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A Complex Case of Bilateral Diffuse Nonnecrotizing Scleritis due to Rheumatoid Arthritis
Published 2020 by Jennifer Reilly
Co-Author(s): NULL
Program Number: 205175
Article Type: Scientific Program
Purpose: This is a case discussion of scleritis due to rheumatoid arthritis in a 43-year-old white man. Scleritis is a rare condition occurring in only 3.9-5.2 per 100,000 people. The condition is due to an underlying systemic disease in up to 50 percent of cases. This case was complicated by a prior misdiagnosis, despite the patient presenting with typical signs and symptoms, and significant side effects from standard of care treatment. This case demonstrates the clinical thinking needed to arrive at the proper diagnosis and management, and the importance of an interdisciplinary approach.
Case Report: A 43-year-old white man with a history of soft contact lens over wear and abuse presented to the clinic with a six-week history of bilateral red eye and eye pain. The patient was previously misdiagnosed with contact lens associated red eye (CLARE) in four prior eye exams and was treated with Tobradex. During his treatment for CLARE, the patient had increased intraocular pressure (IOP) and was identified as a steroid responder. His IOP returned to normal levels upon discontinuation of the drop. At the time of clinical presentation, the patient had moderate diffuse redness and conjunctival chemosis in both eyes. Anterior segment photos and anterior segment optical coherence tomography (AS-OCT) images were obtained and revealed suspected bilateral scleritis. Our team took an interdisciplinary approach and worked with ophthalmology, rheumatology, and dermatology to arrive at a diagnosis of bilateral diffuse non-necrotizing scleritis secondary to rheumatoid arthritis. This diagnosis was confirmed with blood work and the underutilized blood test of cyclic citrullinated peptide antibody IgG (CCP Ab IgG). The multidisciplinary team navigated managing a steroid responder with nonsteroidal anti-inflammatory drugs, topical and oral steroids along with topical ocular anti-hypertensive agents, and eventually methotrexate self-injections. The patient's ocular and systemic condition responded well to treatment.
Results: Scleritis is a rare condition that responds well to treatment when it is targeted at the appropriate underlying cause of the condition. Determining the correct diagnosis and underlying cause was challenging in this case due to prior misdiagnosis. This case scenario was unique in that it involved the use AS-OCT imaging of the sclera demonstrating an underutilized ability of the OCT machine to aid in the proper diagnosis. The case also outlined appropriate management of scleritis with steroids and topical anti-ocular hypertensive medications when the patient is a known steroid responder. Additionally, this case highlights the importance of ordering applicable lab work to uncover the underlying cause of the ocular condition, all while enlisting an interdisciplinary care team.
Case Report: A 43-year-old white man with a history of soft contact lens over wear and abuse presented to the clinic with a six-week history of bilateral red eye and eye pain. The patient was previously misdiagnosed with contact lens associated red eye (CLARE) in four prior eye exams and was treated with Tobradex. During his treatment for CLARE, the patient had increased intraocular pressure (IOP) and was identified as a steroid responder. His IOP returned to normal levels upon discontinuation of the drop. At the time of clinical presentation, the patient had moderate diffuse redness and conjunctival chemosis in both eyes. Anterior segment photos and anterior segment optical coherence tomography (AS-OCT) images were obtained and revealed suspected bilateral scleritis. Our team took an interdisciplinary approach and worked with ophthalmology, rheumatology, and dermatology to arrive at a diagnosis of bilateral diffuse non-necrotizing scleritis secondary to rheumatoid arthritis. This diagnosis was confirmed with blood work and the underutilized blood test of cyclic citrullinated peptide antibody IgG (CCP Ab IgG). The multidisciplinary team navigated managing a steroid responder with nonsteroidal anti-inflammatory drugs, topical and oral steroids along with topical ocular anti-hypertensive agents, and eventually methotrexate self-injections. The patient's ocular and systemic condition responded well to treatment.
Results: Scleritis is a rare condition that responds well to treatment when it is targeted at the appropriate underlying cause of the condition. Determining the correct diagnosis and underlying cause was challenging in this case due to prior misdiagnosis. This case scenario was unique in that it involved the use AS-OCT imaging of the sclera demonstrating an underutilized ability of the OCT machine to aid in the proper diagnosis. The case also outlined appropriate management of scleritis with steroids and topical anti-ocular hypertensive medications when the patient is a known steroid responder. Additionally, this case highlights the importance of ordering applicable lab work to uncover the underlying cause of the ocular condition, all while enlisting an interdisciplinary care team.
A Comprehensive Approach to Sjogren's Syndrome
Published 2020 by Scott Hauswirth
Co-Author(s): Whitney Hauser, Leslie O'Dell, Melissa Barnett
Article Type: Lectures & Workshops
This course presents an overview of Sjogren�s Syndrome and associated ocular complications. Emphasis is to present different aspects of the ocular effects of the disease, as well as to discuss different strategies for improving the ocular surface which are customized to the patient, with the goal of improving patient quality of life.
A Confounding Case of Chorioretinopathy
Published 2020 by Megan Lusignan
Co-Author(s): NULL
Article Type: Residents Day
Abstract: We present a case of a healthy 43 year old patient complaining of sudden vision loss with a serous retinal detachment OS, with no history of trauma, flashes, or floaters prior to vision loss.
Case History: A 43 year old Hispanic male presented to the clinic complaining of sudden onset blackout vision OS for 3 days. The patient denied any previous head trauma, flashes, or floaters. His last eye exam was 7 years ago, and he denied any ocular conditions or medications. The patient also reported good health, and is not currently taking any systemic medications, OTC or prescribed.
Pertinent Findings: Entering visual acuities were 20/20 OD and 20/100- OS uncorrected, PHNI OS. Pupils were equal and reactive, with no RAPD. Confrontation visual fields were FTFC OD with inferior restriction OS. Anterior segment exam was unremarkable, and IOPs were 16 mmHg OD and 15 mmHg OS. Optic nerves were healthy and pink for both eyes. Fundus exam OD revealed a ½ DD PED nasal to the macula and a ¼ DD PED temporal to the macula, with subretinal and intraretinal fluid visible on OCT. Fundus exam OS revealed paracentral RPE hyperpigmentation and exudates, with a central PED and adjacent serous retinal detachment and intraretinal fluid on OCT. A large floater or possible operculum was visible in the posterior chamber just anterior to the area of RPE clumping.
Differential Diagnosis: The main concern for this patient due to the appearance of the fundus and the large vitreous floater was an operculated retinal hole causing a serous retinal detachment OS. While we were unable to locate signs of a retinal hole on the OCT, we felt it important to have this possibility ruled out first due to the narrow window for treatment with the macula off.
Central serous chorioretinopathy (CSR) was also considered due to the OCT appearance and lack of head trauma, flashes, or floaters as stated by the patient.
Diagnosis and Discussion: The patient was referred to ophthalmology for evaluation and management, where he was diagnosed with CSR OS. This condition is characteristically seen in men aged 25-50 years old, and is typically associated with either high stress or systemic/topical steroid use. It typically presents unilaterally with complaints of a central scotoma or central blur/distortion. Visual acuity generally ranges from 20/20 to 20/80, with a small APD possible. OCT imaging for these patients shows localized serous retinal detachments near the macula with possible PEDs as well. F-ANG may show a classic "�smoke-stack"� pattern.
Treatment, Management: The patient was placed under observation only by ophthalmology, the most common management for CSR patients. Visual prognosis is excellent without treatment, with most patients recovering 20/30 or better vision. 3 days after the initial visit (6 days after onset) the patient's visual acuity had improved to 20/60- OS. The patient was educated to avoid oral or topical steroids as well as Viagra. Due to the presence of multiple PEDs in both eyes, the patient was also referred for F-ANG to rule out CNVM or polypoidal choroidal vasculopathy,
Results: pending.
Other treatment options for this condition include laser therapy and photodynamic therapy. Laser therapy may be used in recurrent or chronic cases and has been shown to accelerate visual recovery, although it does not improve the final visual outcome. PDT has also been shown to be affective in patients with chronic CSR, and was found to be superior to laser in visual improvement1.
