Letters to the Editor

Reply to the editor Sir, We read with pleasure the comments on our recent paper, entitled “Outcome of pulmonary embolism and clinicoradiological predictors of mortality: Experience from a university hospital in Saudi Arabia”.[1] We agree that signs of right ventricular dysfunction in computed tomography scan can be more predictive of outcome than the embolic burden based on obstruction score and localization, however in our study we assessd right side overload using echocardiographic criteria.[2] Biochemical markers of myocardial injury, e.g., troponin and pro-brain natriuretic peptide, although they are non specific, can be useful as prognostic markers in normotensive patients[3] and we acknowledge this to be a limitation of our study.

Hadil AK Al Otair

Assistant Professor of Medicine, Consultant Department of Critical Care Medicine, King Saud University. E-mail: [email protected]

References 1.

2.

3.

Al Otair HA, Al-Boukai AA, Ibrahim GF, Al Shaikh MK, Mayet AY, Al-Hajjaj MS. Outcome of pulmonary embolism and clinico-radiological predictors of mortality: Experience from a university hospital in Saudi Arabia. Ann Thorac Med 2014;9:18-22. Schoepf UJ, Kucher N, Kipfmueller F, Quiroz R, Costello P, Goldhaber SZ. Right ventricular enlargement on chest computed tomography: A predictor of early death in acute pulmonary embolism. Circulation 2004;110:3276-80. ten Wolde M, Söhne M, Quak E, Mac Gillavry MR, Büller HR. Prognostic value of echocardiographically assessed right ventricular dysfunction in patients with pulmonary embolism. Arch Intern Med 2004;164:1685-9. Access this article online Quick Response Code:

Website: www.thoracicmedicine.org

DOI: 10.4103/1817-1737.134080

Respiratory morbidity in obesity, beyond obstructive sleep apnea Sir, The original article on obstructive sleep apnea (OSA) being associated with higher health care utilization in the elderly 182

highlights not only the risk of hospitalization in OSA but also the widespread implications of the well-known pandemic — obesity.[1] In this letter, we would like to elucidate other respiratory complications associated with obesity, which often goes unanticipated. Central obesity impairs ventilatory function. Increasing body mass index (BMI) is typically associated with a reduced forced expiratory volume in one second (FEV1), forced vital capacity (FVC), total lung capacity, functional residual capacity, and expiratory reserve volume, with spirometry showing a restrictive pattern more often than obstructive, with low FVC and normal FEV1/FVC. Progressive fat accumulation over the anterior chest wall and abdominal wall is associated with decreased thoracic wall compliance and diaphragmatic excursion and diminished respiratory muscle endurance, leading to increased work of breathing and airway resistance. There is decreased basal inspiratory expansion of the lungs with consequent ventilation-perfusion mismatch and arterial hypoxemia. Hence, obesity leads to increased respiratory complications, especially on exertion and in supine positions of sleep and anesthesia.[2,3] Increasing BMI has been associated with increased frequency of wheezing and breathlessness in asthma although obesity has not been found to be associated with increased airway hyper-responsiveness. The increase in symptoms in obesity is, therefore, most probably due to altered ventilation dynamics and decreased lung compliance. It has also been speculated that the systemic inflammation with elevated IL-6, IL-8, and TNF-α associated with obesity may lead to glucocorticoid unresponsiveness in some patients. Thus, obesity increases hospitalizations due to increased frequency of acute asthmatic exacerbations.[2] Similarly, obesity and chronic obstructive pulmonary disease (COPD) seem to synergize with each other, with decreasing FEV1 associated with both conditions leading to worsening airflow obstruction and hypoxia. In overlap syndrome of COPD with OSA, there is a greater risk for respiratory failure and cor pulmonale as compared to COPD alone, pertaining to increased sympathetic overactivity leading to greater cardiovascular morbidity and mortality.[2,3] Obesity hypoventilation syndrome, associated with hypercapneic respiratory failure and cor pulmonale may be present in one-fifth of patients with OSA, or may occur as an isolated entity due to obesity alone. Sleep-related disturbance and pulmonary hypertension leads to significant morbidity in these patients.[2] Obesity also causes increased respiratory complications in anesthetized and intubated patients. Thicker necks, poorer neck mobility, and smaller upper airway caliber make intubation and ventilation difficult. Increased volume of distribution in adipose tissue makes the required dosages for sedatives and anesthetics unpredictable. There is also a tendency to desaturate faster due to an already low lung reserve and hence need to be intubated faster. The risks for ventilation-associated atelectasis also increases due to decreased FRC and ERV. Extubation also poses Annals of Thoracic Medicine - Vol 9, Issue 3, July-September 2014

Letters to the Editor

difficulties in such patients, who frequently require a high flow of oxygen in the sitting or lateral recumbent position along with continuous or bilevel positive airway pressure to prevent airway collapse, basal atelectasis, and hypoxemia. [2,3] Therefore, it goes without saying that managing obesity would lower health care utilization not only because of OSA but also a vast number of significant other respiratory diseases.

