CC: Headache x 3 days
HPI: The patient is a 48 year-old Hispanic female with history of DM and hypothyroidism who presented to LAC-USC ED with a 3 day history of headache. She states that starting 2 months ago, she began to have symptoms of generalized weakness. By the end of the day, patient felt very fatigued though she is still able to complete her daily tasks. Starting three days prior to presentation, patient experienced sudden onset, severe headache. It is difficult to say what makes it worse or better however the patient has tried over the counter medications of Tylenol with no improvement. The patient denies fevers, chills, neck stiffness, photophobia or phonophobia, but endorses blurry vision. Of note, patient gives a history of irregular menses for the last year as well. On exam, patient has poor visual acuity bilaterally with right temporal vision loss. Otherwise the exam is normal. Labs are significant for Na 130, Serum Osm 275, Urine Osm 376, and Urine Na 147 that in the patient’s euvolemic state is consistent with SIADH versus cortisol deficiency. Further endocrine labs and CT Head ordered are written below.
AM Cortisol: 0.5
ACTH: 5 (Normal 6-50)
TSH 6.14 (H)
Free T4 0.97
Anti-TPO: 355.7 (H)
IGF-I: 45 (normal 52-358)
Luteinizing Hormone: 0.3
FSH: 151.0 (Post-menopausal range 25.8-135)
CT Head: Large bulky sella, supra-sellar, para-sellar mass with involvement of the bilateral cavernous sinuses and sphenoid sinuses with imaging features suggestive of a pituitary macroadenoma
Labs are significant for elevated prolactin likely from the mass causing stalk effect. The elevated FSH, decreased ACTH and random cortisol, indicates likely FSH-secreting tumor with adrenal insufficiency from pituitary compression. Though FSH is difficult to interpret in peri-menopausal state, LH should also be elevated peri-menopausally which is not seen in this case. Patient was started on Hydrocortisone 20mg AM, 10mg PM with significant improvement in energy levels. Sodium did dip to 128 as an inpatient but improved with glucocorticoid replacement. Neurosurgery plans to follow her as an outpatient for tumor removal.
Morning Report Pearls:
Let’s review the work up of hyponatremia which is an important work up in this patient.
Whenever considering SIADH as the etiology, exclude thyroid and adrenal causes which can have similar appearance.
Taking a look at the hypothalamic pituitary axis issue, remember that the first step with a pituitary tumor is identifying size and whether it is functional or non-functional.
- Determining if this is a macroadenoma versus microadenoma will give you an idea if it could potentially be causing compression leading to a panhypopituitary state.
Figuring out if it is a functional tumor versus non-functional is important because management changes.
- The most common functional tumor is a prolactinoma which can be medically managed initially, even if causing neurologic defects. This is unlike the other functional and non-functional tumors where surgery is usually your only option when neurologic defects are present.
- This patient’s prolactin elevation is not very high so unlikely to present a prolactinoma. Usually when a macroadenoma is prolactin producing, the PRL are at least >100 and usually closer to 200. The elevation in this patient is due to stalk compression leading to a blockade of the dopamine inhibitory pathway.
Another interesting part of the case is interpreting the FSH level. This becomes slightly more complicated given the patient’s perimenopausal state, as this is a time when an elevated FSH level is expected. However, the tumor may be FSH producing instead of related to a perimenopausal state as the LH is actually low which is not typical for someone going through menopause. In addition, all other pituitary hormone levels are low or inappropriately normal which confirms that this patient is having pituitary dysfunction from tumor compression.