Optometry Notes

Subconjunctival Hemhorrage

2010-05-20T12:21:00.000-07:00

In highly recurrent cases, testing for blood-tissue abnormalities, clotting disorders, hypertension, diabetes and malignancies should be done.

This includes, but is not limited to, a complete blood count with differential and platelets, prothrombin time, activated partial thromboplastin time, fasting blood sugar, blood pressure
evaluation, echocardiogram, lipid profile, homocysteine levels, antiphosolipid antibodies, protein s, protein c, antithrombin III, factor V Leiden, beta-glycoprotein, sickle cell preparation
and human immunodeficiency virus titres.

In most cases, SCH episodes are not so severe that they warrant cessation of a patient’s necessary systemic medications. However, in cases where the occurrence is substantial, communication and discussion with the internist is advised. As a rule SCH is rarely evacuated.

Blood pressures should be examined in patients with subconjunctival hemorrhages, particularly in older patients.

Any 360° subconjunctival hemorrhage following trauma should invoke a suspicion and investigation to rule out ruptured globe.

Recurrent events may suggest a situation of abuse, tumor or excessive anticoagulation therapy
(Requiring an International Normalized Ratio [INR] evaluation to determine the patient’s sensitivity to clotting).

http://www.revoptom.com/cmsdocuments/2010/4/ro0410_hndbk.pdf

Handbook of Ocular Disease Management

2010-05-20T11:51:00.000-07:00

http://www.revoptom.com/cmsdocuments/2010/4/ro0410_hndbk.pdf

Fish oils

2010-05-20T11:24:00.000-07:00

http://www.revoptom.com/content/d/special_report/i/1104/c/20786/

Oral antivirals

2010-02-21T16:20:00.000-08:00

Active acute infection
-acyclovir (Zovirax) 200mg 5xd for 7-10 day
-famciclovir (famvir) 125mg bid for 7-10 day
-valacyclovir (valtrex) 500mg bid for 7-10 day

Active recurrent infection
-acyclovir 200 mg 5xd for 5 days
-acyclovir 400mg tid for 5 days
-famciclovir 500mg bid for 5 days
-valacyclovir 500mg bid for 5 days

Long-term prophylactic use
-acyclovir 400mg bid
-famciclovir 500mg bid
-valacyclovir 500mg qid

Plaquenil

2009-11-14T12:58:00.001-08:00

http://www.eyeupdate.com/pages/plaquenil.html
plaquenil form: http://www.eyeupdate.com/pages/forms/plaquenil-eval.pdf

1. Best visual acuity.
2. Dilated ophthalmoscopic examination of the macular and paramacular tissues.
3. Zeiss-Humphrey visual field 10-2 testing (using standard white stimulus).

Corneal thinning disorders

2009-10-25T13:34:00.000-07:00

http://www.revophth.com/index.asp?page=1_14448.htm

Thinning in the ‘Quiet’ Eye

Dellen. In the absence of inflammation, one of the more likely causes of the thinning is a dell, or an area of non-wetting that thins and then breaks down. The treatment is lubrication, maybe punctal occlusion, and a bandage contact lens, a temporary tarsorraphy.
Furrow degeneration. This is a variety of peripheral thinning, typically between the limbus and the arcus senilis, that usually occurs in elderly patients. The hallmark signs of furrow degeneration are that the thinning, if it’s present at all, is very shallow, non-progressive and isn’t visually significant; the eye is white and quiet, there’s no vascularization and there’s no possibility for perforation.No actual treatment is necessary.
Pellucid marginal degeneration. This is a cousin to keratoconus, however, where keratoconus tends to mean central or paracentral thinning, pellucid is peripheral. Some patients with pellucid can have severe thinning, usually inferiorly, within a couple of millimeters of the limbus. Though there’s no redness, pain or inflammation, it causes significant irregular astigmatism, so the patient tends to complain of a slow, progressive worsening of vision. On topography, PMD will have an area of inferior steepening that resembles a crab claw. Glasses sometimes help, though the management typically involves a rigid gas permeable contact lens or a hybrid lens like the Synergize. Rarely, you’ll need to do a corneal transplant.
Terrien’s marginal degeneration. This presents as a marginal furrow, usually bilateral, and is most common in men between 20 and 40 years of age. It starts as a non-ulcerated area of thinning located superiorly, and it slowly progresses from there. You’ll see vascularization in addition to the thinning, often with a leading edge of lipid. However, the epithelium is also intact with this condition. The thinning can be progressive, and can progress circumferentially or centrally. And, since it starts superiorly, the patient usually gets against-the-rule astigmatism. You can manage the astigmatism with glasses or, failing that, RGPs or hybrid lenses.

