Correspondence Reliability and interpretation of pulmonary function tests when morbid obesity combines with chronic obstructive pulmonary disease and neuromuscular weakness To the Editor, Association of chronic obstructive pulmonary disease (COPD) and obesity is increasingly being observed nowadays, particularly as part of metabolic syndrome [1]. Perioperative interpretation of pulmonary mechanics may lead to confusion in such mixed pathology. We address this issue with a description of perioperative anesthesia management of a patient of morbid obesity with COPD and quadriparesis for laparoscopic sleeve gastrectomy. A 55-year-old morbidly obese male patient (weight, 103 kg; body mass index, 37.8 kg/m2) was admitted for laparoscopic sleeve gastrectomy. He had history of dyspnoea grade II-III with intermittent exacerbations of cough and expectoration since last 7 years. He was a chronic smoker (40 pack years) presently in abstinence for 7 years. He was on inhaled fluticasone-salmeterol and tablet prednisolone, 5 mg, once daily. There was no history suggestive of obstructive sleep apnea. He underwent cervical spine instrumentation for fracture C5-7 causing quadriparesis, sustained after a fall 7 years back. He had residual weakness in upper and lower limbs (power, 3/5). He was diagnosed to have diabetes mellitus 6 months back and started on tablets glimepiride, metformin, and pioglitazone. He was able to walk less than 10 steps with support in view of the neurologic deficit and the dyspnea. His general and systemic examination was unremarkable. Airway examination revealed modified Mallampati class III and restricted neck movements. Pulmonary function tests (PFTs) revealed forced expiratory volume in 1 second (FEV1), 33%; forced vital capacity (FVC), 48%; and FEV1/FVC, 72%. Room air oxygen blood gas reported PaO2, 82 mm Hg; PaCO2, 43 mm Hg; pH 7.34; and oxygen saturation, 95%. Hemogram; electrolytes; renal, liver, and thyroid function tests; and electrocardiogram were within normal limits. Computed tomographic scan of neck showed a metallic implant in situ with no spinal cord compression. A polysomnography showed an apneahypopnea index of 8, suggesting mild obstructive sleep apnea. An ultrasound Doppler study ruled out any deep venous thrombosis. He was started on a diet regimen, incentive spirometry, deep breathing exercises and nebulization with salmeterol and budesonide. On the morning of surgery, tablet ranitidine, 150 mg was prescribed. Sedative premedication was avoided. In the operating room, all standard monitors were attached and an 18-gauge intravenous access was secured. After pre-oxygenation, anesthesia was induced with fentanyl, 150 mcg; titrated boluses of propofol and vecuronium, 8 mg. Trachea was intubated with orotracheal cuffed tube number 8 mm under fiberoptic bronchoscope guidance. Anesthesia
369 was maintained with oxygen, air, and desflurane; and ventilation was controlled (volume control; tidal volume, 600 mL; rate, 12; positive end-expiratory pressure, 5 cm H2O). Pneumoperitoneum was created, and reverse Trendelenburg position was achieved. However, liver and peritoneum were found studded with numerous granulomatous lesions suggestive of miliary tuberculosis. Biopsy of the granuloma was obtained, and surgery was postponed. Subsequently, neuromuscular blockade was reversed, and trachea was extubated. Patient was shifted to the postanesthesia care unit. He was subsequently started on antitubercular medications and discharged with advice for further follow-up. Combination of restrictive (morbid obesity) and obstructive pulmonary disease (COPD) along with neuromuscular weakness in the same patient may alter pulmonary function unpredictably. Therefore, interpretation