Results: CSR is characterized by sudden onset central vision loss, and presents with serous retinal detachments in the macula with possible PEDs. Visual prognosis is generally excellent without intervention, although patients should be monitored every 6-8 weeks until resolved. Bibliography: 1. van Dijk EHC, Fauser S, Breukink MB, et al. Half-Dose Photodynamic Therapy versus High-Density Subthreshold Micropulse Laser Treatment in Patients with Chronic Central Serous Chorioretinopathy: The PLACE Trial. Ophthalmology. 2018;125(10):1547-1555. doi:10.1016/j.ophtha.2018.04.021
Case History: A 43 year old Hispanic male presented to the clinic complaining of sudden onset blackout vision OS for 3 days. The patient denied any previous head trauma, flashes, or floaters. His last eye exam was 7 years ago, and he denied any ocular conditions or medications. The patient also reported good health, and is not currently taking any systemic medications, OTC or prescribed.
Pertinent Findings: Entering visual acuities were 20/20 OD and 20/100- OS uncorrected, PHNI OS. Pupils were equal and reactive, with no RAPD. Confrontation visual fields were FTFC OD with inferior restriction OS. Anterior segment exam was unremarkable, and IOPs were 16 mmHg OD and 15 mmHg OS. Optic nerves were healthy and pink for both eyes. Fundus exam OD revealed a ½ DD PED nasal to the macula and a ¼ DD PED temporal to the macula, with subretinal and intraretinal fluid visible on OCT. Fundus exam OS revealed paracentral RPE hyperpigmentation and exudates, with a central PED and adjacent serous retinal detachment and intraretinal fluid on OCT. A large floater or possible operculum was visible in the posterior chamber just anterior to the area of RPE clumping.
Differential Diagnosis: The main concern for this patient due to the appearance of the fundus and the large vitreous floater was an operculated retinal hole causing a serous retinal detachment OS. While we were unable to locate signs of a retinal hole on the OCT, we felt it important to have this possibility ruled out first due to the narrow window for treatment with the macula off.
Central serous chorioretinopathy (CSR) was also considered due to the OCT appearance and lack of head trauma, flashes, or floaters as stated by the patient.
Diagnosis and Discussion: The patient was referred to ophthalmology for evaluation and management, where he was diagnosed with CSR OS. This condition is characteristically seen in men aged 25-50 years old, and is typically associated with either high stress or systemic/topical steroid use. It typically presents unilaterally with complaints of a central scotoma or central blur/distortion. Visual acuity generally ranges from 20/20 to 20/80, with a small APD possible. OCT imaging for these patients shows localized serous retinal detachments near the macula with possible PEDs as well. F-ANG may show a classic "�smoke-stack"� pattern.
Treatment, Management: The patient was placed under observation only by ophthalmology, the most common management for CSR patients. Visual prognosis is excellent without treatment, with most patients recovering 20/30 or better vision. 3 days after the initial visit (6 days after onset) the patient's visual acuity had improved to 20/60- OS. The patient was educated to avoid oral or topical steroids as well as Viagra. Due to the presence of multiple PEDs in both eyes, the patient was also referred for F-ANG to rule out CNVM or polypoidal choroidal vasculopathy,
Results: pending.
Other treatment options for this condition include laser therapy and photodynamic therapy. Laser therapy may be used in recurrent or chronic cases and has been shown to accelerate visual recovery, although it does not improve the final visual outcome. PDT has also been shown to be affective in patients with chronic CSR, and was found to be superior to laser in visual improvement1.
Results: CSR is characterized by sudden onset central vision loss, and presents with serous retinal detachments in the macula with possible PEDs. Visual prognosis is generally excellent without intervention, although patients should be monitored every 6-8 weeks until resolved. Bibliography: 1. van Dijk EHC, Fauser S, Breukink MB, et al. Half-Dose Photodynamic Therapy versus High-Density Subthreshold Micropulse Laser Treatment in Patients with Chronic Central Serous Chorioretinopathy: The PLACE Trial. Ophthalmology. 2018;125(10):1547-1555. doi:10.1016/j.ophtha.2018.04.021
A Cryptic Case of Bilateral Optic Neuropathy
Published 2020 by Lucia Yang
Co-Author(s): NULL
Article Type: Residents Day
Abstract:
We report an atypical case of cryptococcal meningitis presenting with bilateral, asymmetric optic disc edema. It is critical to recognize the various ocular manifestations & diagnostic considerations in cryptococcal meningitis with bilateral optic neuropathy.
Case History:
74 YO white male
CC: left eye swelling & pain x 2 days, pain on eye movement
Medical history:
●Small Lymphocytic Leukemia (SLL)/Chronic Lymphocytic Leukemia (CLL) x 2012
●Seizure disorder
●DM
●HTN
●HLD
●BPH
●DVT
Ocular history:
●Acephalgic migraines
●Cataracts
Medications:
●Metformin
●Lisinopril
●Atorvastatin
●Tamsulosin
●Warfarin
Other salient information:
●20lb unintentional weight loss, fatigue, bilateral retro-orbital pain x 2 months
Pertinent Findings:
●Initial VA OD 20/20, OS 20/25, moderate lid edema OS, conj injection & chemosis OS with inflammatory changes of left orbit on CT; pt admitted for IV antibiotics
●F/u revealed reduced VA OS 20/40, 2+RAPD OS, decreased color vision OS, proptosis OS, newly noted disc edema OS>>OD
●Abnormal thickened left optic nerve & leptomeningeal enhancement on MRI
●Positive cryptococcus Ag & CSF yeast culture on LP with normal opening pressure; antifungal treatment initiated
●Pt experienced acute episode of altered mental status with increased leptomeningeal enhancement on MRI after initiating antifungals; improved mental status after initiating steroids
●Serial LPs show improved crypto Ag titer & less yeast on CSF Gram stain (stable protein, glucose, opening pressure)
●All ocular/visual parameters markedly improved after initiating treatment, VA 20/20 each eye, VF improved OU, eye/lid findings resolved
●Pt co-managed by optometry, ophthalmology, infectious disease, neurology, and hematology/oncology specialists during hospital course
Ongoing care: updates to be provided
Differential Diagnosis:
Cryptococcal meningitis (CM)
Orbital cellulitis
Neoplastic optic nerve infiltration
Optic neuritis / perineuritis
Idiopathic orbital inflammation
Diagnosis and Discussion:
●Initial dx of orbital cellulitis & leptomeningeal spread of CLL/SLL but later confirmed as CM after LP
●CM risk factors include HIV (80% of cases), organ transplant, cancer, liver cirrhosis;1 our pt was HIV-negative but had positive history of CLL
●75% of CM cases present with elevated intracranial pressure (ICP)2
●Up to 50% of CM pts have visual loss, typically from papilledema.1 Visual loss in CM with normal ICP can be due to direct infiltration of optic nerve or inflammatory optic neuritis2
●Immune reconstitution inflammatory syndrome (IRIS) occurred in our pt after antifungal initiation, causing a worsened clinical presentation; further discussion will be provided
Treatment, Management:
●CM pts require oral & IV antifungals over a prolonged treatment course with induction, consolidation & maintenance phases3
●ICP should be monitored while treating CM: serial LP recommended; acetazolamide & weight loss are NOT appropriate1
●Steroids are not used to treat CM except with concurrent antifungals in the setting of IRIS3
●Residual neurocognitive impairment may result following CM1
●Serial OCT, fundus photos & HVF illustrate improvement in our pt after initiating antifungals
Results:
●Optometrists must be aware of different ocular presentations of cryptococcus. In our case, the pt demonstrated visual decline due to optic neuropathy without raised ICP, which subsequently improved after appropriate therapy
●Interdisciplinary co-management in CM is critical to improve pt outcomes Bibliography:
1 Rigi M, Khan K, Smith SV, et al. Evaluation & management of the swollen optic disk in cryptococcal meningitis. Survey of ophthalmology. 2017 Mar 1;62(2):150-60.
2 Werner AC, Vuong LN, Hedges TR, et al. Immune reconstitution inflammatory syndrome causing progressive optic nerve edema in cryptococcal meningitis. Retinal Cases & Brief Reports. 2019 Jul 1;13(3):207-10.
3 Perfect JR, Dismukes WE, Dromer F, et al. Clinical practice guidelines for the management of cryptococcal disease: 2010 update by the Infectious Diseases Society of America. Clinical infectious diseases. 2010 Feb 1;50(3):291-322.
We report an atypical case of cryptococcal meningitis presenting with bilateral, asymmetric optic disc edema. It is critical to recognize the various ocular manifestations & diagnostic considerations in cryptococcal meningitis with bilateral optic neuropathy.
