A 56‐year‐old man presented with altered mental status secondary to complex partial seizures. He had a history of neurosarcoidosis diagnosed by imaging. On arrival to the hospital, he was found to be hypotensive, hypothermic, and hyponatremic. On exam, he had a large tongue with a flat affect and nonpitting lower‐extremity edema. His testicles were 2 centimeters in diameter bilaterally. Neurologic exam revealed delayed relaxation of the deep tendon reflexes symmetrically in the upper and lower extremities. Labs revealed a sodium of 120, thyroid‐stimulating hormone level of 2, and a free T4 level of 0.04. Luteinizing hormone was undetectable; serum testosterone levels were 15. A morning cortisol level was 2. A cosyntropin stimulation test showed a cortisol of 16 at 30 minutes and 22 at 60 minutes. Repeat magnetic resonance imaging showed an enlarged empty sella and diffuse enlargement of the ventricular system with microvascular ischemia. He was initially fluid‐resuscitated with normal saline. When his hyponatremia did not improve, he was fluid‐restricted at which point his sodium gradually corrected. First, hydrocortisone was given to avoid precipitating an adrenal crisis. Four days later, levothyroxine was given and his sodium stabilized. Testosterone therapy was initiated with the levothyroxine. His mental acuity dramatically improved over the course of several months.
The hospitalist commonly encounters isolated pituitary disorders. However, the presentation of panhypopituitarism can be more difficult to diagnose and manage. In this case, secondary adrenal insufficiency resulted in hypotension; hypothyroidism in macroglossia, hypothermia, myxedema, hyponatremia, and delayed deep tendon reflexes; and hypogonadism resulted in testicular atrophy. In a hypopituitarism patient with hyponatremia refractory to volume correction, an etiology of hypothyroidism should be considered and fluid restriction initiated. Hyponatremia is caused by an SIADH‐like presentation. The mechanism involves decreased thyroid hormone stimulation of the glomerular filtration rate, resulting in water retention and dilutional hyponatremia. Prevention of an adrenal crisis is an important consideration in panhypopituitarism treatment. Administration of exogenous thyroid hormone increases the metabolic clearance and use of glucocorticoids. A cortisol level and ACTH stimulation test to assess pituitary‐adrenal function must be done prior to initiation of thyroid hormone replacement. In this case, the random cortisol level was likely decreased secondary to impaired pituitary ACTH secretion.
When evaluating a patient with suspected panhypopituitarism, signs and symptoms should be associated with specific pituitary hormone deficits, but the interaction of these hormonal deficits also needs to be considered, especially regarding treatment.