Thinning in the ‘Hot’ Eye

Patients can also present with peripheral thinning accompanied by ulceration and general inflammation. These are the presentations are more concerning since actual tissue is being lost. Since several of the ulcerative conditions have similar appearances, it takes more diagnostic detective work to narrow down the cause in these cases.
If the eye is red and painful, and there’s peripheral thinning with an epithelial defect, then you first assess the defect’s size, location and whether it’s associated with a hypopyon.
None of the immune conditions cause a hypopyon, while the bacterial ones do. If there’s a hypopyon, corneal specialists say to proceed as if it’s a bacterial infection until proven otherwise. Scrape it, culture it and put the patient on antibiotics.
When presented with a non-infectious peripheral ulcerative keratitis, however, first suspect rheumatoid arthritis or another autoimmune condition. If a patient doesn’t already have a diagnosis of rheumatoid, physicians also suspect Wegener’s granulomatosus, a serious vasculitis; or Mooren’s ulcer, which is peripheral ulcerative keratitis of unknown etiology. Unfortunately, all three ulcerative conditions have similar characteristics, and serologic testing is often the key to making the diagnosis. Corneal specialists say many patients who present with PUK often have already been diagnosed with rheumatoid disease and are on some type of systemic medication for it already, which aids the diagnosis.
If the patient doesn’t already have a diagnosis of a systemic disease associated with peripheral corneal thinning with ulceration, order a panel of blood work: check for rheumatoid factor, erythrocyte sedimentation rate, an antinuclear antibody test, an anti-neutrophil cytoplasmic antibody test, a complete blood count, check for hepatitis-C, (because there’s one form of peripheral thinning that looks like peripheral ulcerative keratitis or Mooren’s ulcer but which is actually associated with hepatitis-C and is very responsive to interferon therapy).
If autoimmune disease isn’t the cause, the other two frequent diagnoses, Wegener’s granulomatosus and Mooren’s ulcer
Wegener’s is one of the main differentials in PUK because, if it’s missed, it can kill someone. Wegener’s is a vasculitis that manifests with peripheral corneal ulcers that mimic a Mooren’s ulcer, in which there’s a nasal or temporal immune-looking ulcer—in other words, there’s no hypopyon in the anterior chamber. The patient needs a chest X-Ray or a CAT scan of the chest because the Wegener’s patient will have a classic diagnostic picture in that region. If a mass is observed, a biopsy is necessary in some cases. With Wegener’s in mind, an ANCA is needed in all cases of PUK. If a patient’s ulceration involves the sclera as well as the cornea, suspect Wegener’s.
If the PUK isn’t from an autoimmune condition like RA, Wegener’s or hepatitis, it’s classified as Mooren’s ulcer, or a peripheral ulcerative keratitis of unknown etiology.
Mooren’s is typically more chronic, progressive and very painful. It will begin in the periphery and spread both circumferentially and centripetally. The key sign is that there will be a leading, undermined edge of de-epithelialized tissue. There will also usually be blood vessels crossing the edge. There’s also a milder form of Mooren’s ulcer that’s more limited and actually responds well to medical therapy consisting of lubrication and low-dose steroids and tarsorraphy, if necessary.
There are also less common causes that need to be kept in mind, as well: Corneal melting can occur in the setting of the neurotrophic cornea or from the frequent use of topical anesthetics or topical non-steroidal anti-inflammatories like Acular, Xibrom and Nevanac. Another cause, which was more common when we did more scleral surgery, is surgically induced necrotizing scleritis, in which there’s melting of the sclera from an old cataract wound. This was rare to begin with, and it still is, but it’s worth being aware of.
The cause may also be just staph marginal hypersensitivity, a relatively mild condition. In blepharitis and other lid disease, patients can get small white infiltrates at the limbus. Those infiltrates can be associated with some thinning and, when they heal, they can result in some scarring and thinning, but they’re not that serious.