Case History:
74 YO white male
CC: left eye swelling & pain x 2 days, pain on eye movement
Medical history:
●Small Lymphocytic Leukemia (SLL)/Chronic Lymphocytic Leukemia (CLL) x 2012
●Seizure disorder
●DM
●HTN
●HLD
●BPH
●DVT
Ocular history:
●Acephalgic migraines
●Cataracts
Medications:
●Metformin
●Lisinopril
●Atorvastatin
●Tamsulosin
●Warfarin
Other salient information:
●20lb unintentional weight loss, fatigue, bilateral retro-orbital pain x 2 months
Pertinent Findings:
●Initial VA OD 20/20, OS 20/25, moderate lid edema OS, conj injection & chemosis OS with inflammatory changes of left orbit on CT; pt admitted for IV antibiotics
●F/u revealed reduced VA OS 20/40, 2+RAPD OS, decreased color vision OS, proptosis OS, newly noted disc edema OS>>OD
●Abnormal thickened left optic nerve & leptomeningeal enhancement on MRI
●Positive cryptococcus Ag & CSF yeast culture on LP with normal opening pressure; antifungal treatment initiated
●Pt experienced acute episode of altered mental status with increased leptomeningeal enhancement on MRI after initiating antifungals; improved mental status after initiating steroids
●Serial LPs show improved crypto Ag titer & less yeast on CSF Gram stain (stable protein, glucose, opening pressure)
●All ocular/visual parameters markedly improved after initiating treatment, VA 20/20 each eye, VF improved OU, eye/lid findings resolved
●Pt co-managed by optometry, ophthalmology, infectious disease, neurology, and hematology/oncology specialists during hospital course
Ongoing care: updates to be provided
Differential Diagnosis:
Cryptococcal meningitis (CM)
Orbital cellulitis
Neoplastic optic nerve infiltration
Optic neuritis / perineuritis
Idiopathic orbital inflammation
Diagnosis and Discussion:
●Initial dx of orbital cellulitis & leptomeningeal spread of CLL/SLL but later confirmed as CM after LP
●CM risk factors include HIV (80% of cases), organ transplant, cancer, liver cirrhosis;1 our pt was HIV-negative but had positive history of CLL
●75% of CM cases present with elevated intracranial pressure (ICP)2
●Up to 50% of CM pts have visual loss, typically from papilledema.1 Visual loss in CM with normal ICP can be due to direct infiltration of optic nerve or inflammatory optic neuritis2
●Immune reconstitution inflammatory syndrome (IRIS) occurred in our pt after antifungal initiation, causing a worsened clinical presentation; further discussion will be provided
Treatment, Management:
●CM pts require oral & IV antifungals over a prolonged treatment course with induction, consolidation & maintenance phases3
●ICP should be monitored while treating CM: serial LP recommended; acetazolamide & weight loss are NOT appropriate1
●Steroids are not used to treat CM except with concurrent antifungals in the setting of IRIS3
●Residual neurocognitive impairment may result following CM1
●Serial OCT, fundus photos & HVF illustrate improvement in our pt after initiating antifungals
Results:
●Optometrists must be aware of different ocular presentations of cryptococcus. In our case, the pt demonstrated visual decline due to optic neuropathy without raised ICP, which subsequently improved after appropriate therapy
●Interdisciplinary co-management in CM is critical to improve pt outcomes Bibliography:
1 Rigi M, Khan K, Smith SV, et al. Evaluation & management of the swollen optic disk in cryptococcal meningitis. Survey of ophthalmology. 2017 Mar 1;62(2):150-60.
2 Werner AC, Vuong LN, Hedges TR, et al. Immune reconstitution inflammatory syndrome causing progressive optic nerve edema in cryptococcal meningitis. Retinal Cases & Brief Reports. 2019 Jul 1;13(3):207-10.
3 Perfect JR, Dismukes WE, Dromer F, et al. Clinical practice guidelines for the management of cryptococcal disease: 2010 update by the Infectious Diseases Society of America. Clinical infectious diseases. 2010 Feb 1;50(3):291-322.
A Curious Case of Left Homonymous Hemianopia
Published 2020 by Michelle Espanto
Co-Author(s): NULL
Article Type: Residents Day
Abstract: A patient with complaints of flashes and vision loss in his left visual field, leads to the discovery of an intracranial tumor. The clinical course and ancillary testing used to come to this conclusion are discussed.
Case History: Patient Demographics:
69 year old white male
Chief Complaint:
Flashes in left side of vision for 2 weeks with subsequent constriction in left visual field with resultant complaint of bumping into things on left side a few days later; comcomitant complaint of mild pain behind left eye.
Ocular Hx:
Choroidal nevi OU, HIV without ocular sequelae, presbyopia
Medical Hx:
Prostate cancer, CAD, COPD, anemia, dermatitis, tobacco use
Medications:
Albuterol, aspirin, atorvastatin, biktarvy, budesonide formoterol inh, cholecalciferol, tiotropium
Pertinent Findings: Pupils:
4mm OD, 4.5mm OS
Aniso similar dim and bright, (-)APD
Motility:
FROM OU
CVF:
Complete left side defect OD, OS
IOP:
11mmHg OD, 10mmHg OS
DFE:
C/D: .15-.20, margins sharp
ONH: p/d
A/V: 2/3
Macula: flat
Periphery: pavingstone inf temp OD, 3DD mildly elevated nevus with overlying drusen OS
24-2SS HVF:
Symmetrical left homonymous hemianopsia, denser inferiorly but with significant extension superiorly
ER Imaging:
CT head: 4.2 x 3.3 x 3.1cm bilobed cystic mass along right parieto-occipital convexity with vasogenic edema and mass effect on right lateral ventricle
Chest x-ray: right apical lung mass
Neurology:
Higher coortical functions: AOx3, does not know year even with options presented, follows complex commands in all extremities
Normal langage, naming and repetition intact. Calculation and finger gnosia intact
Normal remote and recent memory
Cranial Nerves:
II: 3mm OD, 4mm OS, round and reactive to light, dense left homonymous hemianopsia
III-XII: normal
Gait:
Not tested due to patient safety
Muscles:
Normal resting tone and bulk
Sensory Exam:
Normal sensation to light touch
Cerebellar Exam:
Normal finger to nose
Reflexes:
Normal
Differential Diagnosis: Metastatic disease (presumably from lung or, less likely, prostate cancer), abcess (given immunocompromised status), CVA, trauma, MS
Diagnosis and Discussion: Diagnosis:
Right parieto-occipital tumor
Discussion:
The most common symptoms of an intracranial tumor are gradual blurred vision, visual disturbances, or visual field defect1. Other symptoms may include headache, diplopia, cranial nerve palsy, and behavioral changes. Homonymous hemianopia (HH) is most commonly caused by CVA (52-70%), trauma (14%), and tumors (11%)2 and is suggestive of a post-chiasmal lesion. Occipital lesions, in particular, cause HH and may cause photopsia in the area of vision loss2, as seen in this patient. This case highlights how optometric testing, neurological testing, and imaging all aided in the diagnosis of a tumor.
Treatment, Management: Optometry:
Patient sent for STAT ER evaluation to rule out CVA.
ER and Neurosurgery:
In-patient work up recommended. Patient refused hospitalization/treatment at this time. An MRI of the brain with and without contrast and CT of the chest, abdomen, and pelvis recommended if/when patient returns. Consult with oncology and infectious disease recommended.
Treatment:
Typically, tumor resection, chemotherapy, and radiation are options for treatment3.
Results: Visual changes are often a primary manifestation of intracranial tumors. Therefore, awareness of ocular signs and symptoms associated with intracranial tumors are integral in promptly obtaining imaging and facilitating co-management to prevent further functional loss or even loss of life. In this case, the optometrist was the first one to initiate further investigation. Bibliography: 1. Sefi-Yurdakul N. Visual findings as primary manifestations in patients with intracranial tumors. International journal of ophthalmology. 2015; 8(4): 800"�803.
2. Goodwin D. Homonymous hemianopia: challenges and solutions. Clinical Ophthalmology. 2014:1919. doi:10.2147/opth.s59452.
3. Leo-Kottler B. (2007) Brain Tumors Relevant to Clinical Neuro-Ophthalmology. In: Schiefer U., Wilhelm H., Hart W. (eds) Clinical Neuro-Ophthalmology. Springer, Berlin, Heidelberg.
Case History: Patient Demographics:
69 year old white male
Chief Complaint:
Flashes in left side of vision for 2 weeks with subsequent constriction in left visual field with resultant complaint of bumping into things on left side a few days later; comcomitant complaint of mild pain behind left eye.
