Floaters, photopsia occur after brain irradiation

Issue: November 2012

A 73-year-old white male was referred from his primary care physician for an evaluation. He had a history of cancer with metastasis. He had recently undergone brain irradiation, and shortly thereafter he began noticing floaters in his vision. The patient stated that they were in both eyes, in the left eye greater than the right, for about 6 weeks. He had noticed intermittent photopsias in the superior portion of his vision. He also reported difficulty focusing with his current glasses.

The patient’s medical history was significant for renal cell carcinoma, for which he underwent right nephrectomy and adrenalectomy; prostatic carcinoma, for which he underwent seed implantation; several mediastinal/lung metastases, for which he was treated with sunitinib; and recent multiple hemorrhagic brain metastatic lesions verified by computed tomography (CT) scan. The patient had opted out of chemotherapy and chose hospice care, but later underwent whole-brain radiation treatment when the brain metastases were found. He also had coronary artery disease, bradycardia, hypertension, dyspnea, osteoarthritis, hemorrhoids, diverticulosis, gastroesophageal reflux disease, anxiety, constipation and insomnia.

First photo: The right eye had a choroidal nevus with slightly irregular borders just superior to the optic nerve; there was no associated drusen or lipofuscin. Second photo: There was an elevation with smoothly transitioning borders in the superior temporal arcade with a large associated serous retinal detachment, about 3 disc diameters in size, extending from the elevated area inferior and including the temporal macula.

The patient’s medications included acetaminophen, albuterol/ipratropium, bisacodyl, citalopram, dexamethasone, diazepam, fentanyl, gabapentin, isosorbide mononitrate, lorazepam, milk of magnesia, morphine, omeprazole, ondansetron, polyethylene glycol, senna/docusate sodium, sodium biphosphate and temazepam. He was allergic to codeine.

The patient’s entering visual acuities with his habitual glasses were 20/50- OD, 20/40- OS. He refracted to 20/40+ OD, 20/25- OS with a 1-D hyperopic shift in the right eye and a minor cylindrical change in the left eye. Pupils were equal, round and reactive without afferent pupillary defect. Motilities were full and smooth, and confrontation visual fields were full in both eyes. He had mild nonsclerotic cataracts. IOPs were 15 mm Hg OD and 17 mm Hg OS via noncontact tonometry.

Third and fourth photos: The left eye had an area of fibrous vitreoretinal traction in the superior temporal arcade but was otherwise unremarkable.

A dilated fundus exam revealed bilateral posterior vitreous detachments, healthy optic nerves with .30/.30 cupping in the right eye and .35/.35 cupping in the left eye. The right eye had a choroidal nevus with slightly irregular borders just superior to the optic nerve; there was no associated drusen or lipofuscin. There was an elevation with smoothly transitioning borders in the superior temporal arcade with a large associated serous retinal detachment, about 3 disc diameters in size, extending from the elevated area inferior and including the temporal macula. The periphery was unremarkable. The left eye had an area of fibrous vitreoretinal traction in the superior temporal arcade but was otherwise unremarkable.

Left OCT. A macular optical coherence tomography in the right eye revealed a serous retinal detachment extending from the subfoveal area temporally.Right OCT. A line scan through the elevation revealed an apparently extraocular lesion causing scleral indentation.

A macular optical coherence tomography in the right eye revealed a serous retinal detachment extending from the subfoveal area temporally. A line scan through the elevation revealed an apparently extraocular lesion causing scleral indentation.

What’s your diagnosis?

The patient presumably had an intraorbital metastasis from either the renal cell or prostatic carcinoma. His records indicated that a head CT scan, with and without contrast, had been completed 2.5 months prior; while several hemorrhagic metastatic brain lesions were described, no orbital findings were noted.

Addressing the patient’s chief complaint of floaters, the likely culprit was posterior vitreous detachment in both eyes with contribution from the fibrous vitreoretinal traction in the left eye.