Vitreous hemorrhage differentials

2009-10-25T13:32:00.000-07:00

blunt trauma
penetrating trauma
abusive head trauma
neoplasm
venous malformations
Terson’s syndrome http://emedicine.medscape.com/article/1227921-overview
inflammation such as pars planitis
regressed retinopathy of prematurity
X-linked retinoschisis
familial exudative vitreoretinopathy

Keratoconus

2009-10-25T10:38:00.000-07:00

http://www.revophth.com/index.asp?page=1_14488.htm

Down’s syndrome, Ehler’s-Danlos syndrome, Leber’s Congenital Amaurosis and atopy associated with KC but are likely secondary to the eye rubbing associated with these conditions instead of genetic link

i..e. secondary association in response to environmental or behavioral factors

only 7 percent of patients report awareness of other family members with this condition

KC is a complex genetic disease that requires interaction with environmental factors to make a genetically determined predisposition clinically apparent

hypothesis that KC includes a genetically altered dose-response curve to eye rubbing

Eye rubbing performed by the purely allergic patients is fairly straightforward. It is in response to allergic symptoms which patients consistently report as “itching.” When asked about eye rubbing, allergic patients are highly aware of their behavior and a typical response might be, “when my eyes itch, I rub them and if they didn’t itch, I wouldn’t rub them.”

KC patients are very different in this regard. While they may have allergies and their symptoms can certainly overlap with allergic complaints, their observations often include comments not typically associated with allergies. The motivation behind their eye rubbing may include itching as a complaint, but unlike the allergic patient, they often report a number of other reasons such as, “burning” or “it just feels good” or commonly, “I need relief.” KC patients also describe motivating factors for eye rubbing that are never offered by the purely allergic patient, such as, “It helps me see better.” (temporary alteration in surface topography or more likely, an improvement in the quantity, quality and distribution of surface lubrication?)

Allergy vs KC patients: different perceived need to rub, timing, contact method, pressure applied, duration, motion, location over the lid and the derived benefit

the purely allergic patient, in response to allergic itching, generally begins by using a flat instrument (back of hand, front of hand or palm applied broadly, rubbing back and forth, horizontally over the eyelids generating eyelid movement and pressure and “traction” within the lid itself with only modest pressure transmitted to the cornea. This is often followed by a transition to using the tip of the index finger as allergic rubbing tends to migrate nasally, concentrating point pressure over the caruncle for the follow through and completion of the effort. Added contact pressure is then applied at this stage when the caruncle is being rubbed and a circular component may also be added to the motion after this transition to the caruncle

The KC patient, on the other hand, has a limited number of favorite techniques, the majority of which begin with a pointed instrument, either a knuckle (middle knuckle more commonly than distal or proximal knuckle or fingertip(s)

The hallmark of the KC rub is the circular motion of this point-like pressure confined over the cornea, often with pronounced pressure transmitted posteriorly—much more than with the allergic rub (apart from the allergic caruncle rub). The intensity and duration (10 to 180 seconds, up to 300 seconds) are much greater in KC patients, as is the repetitive nature. The perceived benefit and relief reported by the KC patient is different from the relief from itching sought and achieved by the allergic patient. Interviewing these patients “in action,” the KC patient is more likely to elucidate an experience of ecstasy and euphoric rapture during and toward the completion of the rub, wanting to do even more.

The purely allergic patient describes the process as filling a need, wishing he did not have to do this, and in the end reports more of a “mission accomplished.”

Allergic patients are highly aware of these episodes and tend to be fairly accurate when reporting their symptoms, as well as the frequency and severity of eye rubbing, in response to these allergic challenges.

KC patients often under-report eye rubbing when first asked about it, perhaps reflecting a desensitized awareness as this repetitive behavior or habit becomes increasingly incorporated into their daily routine.

KC patients may also exhibit repetitive and even ritualistic behavioral tendencies compounding the physical need they feel to rub their eye. This can include profound eye rubbing at certain times of the day or associated with specific activities such as immediately after awakening or after removal of their contact lenses.

It appears directed at a stimulus derived from the cornea or from the interaction between the eyelid and corneal surface in the absence of a contact lens. While eye rubbing facilitates lubrication and the interaction between the eyelid and the corneal surface in the absence of a contact lens, I also wonder if contact lens removal improves oxygenation to corneal nerves that are stretched and stressed from KC but also somewhat hypoxic after contact lens wear.

This improvement in oxygenation immediately after contact lens removal might initiate a pain signal that responds favorably to eye rubbing—perhaps in the same way that the gate-control theory of pain explains the benefits of acupuncture or therapeutic massage.

