We report the case of a 65 year old lady who was admitted to A&E with neurological symptoms (slurred speech, ataxia, intermittent confusion) and she was found to have low sodium (116 mmol/l). She reported 23 week history of lethargy and lightheadedness. There was no history of shortness of breath, cough, haemoptysis, weight loss, night sweats, altered bowel habits or excessive fluid intake. Her past medical history included hip osteoarthritis and dyslipidaemia. She lived with her husband. She was independent, lifelong smoker (20 cig/day) and consumed no alcohol. Her regular medications included Pantoprazole, Celecoxib, Atovastatin and Cetirizine. Pantoprazole was discontinued on admission. On examination, she appeared euvolaemic. Gait was mildly ataxic, but no other focal neurology was noted. Cardiovascular, respiratory and GI systems were unremarkable. She was investigated initially with a CT-head to rule out stroke which revealed no evidence of acute pathology. The blood tests showed normal kidney and liver function, normal FBC and Glucose. To investigate further the hyponatraemia, paired serum/urine osmolalities and urine sodium as well as cortisol and TSH were requested. Serum Osm: 246, Urine Osm: 477, Ur Na: 62. Normal cortisol (521 nmol/l) and TSH (1.77 mu/l). The test was suggestive of SIADH. She was placed on fluid restriction 1 l and her Na increased to 120. However, failing to increase further, she was started on Demeclocycline 300 mg TDS. In view of the above diagnosis, a CT thorax-abdomen-pelvis was performed revealing a pathological right hilar and mediastinal lymphadenopathy. Subsequently, she underwent EBUS to obtain a definite diagnosis. During her inpatient stay, she developed a rash in her legs. This was thought to be a photosensitivity rash secondary to the recent initiation of Demeclocycline (The patient reported spending some time in the hospital yard with her family). The following days her blood tests revealed increasing inflammatory markers and therefore she was covered for possible cellulitis with antibiotics as per Trust guidelines. In the meanwhile, her sodium had improved, but she developed acute kidney injury stage 3. As a result, fluid restriction and demeclocycline were discontinued. US Kidneys was normal. EBUS guided FNA cytology revealed small cell lung cancer. She was referred to oncology services with sodium of 143 on discharge.
Conclusion: This is a case of ectopic ADH production secondary to small cell lung cancer. It highlights the diagnostic considerations in SIADH and side effects of treatment with Demeclocycline.
08 - 10 Apr 2019
Society for Endocrinology