Ocular Hx:
Choroidal nevi OU, HIV without ocular sequelae, presbyopia
Medical Hx:
Prostate cancer, CAD, COPD, anemia, dermatitis, tobacco use
Medications:
Albuterol, aspirin, atorvastatin, biktarvy, budesonide formoterol inh, cholecalciferol, tiotropium
Pertinent Findings: Pupils:
4mm OD, 4.5mm OS
Aniso similar dim and bright, (-)APD
Motility:
FROM OU
CVF:
Complete left side defect OD, OS
IOP:
11mmHg OD, 10mmHg OS
DFE:
C/D: .15-.20, margins sharp
ONH: p/d
A/V: 2/3
Macula: flat
Periphery: pavingstone inf temp OD, 3DD mildly elevated nevus with overlying drusen OS
24-2SS HVF:
Symmetrical left homonymous hemianopsia, denser inferiorly but with significant extension superiorly
ER Imaging:
CT head: 4.2 x 3.3 x 3.1cm bilobed cystic mass along right parieto-occipital convexity with vasogenic edema and mass effect on right lateral ventricle
Chest x-ray: right apical lung mass
Neurology:
Higher coortical functions: AOx3, does not know year even with options presented, follows complex commands in all extremities
Normal langage, naming and repetition intact. Calculation and finger gnosia intact
Normal remote and recent memory
Cranial Nerves:
II: 3mm OD, 4mm OS, round and reactive to light, dense left homonymous hemianopsia
III-XII: normal
Gait:
Not tested due to patient safety
Muscles:
Normal resting tone and bulk
Sensory Exam:
Normal sensation to light touch
Cerebellar Exam:
Normal finger to nose
Reflexes:
Normal
Differential Diagnosis: Metastatic disease (presumably from lung or, less likely, prostate cancer), abcess (given immunocompromised status), CVA, trauma, MS
Diagnosis and Discussion: Diagnosis:
Right parieto-occipital tumor
Discussion:
The most common symptoms of an intracranial tumor are gradual blurred vision, visual disturbances, or visual field defect1. Other symptoms may include headache, diplopia, cranial nerve palsy, and behavioral changes. Homonymous hemianopia (HH) is most commonly caused by CVA (52-70%), trauma (14%), and tumors (11%)2 and is suggestive of a post-chiasmal lesion. Occipital lesions, in particular, cause HH and may cause photopsia in the area of vision loss2, as seen in this patient. This case highlights how optometric testing, neurological testing, and imaging all aided in the diagnosis of a tumor.
Treatment, Management: Optometry:
Patient sent for STAT ER evaluation to rule out CVA.
ER and Neurosurgery:
In-patient work up recommended. Patient refused hospitalization/treatment at this time. An MRI of the brain with and without contrast and CT of the chest, abdomen, and pelvis recommended if/when patient returns. Consult with oncology and infectious disease recommended.
Treatment:
Typically, tumor resection, chemotherapy, and radiation are options for treatment3.
Results: Visual changes are often a primary manifestation of intracranial tumors. Therefore, awareness of ocular signs and symptoms associated with intracranial tumors are integral in promptly obtaining imaging and facilitating co-management to prevent further functional loss or even loss of life. In this case, the optometrist was the first one to initiate further investigation. Bibliography: 1. Sefi-Yurdakul N. Visual findings as primary manifestations in patients with intracranial tumors. International journal of ophthalmology. 2015; 8(4): 800"�803.
2. Goodwin D. Homonymous hemianopia: challenges and solutions. Clinical Ophthalmology. 2014:1919. doi:10.2147/opth.s59452.
3. Leo-Kottler B. (2007) Brain Tumors Relevant to Clinical Neuro-Ophthalmology. In: Schiefer U., Wilhelm H., Hart W. (eds) Clinical Neuro-Ophthalmology. Springer, Berlin, Heidelberg.
A Curious Case of SUNCT Syndrome
Published 2020 by Tina Khieu
Co-Author(s): NULL
Article Type: Residents Day
Abstract: Short-lasting Unilateral Neuralgiform headache attacks with Conjunctival injection and Tearing is a rare headache syndrome not commonly known to many optometrists. This case highlights the recognition of the disorder and it's unique clinical management.
Case History: 51 yo WM presents w/ long-standing h/o short-lasting, "�stabbing-like"� headaches around OD w/ associated redness and tearing. Headaches occur 300x per week lasting 5-30 sec every 20 min. Pain is generally well-controlled by implanted nerve stimulators but pt has recently been experiencing increasing discomfort in R gaze.
OHx: R-sided SUNCT Syndrome, Glaucoma suspect vs. OHTN OS
MHx: DMT2, PTSD, Depression, Erectile Dysfunction
Meds: Timolol 0.5% gel OS, Lisinopril, Omeprazole, Galcanezumab-Gnlm inj, Semaglutide, Metformin, Vardenafil
Other Salient Information:
1. Occipital and supraorbital nerve stimulators implanted 2017 to reduce frequency and magnitude of Sxs
2. H/o occipital nerve block x4 2016
Pertinent Findings: BCVA: 20/20 OD & OS
EOMs: SAFE OU, Pain (6/10) in all R gazes OD>OS w/ mild tearing OD
Slit Lamp: Tr diffuse conjunctival injection OD=OS
Imaging:
1. MRI highlighting vascular loop compressing CN V
2. X-Ray of nerve stimulators w/ positioning of leads
3. Photos of incision and location of implants in pt's head and chest
Differential Diagnosis: Trigeminal Neuralgia, Cluster Headaches, Paroxysmal Hemicrania
Diagnosis and Discussion: SUNCT syndrome is a rare primary headache disorder in the classification of trigeminal autonomic celphias. These headaches can also have secondary etiologies due to posterior fossa lesions. Pts frequently experience severe, short, stabbing-like unilateral pain in the V1 distribution that can last up to 600 sec 1-600x/day around the orbit. Pts experience ipsilateral cranial autonomic symptoms due to CN V stimulation"�specifically conjunctival injection and tearing that vary in intensity.
Often SUNCT can be confused with other forms of headaches due to similarities between these disorders. However, recognizing the autonomic features and absence of having refractory periods are paramount in diagnosing SUNCT. MRIs also aid in finding causes for secondary SUNCT, e.g. vascular loop compressions.
First line Tx includes oral lamotrigine and/or IV lidocaine (occipital nerve block). Microvascular decompression (MVD) can effectively treat secondary SUNCT caused by compression of CN V by a major blood vessel. Occipital Nerve Stimulation (ONS) is another method that can reduce the intensity and frequency of attacks. If ONS fails, Deep Brain Stimulation can be an alternative method.
Our pt was diagnosed w/ SUNCT after his MRI revealed a vascular loop compressing on CN V in 2014. He has failed multiple medication interventions and though occipital nerve blocks were once useful, those effects wore off. Since then, he has responded well to ONS, but his symptoms are now worsening in all right gazes. Though MVD was offered, he chose to not proceed with the surgery due to complication risks.
Treatment, Management:
1. Continue Galcanezumab-Gnlm injections, ONS, and periodic adjustment of leads
2. MVD may serve as a possible choice if ONS fails, but
Results: do not come without risk.
Results: SUNCT syndrome is a rare headache disorder that may not be commonly known or recognized by optometrists. It can be misdiagnosed w/ other similar headaches. S/Sxs are limited to manifesting when attacks are present and may be missed during ocular examinations. However, it is important to consider this condition as a differential diagnosis w/ pts that present w/ unilateral headaches surrounding or occurring within the orbit and to ask about autonomic symptoms associated w/ their condition. Even w/ the lack of ocular evidence upon evaluation, it can be beneficial to seek care with neurology for further testing in order to confirm the diagnosis and guide pts to the proper course of treatment as pain and frequency of this condition can be debilitating. Bibliography: 1. Lambru, G., et al. SUNCT and SUNA: medical and surgical treatments. Neurol Sci 34, 75"�81 (2013)
Case History: 51 yo WM presents w/ long-standing h/o short-lasting, "�stabbing-like"� headaches around OD w/ associated redness and tearing. Headaches occur 300x per week lasting 5-30 sec every 20 min. Pain is generally well-controlled by implanted nerve stimulators but pt has recently been experiencing increasing discomfort in R gaze.
