperresponsiveness associated to emphysema in smokers with both asthma and COPD.
METHODS::The interim results from this 90-day multi-dose, inhalation toxicology study with life-time post-exposure observation has shown an important fundamental difference in persistence and pathological response in the lung between brake dust derived from brake-pads manufactured with chrysotile, TiO2 or chrysotile alone in comparison to the amphiboles, crocidolite and amosite asbestos. In the brake dust exposure groups no significant pathological response was observed at any time. Slight macrophage accumulation of particles was noted. Wagner-scores, were from 1 to 2 (1 = air-control group) and were similar to the TiO2 group. Chrysotile being biodegradable, shows a weakening of its matrix and breaking into short fibers & particles that can be cleared by alveolar macrophages and continued dissolution. In the chrysotile exposure groups, particle laden macrophage accumulation was noted leading to a slight interstitial inflammatory response (Wagner-score 1-3). There was no peribronchiolar inflammation and occasional very slight interstitial fibrosis. The histopathology and the confocal analyses clearly differentiate the pathological response from amphibole asbestos, crocidolite and amosite, compared to that from the brake dust and chrysotile. Both crocidolite and amosite induced persistent inflammation, microgranulomas, and fibrosis (Wagner-scores 4), which persisted through the post exposure period. The confocal microscopy of the lung and snap-frozen chestwalls quantified the extensive inflammatory response and collagen development in the lung and on the visceral and parietal surfaces. The interim results reported here, provide a clear basis for differentiating the effects from brake dust exposure from those following amphibole asbestos exposure. The subsequent results through life-time post-exposure will follow.
METHODS::The respiratory tract is lined by a pseudo-stratified epithelium from the nose to terminal bronchioles. This first line of defense of the lung against external stress includes five main cell types: basal, suprabasal, club, goblet and multiciliated cells, as well as rare cells such as ionocytes, neuroendocrine and tuft/brush cells. At homeostasis, this epithelium self-renews at low rate but is able of fast regeneration upon damage. Airway epithelial cell lineages during regeneration have been investigated in the mouse by genetic labeling, mainly after injuring the epithelium with noxious agents. From these approaches, basal cells have been identified as progenitors of club, goblet and multiciliated cells, but also of ionocytes and neuroendocrine cells. Single-cell RNA sequencing, coupled to lineage inference algorithms, has independently allowed the establishment of comprehensive pictures of cell lineage relationships in both mouse and human. In line with genetic tracing experiments in mouse trachea, studies using single-cell RNA sequencing (RNAseq) have shown that basal cells first differentiate into club cells, which in turn mature into goblet cells or differentiate into multiciliated cells. In the human airway epithelium, single-cell RNAseq has identified novel intermediate populations such as deuterosomal cells, 'hybrid' mucous-multiciliated cells and progenitors of rare cells. Novel differentiation dynamics, such as a transition from goblet to multiciliated cells have also been discovered. The future of cell lineage relationships in the respiratory tract now resides in the combination of genetic labeling approaches with single-cell RNAseq to establish, in a definitive manner, the hallmarks of cellular lineages in normal and pathological situations.