Patients with obstructive sleep apnea (OSA) have an increased risk of cardiovascular morbidity. This study aimed to determine circulating carbon monoxide (CO) levels, which have been suggested to be a marker of cardiovascular risk in patients with OSA.
Venous blood samples were obtained from 35 patients with OSA and 17 age-matched, healthy control subjects before and after polysomnography. Concentrations of venous CO and serum heme oxygenase (HO)-1 were determined by gas chromatography and enzyme-linked immunosorbent assay, respectively.
Circulating CO levels in OSA patients were significantly increased in the morning, but not in the evening. The change in CO level, which was defined as a gap between the presleep and postsleep CO levels, correlated with apnea-hypopnea index and hypoxia duration as a percentage of total sleep time. No difference was found in serum HO-1 levels between OSA patients and control subjects. Treatment with continuous positive airway pressure (CPAP) resulted in normalization of the postsleep CO level.
The postsleep circulating CO level is helpful for assessing the clinical severity of OSA. Moreover, treatment of OSA with CPAP can potentially reduce the risk of the disease associated cardiovascular events.
Inflammatory changes such as subepithelial edema and excessive inflammatory cell infiltration have been observed in uvular tissues of obstructive sleep apnea (OSA) subjects. The levels of proinflammatory cytokines such as tumor necrosis factor (TNF)- and interleukin-6 are elevated in the serum of apneic patients and have been proposed as mediators of muscle weakness. TNF- has been shown to affect diaphragm contractility in mice and rabbit in vivo.
To assess total and compartmental TNF- expression in uvular tissues of apneic and nonapneic patients.
Uvular tissues were collected from 14 snorers without sleep disorders breathing, 14 subjects with OSA (OSA 1 group) whose body mass index (BMI) was similar to that of snorers, and 12 additional obese OSA subjects (OSA 2 group) who underwent an uvulopalatopharyngoplasty. Sections were examined using immunohistochemistry and Western blot analysis. TNF- expression was evaluated in the musculus uvulae (MU), epithelial layer, and perimuscular tissues from proximal uvular sections.
TNF- was more highly expressed in whole uvular protein extracts of apneic groups than in snorers ([mean ± SEM] snorers, 100.5 ± 3.0%; OSA 1 group, 127.1 ± 6.9%; OSA 2 group, 140.7 ± 11.0%; p = 0.01). In the muscular area, TNF- levels were higher in the more obese OSA subjects than in the other two groups (snorers, 100.3 ± 3%; OSA 1 group, 107.4 ± 0.7%; OSA 2 group, 124.1 ± 4.2%; p = 0.007). In the muscular area, TNF- was correlated with BMI, but no relationship was found with the apnea-hypopnea index.
We conclude that MU is the major TNF- source in uvular tissue and that TNF- is more highly expressed in the heaviest OSA patients compared to less obese OSA patients and nonapneic snorers.
The aim was to investigate the significance of snoring and sleep apnea on daytime symptoms in a population-based sample of women.
From the general population, 400 women aged 20 to 70 years were randomly selected, with oversampling of habitually snoring women. The women were investigated using full-night polysomnography and a questionnaire. The apnea-hypopnea index (AHI) was calculated, and women who acknowledged snoring loudly and disturbingly often or very often were considered habitual snorers.
Habitual snoring was independently related to excessive daytime sleepiness (odds ratio [OR], 2.28; 95% confidence interval [CI], 1.31 to 3.99), to falling asleep involuntarily during the day (OR, 2.11; 95% CI, 1.06 to 4.21), to waking up unrefreshed (OR, 2.14; 95% CI, 1.30 to 3.52), to daytime fatigue (OR, 2.77; 95% CI, 1.54 to 4.99), and to a dry mouth on awakening (OR, 2.00; 95% CI, 1.22 to 3.27) after adjustment for AHI, age, body mass index (BMI), smoking, total sleep time, percentage of slow-wave sleep, and percentage of rapid eye movement (REM) sleep. An AHI ≥ 15/h was only related to a dry mouth on awakening after adjustment for snoring, age, BMI, smoking, total sleep time, percentage of slow-wave sleep, and percentage of REM sleep (OR, 2.24; 95% CI, 1.14 to 4.40). An AHI of 5 to 15/h was not related to any daytime symptom.
