Contemporary management of benign parotid tumours – the increasing evidence for extracapsular dissection

Benign parotid tumours have historically often been managed surgically by superficial parotidectomy. While this approach usually gives a generous cuff of surrounding normal parotid tissue to increase tumour margins, it requires a much larger incision than the increasingly used extracapsular dissection (ECD) technique. Furthermore, superficial parotidectomy can result in marked facial hollowing, Frey syndrome and an increased risk of both temporary and permanent facial nerve weakness. ECD has been popularised as a safe alternative to parotidectomy primarily for the removal of mobile, benign parotid tumours with safe outcomes and reduced risk to the facial nerve. In this article, we review the growing body of evidence for ECD and include our own experience confirming the move away from superficial parotidectomy in contemporary practice for the treatment of benign parotid tumours.     

CT‐measured bone attenuation in patients with chronic obstructive pulmonary disease: Relation to clinical features and outcomes

Osteoporosis is highly prevalent in chronic obstructive pulmonary disease (COPD) patients and has been related to several clinical features. However, most studies have been in relatively small COPD cohorts. Therefore, the objectives of this study were to compare bone attenuation measured on low‐dose chest computed tomography (CT) between COPD subjects and smoker and nonsmoker controls, and to relate bone attenuation to clinical parameters, inflammatory biomarkers, and outcomes in a large, well‐characterized COPD cohort. We studied 1634 COPD subjects, 259 smoker controls, and 186 nonsmoker controls who participated in a large longitudinal study (ECLIPSE). We measured bone attenuation, extent of emphysema, and coronary artery calcification (Agatston score) on baseline CT scans, and clinical parameters, inflammatory biomarkers, and outcomes. Bone attenuation was lower in COPD subjects compared with smoker and nonsmoker controls (164.9 ± 49.5 Hounsfield units [HU] versus 183.8 ± 46.1 HU versus 212.1 ± 54.4 HU, p < 0.001). Bone attenuation was not significantly different between COPD subjects and smoker controls after adjustment for age, sex, and pack‐years of smoking. In the COPD subjects, bone attenuation correlated positively with forced expiratory volume in 1 second (FEV₁, r = 0.062, p = 0.014), FEV₁/forced vital capacity (FVC) ratio (r = 0.102, p < 0.001), body mass index (r = 0.243, p < 0.001), fat‐free mass index (FFMI, r = 0.265, p < 0.001), and C‐reactive protein (r = 0.104, p < 0.001), and correlated negatively with extent of emphysema (r = ?0.090, p < 0.001), Agatston score (r = ?0.177, p < 0.001), and interleukin‐8 (r = ?0.054, p = 0.035). In a multiple regression model, older age, lower FFMI and higher Agatston score were associated with lower bone attenuation. Lower bone attenuation was associated with higher exacerbation (r = ?0.057, p = 0.022) and hospitalization (r = ?0.078, p = 0.002) rates but was not associated with all‐cause mortality. In conclusion, CT‐measured bone attenuation was lower in COPD subjects compared with nonsmoker controls but not compared with smoker controls, after adjustment for age, sex, and pack‐years of smoking. In the COPD subjects, bone attenuation was associated with age, body composition, and coronary artery calcification but was not associated with all‐cause mortality.