Endocrine Abstracts

Introduction: Hyponatraemia is a common electrolyte abnormality seen among hospitalised patients. We describe below, an inpatient seen with severe hyponatraemia.

Case description: 71yr old gentleman with no co-morbidities, admitted with acute confusion and slurred speech. Physical examination: Observations: Temperature 35C, heart rate 53/min, otherwise stable. GCS 15/15, no focal neurology except slurred speech and broad-based gait. Investigations: ECG: Sinus bradycardia, 47/min with PR-313ms, CXR-unremarkable CT head-nil acute. Hb 119g/l, WCC 3.0x10^9/l, platelet 120x 10^9/l, CRP 10mg/l Na 109 mmol/l with other electrolytes, renal and liver function tests within normal limits. Stroke team review- Treated with thrombolysis for left MCA stroke. Further investigations- MRI brain and carotid Doppler excluded stroke. During ward round, he was examined and noted to be euvolemic and so fluid restricted to <1.5L/day and further test related to hyponatraemia requested. Cardiologist also reviewed for bradycardia and advised he may need a pacemaker if PR prolongation persisted. Haematological investigations for pancytopenia were unremarkable.

Results: Serum cortisol 549 nmol/l; Na 112 mmol/l; osmolality 235mOsm/kg Urine osmolality 481mOsm/kg; sodium 30 mmol/l TSH 45mu/l, FT4 4pmol/l Next day, his BP dropped to 68/46mmHg with minimal response to fluid challenge, blood sugars remained normal, sodium had improved to from 109 mmol/l to 112 mmol/l, and was also given stat dose of Hydrocortisone(100mg) intravenously but no significant improvement in his BP noted. He was then commenced on 0.9%NaCl 8-hourly with electrolytes monitored daily. He was started on Levothyroxine 50micrograms a day after discussing with endocrinology team. Patient remained stable but with confusion and no improvement. On 7th day, TSH worsened (54.4mu/l and FT4-5.8pmol/l). Levothyroxine was increased to 75micrograms a day and, sodium continued to increase gradually (109—112—115—116—117—119—118). On the dawn of 8th day, crash call was put out as patient became unresponsive, GCS 3/15, with compromised airway, BP-68mmHg (systolic), hypothermic (30.3C), bradycardic (36/min), normal blood glucose. His airway was secured, resuscitated with intravenous fluids, Hydrocortisone 200mg stat, and transferred to ITU for intubation and vasopressor support. He was started on intravenous Liothyronine 20 mg TDS, and then switched to oral levothyroxine after one week. His TFTs improved gradually (45--54.4--95.4--12.8--9.8).

Questions/Discussion: Was this Myxoedema coma? Why did it happen after one week of being on Levothyroxine? Does hypertonic saline have any role in hypothyroidism related hyponatraemia? MRI head done 2weeks into admission was reported as central pontine myelinosis. Why did this happen in spite of gradual increase in sodium levels?