Excessive daytime sleepiness and daytime fatigue are related to habitual snoring independent of the apnea-hypopnea frequency, age, obesity, smoking, and sleep parameters in a population-based sample of women, but not to the AHI. This indicates that snoring is an independent cause of excess daytime sleepiness and not merely a proxy for sleep apnea.
Cardiac events are the predominant cause of late mortality in patients with peripheral arterial disease (PAD). In these patients, mortality decreases with increasing body mass index (BMI). COPD is identified as a cardiac risk factor, which preferentially affects underweight individuals. Whether or not COPD explains the obesity paradox in PAD patients is unknown.
We studied 2,392 patients who underwent major vascular surgery at one teaching institution. Patients were classified according to COPD status and BMIs (ie, underweight, normal, overweight, and obese), and the relationship between these variables and all-cause mortality was determined using a Cox regression analysis. The median follow-up period was 4.37 years (interquartile range, 1.98 to 8.47 years).
The overall mortality rates among underweight, normal, overweight, and obese patients were 54%, 50%, 40%, and 31%, respectively (p < 0.001). The distribution of COPD severity classes showed an increased prevalence of moderate-to-severe COPD in underweight patients. In the entire population, BMI (continuous) was associated with increased mortality (hazard ratio [HR], 0.96; 95% confidence interval [CI], 0.94 to 0.98). In addition, patients who were classified as being underweight were at increased risk for mortality (HR, 1.42; 95% CI, 1.00 to 2.01). However, after adjusting for COPD severity the relationship was no longer significant (HR, 1.29; 95% CI, 0.91 to 1.93).
The excess mortality among underweight patients was largely explained by the overrepresentation of individuals with moderate-to-severe COPD. COPD may in part explain the "obesity paradox" in the PAD population.
Lung densitometry is an effective method to assess overall progression of emphysema, but generally the location of the progression is not estimated. We hypothesized that progression of emphysema is the result of extension from affected areas toward less affected areas in the lung. To test this hypothesis, a method was developed to assess emphysema severity at different levels in the lungs in order to estimate regional changes.
Fifty subjects with emphysema due to 1-antitrypsin deficiency (AATD) [AATD deficiency of phenotype PiZZ (PiZ) group] and 16 subjects with general emphysema (general emphysema without phenotype PiZZ [non-PiZ] group) were scanned with CT at baseline and after 30 months. Densitometry was performed in 12 axial partitions of equal volumes. To indicate predominant location, craniocaudal locality was defined as the slope in the plot of densities against partitions. Regional progression of emphysema was calculated after volume correction, and its slope identifies the area of predominant progression. The hypothesis was tested by investigating the correlation between predominant location and predominant progression.
As expected, the PiZ patients showed more basal emphysema than the non-PiZ group (craniocaudal locality, – 40.0 g/L vs – 6.2 g/L). Overall progression rate in PiZ patients was lower than in non-PiZ subjects. A significant correlation was found between craniocaudal locality and progression slope in PiZ subjects (R = 0.566, p < 0.001). In the non-PiZ group, no correlation was found.
In the PiZ group, the more emphysema is distributed basally, the more progression was found in the basal area. This finding suggests that emphysema due to AATD spreads out from affected areas.
Aspiration of endotracheal secretions is a major step in the prevention of ventilator-associated pneumonia (VAP). We compared conventional and continuous aspiration of subglottic secretions (CASS) procedures in ventilated patients after major heart surgery (MHS).
Randomized comparison during a 2-year period.
A total of 714 patients were randomized (24 patients were excluded from the study; 359 CASS patients; 331 control subjects). The results for CASS patients and control subjects (per protocol and intention-to-treat analysis) were as follows: VAP incidence, 3.6% vs 5.3% (p = 0.2) and 3.8% vs 5.1%, respectively; incidence density, 17.9 vs 27.6 episodes per 1,000 days of mechanical ventilation (MV) [p = 0.18] and 18.9 vs 28.7 episodes per 1,000 days of MV, respectively; hospital antibiotic use in daily defined doses (DDDs), 1,213 vs 1,932 (p < 0.001) and 1,392 vs 1,932, respectively (p < 0.001). In patients who had received mechanical ventilation for > 48 h, the comparisons of CASS patients and control subjects were as follows: VAP incidence, 26.7% vs 47.5% (p = 0.04), respectively; incidence density, 31.5 vs 51.6 episodes per 1,000 days of MV, respectively (p = 0.03); median length of ICU stay, 7 vs 16.5 days (p = 0.01), respectively; hospital antibiotic use, 1,206 vs 1,877 DDD (p < 0.001), respectively; Clostridium difficile-associated diarrhea, 6.7% vs 12.5% (p = 0.3), respectively; and overall mortality rate, 44.4% vs 52.5% (p = 0.3), respectively. Reintubation increased the risk of VAP (relative risk [RR], 6.07; 95% confidence interval [CI], 2.20 to 16.60; p < 0.001), while CASS was the only significant protective factor (RR, 0.40; 95% CI, 0.16 to 0.99; p = 0.04). No complications related to CASS were observed. The cost of the CASS tube was 9 vs 1.5 for the conventional tube.