Chatterjee Krishnarpan, Sen Chetana1

Department of Medicine, Dr. Ram Manohar Lohia Hospital, Guru Gobind Singh Indraprastha University, New Delhi, 1Department of Internal Medicine, Medical College and Hospital, Kolkata, West Bengal, India E-mail: [email protected]

References 1.

2. 3.

Diaz K, Faverio P, Hospenthal A, Restrepo MI, Amuan ME, Pugh MJ. Obstructive sleep apnea is associated with higher healthcare utilization in elderly patients. ATM 2014;9:92-8. Zammit C, Liddicoat H, Moonsie I, Makker H. Obesity and respiratory diseases. Int J Gen Med 2010;3:335-43. Poulain M, Doucet M, Major GC, Drapeau V, Sériès F, Boulet LP, et al. The effect of obesity on chronic respiratory diseases: Pathophysiology and therapeutic strategies. CMAJ 2006;174:1293-9. Access this article online Quick Response Code:

Website: www.thoracicmedicine.org

DOI: 10.4103/1817-1737.134081

Reply to the editor Sir, The original article on obstructive sleep apnea (OSA) being associated with higher health care utilization in the elderly highlights not only the risk of hospitalization in OSA, but also the widespread implications of the well-known pandemic — obesity.[1] In this letter, we would like to elucidate other respiratory complications associated with obesity, which often goes unanticipated. Central obesity impairs ventilatory function. Increased body mass index (BMI) is typically associated with a reduced forced expiratory volume in one second (FEV1), forced vital capacity (FVC), total lung capacity, functional residual capacity (FRC), and expiratory reserve volume (ERV), with spirometry showing a restrictive pattern more often than obstructive, with Annals of Thoracic Medicine - Vol 9, Issue 3, July-September 2014

low FVC and normal FEV1/FVC. Progressive fat accumulation over the anterior chest wall and abdominal wall is associated with decreased thoracic wall compliance and diaphragmatic excursion and diminished respiratory muscle endurance, leading to increased work of breathing and airway resistance. There is decreased basal inspiratory expansion of the lungs with consequent ventilation-perfusion mismatch and arterial hypoxemia. Hence, obesity leads to increased respiratory complications, especially on exertion and in supine positions of sleep and anesthesia.[2,3] Increased BMI has been associated with increased frequency of wheezing and breathlessness in asthma although obesity has not been found to be associated with increased airway hyper-responsiveness. The increase in symptoms in obese patients is most probably due to altered ventilation dynamics and decreased lung compliance. It has also been speculated that the systemic inflammation with elevated IL-6, IL-8, and TNF-α associated with obesity may lead to glucocorticoid unresponsiveness in some patients. Thus, obesity increases hospitalizations due to increased frequency of acute asthmatic exacerbations.[2] Similarly, obesity and chronic obstructive pulmonary disease (COPD) seem to synergize with each other, with decrease FEV1 associated with both conditions leading to worsening airflow obstruction, and hypoxia. In overlap syndrome (COPD with OSA), there is a greater risk for respiratory failure and cor pulmonale as compared to COPD alone, pertaining to increased sympathetic overactivity leading to greater cardiovascular morbidity and mortality.[2,3] Obesity hypoventilation syndrome, associated with hypercapneic respiratory failure and cor pulmonale, may be present in one-fifth of patients with OSA, or may occur as an isolated entity due to obesity alone. Sleep-related disturbance and pulmonary hypertension leads to significant morbidity in these patients.[2] Obesity also causes increased respiratory complications in anesthetized and intubated patients. Thicker necks, poorer neck mobility, and smaller upper airway caliber, make intubation and ventilation difficult. Increased volume of distribution in adipose tissue, makes the required dosages for sedatives and anesthetics unpredictable. There is also a tendency to desaturate faster due to an already low lung reserve and hence need to be intubated faster. The risks for ventilation associated atelectasis also increases due to decreased FRC and ERV. Extubation also poses difficulties in these patients, who frequently require a high flow of oxygen in the sitting or lateral recumbent position along with continuous or bilevel positive airway pressure to prevent airway collapse, basal atelectasis, and hypoxemia.[2,3] Therefore, it goes without saying that managing obesity would lower health care utilization not only because of OSA but also a vast number of significant other respiratory diseases.

Paola Faverio

University of Texas Health Science Center, San Antonio, TX, USA E-mail: [email protected] 183

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