OHx: R-sided SUNCT Syndrome, Glaucoma suspect vs. OHTN OS
MHx: DMT2, PTSD, Depression, Erectile Dysfunction
Meds: Timolol 0.5% gel OS, Lisinopril, Omeprazole, Galcanezumab-Gnlm inj, Semaglutide, Metformin, Vardenafil
Other Salient Information:
1. Occipital and supraorbital nerve stimulators implanted 2017 to reduce frequency and magnitude of Sxs
2. H/o occipital nerve block x4 2016
Pertinent Findings: BCVA: 20/20 OD & OS
EOMs: SAFE OU, Pain (6/10) in all R gazes OD>OS w/ mild tearing OD
Slit Lamp: Tr diffuse conjunctival injection OD=OS
Imaging:
1. MRI highlighting vascular loop compressing CN V
2. X-Ray of nerve stimulators w/ positioning of leads
3. Photos of incision and location of implants in pt's head and chest
Differential Diagnosis: Trigeminal Neuralgia, Cluster Headaches, Paroxysmal Hemicrania
Diagnosis and Discussion: SUNCT syndrome is a rare primary headache disorder in the classification of trigeminal autonomic celphias. These headaches can also have secondary etiologies due to posterior fossa lesions. Pts frequently experience severe, short, stabbing-like unilateral pain in the V1 distribution that can last up to 600 sec 1-600x/day around the orbit. Pts experience ipsilateral cranial autonomic symptoms due to CN V stimulation"�specifically conjunctival injection and tearing that vary in intensity.
Often SUNCT can be confused with other forms of headaches due to similarities between these disorders. However, recognizing the autonomic features and absence of having refractory periods are paramount in diagnosing SUNCT. MRIs also aid in finding causes for secondary SUNCT, e.g. vascular loop compressions.
First line Tx includes oral lamotrigine and/or IV lidocaine (occipital nerve block). Microvascular decompression (MVD) can effectively treat secondary SUNCT caused by compression of CN V by a major blood vessel. Occipital Nerve Stimulation (ONS) is another method that can reduce the intensity and frequency of attacks. If ONS fails, Deep Brain Stimulation can be an alternative method.
Our pt was diagnosed w/ SUNCT after his MRI revealed a vascular loop compressing on CN V in 2014. He has failed multiple medication interventions and though occipital nerve blocks were once useful, those effects wore off. Since then, he has responded well to ONS, but his symptoms are now worsening in all right gazes. Though MVD was offered, he chose to not proceed with the surgery due to complication risks.
Treatment, Management:
1. Continue Galcanezumab-Gnlm injections, ONS, and periodic adjustment of leads
2. MVD may serve as a possible choice if ONS fails, but
Results: do not come without risk.
Results: SUNCT syndrome is a rare headache disorder that may not be commonly known or recognized by optometrists. It can be misdiagnosed w/ other similar headaches. S/Sxs are limited to manifesting when attacks are present and may be missed during ocular examinations. However, it is important to consider this condition as a differential diagnosis w/ pts that present w/ unilateral headaches surrounding or occurring within the orbit and to ask about autonomic symptoms associated w/ their condition. Even w/ the lack of ocular evidence upon evaluation, it can be beneficial to seek care with neurology for further testing in order to confirm the diagnosis and guide pts to the proper course of treatment as pain and frequency of this condition can be debilitating. Bibliography: 1. Lambru, G., et al. SUNCT and SUNA: medical and surgical treatments. Neurol Sci 34, 75"�81 (2013)
A Model of Visual Impairment as a Function of Age and Axial Length
Published 2020 by Mark Bullimore
Co-Author(s): Noel Brennan
Program Number: 200035
Article Type: Scientific Program
Purpose: Tideman et al. have published comprehensive data on visual impairment as a function of axial length for 9,074 subjects (JAMA Ophthalmology 2016;134:1355-63). Here we present a model of visual impairment as a function of age and axial length.
Methods: Tideman et al.’s Figure 2 of cumulative risk of visual impairment as a function of age for five ranges of axial lengths was digitized. The midpoint of each axial length range was used, and a value of 31 mm chosen for the highest range. From these the logarithm of the odds of visual impairment (based on reference prevalence of 1.3% for the WHO criterion of 20/60) was plotted as a function of age for five axial lengths. These data were fit by multiple linear regression and used to calculate the cumulative risk of visual impairment (based on reference prevalence of 3.6% for the US criterion of 20/40). The impact was further assessed by combining the model with life expectancy data for the US population to calculate the probability of an individual living with visual impairment as a function of age and axial length.
Results: The cumulative risk of visual impairment increases exponentially with both age and axial length—on average 54% per mm of axial length. The equation for the odds of visual impairment is:
Log10Odds of Visual Impairment = 0.067Age + 0.234AL – 9.89
Thus:
Odds of Visual Impairment = 10(0.067Age + 0.234AL – 9.89)
Note that the coefficients show that the impact of 1 mm of axial length (AL) is almost four times that of one year of aging. Using this equation, the age-related risk of visual impairment was calculated for different axial lengths, showing the expected sigmoidal pattern (Figure A). The percentage of individuals living with visual impairment as a function of age and axial length follows an asymmetric bell curve (Figure B). The peak of the distribution shifts from 86 years for an axial length of 23 mm to 80 years for 27 mm. Beyond the peak, the influence of mortality outweighs the increased risk of visual impairment. The mean number of years of visual impairment experienced by a patient over their lifetime may be estimated by simply integrating the area under each curve. For example, a patient with an axial length of 26 mm will experience an average of 8.25 years of visual impairment whereas someone with an axial length of 24 mm will experience only 4.79 years of visual impairment.
Conclusion: Our model shows the cumulative risk of visual impairment as a function of age and axial length. The model allows the benefits of myopia control to be explored, for example, slowing axial elongation such that a patient destined to have an axial length of 26 mm instead ends up at 25.5 mm should prevent 1 year of visual impairment.
Methods: Tideman et al.’s Figure 2 of cumulative risk of visual impairment as a function of age for five ranges of axial lengths was digitized. The midpoint of each axial length range was used, and a value of 31 mm chosen for the highest range. From these the logarithm of the odds of visual impairment (based on reference prevalence of 1.3% for the WHO criterion of 20/60) was plotted as a function of age for five axial lengths. These data were fit by multiple linear regression and used to calculate the cumulative risk of visual impairment (based on reference prevalence of 3.6% for the US criterion of 20/40). The impact was further assessed by combining the model with life expectancy data for the US population to calculate the probability of an individual living with visual impairment as a function of age and axial length.
Results: The cumulative risk of visual impairment increases exponentially with both age and axial length—on average 54% per mm of axial length. The equation for the odds of visual impairment is:
Log10Odds of Visual Impairment = 0.067Age + 0.234AL – 9.89
Thus:
Odds of Visual Impairment = 10(0.067Age + 0.234AL – 9.89)
Note that the coefficients show that the impact of 1 mm of axial length (AL) is almost four times that of one year of aging. Using this equation, the age-related risk of visual impairment was calculated for different axial lengths, showing the expected sigmoidal pattern (Figure A). The percentage of individuals living with visual impairment as a function of age and axial length follows an asymmetric bell curve (Figure B). The peak of the distribution shifts from 86 years for an axial length of 23 mm to 80 years for 27 mm. Beyond the peak, the influence of mortality outweighs the increased risk of visual impairment. The mean number of years of visual impairment experienced by a patient over their lifetime may be estimated by simply integrating the area under each curve. For example, a patient with an axial length of 26 mm will experience an average of 8.25 years of visual impairment whereas someone with an axial length of 24 mm will experience only 4.79 years of visual impairment.
Conclusion: Our model shows the cumulative risk of visual impairment as a function of age and axial length. The model allows the benefits of myopia control to be explored, for example, slowing axial elongation such that a patient destined to have an axial length of 26 mm instead ends up at 25.5 mm should prevent 1 year of visual impairment.
A Multitherapy Approach to Functional Vision Deficits
Published 2020 by David Spengler
Co-Author(s): NULL
Article Type: Residents Day
Abstract: In a case of acute functional vision deficits, supplementing vision therapy (VT) with optometric phototherapy (OPT) yields quick
Results:.
Case History: 10 year old white female presents complaining of distance vision blur OD & OS with her glasses.