CASS is a safe procedure that reduces the use of antimicrobial agents in the overall population and the incidence of VAP in patients who are at risk. CASS use should be encouraged, at least in patients undergoing MHS.
High cortisol levels are frequent in patients with severe infections. However, the predictive value of total cortisol and of the presence of critical illness-related corticosteroid insufficiency (CIRCI) in severe community-acquired pneumonia (CAP) remains to be thoroughly evaluated. The aim of this study was to investigate the predictive value of adrenal response in patients with severe CAP admitted to the ICU.
Baseline and postcorticotropin cortisol levels C-reactive protein (CRP), d-dimer, clinical variables, sequential organ failure assessment (SOFA), APACHE (acute physiology and chronic health evaluation) II, and CURB-65 (confusion, urea nitrogen, respiratory rate, BP, age ≥ 65 years) scores were measured in the first 24 h. Results are shown as median (interquartile range [IQR]). The major outcome measure was hospital mortality.
Seventy-two patients with severe CAP admitted to the ICU were evaluated. Baseline cortisol levels were 18.1 µg/dL (IQR, 14.4 to 26.7 µg/dL), and the difference between baseline and postcorticotropin cortisol after 250 µg of corticotropin was 19 µg/dL (IQR, 12.8 to 27 µg/dL). Baseline cortisol levels presented positive correlations with scores of disease severity, including CURB-65, APACHE II, and SOFA (p < 0.05). Cortisol levels in nonsurvivors were higher than in survivors. CIRCI was diagnosed in 29 patients (40.8%). In univariate analysis, baseline cortisol, CURB-65, and APACHE II were predictors of death. The discriminative ability of baseline cortisol (area under receiver operating characteristic curve, 0.77; 95% confidence interval, 0.65 to 0.90; best cutoff for cortisol, 25.7 µg/dL) for in-hospital mortality was better than APACHE II, CURB-65, SOFA, d-dimer, or CRP.
Baseline cortisol levels are better predictors of severity and outcome in severe CAP than postcorticotropin cortisol or routinely measured laboratory parameters or scores as APACHE II, SOFA, and CURB-65.
The etiology of clinical failure in hospitalized patients with community-acquired pneumonia (CAP) may be related or unrelated to pulmonary infection. The objective of this study was to define the incidence, etiology, timing, and risk factors associated with clinical failures related to CAP vs those unrelated to CAP.
Observational retrospective study of consecutive CAP patients. All patients who experienced clinical failure were identified. Cases were presented to a review committee that defined, by consensus, etiology, timing, and risk factors for clinical failures related to CAP.
Among 500 patients who were enrolled in the study, clinical failure was identified in 67 (13%). Clinical failure was related to CAP in 54 patients (81%). The most common etiologies for clinical failure related to CAP were severe sepsis (33%), acute myocardial infarction (28%), and progressive pneumonia (19%). All cases of severe sepsis occurred in the first 72 h of hospitalization. The most common etiology for clinical failure unrelated to CAP was the development of hospital-acquired pneumonia (45%). At the time of hospital admission, factors associated with clinical failure related to CAP were advanced age, congestive heart failure, hypotension, abnormal gas exchange, acidosis, hypothermia, thrombocytopenia, and pleural effusion.
The development of severe sepsis early during hospitalization is the primary etiology for clinical failure related to CAP. To achieve early treatment intervention, physicians should maintain a high index of suspicion for severe sepsis in hospitalized patients with CAP. To decrease the number of clinical failures unrelated to CAP, interventions need to be developed at the local level to improve the processes of care for patients with pneumonia.