of clinical and various investigation parameters and risk stratification in such a patient may lead to significant dilemma. Perioperative risk stratification based on PFT may be erroneous in such patients. Neuromuscular weakness significantly reduces FVC and FEV1 due to reduction in contribution from expiratory and inspiratory muscles other than diaphragm [2]. Morbid obesity predominantly reduces FVC, and COPD mainly reduces FEV1 [3]. Thereby, in combined clinical scenario as in the current patient, greater reduction of FVC may lead to false high FEV1/FVC ratio, and COPD may be missed (COPD is defined as FEV1/FVC ratio, b 0.7) [4]. On the contrary, low values of FEV1 and FVC may lead to overestimation of perioperative risk, overuse of planned mechanical ventilation, and even postponement or cancellation of cases. Preoperative estimation of arterial blood gas may provide clear picture of oxygenation or ventilation status when measures of estimating pulmonary mechanics are at stake. In the present case, poor PFT (FVC, b 50% and FEV1, b 40%) may independently predict requirement of postoperative mechanical ventilation after major surgery [2]. However, room air arterial blood gas suggested otherwise. Treating morbid obesity could undo 1 of the 3 pathologies in this patient and thereby improve his functional status as observed that obese COPD patients have increased activityrelated dyspnea, restriction of daily activities, and chance of respiratory failure [3] and they fare worse in 6-minute walk test than their nonobese counterparts [5]. Surgery was justified given the neuromuscular weakness prohibited instituting any exercise regimen. Positive pressure ventilation during pneumoperitoneum could be challenging in morbidly obese COPD patient. However, restriction imposed by increased fat of obesity was perhaps negated by compliant chest wall muscles in neuromuscular weakness. Reverse Trendelenburg position made mechanical ventilation easier. Postoperative head elevated position along with continuous positive airway pressure if required helps by unloading of respiratory muscles and prevents dynamic expiratory midtracheal collapse in supine position observed in morbidly obese COPD patients [1].
370 To conclude, in the setting of mixed respiratory comorbidities, PFT should always be interpreted with caution, and correlation should be made with blood gas and clinical condition of the patient before risk stratification.
Ajisha Aravindan, MD (Senior Resident) Rajeshwari Subramaniam, MD (Professor) Dalim Kumar Baidya, MD (Assistant Professor) Department of Anesthesia and Intensive Care, All India Institute of Medical Sciences, New Delhi E-mail address: [email protected]
http://dx.doi.org/10.1016/j.jclinane.2015.03.015
Correspondence
References [1] Boiselle PM, Litmanovich DE, Michaud G, Roberts DH, Loring SH, Womble HM, et al. Dynamic expiratory tracheal collapse in morbidly obese COPD patients. Int J Chron Obstruct Pulmon Dis 2013;10:604-10. [2] Kang GR, Suh SW, Lee IO. Preoperative predictors of postoperative pulmonary complications in neuromuscular scoliosis. J Orthop Sci 2011;16:139-47. [3] O'Donnell DE, Ciavaglia CE, Nader JA. When obesity and chronic obstructive pulmonary disease collide: physiological and clinical consequences. Ann Am Thorac Soc 2014;11:635-44. [4] Price DB, Baker CL, Zou KH, Higgins VS, Bailey JT, Pike JS. Real-world characterization and differentiation of the Global Initiative for Chronic Obstructiv Lung Disease strategy classification. Int J Chron Obstruct Pulmon Dis 2014;28:551-61. [5] Bautista J, Ehsan M, Normandin E, Zuwallack R, Lahiri B. Physiological response during the six minute walk test in obese and non-obese COPD patients. Respir Med 2011;105:1189-94.
