Imaging in alpha-1 antitrypsin deficiency: a window into the disease.

Imaging modalities such as plain chest radiograph and computed tomography (CT) are important tools in the assessment of patients with chronic obstructive pulmonary disease (COPD) of any etiology. These methods facilitate differential diagnoses and the assessment of individual lung pathologies, such as the presence of emphysema, bullae, or fibrosis. However, as emphysema is the core pathological consequence in the lungs of patients with alpha-1 antitrypsin deficiency (AATD), and because AATD is associated with the development of other lung pathologies such as bronchiectasis, there is a greater need for patients with AATD than those with non-AATD-related COPD to undergo more detailed assessment using CT. In the field of AATD, CT provides essential information regarding the presence, distribution, and morphology of emphysema. In addition, it offers the option to quantify the extent of emphysema. These data have implications for treatment decisions such as initiation of alpha-1 antitrypsin (AAT) therapy, or suitability for surgical or endoscopic interventions for reducing lung volume. Furthermore, CT has provided vital insight regarding the natural history of emphysema progression in AATD, and CT densitometry has underpinned research into the efficacy of AAT therapy. Moving forward, hyperpolarized xenon gas (129Xe) lung magnetic resonance imaging (MRI) is emerging as a promising complement to CT by adding comprehensive measures of regional lung function. It also avoids the main disadvantage of CT: the associated radiation. This chapter provides an overview of technological aspects of imaging in AATD, as well as its role in the management of patients and clinical research. In addition, perspectives on the future potential role of lung MRI in AATD are outlined.

The effect of tracheostomy delay time on outcome of patients with prolonged mechanical ventilation: A STROBE-compliant retrospective cohort study.

The tracheostomy timing for patients with prolonged mechanical ventilation (PMV) was usually delayed in our country. Both physician decision time and tracheostomy delay time (time from physician's suggestion of tracheostomy to procedure day) affect tracheostomy timing. The effect of tracheostomy delay time on outcome has not yet been evaluated before.Patients older than 18 years who underwent tracheostomy for PMV were retrospectively collected. The outcomes between different timing of tracheostomy (early: ≤14 days; late: >14 days of intubation) were compared. We also analyzed the effect of physician decision time, tracheostomy delay time, and procedure type on clinical outcomes.A total of 134 patients were included. There were 57 subjects in the early tracheostomy group and 77 in the late group. The early group had significantly shorter mechanical ventilation duration, shorter intensive care unit stays, and shorter hospital stays than late group. There was no difference in weaning rate, ventilator-associated pneumonia, and in-hospital mortality. The physician decision time (8.1 ±â€Š3.4 vs 18.2 ±â€Š8.1 days, P < .001) and tracheostomy delay time (2.1 ±â€Š1.9 vs 6.1 ±â€Š6.8 days, P < .001) were shorter in the early group than in the late group. The tracheostomy delay time [odds ratio (OR) = 0.908, 95% confidence interval (CI) = 0.832-0.991, P = .031) and procedure type (percutaneous dilatation, OR = 2.489, 95% CI = 1.057-5.864, P = .037) affected successful weaning. Platelet count of >150 × 10/µL (OR = 0.217, 95% CI = 0.051-0.933, P = .043) and procedure type (percutaneous dilatation, OR = 0.252, 95% CI = 0.069-0.912, P = .036) were associated with in-hospital mortality.Shorter tracheostomy delay time is associated with higher weaning success. Percutaneous dilatation tracheostomy is associated with both higher weaning success and lower in-hospital mortality.

Monitoring oxygen delivery in the critically ill.

An accurate assessment of regional tissue oxygen delivery (DO(2)) may help the intensivist to attenuate end-organ damage in critically ill patients. Transport of oxygen from the ambient air to the mitochondria occurs by convection and diffusion, and is tightly regulated by neural and humoral factors. This article reviews the basic principles of DO(2) and the abnormal oxygen supply-demand relationship seen in patients with shock. It also discusses approaches to monitoring DO(2), including clinical symptoms/signs, acid-base status, and gas exchange, which provide global assessment, as well as gastric tonometry, which may reflect regional DO(2). Some new experimental methods, such as near-infrared spectroscopy and positron emission tomography, are still in development but may in the future provide useful clinical devices for quantifying the adequacy of regional tissue oxygenation in critically ill patients.