Ocular History: myopia OD & OS; pt takes her glasses off to read
Family Ocular History: Father is 11D myope; birth mother was a myope (level unknown)
Medical History: unremarkable, (-)medications
Family Medical History: birth mother is deceased from cancer
Pertinent Findings:
Lensometry: -1.00sph OD & OS
Autorefraction OD: -1.50sph, OS: -1.50-0.25x120
Distance VAcc OD: 20/60-2, OS: 20/60-, OU: 20/50
Near VAcc OD: 20/20, OS: 20/20, OU: 20/20
Stereo: 20" of arc
Pupils: PERRL, (-)APD
EOMs: full OU
CVF: FTFC OD & OS
Pusuits: smooth with minor head movements
Saccades: slight undershoot
DCTcc: Ortho
NCTcc: Ortho
NPCcc: 1"/2"
Retinoscopy OD: -1.25sph, OS: -1.25sph
Refraction OD: -2.00sph VAdist: 20/30, VAnear 20/60
Refraction OS: -2.00sph VAdist: 20/25, VAnear 20/60
Note on refraction: Pt was unable to see all the letters on a given Snellen chart line; She needed single letter isolation
Distance Phoria: Ortho
Dist BI: X/8/6
Dist BO: 20/24/16
FCC: +1.25
Near Phoria: 5 exo
Near BI: X/16/14
Near BO: X/24/19
NRA: +0.25
PRA: -1.75
Accommodative Amplitudes: 2.75D OD & OS
Supplemental Testing: functional color visual field testing revealed severely constricted fields OD & OS; kinetic form fields measured at ~6°, blue fields were ~4°, red fields were ~3°, and green fields were ~2.5°.
Differential Diagnosis:
Primary: Streff Syndrome
Secondary: Accommodative Insufficiency
Others: Hysterical Amblyopia, Malingering
Diagnosis and Discussion: Streff Syndrome is a functional vision problem most frequently exhibited by children age 8-18. It effects females at a 2:1 ratio compared to males. While there is no formal, accepted guideline for a diagnosis of Streff Syndrome, this patient exhibits many of the commonly reported symptoms. She was correctable to 20/20 distance and near at her comprehensive exam 1 year ago. However, at her 10 year old comprehensive exam she was unable to be corrected to 20/20 at distance and through her distance subjective she was 20/60 at near. Her accommodative amplitudes were reduced and a lag of accommodation was found. Functional color visual field testing found very constricted fields OD & OS. Interestingly, this patient had FTFC confrontation visual fields, implying a difference between gross visual field testing and functional visual field testing. While Streff syndrome as a diagnosis is controversial, at a minimum this patient was exhibiting acute functional vision problems, with reduced BCVA, and accommodative insufficiency. It is worth noting Streff syndrome theorists often identify a coinciding emotional stressor in the patient's life at the time of the visual deficits. In this patient's case, her visual symptoms coincide with the initial COVID-19 outbreak in her area and the subsequent closing of her school and shift to virtual learning.
Treatment, Management: The patient is enrolled in 10 sessions of weekly VT and is using OPT as supplemental therapy. She is using αΩ and μΔ filters each for 10 minutes daily. By week 5 of VT the patient was easily clearing +2.50/-6.00 monocular accommodative rock. By week 8 of VT she is easily clearing +/-2.50 binocular accommodative rock. A repeat functional color visual field was administered and all fields have tripled in their extent of degrees from fixation. She is now best corrected to 20/20 at both distance and near. She has a full sensorimotor progress exam scheduled.
Results: It is imperative to include a sensorimotor evaluation in the case of young patients with reduced BCVA in the absence of amblyogenic factors and ocular pathology. Bibliography: Erickson, G.B., Griffin, J.R., and Kurihara, J.R. (1994). Streff Syndrome: A Literature Review. Journal of Optometric Vision Development, 25(2), 101-106.
Caughell, S.J. (2010). Clinical Diagnosis and Management of Streff Syndrome: A Case Report. Indiana Journal of Optometry, 13(1/2), 8-12.
Results:.
Case History: 10 year old white female presents complaining of distance vision blur OD & OS with her glasses.
Ocular History: myopia OD & OS; pt takes her glasses off to read
Family Ocular History: Father is 11D myope; birth mother was a myope (level unknown)
Medical History: unremarkable, (-)medications
Family Medical History: birth mother is deceased from cancer
Pertinent Findings:
Lensometry: -1.00sph OD & OS
Autorefraction OD: -1.50sph, OS: -1.50-0.25x120
Distance VAcc OD: 20/60-2, OS: 20/60-, OU: 20/50
Near VAcc OD: 20/20, OS: 20/20, OU: 20/20
Stereo: 20" of arc
Pupils: PERRL, (-)APD
EOMs: full OU
CVF: FTFC OD & OS
Pusuits: smooth with minor head movements
Saccades: slight undershoot
DCTcc: Ortho
NCTcc: Ortho
NPCcc: 1"/2"
Retinoscopy OD: -1.25sph, OS: -1.25sph
Refraction OD: -2.00sph VAdist: 20/30, VAnear 20/60
Refraction OS: -2.00sph VAdist: 20/25, VAnear 20/60
Note on refraction: Pt was unable to see all the letters on a given Snellen chart line; She needed single letter isolation
Distance Phoria: Ortho
Dist BI: X/8/6
Dist BO: 20/24/16
FCC: +1.25
Near Phoria: 5 exo
Near BI: X/16/14
Near BO: X/24/19
NRA: +0.25
PRA: -1.75
Accommodative Amplitudes: 2.75D OD & OS
Supplemental Testing: functional color visual field testing revealed severely constricted fields OD & OS; kinetic form fields measured at ~6°, blue fields were ~4°, red fields were ~3°, and green fields were ~2.5°.
Differential Diagnosis:
Primary: Streff Syndrome
Secondary: Accommodative Insufficiency
Others: Hysterical Amblyopia, Malingering
Diagnosis and Discussion: Streff Syndrome is a functional vision problem most frequently exhibited by children age 8-18. It effects females at a 2:1 ratio compared to males. While there is no formal, accepted guideline for a diagnosis of Streff Syndrome, this patient exhibits many of the commonly reported symptoms. She was correctable to 20/20 distance and near at her comprehensive exam 1 year ago. However, at her 10 year old comprehensive exam she was unable to be corrected to 20/20 at distance and through her distance subjective she was 20/60 at near. Her accommodative amplitudes were reduced and a lag of accommodation was found. Functional color visual field testing found very constricted fields OD & OS. Interestingly, this patient had FTFC confrontation visual fields, implying a difference between gross visual field testing and functional visual field testing. While Streff syndrome as a diagnosis is controversial, at a minimum this patient was exhibiting acute functional vision problems, with reduced BCVA, and accommodative insufficiency. It is worth noting Streff syndrome theorists often identify a coinciding emotional stressor in the patient's life at the time of the visual deficits. In this patient's case, her visual symptoms coincide with the initial COVID-19 outbreak in her area and the subsequent closing of her school and shift to virtual learning.
Treatment, Management: The patient is enrolled in 10 sessions of weekly VT and is using OPT as supplemental therapy. She is using αΩ and μΔ filters each for 10 minutes daily. By week 5 of VT the patient was easily clearing +2.50/-6.00 monocular accommodative rock. By week 8 of VT she is easily clearing +/-2.50 binocular accommodative rock. A repeat functional color visual field was administered and all fields have tripled in their extent of degrees from fixation. She is now best corrected to 20/20 at both distance and near. She has a full sensorimotor progress exam scheduled.
Results: It is imperative to include a sensorimotor evaluation in the case of young patients with reduced BCVA in the absence of amblyogenic factors and ocular pathology. Bibliography: Erickson, G.B., Griffin, J.R., and Kurihara, J.R. (1994). Streff Syndrome: A Literature Review. Journal of Optometric Vision Development, 25(2), 101-106.
Caughell, S.J. (2010). Clinical Diagnosis and Management of Streff Syndrome: A Case Report. Indiana Journal of Optometry, 13(1/2), 8-12.
A New Lens on IOL Dislocation Reevaluating Risk Factors to Improve Patient Care
Published 2020 by Gail Bojarski
Co-Author(s): NULL
Article Type: Residents Day
Abstract: An elderly patient presents with new onset vision loss secondary to intraocular lens dislocation, a rare event. Identification of risk factors and proper assessment can help with diagnosis, prevention and management as frequency increases.