©2015 Elsevier
369 was maintained with oxygen, air, and desflurane; and ventilation was controlled (volume control; tidal volume, 600 mL; rate, 12; positive end-expiratory pressure, 5 cm H2O). Pneumoperitoneum was created, and reverse Trendelenburg position was achieved. However, liver and peritoneum were found studded with numerous granulomatous lesions suggestive of miliary tuberculosis. Biopsy of the granuloma was obtained, and surgery was postponed. Subsequently, neuromuscular blockade was reversed, and trachea was extubated. Patient was shifted to the postanesthesia care unit. He was subsequently started on antitubercular medications and discharged with advice for further follow-up. Combination of restrictive (morbid obesity) and obstructive pulmonary disease (COPD) along with neuromuscular weakness in the same patient may alter pulmonary function unpredictably. Therefore, interpretation of clinical and various investigation parameters and risk stratification in such a patient may lead to significant dilemma. Perioperative risk stratification based on PFT may be erroneous in such patients. Neuromuscular weakness significantly reduces FVC and FEV1 due to reduction in contribution from expiratory and inspiratory muscles other than diaphragm [2]. Morbid obesity predominantly reduces FVC, and COPD mainly reduces FEV1 [3]. Thereby, in combined clinical scenario as in the current patient, greater reduction of FVC may lead to false high FEV1/FVC ratio, and COPD may be missed (COPD is defined as FEV1/FVC ratio, b 0.7) [4]. On the contrary, low values of FEV1 and FVC may lead to overestimation of perioperative risk, overuse of planned mechanical ventilation, and even postponement or cancellation of cases. Preoperative estimation of arterial blood gas may provide clear picture of oxygenation or ventilation status when measures of estimating pulmonary mechanics are at stake. In the present case, poor PFT (FVC, b 50% and FEV1, b 40%) may independently predict requirement of postoperative mechanical ventilation after major surgery [2]. However, room air arterial blood gas suggested otherwise. Treating morbid obesity could undo 1 of the 3 pathologies in this patient and thereby improve his functional status as observed that obese COPD patients have increased activityrelated dyspnea, restriction of daily activities, and chance of respiratory failure [3] and they fare worse in 6-minute walk test than their nonobese counterparts [5]. Surgery was justified given the neuromuscular weakness prohibited instituting any exercise regimen. Positive pressure ventilation during pneumoperitoneum could be challenging in morbidly obese COPD patient. However, restriction imposed by increased fat of obesity was perhaps negated by compliant chest wall muscles in neuromuscular weakness. Reverse Trendelenburg position made mechanical ventilation easier. Postoperative head elevated position along with continuous positive airway pressure if required helps by unloading of respiratory muscles and prevents dynamic expiratory midtracheal collapse in supine position observed in morbidly obese COPD patients [1].
370 To conclude, in the setting of mixed respiratory comorbidities, PFT should always be interpreted with caution, and correlation should be made with blood gas and clinical condition of the patient before risk stratification.
Ajisha Aravindan, MD (Senior Resident) Rajeshwari Subramaniam, MD (Professor) Dalim Kumar Baidya, MD (Assistant Professor) Department of Anesthesia and Intensive Care, All India Institute of Medical Sciences, New Delhi E-mail address: [email protected]
http://dx.doi.org/10.1016/j.jclinane.2015.03.015
Correspondence
References [1] Boiselle PM, Litmanovich DE, Michaud G, Roberts DH, Loring SH, Womble HM, et al. Dynamic expiratory tracheal collapse in morbidly obese COPD patients. Int J Chron Obstruct Pulmon Dis 2013;10:604-10. [2] Kang GR, Suh SW, Lee IO. Preoperative predictors of postoperative pulmonary complications in neuromuscular scoliosis. J Orthop Sci 2011;16:139-47. [3] O'Donnell DE, Ciavaglia CE, Nader JA. When obesity and chronic obstructive pulmonary disease collide: physiological and clinical consequences. Ann Am Thorac Soc 2014;11:635-44. [4] Price DB, Baker CL, Zou KH, Higgins VS, Bailey JT, Pike JS. Real-world characterization and differentiation of the Global Initiative for Chronic Obstructiv Lung Disease strategy classification. Int J Chron Obstruct Pulmon Dis 2014;28:551-61. [5] Bautista J, Ehsan M, Normandin E, Zuwallack R, Lahiri B. Physiological response during the six minute walk test in obese and non-obese COPD patients. Respir Med 2011;105:1189-94.
©2015 Elsevier
