Hyponatremia after Thyroid Hormone Withdrawal in a Patient with Papillary Thyroid Carcinoma
A 76-year-old female visited the emergency room with symptoms of communication disability, mumbling, and impatience. She was treated with total thyroidectomy and radioiodine therapy for papillary thyroid carcinoma in October 2001. In April 2011, she was treated with cervical lymphadenectomy for left cervical lymph node metastasis of papillary thyroid carcinoma, radical nephrectomy for left renal tubular carcinoma, and finally radioiodine therapy in July 2011. She was initially administered levothyroxine 0.1 mg daily and in April 2012 blood examination showed a high level of thyroglobulin at 14.67 ng/mL. The thyroid hormone was replaced by liothyronin sodium, and after 2 weeks of complete thyroid hormone withdrawal an iodine whole-body scan was conducted 5 days before admission. The level of free T4 was decreased to 0.25 ng/dL (normal range, 0.93 to 1.7) and thyrotropin (TSH) was increased to 106 µIU/mL (normal range, 0.27 to 4.2). After examination, levothyroxine 0.1 mg daily was readministered. Because cervical node metastasis was suspected, a fine needle aspiration test was reserved before release. Dizziness and weakness were present before the iodine whole body scan, but no particular treatment was given due to its low level of severity. However, 2 days after the iodine whole body scan and 3 days before admission, she visited another hospital for pain in her heels where drugs including nonsteroidal anti-inflammatory were given twice. Her dizziness and nausea worsened after which she reported vomiting that occurred more than 10 times a day. A day before admission, the patient visited the emergency room and was examined for a suspicious gastrointestinal tract reaction induced by nonsteroidal anti-inflammatory drugs. She was administered antiemetic drugs, and sent home with a serum sodium level of 121 mEq/L. After getting home, her nausea continued despite the antiemetics and she was hospitalized in the same night from the emergency room with symptoms of communication disability, mumbling, and impatience.\nThe patient was diagnosed with diabetes and hypertension about 20 years ago and was on medication including oral hypoglycemic agents (pioglitazone 15 mg daily, metformin 250 mg daily) and oral antihypertensive drugs (perindopril tert-butylamine 8 mg daily, amlodipine besylate 5 mg daily). In 1999, she underwent hip bipolar hemiarthroplasty and right total knee arthroplasty (TKA) and, in 2000, left TKA.\nAt admission, she presented with signs of delirium and disorientation and her vital signs were as follows: blood pressure 160/80 mm Hg, pulse rate 66 times per minute, breathing rate 20 times per minute, body temperature 36.8℃, and oxygen saturation on room air was 95%. There were no reported changes in body weight.\nSkin tension was not decreased, there was no conjunctival pallor or sclera jaundice, and the papillary reflex was normal. Cervical lymphadenopathy was not diagnosed, and both cardiac and breathing sounds were normal on chest examination. On abdominal examination, bowel sound was normal, and there were no masses or pain. There was no limb edema on examination of the peripheral extremities.\nPeripheral blood examination showed a white blood cell count, hemoglobin concentration, and platelet count as 7,700/mm3, 9.7 g/dL, and 144,000/mm3, respectively. Electrolyte tests showed a sodium of 110 mEq/L, a potassium of 3.9 mEq/L, and a chloride of 82 mEq/L which suggested hyponatremia. Serum osmolality was 233 mOsm/kg and a urine osmolality was 418 mOsm/kg, indicating a severe hypotonic hyponatremia. Biochemical blood tests showed a blood glucose of 133 mg/dL, a blood urea nitrogen of 11 mg/dL, a creatinine of 1.2 mg/dL, a total protein of 6.7 g/dL, albumin of 4.0 g/dL, total bilirubin of 0.71 mg/dL, aspartate aminotransferase 61 IU/L, alanine aminotransferase 25 IU/L, alkaline phosphatase 175 IU/L, r-guanosine triphosphate 11 IU/L, creatine kinase 1,380 IU/L, lactic dehydrogenase 779 IU/L, and total cholesterol was 206 mg/dL. Serum C-reactive protein, PT, and aPTT was 0.1 mg/dL, 11.5 seconds (INR 1.06), 28.1 seconds, respectively.\nHepatitis testing was hepatitis B surface antigen negative, antihepatitis B surface antibody negative, and antihepatitis C virus negative. Chemical urinalysis showed sodium, potassium, chloride, and creatinine to be 50, 41.6, 58.1 mEq/L, and 63.65 mg/dL respectively. Electrocardiogram showed normal sinus rhythm (66 times per minute).\nA hormone test was conducted to identify the cause of hypoosmolar hyponatremia, and the result showed that the TSH was 90.78 µIU/mL with a free T4 of 0.61 ng/dL, an ACTH of 33.3 pg/mL, and a cortisol of 341.84 ng/mL ().\nBrain magnetic resonance imaging and computed tomographic features showed no signs of acute lesions, and chest and abdominal X-ray, and echocardiography results gave no significant diagnosis.\nThe patient showed signs of severe hyponatremia with continuous nausea and disorientation and had a serum sodium level of 110 mEq/L, so 3% normal saline was injected. On the second day after admission, levothyroxine 0.2 mg was administered for 3 days at 6 hours intervals, then reduced to 0.1 mg every 12 hours for 8 days, and finally maintained at 0.1 mg every 24 hours. On the third day of admission, consciousness and nausea had improved. The electrolyte levels gradually improved, and normalized by the 12th day. On the fifth day of admission, external tube feeding began. On the sixth day, full consciousness returned enabling oral feeding. On the 13th day, after the volume of food had increased and the serum sodium level normalized, fluid infusion was stopped, and the serum sodium level was maintained without fluid infusion.