Patients with health-care–associated pneumonia (HCAP) are frequently infected with a resistant pathogen and receive inappropriate empiric antibiotics (ie, pathogens resistant to administered treatment). Initial inappropriate treatment has been shown to increase hospital mortality. It is not known whether escalation in response to culture results mitigates this risk.
We identified patients admitted with a culture-positive pneumonia between January 2003 and December 2005. HCAP patients met one or more of the following criteria indicating ongoing contact with the health-care system: recent hospitalization (≤ 12 months), admission from a nursing home, immunosuppression, or long-term dialysis. We compared survivors to nonsurvivors among those patients with HCAP still hospitalized beyond 48 h.
Of 431 HCAP patients, 396 patients (92%) were alive and still hospitalized beyond 48 h. The crude mortality rate was 21.5%. Compared to survivors, nonsurvivors were significantly more likely to be treated with inappropriate empiric antibiotics (37.6% vs 24.1%, p = 0.013). Although mortality was higher among patients receiving inappropriate than appropriate therapy (30.0% vs 18.3%, p = 0.013), this difference was more pronounced among nonbacteremic patients (odds ratio [OR], 2.45; 95% confidence interval [CI], 1.26 to 4.75) than bacteremic patients (OR, 1.25; 95% CI, 0.41 to 3.57). In a logistic regression, inappropriate empiric antibiotic treatment among nonbacteremic patients was independently associated with mortality (OR, 2.88; 95% CI, 1.46 to 5.67); treatment escalation did not attenuate the risk of death.
Among HCAP patients alive and hospitalized beyond 48 h, hospital mortality was high and, in the absence of bacteremia, greater with initial inappropriate antibiotic treatment. Despite subsequent escalation, initial inappropriate antibiotic choice nearly tripled the risk of hospital death.
To compare pressure characteristics of mechanical ventilation and their impact on pediatric patients with severe ARDS in the pre-protective lung strategy (PLS) and post-PLS eras.
Medical records of 33 patients admitted to our pediatric ICU with ARDS from 1992 through 1994 (pre-PLS) and 52 patients with ARDS admitted from 2000 through 2003 (post-PLS) were retrospectively reviewed.
Patient age and gender distribution were identical in both eras. Fifty-five percent of the patients in the pre-PLS era had pneumothorax, compared to 17% in the post-PLS era (p < 0.05). Overall mortality rates for patients in the pre-PLS and post-PLS eras were 42% and 25%, respectively (p = 0.09; not significant). Mean duration of exposure to peak inspiratory pressure (PIP) values > 40 cm H2O was significantly longer in the pre-PLS era than in the post-PLS era. Pre-PLS patients with pneumothorax received mean maximum PIP of 72 ± 17 cm H2O, mean maximum positive end-expiratory pressure (PEEP) of 20 ± 5 cm H2O, and maximum mean airway pressure (MAP) of 46 ± 8 cm H2O, while patients in the post-PLS era required mean maximum PIP of 42 ± 2 cm H2O, mean maximum PEEP of 14 ± 2 cm H2O, and maximum MAP of 30 ± 6 cm H2O, respectively (p < 0.05 for all pressure parameters). There were no significant differences in mechanical ventilation pressure characteristics among patients who did not have pneumothorax during their course of management in both eras.
A significantly more aggressive use of ventilator pressure characteristics distinguished the pre-PLS era from the post-PLS era, and was found to be associated with a markedly higher incidence of pneumothorax. Outcome in both eras did not differ significantly, presumably due to insufficient statistical power.
Pulmonary complications following injury significantly contribute to subsequent mortality. Obese patients have preexisting risk factors for pulmonary complications, and are at risk for these complications following elective surgery. Whether or not obesity contributes to pulmonary complications after critical injury is poorly understood.
A secondary analysis of a prospective cohort study of critically injured adults requiring at least 48 h of intensive care was performed. Patients were classified into the following body mass index groups: ≤ 18.5 kg/m2 (underweight); 18.5 to 24.9 kg/m2 (normal); 25 to 29.9 kg/m2 (overweight); 30.0 to 39.9 kg/m2 (obese); and ≥ 40.0 kg/m2 (severely obese). Outcomes included the rates of ARDS and pneumonia, the placement of a tracheostomy tube, and in-hospital mortality rate.
