SESSION TITLE: Pulmonary Manifestations of Systemic Disease Case Report Posters
SESSION TYPE: Affiliate Case Report Poster
PRESENTED ON: Tuesday, October 27, 2015 at 01:30 PM - 02:30 PM
INTRODUCTION: Dyspnea and orthopnea has been described to be due to diaphragmatic dysfunction.
CASE PRESENTATION: A 68 year-old diabetic female, presented with progressive shortness of breath for 3 months associated with orthopnea. She did not have any clinical features of congestive heart failure. Neurological examination revealed reduced power in both upper and lower limbs. She was recently diagnosed with hyperplastic colloid thyroid nodules for which she was started on thyroxine by her endocrinologist to suppress the thyroid stimulating hormone. Chest radiograph showed raised bilateral hemidiaphragms (Fig.1). 2D echocardiography was normal. Spirometry showed a restrictive pattern with a 43% reduction in FVC on lying down from a sitting position (Table 1). Maximal inspiratory and maximal expiratory pressures were both reduced. Serum thyroid stimulating hormone was low, while serum free thyroxine was high; consistent with hyperthyroidism due to thyroxine therapy. Electrophysiological studies showed no evidence of peripheral neuropathy or decremental response in the repetitive nerve stimulation. EMG was suggestive of an underlying myopathy with phrenic nerve conduction demonstrating bilateral small compound muscle action potential amplitudes. Deltoid muscle biopsy showed moderate type 2 fiber atrophy with no evidence of an underlying inflammatory or mitochondrial myopathy. She was diagnosed to have hyperthyroidism with myopathy and bilateral diaphragmatic muscle weakness. Her thyroxine was stopped, with complete resolution of her dyspnea and orthopnea.
DISCUSSION: Patient with bilateral diaphragmatic dysfunction may have 30% to 50% reduction in vital capacity from cephalic displacement of diaphragm in supine position1, 2 resulting in clinical presentation of dyspnea and orthopnea. Significant diaphragmatic weakness has been described in Grave’s disease3 with improvement following carbimazole therapy.
CONCLUSIONS: This case highlights the importance of excluding hyperthyroidism in the evaluation of patients with dyspnea due to diaphragmatic weakness.
Reference #1: Mier-Jedrzejowicz A, Brophy C, Moxham J, Green M., Assessment of diaphragm weakness. Am Rev Respir Dis 1988; 137:877-883.
Reference #2: F. Dennis McCool, George E. Tzelepis. Dysfunction of diaphragm. N Engl J Med 2012; 366:932-942.
Reference #3: Ravinder Goswami et al, Prevalence of diaphragmatic muscle weakness and dyspnoea in Graves’ disease and their reversibility with carbimazole therapy, European Journal of Endocrinology 2002; 147:299-303.
DISCLOSURE: The following authors have nothing to disclose: Aza AM Taha, Yew-Long Lo, Su Ying Low, Keng Leong Tan
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