This patient’s treatment

His primary care physician was alerted to the findings, and the patient was referred to the facility’s ophthalmology clinic. Because the patient was under hospice care, the ophthalmologist deemed surgical intervention for the orbital mass unwarranted; however, he suggested that orbital radiation may alleviate the patient’s symptoms and help the retinal detachment resolve over the course of several weeks. He noted a risk of visual loss and proliferative vitreoretinopathy with this option, but stated that this would likely not occur for 18 months or more.

The patient was then referred to an ocular oncologist. Per the provider’s correspondence, at that exam the patient reported relatively stable vision. Visual acuity was 20/30 OD and 20/25 OS, IOPs were 17 mm Hg OU and slit lamp exam was unremarkable. The amelanotic lesion along the superotemporal arcade of the right eye remained, measuring 3 mm x 3 mm x 0.9 mm. The subretinal fluid inferior to the lesion and involving the macula persisted, basically unchanged. The choroidal nevus in the right eye was stable. The provider recommended monitoring, with a 3-month return visit scheduled.

Follow-up

Since that time, additional metastatic disease was found in the patient’s right hip, for which he underwent palliative radiation treatment. Shortly thereafter, he suffered several broken bones after a fall while attempting independent ambulation; the breaks were reportedly a result of decreased bone density due to additional bone metastases.

Sara L. Weidmayer

The patient began suffering with delirium, likely a result of decreased brain function from metastatic lesions in his brain, complicated by widespread cancer and anemia. He remained under hospice care until his death.

Discussion of diagnosis

Orbital metastasis accounts for 3% to 10% of orbital masses (George et al.) and 12% of all orbital malignancies (Isshiki et al.). They typically originate from carcinomas with the primary tumor located in the breast or lung, but may also be secondary to prostatic, renal or several other cancers (Young Lee et al.); one third of cases have an unidentified primary source (Shome et al.).

Presenting symptoms most often are proptosis or diplopia, but also include pain, decreased vision, ptosis, globe displacement, exophthalmos and occasionally enophthalmos (Young Lee et al.). Unfortunately, orbital metastasis usually represents late metastatic disease and rarely is the first sign of disseminate cancer, so the prognosis is generally poor.

In this case, additional orbital imaging and biopsy or other testing of the mass was not conducted due to the patient’s advanced disease and his election of hospice care. However, given the patient’s systemic history and metastatic status, the lesion is highly suggestive of metastasis, with the primary tumor most likely being prostatic or renal cell carcinoma, despite ocular or orbital metastasis from prostatic or renal cell carcinoma being very rare (Mezer et al.). MRI and CT scans usually show nonspecific features for orbital metastases, but are helpful for determining the size and extent of tumor involvement; MRI offers better resolution. Orbital metastases may involve the globe and optic nerve and intraconal, conal and extraconal spaces (Chong).

Prostate cancer typically affects men older than 50, more commonly black men, with primary risk factors being increasing age, positive family history and hypertension. It is often a nonaggressive cancer, though it does metastasize, primarily to bone and lymph nodes. Though prostatic carcinoma rarely metastasizes to the orbit, it is the third leading primary site for orbital metastasis; orbital bone is typically affected in such cases (Gupta et al.).

Renal cell carcinoma (RCC) accounts for more than 80% of renal malignancy. Consistent with this patient’s demographics, RCC occurs predominantly in men in their seventh and eighth decade (Shome et al.). RCC typically metastasizes to the lungs, bones, liver and brain, but can affect any organ system and often involves unusual sites, often several years after RCC diagnosis. Still, orbital metastasis from RCC is rare. One series from Ferry and Font reported ocular metastatic tumor to be caused by a RCC primary in only 3% of cases.

Though RCC rarely affects ocular structures, the orbit, choroid, iris, ciliary body, lacrimal gland conjunctiva, eyelid, eyebrow and extraocular muscles have been reported to be involved. Orbital metastasis from RCC generally causes a diffuse orbital mass, typically involving the orbital fat, muscle or bone. RCC metastases are characteristically vascular, which may lead to pulsatile exophthalmos (Shome et al.).

