Amiodarone
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Syndrome of inappropriate antidiuretic hormone: case report An 88-year-old man experienced syndrome of inappropriate antidiuretic hormone (SIADH) during treatment with amiodarone for atrial fibrillation. The man presented to hospital due to trauma after falling down the stairs backwards. He reported back pain without loss of consciousness. He was neurologically intact; his Glasgow coma scale (GCS) score was 15. His vital signs were as follows: normal sinus rhythm, HR 59 beats per minute, RR 20 breaths per minute, temperature 36.1°C, BP 90/60mm Hg and oxygen saturation 100% on room air. His medical history was notable for atrial fibrillation, for which he had been receiving amiodarone [Cordarone; route not stated] 200mg once daily for 9 months. He was also receiving aspirin and metoprolol succinate for other co-morbidities. He denied recent history of diarrhoea, vomiting, polydipsia or decreased oral intake, and his physical examination was unremarkable. A CT scan of his cervical spine revealed a C4 extension teardrop fracture, whereas a CT scan of his abdomen and pelvis revealed an active arterial extravasation into the left gluteal region and a right ninth rib fracture. Laboratory test results were notable for decreased serum sodium levels, serum osmolality, anion gap, phosphate, serum creatinine and GFR. His blood urea nitrogen was found increased. His high urine sodium and urine osmolality [sic] led to the diagnosis of SIADH. Apart from amiodarone, he was taking no other medications which could have contributed to the development of SIADH, and he had no history of malignancies, pneumonia or HIV infection. The man’s amiodarone and metoprolol therapies were withheld due to bradycardia and hypotension secondary to acute bleeding. In the setting of declining haemoglobin and haematocrit, hypotension and thrombocytopenia, angioembolisation was performed for arterial extravasation into the left gluteal region. He was shifted to the ICU for blood transfusion and haemodynamic monitoring. He was administered two units of packed RBCs, following which his BP normalised. Thromboelastography revealed platelet dysfunction, which indicated increased platelet inhibition, likely due to aspirin. Therefore, aspirin was held due to active haemorrhaging, and he was treated with platelets and desmopressin. About 2 hours post admission, he experienced a tonic-clonic seizure, which lasted for about one minute. He was administered levetiracetam and monitored. He experienced no further seizures (days 2 and 3). The seizure was thought to have resulted from the concussion, fall, or the rapid decrease in serum sodium. Therefore, his sodium levels were closely monitored every 2 hours. Within 19 hours, his serum sodium levels improved (from 123 mEq/L on day 1 to 130 mEq/L on day 4). The man resumed amiodarone on day 4. His serum sodium levels remained unaltered. He was discharged on day 7. Two months following discharge, he remained adherent on amiodarone. His serum sodium level ranged from 126–131 mEq/L over a two-week period after disc
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