A total of 1,291 patients were available for analysis, and 30% of these patients were classified as either obese or severely obese. The age-, gender-, and severity-adjusted rate of ARDS was lower in severely obese patients (odds ratio, 0.36; 95% confidence interval [CI], 0.13 to 0.99) compared to normal weight patients. The rates of pneumonia (37%), tracheostomy (10%), and in-hospital mortality (11%) did not differ among the groups. Despite no difference in pulmonary complications, the severely obese group had an ICU length of stay that was 4.8 days (95% CI, 1.8 to 7.7 days) longer than the normal weight group.
Obesity does not appear to be an independent risk factor for increased pulmonary complications after critical injury, but severely obese patients are likely to require longer ICU stays.Trial registration: Clinicaltrials.gov Identifier: NCT00170560
Because interpatient variability in bronchodilation from inhaled albuterol is large and clinically important, we characterized the albuterol dose/response relationship by pharmacodynamic modeling and quantified variability.
Eighty-one patients with asthma (24% African American [AA]; 8 to 65 years old; baseline FEV1, 40 to 80% of predicted) received 180 µg of albuterol from a metered-dose inhaler (MDI), and then 90 µg every 15 min until maximum improvement or 540 µg was administered; all then received 2.5 mg of nebulized albuterol. FEV1 was measured 15 min after each dose. The population cumulative dose/response data were fitted with a sigmoid maximum effect of albuterol (Emax) [maximum percentage of predicted FEV1 effect] model by nonlinear mixed-effects modeling. The influence of covariates on maximum percentage of predicted FEV1 reached after albuterol administration (Rmax) and cumulative dose of albuterol required to bring about 50% of maximum effect of albuterol (ED50) and differences between AA and white patients were explored.
ED50 was 141 µg, and Emax was 24.0%. Coefficients of variation for ED50 and Emax were 40% and 56%, respectively. Ethnicity was a statistically significant covariate (p < 0.05). AA and white patients reached 82.4% and 91.9% of predicted FEV1, respectively (p = 0.0004); and absolute improvement in percentage of predicted FEV1 was 16.6% in AA patients vs 26.7% in white patients (p < 0.0003). There were no baseline characteristic differences between AA and white patients. Nebulized albuterol increased FEV1 ≥ 200 mL in 21% of participants. Heart rate and BP were unchanged from baseline after maximal albuterol doses.
Our model predicts that 180 µg of albuterol by MDI produces a 14.4% increase in percentage of predicted FEV1 over baseline (11.7% in AA patients, and 17.5% in white patients). Emax varies widely between asthmatic patients. AA patients are less responsive to maximal doses of inhaled albuterol than white patients.
Nonasthmatic eosinophilic bronchitis (NAEB) is an important cause of chronic cough, and it can be diagnosed by an induced-sputum (IS) examination. However, an IS examination is a complex and time-consuming procedure, and it has limited clinical application. This study aimed to evaluate the role of exhaled nitric oxide (NO) for the investigation of chronic cough, especially of NAEB.
Two hundred eleven nonsmoking patients with a cough lasting > 3 weeks were enrolled in the study. The patients were examined and investigated with conventional diagnostic tools, including an IS examination. Exhaled NO was measured by a chemoluminescent analyzer.
One hundred seventeen patients with adequate IS results were analyzed: asthma, n = 14; NAEB, n = 21; and "others," n = 82. Exhaled NO and IS eosinophils were significantly higher in the asthma group and NAEB group than in the others group. Exhaled NO and IS eosinophils were significantly correlated in the asthma and NAEB groups. In the nonasthmatic group, the sensitivity and specificity of exhaled NO for detecting NAEB, using 31.7 parts per billion as the exhaled NO cutoff point, were 86% and 76%, respectively. Positive and negative predictive values were 47% and 95%, respectively, and positive and negative likelihood ratios were 3.51 and 0.19, respectively.
We concluded that exhaled NO measurement may be useful as part of the initial evaluation for chronic cough, especially for the exclusion of NAEB. A low level of exhaled NO suggested little likelihood of NAEB for the nonasthmatic patients with chronic cough.
