An 80–year–old woman presented to the hospital with syncope and several weeks of headache, nausea, dizziness, generalized weakness and anorexia. Vital signs were stable and physical exam was unremarkable except bilateral maxillary sinus tenderness. Labs revealed sodium 122 meq/L (135–146 meq/L), potassium 2.7 meq/L (3.5–5 meq/L), serum uric acid 2 mg/dl (2.6–8 mg/dl), serum osmolality 266 mOsm/kg (282–303 mOsm/kg), urine osmolality 433 mOsm/kg (50–1400 mOsm/kg) and urine sodium 149 mmol/L. Renal and thyroid function were normal. Computed Tomography (CT) of head was negative. Chest X–ray showed right lower lobe infiltrate. Patient was admitted to the hospital and started on intravenous (IV) moxifloxacin. Hyponatremia was thought to be secondary to SIADH from pneumonia. Patient was placed on fluid restriction but her hyponatremia persisted. She also developed fever, photophobia, lethargy and confusion. CSF analysis ruled out meningitis. Due to change in mental status, 3% saline infusion was started which resulted in only slight improvement in sodium level from 122 to 128 mEq/L. CT chest and abdomen/pelvis done to detect any underlying malignancy as a potential cause of SIADH, was negative. MRI brain performed as a part of work up for persistent neurologic symptoms, revealed a 2.1x.0.9×1.3cm pituitary macroadenoma. Further tests revealed Prolactin of 5.04 ng/ml (3–19 ng/ml), TSH of 0.04 mIU/L (0.34–5.6 mIU/L), Free T4 of 0.9 ng/dl (0.75–2 ng/dl), Free T3 of 238 pg/dl (230–420 pg/dl), LH of <0.2 mIU/ml (postmenopausal 30–72 mIU/ml), FSH of 2.56 mIU/ml (postmenopausal 27.6–133 mIU/ml), Cortisol of 2.2 mg/dl (l6.2–29 mg/dl) and ACTH of <5pg/ml (9–52 pg/ml). Diagnosis of panhypopitutarism was established. She was started on IV hydrocortisone and oral levothyroxine which resulted in normalization of serum sodium level and resolution of symptoms within a day. Hypertonic saline was discontinued and patient was discharged on oral hydrocortisone and levothyroxine.
Hyponatremia is a frequent cause of hospitalization in the elderly and may prove fatal. Neurologic symptoms can be vague and confused for those due to infectious or vascular etiology. Such symptoms should be carefully evaluated in a hyponatremic patient as they could be a manifestation of an underlying CNS pathology instead of the hyponatremia itself. Pituitary dysfunction should be considered in cases of unexplained persistant hyponatremia with little response to hypertonic saline and a clinical picture consistent with SIADH. Panhypopitutarism can be easily missed, especially in elderly patients, due to its non specific presentation. A high index of suspicion is needed as it can be life threatening in the absence of prompt glucocorticoid initiation. As such, this uncommon diagnosis is often overlooked due to its vague clinical features and subtle findings.
Hyponatremia as a part of SIADH can be a presenting feature of panhypopitutarism.