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Atypical asymptomatic presentation of advanced pituitary adenoma that advances Rapidly to Apoplexy I. Case History A. Patient Demographics 48 yo/AA/F B. Referred in for glaucoma consultation, no complaints C. OCULAR HISTORY: questionable past history of glaucoma, was taking Timoptic 0.5% (in mid 1990's) but stopped drops as recommended by another doctor. Borderline IOP, high myopia OU. D. Medical history: cardiac arrhythmia, hypothyroidism, partial hysterectomy, carpel tunnel, breast Bx. June 2009 (-) II. Pertinent findings A. Clinical 1. DVA CC 20/30 OD Ph 20/25 20/25 OS Ph 20/20 2 Pupils: PERRL (-) APD 3. SLE: Nml OU Cl cornea, conjunctiva, A/C, lens, vitreous OU 4. Ta OD 23 OS 23 @ 9:45 AM 5. DFE: Vitreous and macula clear OU, C/D .85/.70 OD .70/.75 OS with slight temporal pallor OU, drance heme OS 6. Initial VF 24-2: high false positives essentially full OU; retest OS 2 months later paracentral scotoma OS 7. OCT/NFL looked slightly thinned OD; nml OS 8. Neuro-imaging study ordered MRI of the brain and orbits with contrast thin sections through orbits. B. Physical 1.Patient in normal shape, slightly overweight,(-) headaches,normal gait, nothing significant on Neuro-symptom inventory . C. lab studies: CBC with differential, prolactin levels elevated D. Neuro-imaging studies: notable for a large sellar mass that extends into the suprasellar region compressing the intracranial portion of the left ON. Likely represents a large pituitary macroadenoma. See films III. Differential Dx. A. primary diagnosis: Bilateral optic atrophy subtle secondary to chiasmal compression. B. others within differential: Likely COAG OS>OD IV. Diagnosis and Discussion: The patient was brought back in a month after the initial visit for diurnal IOP check and gonio and to review the results of MRI with the patient. The patient was told she had a large macroadenoma that would likely need surgery rather soon. What is atypical about this case is despite the enormous macroadenoma there was no significant bitemporal VF loss. This was because the tumor growth was in a downward direction into the soft palate and not entirely upward compressing the mid-chiasm, although there was obviously some ON compression as the pallor would indicate. It also appears that the patient has a glaucoma diagnosis overlapping this compressive atrophy. She presented a month later when she was told the news, and she was started on Travatan-Z for COAG. She was referred to neuro-surgery for surgical consultation.The neurosurgeon she was referred to did not feel comfortable with doing her surgery as the tumor was very large and extending in a downward (atypical direction). He then referred her to an academic institution and she had to wait another month until she could be seen. In the meantime our patient came back for an unscheduled urgent visit with acute onset of the worst headache of her life, nausea and vomiting profusely and diplopia. On motility she presented with multiple CN deficits and ophthalmoplegia OS>OD, and ptosis OS. She was Dx. with a cavernous sinus syndrome, likely due to pituitary apoplexy, and she was rushed to the ER for emergent imaging studies. These studies confirmed apoplexy and the patient was air lifted to the regional hospital with neuro-surgical back-up. She was urgently operated on that day and is in recovery. V. Treatment: The patient underwent complete removal of the hemorrhagic pituitary, and will require hormone replacement therapy. She also has constant diplopia due to persistent ophthalmoplegia which is improving slowly. We suggested patching one eye for now to eliminate diplopia. She has continued her Travatan -Z for her glaucoma. It is possible the increased cupping is due at least in part to the compression of the chiasm, but given the borderline IOP, and compromised ON I decided to leave her on it for now. VI. Conclusion/ Take Away Points A. Pituitary apoplexy is a vision threatening and life threatening condition that occurs when pituitary adenoma grows suddenly and rapidly outstripping its blood supply. This causes a sudden and profound intracranial hemorrhage which leads to the headache and ultimately the cavernous sinus syndrome. The two key things to point out here are the fact that you can have an enormous pituitary macroadenoma and not have bi-temporal VF loss. Infact from the standpoint of the tumor there was essentially only central scotoma OS, which could also be from old glaucoma. The other key point is to always investigate pallor of the ON. Glaucoma does not cause pallor, and if you right optic atrophy in your chart you better have a reason for it ;either ischemia or compression. Lastly a sudden onset cavernous sinus syndrome, in a patient with known pituitary neoplasm, is apoplexy until proven otherwise. Resources: Walsh and Hoyt's Clinical Neuro-Ophthalmology 5th Edition Neuro-Ophthalmology 2nd Edition ,Bert Glaser, MD