Different types of immune cells are involved in the formation of granulomas, a hallmark of pulmonary sarcoidosis. Proinflammatory monocytes are activated circulating monocytes thought to be related to the initial events of granuloma formation. We tested the hypothesis that peripheral blood monocytes in patients with active pulmonary sarcoidosis have an activated phenotype and, secondly, that measuring this activation status can provide a new tool for monitoring disease activity.
Blood was collected of 23 steroid-naive patients presenting with pulmonary sarcoidosis and 10 healthy control subjects. Expression of CD16 (Fc- type III receptor), CD69 (a general activation marker of cells of the hematopoietic lineage), and the integrin very late antigen (VLA)-1 (on interaction with extracellular matrix compounds mediates cell adhesion) was measured by flow cytometry.
Percentages of monocytes expressing CD16, CD69, and VLA-1 in patients vs control subjects were 56.2 ± 4.1% vs 12.2 ± 2.4% (p < 0.0001), 87.3 ± 2.1% vs 8.6 ± 3.3% (p < 0.0001), and 66.5 ± 3.6% vs 11.2 ± 2.3% (p < 0.0001), respectively. Moreover, the CD69+VLA-1+ monocyte subset, abundantly present at disease presentation, was found to decrease to normal levels during follow-up with disease remission.
Peripheral blood monocytes from patients with pulmonary sarcoidosis show a highly activated phenotype. Phenotyping circulating monocytes might be a promising tool for monitoring sarcoidosis disease activity but needs further investigation.
Spirometry plays an essential role in the diagnosis and management of pulmonary diseases. The accurate interpretation of spirometric data depends on comparison to a reference population to identify abnormalities in ventilatory function. National guidelines recommended the use of the National Health and Nutrition Examination Study (NHANES) III data set as the preferred reference population for those persons 8 to 80 years of age in the United States.
To determine the effect of using NHANES III reference equations, compared to those of Crapo et al (Crapo), Knudson et al (Knudson), or Morris et al (Morris), on spirometric interpretations in non-Hispanic white patients.
We conducted a cross-sectional study of all white patients undergoing spirometry testing at our hospital from January 2000 through May 2007. Patients were classified as normal, restricted, obstructed, or mixed, based on the American Thoracic Society (ATS)/European Respiratory Society (ERS) guidelines, using the Crapo, Knudson, Morris, and NHANES III prediction equations. Differences in the classifications based on the reference data set were evaluated.
At total of 8,733 subjects (62.4% male subjects) were identified, with a mean age of 53 years. Discordance was most common when the results from prediction equations by Knudson and Morris were compared to those of NHANES III (45.5% and 35.3%, respectively). Diagnostic recategorizations occurred less frequently when the prediction equations by Crapo were compared with those of NHANES III (15.9%). Relative to NHANES III, the prediction equations by Knudson, Crapo, and Morris tend to overclassify obstruction and underclassify restriction.
There is significant discordance between the prediction equations put forth by Crapo, Knudson, Morris, and the NHANES III. Our data suggest that the diagnostic reclassification of many patients undergoing pulmonary function testing will occur when ATS/ERS guidelines are implemented. Pulmonologists and other physicians interpreting spirometry need to be aware of the presence and nature of these changes.
Ultrathin bronchoscopy guided by virtual bronchoscopy (VB) techniques show promise for the diagnosis of peripheral lung lesions. In a phantom study, we evaluated a new real-time, VB-based, image-guided system for guiding the bronchoscopic biopsy of peripheral lung lesions and compared its performance to that of standard bronchoscopy practice.
Twelve bronchoscopists of varying experience levels participated in the study. The task was to use an ultrathin bronchoscope and a biopsy forceps to localize 10 synthetically created lesions situated at varying airway depths. For route planning and guidance, the bronchoscopists employed either standard bronchoscopy practice or the real-time image-guided system. Outcome measures were biopsy site position error, which was defined as the distance from the forceps contact point to the ground-truth lesion boundary, and localization success, which was defined as a site identification having a biopsy site position error of ≤ 5 mm.
