OPTOMETRIC EDUCATION CONSULTANTS CLINICAL CASE CHALLENGE

Case Challenge 08 – March 2019

A 53 year old man who had been treated for advanced glaucoma presented with slowly progressive, painless vision loss in his right eye. He had missed his visits for the past year, though he had been obtaining medication refills through his pharmacy. His vision in this eye is Light Perception. A year earlier, it was 20/200 and 3 years earlier it was 20/70 with fixation loss from glaucoma.

His recent vision reduction was due to a hypermature cataract that fully developed in the year between visits.  His intraocular pressure was 14 mm Hg OD and 16 mm Hg OS. He had neither pain nor inflammation and gonioscopically his anterior chamber angles were open and normal. However, with mature and hypermature cataracts, concern must be for phacomorphic and phacolytic glaucoma.

Phacomorphic glaucoma develops as the lens becomes intumescent and thickened through the process of cataractogenesis.  This can cause a relative pupil block with secondary angle closure with all of the attendant signs and symptoms of an acute angle closure attack. The glaucomatous mechanism is secondary angle closure with pupil block. However, intermittent angle closure with sporadic symptoms or asymptomatic chronic angle closure can also commonly occur.

Alternately, upon cataract hypermaturation, the lens cortex undergoes spontaneous lysis and absorption with secondary lens nucleus shrinkage and capsule wrinkling.  This allows internal lens proteins to leak out through an intact though permeable lens capsule.   While the internal lens proteins are the host’s own body tissue, they have never been exposed to the anterior chamber due to their envelopment by the lens capsule.  Thus, when the body detects these internal lens proteins, it interprets them as foreign and antigenic.  Subsequently, a lens-induced inflammatory reaction ensues. This is the phacolytic response.  Macrophages are scavenger cells that attempt to remove lens material and re-establish normal aqueous outflow. 

Elevated levels of high molecular weight (HMW) soluble lens proteins can directly obstruct aqueous outflow.  Further, during the uveitic process, breakdown of the blood-ocular barrier occurs with subsequent influx of proteins as well as inflammatory cells. These constituents are considered to have a major impact on IOP elevation as well. Obstruction of the trabecular meshwork by inflammatory cells and proteins, as well as trabeculitis (inflammation of the trabecular meshwork), likely contribute to the secondary open angle glaucoma.

Pupil block angle closure in phacomorphic glaucoma is initially addressed in much the same way as primary angle closure. The inflammatory response in phacolytic glaucoma is initially treated with steroids, cycloplegics, and aqueous suppressants. When lens-induced glaucoma develops, the logical approach is to remove the lens. These hypermature lens conditions develop typically when a patient is deemed a poor candidate for surgery or otherwise cannot obtain or undergo cataract extraction. In the patient presented here, he already had longstanding severe vision loss from advanced glaucoma; thus his developing cataract was never addressed. With no future visual potential in this eye from pre-existing glaucoma, he will be monitored for the possible development of phacomorphism and phacolysis.

READ MORE CASE CHALLENGES

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Case Challenge 07 – January 2019

A 25 year old woman was involved in a minor automobile accident where she was hit by another driver. The accident was reportedly minor, with no initial injury to either driver, and both cars were able to be driven away. She felt that she experienced only a...

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Case Challenge 06 – November 2018

Optometric Education Consultants Clinical Case Challenge A 21 year old male plumber called in requesting an urgent appointment. He was working on a job and trying to dislodge a drain coupling by hammering it with the blunt end of a screw driver. He missed,...

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Case Challenge 05, Explained – October 2018

  A 47-year-old man presented complaining of gradually decreasing vision and monocular diplopia in his right eye for approximately the past 18 months. He had undergone LASIK vision correction over 13 years earlier with an excellent emmetropic...

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Case Challenge 05 – September 2018

A 65 year old woman previously diagnosed with primary open angle glaucoma presented for ongoing care. She was using latanoprost in each eye and had bilateral selective laser trabeculoplasty performed two years earlier. Her medical history was significant for hypertension, elevated cholesterol, and arthritis.  Her vision was 20/20 OD and 20/25 OS. She had an inferior retinal nerve fiber layer defect in the right eye and significant superior rim damage in the left eye. Threshold perimetry showed the above corresponding visual field defects.

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Case Challenge 04 – August 2018

The first patient is a 16 year old male whose vision has been fluctuating for 6 weeks. He also complains about headaches. His primary care physician feels it’s a normal growth spurt and Mom feels it’s migraines as there is a strong family history, but she still wants eyes checked. His vision is 20/20 OD/OS uncorrected and he has bilateral optic disc edema.

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Case Challenge 03 – July 2018

A 35 year old man presents wanting another opinion due to “blood on my right eye”. He says that everything happened 3 days ago after violently vomiting, reportedly due to food poisoning from chicken Caesar salad. He still feels a little nauseated and somewhat “not himself”. He saw another practitioner 3 days ago, was told he had a ‘bruise’ on his eye and it should go away in 1-2 weeks. From the outward appearance, he seems to simply have just a subconjunctival hemorrhage…or does he?

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Case Challenge 02 – June 2018

A 13 year old female was referred for painless reduced vision (20/40) in her left eye with a concurrent abnormal screening visual field, reportedly elevated intraocular pressure (IOP), and an afferent pupillary defect. Her previous exam was 3 weeks earlier and she had been previously referred to an ophthalmologist over a year earlier by another optometrist, but her mother did not know why and did not take her. When presented with painless vision loss in a young patient with these findings, there are numerous diagnostic possibilities.

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Case Challenge 01 – June 2018

A 27 year old woman presents urgently complaining of painful vision loss in her right eye. She has no known medical history and this has never occurred before. She has an edematous optic nerve with hemorrhaging, an afferent pupil defect, superior arcuate scotoma, pain when she moves her eye, and 20/70 visual acuity. A clear-cut case of optic neuritis possibly as the first manifestation of multiple sclerosis? Perhaps…perhaps not.

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