Non-anemic iron deficiency has been studied in heart failure, but studies are lacking in chronic obstructive pulmonary disease (COPD). The potential clinical implications of association of iron deficiency with the severity of COPD warrant research in this direction. This was an observational, cross-sectional study on patients with COPD to compare disease severity, functional status and quality of life in non-anemic patients with COPD between two groups - iron deficient and non-iron deficient. Stable non-anemic COPD with no cause of bleeding were evaluated for serum iron levels, ferritin levels, TIBC, 6MWD, SGRQ, spirometry, and CAT questionnaire. The study patients were divided into iron replete (IR) and iron deficient (ID) groups. A total of 79 patients were studied, out of which 72 were men and seven were women. The mean age was 61.5±8.42 years. Of these, 36 (45.5%; 95% CI, 34.3-56.8%) had iron deficiency. Mean 6-minute-walk distance was significantly shorter in ID (354.28±82.4 meters vs 432.5±47.21 meters; p=0.001). A number of exacerbations in a year were more in ID group (p=0.003), and more patients in ID had at least two exacerbations of COPD within a year (p=0.001). However, the resting pO2, SaO2, and SpO2 levels did not differ significantly between the two groups (p=0.15 and p=0.52, respectively). Also, there was no significant difference in the distribution of patients of a different class of airflow limitations between the two groups. Non-anemic iron deficiency (NAID) is an ignored, yet easily correctable comorbidity in COPD. Patients with iron deficiency have a more severe grade of COPD, had lesser exercise capacity and more exacerbations in a year as compared to non-iron deficient patients. So, foraying into the avenue of iron supplementation, which has shown promising results in improving functional capacity in heart failure and pulmonary hypertension, may well lead to revolutionary changes in the treatment of COPD.

Background: Ultrasound elastography noninvasively estimates tissue hardness. Studies have evaluated elastography for differentiating malignant from benign lymph nodes during endobronchial ultrasound-guided transbronchial needle aspiration. Several methods of performing elastography are described with variable diagnostic accuracy.Methods: The aim of this study was to evaluate endobronchial ultrasound-guided elastography in differentiating malignant from benign mediastinal lymphadenopathy. We performed a systematic search of the PubMed and Embase databases to extract the relevant studies. A diagnostic accuracy meta-analysis was carried out to calculate the pooled sensitivity and specificity [with 95% confidence intervals (CIs)], and positive and negative likelihood ratios of elastography.Results: After a systematic search, 20 studies (1600 patients, 2712 nodes) were selected. The pooled sensitivity and specificity of elastography were 0.90 (95% CI, 0.84-0.94) and 0.79 (95% CI, 0.73-0.84), respectively. The summary receiver operating curve demonstrated an area under the curve for elastography of 0.90 (0.88-0.93). The positive and negative likelihood ratios and the diagnostic odds ratio were 4.3 (95% CI, 3.3-5.5), 0.12 (95% CI, 0.07-0.20), and 35 (95% CI, 19-63), respectively. Of the most commonly described methods, the color classification method (type 3 malignant vs. type 1 benign) demonstrated the highest area under the curve of 0.91 (0.88-0.93). There was significant heterogeneity and publication bias. Subgroup analyses indicated no significant difference between the sensitivity and specificity of quantitative and qualitative elastography methods.Conclusions: Ultrasound elastography is useful in differentiating malignant and benign lymph nodes during endobronchial ultrasound-guided transbronchial needle aspiration. However, elastography does not replace the requirement of lymph node aspiration.

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Introduction:The diagnosis of obstructive sleep apnea (OSA) requires polysomnography (PSG). The screening of OSA utilizes questionnaires like the Epworth sleepiness scale (ESS) and the STOP-BANG questionnaire (SBQ) that have variable predictive value, as reported from the Western literature. Materials and methods: A retrospective cohort study was done in adult subjects (n = 80) presenting with symptoms of OSA. The demographic profile, ESS, and SBQ scores were evaluated. The level one recorded PSG was evaluated for apnea-hypopnea index (AHI) and positive airway pressure (PAP) therapy prescribed. Results: Of the 80 subjects, 75 were diagnosed as OSA on PSG. The mean age of the study group was 49 years, with 71% men and a mean BMI of 28.25 kg/m 2 . Epworth sleepiness scale ≥11 was in 62.66%, and SBQ ≥ 5 in 53% of the 75 subjects. Hence, both questionnaires failed to predict OSA in nearly half of the population. The mean AHI was 33.8/hour, and the mean continuous positive airway pressure (CPAP) was 10.05 cm H 2 O. The AHI had a significant correlation with BMI, ESS score, and CPAP. Epworth sleepiness scale had a 53% sensitivity and 60% specificity for diagnosing OSA using a cutoff of 11, whereas SBQ had a 68% sensitivity and 100% specificity using a cutoff of 5. Conclusion:The SBQ has a higher sensitivity and specificity to detect OSA than ESS as it envisages distinct clinical manifestations and risk factors of OSA. However, neither of the two can replace PSG.

Obesity hypoventilation syndrome (OHS) is a highly underdiagnosed and undertreated condition, especially in developing countries like India. We present a case of a young 26-year-old male with Metabolic syndrome along with severe OSA with OHS, who after weight reduction of 50 kgs over 2 years was practically cured of the same; with no requirement of PAP, insulin and oral medications in follow-up. This case highlights the importance of evaluating obstructive sleep apnea by a phenotypic approach so that appropriate treatment is given.

High flow nasal cannula (HFNC) provides warmed and humidified air with flow rates up to 60 liters/min with relatively fixed oxygen content (FiO2). It has been extensively evaluated for hypoxemic respiratory failure and has been used in mild acute respiratory distress syndrome, pre-intubation, bronchoscopy and pediatric obstructive sleep apnea. Recent data has suggested a role in stable hypercapnic chronic obstructive pulmonary disease (COPD) and even in acute exacerbations, though, the use has not been advocated by any guidelines yet. We present a case of acute hypercapnic exacerbation of COPD, intolerant to non-invasive ventilation, showing response and improvement on use of HFNC. This case highlights this potential mechanisms and prospects for the same.

A 37-year male presented with cough and dyspnoea for 9 months that had worsened over the past 7 days and was complicated by haemoptysis. Haemoptysis was moderate in amount with 3-4 episodes per day consisting of fresh red blood and was not associated with bleeding from any other site. There was no history of fever or weight loss. Dyspnoea was persistent and progressive to dyspnoea at rest on presentation. Two years ago, the patient had undergone 6 months of anti-tubercular therapy for sputum positive pulmonary tuberculosis. On examination, the patient was conscious and oriented. His blood pressure was 110/70 mm Hg, pulse was 120/minute and respiratory rate was 34/min. Pallor was present but without any icterus, pedal oedema or lymphadenopathy. Respiratory system examination revealed vesicular breath sounds with bilateral crackles. Investigations revealed Haemoglobin 9 gram% with normal organ function tests and hypoxemic respiratory failure. Chest X-ray and a CT examination of the chest are provided below (Figure 1 A-E). Flexible bronchoscopy was essentially normal. Sequential bronchoalveolar lavage (BAL) fluid instillation became progressively bloodier upon aspiration and contained hemosiderin-laden macrophages confirming diffuse alveolar haemorrhage (DAH). BAL was negative for acid-fast bacilli (AFB), pneumocystis pneumonia (PCP), fungal mount, malignant cytology, and pyogenic/mycobacterial culture.

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