Treatment

Radiotherapy is generally used to treat orbital metastasis and alleviate symptoms, including pain, by reducing the tumor size. Other options include steroid treatment to reduce orbital edema, evisceration and hormonal or chemotherapy. Surgical removal is not recommended.

Significant symptomatic relief occurs in most patients treated with irradiation, and the treatment is generally effective for orbital metastasis from prostatic carcinoma (Green et al.). Despite local tumor control, systemic prognosis remains poor if the metastasis is caused by RCC (Shome et al.).

Again, orbital metastasis usually occurs in patients with advanced disease, so survival times are low; studies vary from about 7 to 16 months, with a 2-year survival rate of 27%, which does not vary much regardless of primary malignancy (Young Lee et al. and Quick et al.). In this case, palliative treatment was considered but was not instituted due to stability of symptoms and bleak systemic prognosis.

References:

Chong VFH. The orbits in cancer imaging. Cancer Imaging. 2006;6(Special Issue A):S27-31. doi: 10.1102/1470-7330.2006.9003. Accessed October 2, 2012.
Ferry AP, Font RL. Carcinoma metastatic to the eye and orbit II. A clinicopathological study of 26 patients with carcinoma metastatic to the anterior segment of the eye. Arch Ophthalmol. 1975;93:472-482.
George S, Cooke CA, McGinnity GF, White S, Venkatraman L. Treated choroidal melanoma with late metastases to the contralateral orbit. Clinical Medicine Insights: Pathology. 2009;2:5-8.
Green S, Som PS, Lavagnini PG. Bilateral orbital metastases from prostate carcinoma: case presentation and CT findings. Am J Neuroradiol. 1995;16:417-419.
Gupta N, Kashyap S, Nayyar N, Panda S, Singh P. Proptosis due to “isolated” soft tissue orbital metastasis of prostate carcinoma. Ind J Cancer. 2010;47(1):74.
Hassane S, Fouad E, Said I, et al. Orbital metastatic angiosarcoma. Korean J Ophthalmol. 2010;24(6):364-366.
Isshiki S, Cho S, Matsuno D, Sato N, Furuya Y. A case of orbital metastasis from prostatic carcinoma as an initial symptom. Hinyokika Kiyo. 2007;53:193-195.
Mezer E, Gdal-On M, Miller B. Orbital metastasis of renal cell carcinoma masquerading as amaurosis fugax. Eur J Ophthalmol. 1997;7(3):301-304.
Quick AM, Bloomston M, Kim EY, Hall NC, Mayr NA. Complete response to radiation therapy of orbital metastasis from hepatocellular carcinoma. World J Gastroenterol. 2009;15(47):6000-6003.
Shome D, Honavar S, Gupta P, Vemuganti G, Reddy P. Metastasis to the eye and orbit from renal cell carcinoma — A report of three cases and review of literature. Surv Ophthalmol. 2007;52(2):213-223.
Tertzakian GM, Herr HW, Mehta MB. Orbital metastases from prostatic carcinoma. Urology. 1982;19(4):427-429.
Young Lee J, Lee HJ, Jung MS, Kim SY. Metastatic esophageal squamous cell carcinoma to the orbit and periorbit masquerading as periorbital abscess. Korean J Ophthalmol. 2010;24(2):123-125.

For more information:

Sara L. Weidmayer, OD, FAAO, is a graduate of the Michigan College of Optometry and practices at Eye Center of Lenawee, PC, in Adrian, Mich. She can be reached at 1400 W. Maumee St., Adrian, MI 49221; saraweidmayer@gmail.com.
Edited by Leo P. Semes, OD, a professor of optometry, University of Alabama at Birmingham and a member of the Primary Care Optometry News Editorial Board. He may be contacted at 1716 University Blvd., Birmingham, AL 35294-0010; (205) 934-6773; fax: (205) 934-6758; lsemes@uab.edu.

Disclosure: Weidmayer has no relevant financial interests to disclose.