Case History: 75 YO Black male
Chief complaint: loss of vision OD x 2-3 days (-) trauma, transient/absolute vision loss
Ocular hx:
Atrophic macular hole worse OD than OS of unknown etiology (Stargardt's v. toxo v. trauma v. histo)
Cataract extraction OU ~2012 (Wilmer Eye)
Medications: Atorvastatin, nicotine patch, amlodipine, meclizine, tamsulosin, tiotropium, omeprazole
Systemic conditions: Peripheral vascular disease, nicotine dependence, alcohol dependence, HTN, seizure disorder
Pertinent Findings: Entering acuity cc
OD: CF @ 2ft PH 20/800-3 (last: 20/800 with EV)
OS: 20/60+2 PH NI (last: 20/100-2)
Retinoscopy
OD: +12.75-1.25x090 20/350
OS: not performed
Last MRx
OD: +3.00-0.25x040 20/400
OS: +1.75-1.00x025 20/100-2
SLE
OD: aphakia
OS: PAS, pseudophakia
OU: iris atrophy, iridodonesis
IOP: 11, 8
DFE
OD: large central macular scar, 3-piece IOL inferior periphery
OS: macular scar, ERM
OU: reticular degeneration resembling bone-spicules
Differential Diagnosis: Primary: Geographic atrophy
Others: CRAO, GCA
Diagnosis and Discussion: Although rare (0.2-3% reported cases), PCIOL dislocation has been increasing in frequency with a cumulative risk following cataract surgery of 0.1% after 10 years and 1.7% after 25 years, possibly due to the popularization of capsulorrhexis (2)
Thought to be due to:
Progressive zonular dehiscence and contraction of the capsular bag years after an apparently uneventful surgery (2)
Zonular stress during surgery (2)
Increase in post-op anterior capsular fibrosis (2)
Zonular stress from increase in IOL capsular bag mass due to lens epithelial cell proliferation, and subsequent additional burden on already compromised zonules with the application of laser energy (1)
Predisposition identified in 90% of reviewed cases (2)
Most common: PXE (>50%) (2)
Others: aging, high myopia/increased axial length, uveitis, trauma, previous vitreoretinal surgery, RP, DM, atopic dermatitis, previous acute angle closure glaucoma attack, and connective tissue disorders (2)
Only identifiable risk factor in this patient is age
Possible bilateral event with short period of time between eyes (2)
Most cases of IOL decentration present in the first few weeks following CE (1)
Treatment, Management: Monitor if asymptomatic. If symptomatic, vitrectomy and IOL removal/replacement/repositioning to iris/sulcus/pars plana (1).
Results: While PCIOL dislocation is rare, its incidence has been growing with the advent of capsulorrhexis. As cases continue to rise, it is important to identify risk factors, and evaluate alternative forms of cataract extraction and the potential risk of YAG capsulotomy in this patient population. In the event that a PCIOL dislocation occurs, a thorough evaluation is imperative. While it may be easy to discount a patient's complaint of vision loss when vision is already greatly reduced, an accurate retinoscopy suggests the diagnosis within minutes. Similarly, in cases where visualization of the intraocular lens is difficult on dilated fundus exam, taking advantage of the B-scan is invaluable. Once a diagnosis of PCIOL dislocation is made, it would be wise to consider reports of bilateral cases, and keep a closer eye on these patients than was previously thought necessary. Bibliography: 1. Gimbel, Howard V. MD, MPH; Condon, Garry P. MD; Kohnen, Thomas MD; Olson, Randall J. MD; Halkiadakis, Ioannis MD Late in-the-bag intraocular lens dislocation: Incidence, prevention, and management, Journal of Cataract & Refractive Surgery: November 2005 - Volume 31 - Issue 11 - p 2193-2204 doi: 10.1016/j.jcrs.2005.06.053
2. Pueringer, S. L., Hodge, D. O., & Erie, J. C. (2011). Risk of late intraocular lens dislocation after cataract surgery, 1980-2009: a population-based study. American journal of ophthalmology, 152(4), 618"�623. https://doi.org/10.1016/j.ajo.2011.03.009
Case History: 75 YO Black male
Chief complaint: loss of vision OD x 2-3 days (-) trauma, transient/absolute vision loss
Ocular hx:
Atrophic macular hole worse OD than OS of unknown etiology (Stargardt's v. toxo v. trauma v. histo)
Cataract extraction OU ~2012 (Wilmer Eye)
Medications: Atorvastatin, nicotine patch, amlodipine, meclizine, tamsulosin, tiotropium, omeprazole
Systemic conditions: Peripheral vascular disease, nicotine dependence, alcohol dependence, HTN, seizure disorder
Pertinent Findings: Entering acuity cc
OD: CF @ 2ft PH 20/800-3 (last: 20/800 with EV)
OS: 20/60+2 PH NI (last: 20/100-2)
Retinoscopy
OD: +12.75-1.25x090 20/350
OS: not performed
Last MRx
OD: +3.00-0.25x040 20/400
OS: +1.75-1.00x025 20/100-2
SLE
OD: aphakia
OS: PAS, pseudophakia
OU: iris atrophy, iridodonesis
IOP: 11, 8
DFE
OD: large central macular scar, 3-piece IOL inferior periphery
OS: macular scar, ERM
OU: reticular degeneration resembling bone-spicules
Differential Diagnosis: Primary: Geographic atrophy
Others: CRAO, GCA
Diagnosis and Discussion: Although rare (0.2-3% reported cases), PCIOL dislocation has been increasing in frequency with a cumulative risk following cataract surgery of 0.1% after 10 years and 1.7% after 25 years, possibly due to the popularization of capsulorrhexis (2)
Thought to be due to:
Progressive zonular dehiscence and contraction of the capsular bag years after an apparently uneventful surgery (2)
Zonular stress during surgery (2)
Increase in post-op anterior capsular fibrosis (2)
Zonular stress from increase in IOL capsular bag mass due to lens epithelial cell proliferation, and subsequent additional burden on already compromised zonules with the application of laser energy (1)
Predisposition identified in 90% of reviewed cases (2)
Most common: PXE (>50%) (2)
Others: aging, high myopia/increased axial length, uveitis, trauma, previous vitreoretinal surgery, RP, DM, atopic dermatitis, previous acute angle closure glaucoma attack, and connective tissue disorders (2)
Only identifiable risk factor in this patient is age
Possible bilateral event with short period of time between eyes (2)
Most cases of IOL decentration present in the first few weeks following CE (1)
Treatment, Management: Monitor if asymptomatic. If symptomatic, vitrectomy and IOL removal/replacement/repositioning to iris/sulcus/pars plana (1).
Results: While PCIOL dislocation is rare, its incidence has been growing with the advent of capsulorrhexis. As cases continue to rise, it is important to identify risk factors, and evaluate alternative forms of cataract extraction and the potential risk of YAG capsulotomy in this patient population. In the event that a PCIOL dislocation occurs, a thorough evaluation is imperative. While it may be easy to discount a patient's complaint of vision loss when vision is already greatly reduced, an accurate retinoscopy suggests the diagnosis within minutes. Similarly, in cases where visualization of the intraocular lens is difficult on dilated fundus exam, taking advantage of the B-scan is invaluable. Once a diagnosis of PCIOL dislocation is made, it would be wise to consider reports of bilateral cases, and keep a closer eye on these patients than was previously thought necessary. Bibliography: 1. Gimbel, Howard V. MD, MPH; Condon, Garry P. MD; Kohnen, Thomas MD; Olson, Randall J. MD; Halkiadakis, Ioannis MD Late in-the-bag intraocular lens dislocation: Incidence, prevention, and management, Journal of Cataract & Refractive Surgery: November 2005 - Volume 31 - Issue 11 - p 2193-2204 doi: 10.1016/j.jcrs.2005.06.053
2. Pueringer, S. L., Hodge, D. O., & Erie, J. C. (2011). Risk of late intraocular lens dislocation after cataract surgery, 1980-2009: a population-based study. American journal of ophthalmology, 152(4), 618"�623. https://doi.org/10.1016/j.ajo.2011.03.009
A New Look at Visual Recovery Transsphenoidal Decompression of the Optic Chiasm from Pituitary Macroadenoma
Published 2020 by Rick Walker
Co-Author(s): NULL
Article Type: Residents Day
Abstract: This case emphasizes the physiology of visual recovery following chiasmal decompression and recent changes in visual field analysis from an intracranial mass. This outline details case information, differential diagnosis and proper testing following field loss.