Mean (± SD) localization success more than doubled from 43 ± 16% using standard practice to 94 ± 7.9% using image guidance (p < 10–15 [McNemar paired test]). The mean biopsy site position error dropped from 9.7 ± 9.1 mm for standard practice to 2.2 ± 2.3 mm for image guidance. For standard practice, localization success decreased from 56% for generation 3 to 4 lesions to 31% for generation 6 to 8 lesions and also decreased from 51% for lesions on a carina vs 23% for lesions situated away from a carina. These factors were far less pronounced when using image guidance, as follows: success for generation 3 to 4 lesions, 97%; success for generation 6 to 8 lesions, 91%; success for lesions on a carina, 98%; success for lesions away from a carina, 86%. Bronchoscopist experience did not significantly affect performance using the image-guided system.
Real-time, VB-based image guidance can potentially far exceed standard bronchoscopy practice for enabling the bronchoscopic biopsy of peripheral lung lesions.
Tuberculosis (TB) is a worldwide infectious disease. Recently, standard therapy has become very effective for treating patients with TB; however, as a result of this powerful regimen, serious side effects have become an important problem. The aim of this prospective study was to evaluate the usefulness of the drug lymphocyte stimulation test (DLST) to determine anti-TB drugs causing side effects.
Four hundred thirty-six patients with TB were admitted to our hospital for treatment between January 2002 and August 2007. DLST was performed in patients who had certain adverse drug reactions during TB treatment. The causative drug was identified by the drug provocation test (DPT). The tested drugs were mainly isoniazid (INH), rifampin (RIF), ethambutol (EMB) and pyrazinamide (PZA).
Of 436 patients, 69 patients (15.8%) had certain adverse drug reactions to anti-TB drugs. Of the 261 agents that underwent the DLST and DPT, 28 agents (10.7%) in 20 patients (28.9%) were positive by DLST, and 67 agents (25.7%) in 46 patients (66.6%) were identified as causative drugs by DPT. The sensitivity of DLST was only 14.9% for all drugs (INH, 14.3%; RIF, 13.6%; EMB, 14.3%; PZA, 0%).
DLST offers little contribution to the detection of causative agents in patients with adverse anti-TB drug reactions.
International guidelines for the management of primary spontaneous pneumothorax (PSP) vary, and there is growing opinion that more patients could be successfully managed with observation alone. There is little published evidence detailing the outcomes of emergency department (ED) patients who have been treated for PSP. The aim of this study was to describe the clinical outcomes for patients with PSP.
This was a retrospective cohort study that was conducted by explicit medical record review that investigated adult patients with PSP who had been treated at two urban teaching hospital EDs from 1996 to 2005. The data collected included demographics, clinical data at presentation, and outcome data. The outcome of interest was the proportion of patients who were successfully treated with the initial management strategy (ie, conservative, aspiration, and tube thoracostomy). Data analysis was performed using descriptive statistics.
A total of 203 episodes of PSP in 154 patients (70% male; median age, 24 years) was identified. PSP size ranged from 5 to 100%. Ninety-one PSP patients (45%) were treated with outpatient observation, 48 patients (24%) were treated with aspiration, and 64 patients (31%) were treated with tube thoracostomy. In total, the conditions of 79% of patients (82 of 91 patients) who were treated with observation resolved without additional intervention. Aspiration was successful in 50% of cases (24 of 48 cases) where it was attempted; the conditions of 73% of PSP patients who were treated with tube thoracostomy (47 of 64) resolved without additional intervention.
These data suggest that observation alone is an effective initial treatment strategy for selected patients with PSP. They support the inclusion of an observation arm in planned prospective studies comparing different management approaches.
Approximately 60 million people in the United States live with one of four chronic conditions: heart disease, diabetes, chronic respiratory disease, and major depression. Anxiety and depression are very common comorbidities in COPD and have significant impact on patients, their families, society, and the course of the disease.
We report the proceedings of a multidisciplinary workshop on anxiety and depression in COPD that aimed to shed light on the current understanding of these comorbidities, and outline unanswered questions and areas of future research needs.
Estimates of prevalence of anxiety and depression in COPD vary widely but are generally higher than those reported in some other advanced chronic diseases. Untreated and undetected anxiety and depressive symptoms may increase physical disability, morbidity, and health-care utilization. Several patient, physician, and system barriers contribute to the underdiagnosis of these disorders in patients with COPD. While few published studies demonstrate that these disorders associated with COPD respond well to appropriate pharmacologic and nonpharmacologic therapy, only a small proportion of COPD patients with these disorders receive effective treatment.
Future research is needed to address the impact, early detection, and management of anxiety and depression in COPD.