La spécificité de la chirurgie pulmonaire chez l’enfant s’explique à la fois par des conditions techniques et anatomiques particulières et la nécessité d’un suivi long, le plus souvent sur plusieurs années.

En dehors des résections carcinologiques, les principales indications de cette chirurgie sont les malformations congénitales (malformations adénomatoïdes kystiques, séquestrations, emphysèmes), les séquelles infectieuses symptomatiques (dilatations des bronches, atélectasies, abcès) et les pneumothorax. Les progrès de la miniaturisation du matériel permettent de réaliser la majorité de ces interventions entièrement par voie thoracoscopique, à la restriction de la période néonatale. Chez le nouveau-né, pour lequel les indications opératoires restent exceptionnelles, les conditions ventilatoires et la relative étroitesse du thorax font encore préférer la chirurgie à ciel ouvert.

Les malformations pulmonaires peuvent également être prises en charge in utero, dès lors qu’elles retentissent sur le développement pulmonaire ou qu’elles sont à l’origine d’une défaillance cardiaque. Ces interventions, proposées après la 30^e semaine de gestation, n’ont pas pour but l’exérèse des lésions mais la levée de la compression. Mais ces prises en charges sont encore en phase d’évaluation et, compte tenu des possibles complications fœtales et maternelles, elles ne peuvent être réalisées que dans des centres experts et dans le cadre de protocoles précis.

Apart from the oncological resections, the main indications for this surgery are congenital lung anomalies (cystic adenomatoid malformation, bronchopulmonary sequestration, lobar emphysema), symptomatic postinfectious lesions (bronchiectasis, atelectasis, abscess) and pneumothorax. Advances in miniaturization of the surgical equipment are used to carry the majority of these interventions by thoracoscopy, except when performed at the neonatal period. In the newborn, for which the indications for lung surgical resections are exceptional, ventilatory conditions and the tightness of the chest lead to still prefer open surgery.

Pulmonary malformations can also be managed prenatally when they affect lung development or cause heart failure because of compressive complications. These interventions, performed after the 30th week of gestation, are not intended to remove the lesions, but to release the compression. But these procedures are still under evaluation and, in light of possible fetal and maternal complications, they should only be performed in tertiary centers and in the context of specific protocols.

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The BODE index has been shown to predict mortality in COPD. The index includes the 6 min walking test as the measure of exercise capacity. The incremental shuttle walking test (ISWT) is an alternative measure of exercise capacity which can be used to prescribe exercise and has been found to correlate well with peak VO2. The objective of the study was to evaluate the incorporation of the ISWT within the BODE index (named the i-BODE) to predict mortality in COPD.

Methods Data was analysed from 633 patients with COPD attending pulmonary rehabilitation over an 11 year period, and mortality determined a minimum of one year on from initial assessment. An i-BODE score was calculated using ISWT(m) then Cox regression analysis evaluated the capacity of the index to predict risk of death.

Results BMI, ISWT (m), MRC dyspnoea score, pack years and age were all significantly associated with mortality. Cox regression revealed the i-BODE index was an independent and significant predictor of mortality (hazard ratio 1.27 (CI 1.17–1.35), p < 0.001) and Kaplan Meier survival analysis showed each quartile increase in severity in i-BODE score was significantly associated with increased mortality (p < 0.001 by log rank test).

Conclusion We have found the i-BODE index to be an independent predictor of mortality in COPD, even when other strong predictors such as age and pack years are adjusted for. We conclude that the ISWT can be successfully substituted for the 6MWT as an alternative measure of exercise capacity within the BODE index.

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Background Despite efforts to disseminate guidelines for managing chronic obstructive pulmonary disease (COPD), adherence to COPD guidelines remains suboptimal. Barriers to adhering to guidelines remain poorly understood.

Methods Clinicians from two general medicine practices in New York City were surveyed to identify barriers to implementing seven recommendations from the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines. Barriers assessed included unfamiliarity, disagreement, low perceived benefit, low self-efficacy, and time constraints. Exact conditional regression was used to identify barriers independently associated with non-adherence.

Results The survey was completed by 154 clinicians. Adherence was lowest to referring patients with a forced expiratory volume in 1 s (FEV1) <80% predicted to pulmonary rehabilitation (5%); using FEV1 to guide management (12%); and ordering pulmonary function tests (PFTs) in smokers (17%). Adherence was intermediate to prescribing inhaled corticosteroids when FEV1 <50% predicted (41%) and long-acting bronchodilators when FEV1 <80% predicted (54%). Adherence was highest for influenza vaccination (90%) and smoking cessation counseling (91%). In unadjusted analyses, low familiarity with the guidelines, low self-efficacy, and time constraints were significantly associated with non-adherence to ≥2 recommendations. In adjusted analyses, low self-efficacy was associated with less adherence to prescribing inhaled corticosteroids (OR: 0.28; 95% CI: 0.10, 0.74) and time constraints were associated with less adherence to ordering PFTs in smokers (OR: 0.31; 95% CI: 0.08, 0.99).

Conclusions Poor familiarity with recommendations, low self-efficacy, and time constraints are important barriers to adherence to COPD guidelines. This information can be used to develop tailored interventions to improve guideline adherence.

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Asthma and COPD are two chronic inflammatory disorders of the airway characterized by airflow limitation. While many similarities exist between these two diseases, they are pathologically distinct due to the involvement of different inflammatory cells; predominantly neutrophils, CD8 lymphocytes in COPD and eosinophils and CD4 lymphocytes in asthma.

Cigarette smoking is associated with accelerated decline of lung function, increased mortality, and worsening of symptoms in both asthma and COPD. Furthermore, exposure to cigarette smoke can alter the inflammatory mechanisms in asthma to become similar to that seen in COPD with increasing CD8 cells and neutrophils and may therefore alter the response to therapy. Cigarette smoke exposure has been associated with a poor response to inhaled corticosteroids which are recommended as first line anti-inflammatory medications in asthma and as an add-on therapy in patients with severe COPD with history of exacerbations. While the main proposed mechanism for this altered response is the reduction of the histone deacetylase 2 (HDAC2) enzyme system, other possible mechanisms include the overexpression of GR-β, activation of p38 MAPK pathway and increased production of inflammatory cytokines such as IL-2, 4, 8, TNF-α and NF-Kß.

Few clinical trials suggest that leukotriene modifiers may be an alternative to corticosteroids in smokers with asthma but there are currently no drugs which effectively reduce the progression of inflammation in smokers with COPD. However, several HDAC2 enhancers including low dose theophylline and other potential anti-inflammatory therapies including PDE4 inhibitors and p38 MAPK inhibitors are being evaluated.

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