Case History: Demographics: 62-year-old African American Male
Chief Complaint: Blur OD>OS
Ocular History: Myopia
Medical History: Hyperlipidemia
Medications: Cholecalciferol
Pertinent Findings: Entrance Testing:
Best Corrected Visual Acuities(VA): 20/30OD, 20/20OS
Pupils: Equal, round, reactive OU, no relative afferent pupillary defect
Tonometry: 16mmHg OU@10:15 AM
Extraocular Muscles: Full, no restrictions OU
Confrontations: Constriction nasal OD, Mild constriction 360 OS
Anterior Segment:
Lens: 1+ cortical cataracts OU
Unremarkable OU
Posterior Segment:
Macula: Normal OU
Optic Disc:
0.45h/0.45v OD with pallor superior, inferior and temporal
0.35h/0.35v OS with pallor temporal
Disc margins distinct, no notching or hemes OU
Periphery: Normal OU
Auxiliary Testing:
Spectral Domain OCT(SD-OCT) Nerve Fiber Layer:
OD: Thinning superior, inferior and temporal quadrants with global thickness of 44 microns
OS: Thinning inferior and temporal quadrants, global thickness thinned to 63 microns
SD-OCT Macula: Normal foveal contour and thickness OU
30-2 Octopus Visual Field(VF)
OD: Left-sided hemianopic defect with some superior and inferior temporal defects
OS: Left-sided hemianopic defect with mild superior nasal defect
Radiology:
Carotid Doppler Ultrasound
No hemodynamically significant stenosis
Magnetic Resonance Imaging(MRI)
Pituitary macroadenoma
Differential Diagnosis: Stroke
-R/o with carotid doppler ultrasound
Trauma
-R/o with case history
Migraine
-R/o with case history
Diagnosis and Discussion: Case Diagnosis: Pituitary Macroadenoma
Secondary Diagnoses: Homonymous bilateral field defects, left side
Discussion:
Typically slow growing and benign tumors larger than 10mm
Tumors causing visual deterioration are often non-functioning macroadenomas
Smaller than 2cm in size have minimal effect on vision
Signs/Symptoms:
Headaches, peripheral vision loss, hormonal changes
Optic nerve pallor, bow-tie atrophy
Scotomas more severe in upper quadrant of temporal hemifield and lower quadrant of nasal hemifield
Diagnostic techniques:
SD-OCT RNFL: Nerve thinning secondary to chiasmal compression
30-2 VF: characteristic bi-temporal field defect
MRI with and without contrast
Recovery:
75-85% of patients have improvement in VF following tumor resection
Preoperative VA shown to be a good prognostic factor for postoperative VA and VF
Treatment, Management: Transsphenoidal adenectomy "� elective tumor resection
Patient education and regular follow ups with SD-OCT and VF
Results: Confrontations and VF testing are vital to detection of scotomas from a pituitary mass
Pituitary tumors often do not present with the classic bitemporal field defect
Preoperative VA and VF can be prognostic factors for postoperative VA and VF following surgery Bibliography: Kotoda, Yumi, et al. "�Left-Right and Upper"�Lower Light Sensitivity Asymmetry in Visual Field Defects Caused by Pituitary Adenoma: A Retrospective Observational Study."� Clinical Ophthalmology, Vol. 14, 2020, p. 317"�324., doi:10.2147/opth.s234422
Ho, Ren-Wen, et al. "�The Influence of Pituitary Adenoma Size on Vision and Visual Outcomes after Trans-Sphenoidal Adenectomy: A Report of 78 Cases."� Journal of Korean Neurosurgical Society, vol. 57, no. 1, 2015, p. 23., doi:10.3340/jkns.2015.57.1.23
Alan Cohen, M.D., Paul Cooper, M.D., Mark Kupersmith, M.D., Eugene Flamm, M.D., Joseph Ransohoff, M.D., Visual Recovery after Transsphenoidal Removal of Pituitary Adenomas, Neurosurgery, Vol 17, Issue 3, Sept. 1985, p 446"�452, https://doi.org/10.1227/00006123-198509000-00008
McIlwaine, Gawn FRCS, FRCOphth; Carrim, Zia I. MB, ChB; Lueck, Christian J. PhD, FRCP(UK), FRCP(Ed), FRACP; Chrisp, T. Malcolm PhD A Mechanical Theory to Account for Bitemporal Hemianopia From Chiasmal Compression, Journal of Neuro-Ophthalmology: March 2005"�Vol. 25-Issue 1-p 40-43
Case History: Demographics: 62-year-old African American Male
Chief Complaint: Blur OD>OS
Ocular History: Myopia
Medical History: Hyperlipidemia
Medications: Cholecalciferol
Pertinent Findings: Entrance Testing:
Best Corrected Visual Acuities(VA): 20/30OD, 20/20OS
Pupils: Equal, round, reactive OU, no relative afferent pupillary defect
Tonometry: 16mmHg OU@10:15 AM
Extraocular Muscles: Full, no restrictions OU
Confrontations: Constriction nasal OD, Mild constriction 360 OS
Anterior Segment:
Lens: 1+ cortical cataracts OU
Unremarkable OU
Posterior Segment:
Macula: Normal OU
Optic Disc:
0.45h/0.45v OD with pallor superior, inferior and temporal
0.35h/0.35v OS with pallor temporal
Disc margins distinct, no notching or hemes OU
Periphery: Normal OU
Auxiliary Testing:
Spectral Domain OCT(SD-OCT) Nerve Fiber Layer:
OD: Thinning superior, inferior and temporal quadrants with global thickness of 44 microns
OS: Thinning inferior and temporal quadrants, global thickness thinned to 63 microns
SD-OCT Macula: Normal foveal contour and thickness OU
30-2 Octopus Visual Field(VF)
OD: Left-sided hemianopic defect with some superior and inferior temporal defects
OS: Left-sided hemianopic defect with mild superior nasal defect
Radiology:
Carotid Doppler Ultrasound
No hemodynamically significant stenosis
Magnetic Resonance Imaging(MRI)
Pituitary macroadenoma
Differential Diagnosis: Stroke
-R/o with carotid doppler ultrasound
Trauma
-R/o with case history
Migraine
-R/o with case history
Diagnosis and Discussion: Case Diagnosis: Pituitary Macroadenoma
Secondary Diagnoses: Homonymous bilateral field defects, left side
Discussion:
Typically slow growing and benign tumors larger than 10mm
Tumors causing visual deterioration are often non-functioning macroadenomas
Smaller than 2cm in size have minimal effect on vision
Signs/Symptoms:
Headaches, peripheral vision loss, hormonal changes
Optic nerve pallor, bow-tie atrophy
Scotomas more severe in upper quadrant of temporal hemifield and lower quadrant of nasal hemifield
Diagnostic techniques:
SD-OCT RNFL: Nerve thinning secondary to chiasmal compression
30-2 VF: characteristic bi-temporal field defect
MRI with and without contrast
Recovery:
75-85% of patients have improvement in VF following tumor resection
Preoperative VA shown to be a good prognostic factor for postoperative VA and VF
Treatment, Management: Transsphenoidal adenectomy "� elective tumor resection
Patient education and regular follow ups with SD-OCT and VF
Results: Confrontations and VF testing are vital to detection of scotomas from a pituitary mass
Pituitary tumors often do not present with the classic bitemporal field defect
Preoperative VA and VF can be prognostic factors for postoperative VA and VF following surgery Bibliography: Kotoda, Yumi, et al. "�Left-Right and Upper"�Lower Light Sensitivity Asymmetry in Visual Field Defects Caused by Pituitary Adenoma: A Retrospective Observational Study."� Clinical Ophthalmology, Vol. 14, 2020, p. 317"�324., doi:10.2147/opth.s234422
Ho, Ren-Wen, et al. "�The Influence of Pituitary Adenoma Size on Vision and Visual Outcomes after Trans-Sphenoidal Adenectomy: A Report of 78 Cases."� Journal of Korean Neurosurgical Society, vol. 57, no. 1, 2015, p. 23., doi:10.3340/jkns.2015.57.1.23
Alan Cohen, M.D., Paul Cooper, M.D., Mark Kupersmith, M.D., Eugene Flamm, M.D., Joseph Ransohoff, M.D., Visual Recovery after Transsphenoidal Removal of Pituitary Adenomas, Neurosurgery, Vol 17, Issue 3, Sept. 1985, p 446"�452, https://doi.org/10.1227/00006123-198509000-00008
McIlwaine, Gawn FRCS, FRCOphth; Carrim, Zia I. MB, ChB; Lueck, Christian J. PhD, FRCP(UK), FRCP(Ed), FRACP; Chrisp, T. Malcolm PhD A Mechanical Theory to Account for Bitemporal Hemianopia From Chiasmal Compression, Journal of Neuro-Ophthalmology: March 2005"�Vol. 25-Issue 1-p 40-43