STATIN-INDUCED DIAPHRAGMATIC MUSCLE WEAKNESS CAUSING HYPERCAPNIA AND SHORTNESS OF BREATH

Abstract

SESSION TITLE: Tuesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM INTRODUCTION: Statins are commonly used medications in medicine. One of their side effects is muscle injury. We present a case of a patient (PT) who presented with chronic shortness of breath (SOB) and hypercapnia secondary to statin therapy. CASE PRESENTATION: A 77 y/o male with history of DM, HTN, HLD and Asthma; no smoking or toxic exposures presented to the hospital due to SOB on exertion for the last 5-6 months. His SOB was relieved by rest, but noted hoarseness and weakness with discomfort of his legs. Upon admission PT had stable VS, physical exam was unremarkable with no muscle tenderness and clear lungs. Chest X-ray and CT scan (Fig. 1) showed only bibasilar atelectasis and small lung volumes. Cardiovascular work up was negative. Laboratory evaluation was significant for an elevated Creatinine Kinase of 470 U/L. He had been on Atorvastatin with increased dosage by his PCP a few months prior. Serum HCO3 level was elevated at 35 mmol/L without diuretic use. An arterial blood gas confirmed hypercapnia(pH 7.37, PCO2 58, PO2 67, O2 saturation at 92% at room air). Thyroid function test were normal and myositis work up was sent for ESR, Anti-Jo, Anti-Ro, Anti-La antibody, Lactate levels, ANA and were found to negative. BMI was calculated to 28. Aldolase was elevated at 21 U/L. Pulmonary Function testing (PFT) were performed showing a restrictive lung pattern with FEV1/FVC ratio of 89% with FVC 41% predicted, TLC was 3.39 L (68% predicted) (Fig.2), DLCO was 49% predicted with a normal DLCO/VA. Tidal-flow volume loop was almost completely shifted to the left suggesting that the PT couldn’t take a deeper breath as there was no airway obstructive pattern. After workup was completed, the statin was discontinued and the PT's SOB slowly improved over the course of a few days. He was successfully discharged without additional intervention. DISCUSSION: Statin induced myopathy is the most common side effect associated to statin therapy(1). Hypercapnia secondary to statin therapy causing diaphragmatic muscle weakness is uncommon in the literature.(2) Most people associate statin myopathies with skeletal muscle and diaphragmatic involvement is not routinely considered. In our PT any underlying lung pathology was ruled out by imaging studies along with central causes for hypoventilation. Autoimmune myositis work up was negative, thyroid function was normal and PFT were consistent with a restrictive lung defect suggesting muscle weakness given negative CT findings for interstitial lung disease or other extra-thoracic causes of restriction. Cognitive biases can frequently limit consideration of rarer causes of dyspnea. CONCLUSIONS: Hypercapnia in the hospital setting is mistakenly attributed to COPD without other causes being considered. We suggest statin induced myopathy causing diaphragmatic weakness to be considered as a differential on PTs on statin and unexplained SOB especially due to the frequency of their use. Reference #1: Upreti, Sunita, Beenish Fayyaz, and Ramchandran P. Bongu. "Anti-HMG-CoA reductase myopathy, an undesirable evolution of statin induced myopathy: a case report.” Journal of Community Hospital Internal Medicine Perspectives 9.1 (2019): 33-35 Reference #2: Biagioni, Bradly, et al. "Diaphragmatic Weakness Due to Statin Myopathy.” Chest 150.4 (2016): 1085A. DISCLOSURES: No relevant relationships by Walter Chua, source=Web Response No relevant relationships by Christian Lopez-Padilla, source=Web Response