Relative hypoxia from eyelid closure and the need for better surface lubrication are both factors that might also explain why some patients report early morning as another favorite time to rub their eyes.

Eye rubbing may also be incorporated in behavioral tendencies associated with obsessive compulsive disease (OCD) as some of these patients reveal these tendencies in other activities in their life.

It is not uncommon for KC patients to report their eye rubbing more accurately when they return for a follow-up visit, noting that it was called to their attention either by the eye doctor raising the question during the first visit or by family, friends or co-workers the patients might survey with regard to their behavior. Another reason for under-reporting this behavior is an embarrassment that some of these patients feel; they may have been chastised growing up or told over the years to stop rubbing their eyes by their peers or by those in authority. For these patients, it is like nail biting, and when asked to demonstrate their eye rubbing technique, they will often blush and remark on the embarrassment this brings.

If the patient and their family denies history of rubbing, another theory is that there may be a tendency toward putting pressure on or around the more severely affected eye while they sleep at night.

position was exclusively on the affected side and involved a hand position that placed considerable pressure on the eye itself.

consistent tendency for patients to sleep on the side that is more severely affected or progressing more rapidly.

Some of these patients like to sleep with their hand or fist directly against their eyelid and are more likely to hug their pillow in a manner that generates some compression around their eyes

While some generate substantial pressure—in effect, grinding their eye into the pillow—even the milder forms of pressure can deliver considerable cumulative effect over time.

Adding further to this is the thermal impact of compressing a pillow against the closed eyelid, reducing the normal dissipation of heat.

These patients with asymmetric KC are also more likely to develop floppy eyelids to a greater degree on their sleeping side.

Also patients are more likely to have undiagnosed obstructive sleep apnea (OSA), a condition that may lead to a host of cardiac and pulmonary problems, hypertension, esophageal reflux, weight gain and shortened lifespan.

Some KC patients develop OSA symptoms prior to acquiring their weight gain, further supporting the need for a heightened sense of awareness among clinicians who may otherwise overlook this condition.

Referring these patients to a sleep lab for formal study if they report restless sleep, snoring, periodic apnea, daytime restlessness, unexplained hypertension or any of the other symptoms commonly associated with OSA.

For those patients already diagnosed with OSA, one should be aware that their favorite sleeping position may be altered by their need to wear a CPAP or BiPAP mask, some of which require patients to sleep on their back to maintain an adequate seal.

link between KC and obesity. These heavier patients were also more likely to demonstrate a floppy eyelid.

a hypothesis that a subset of KC patients represents a syndrome that includes a floppy eyelid, “floppy” keratoconic cornea, and floppy soft palate leading to OSA is intriguing and worth pursuing as we try to better understand aging and mortality among our KC patients

this still does not fully account for the observed reduction in disease prevalence with advancing age.

patients usually point to the moreadvanced eye as their favorite eye to rub prior to PK. After PK; however, patients often switch so that the other eye becomes the favorite eye to rub

Their need for relief diminishes, further supporting that it is not the conjunctiva or eyelids producing this need to eye rub, in contrast to what we see with allergic patients. Instead, this may be a product of neurotrophism making the dry-eye symptoms of lid wiper epitheliopathy less symptomatic. Alternatively, this may provide added support to the gate-control theory of pain with neurogenic factors originating in the cornea “short-circuited” by vigorous eye rubbing and then dramatically reduced when tissue containing these stretched or altered nerves is eventually removed with PK.

Do the prominent corneal nerves seen by slit-lamp biomicroscopy anatomically represent either a response or a contribution to the viscious eye rubbing cycle we see clinically?

The case is strong that eye-rubbing tendencies of KC patients are overall quite distinct from those seen in the purely allergic patient. Interestingly, these same tendencies are seen in a number of patients with post-LASIK keratoectasia.

Perhaps the best model for KC is a genetic condition that is particularly susceptible and even accelerated by trauma resulting from eye rubbing or mechanical weakening from LASIK surgery?

The observed association with OSA brings to mind a number of plausible hypotheses, the most intriguing of which would be a syndrome that includes KC, floppy eyelid and OSA.

Consider the genetically susceptible host with the environmental “second hit” provided as follows: a) eye rubbing or nocturnal eye pressure leading to the “floppy” keratoconic cornea; b) sleeping position and eye rubbing leading to the floppy upper eyelid; and c) the genetically affected soft palate that has a greater propensity for developing OSA due to a greater susceptibility to become “floppy” and obstruct from airway turbulence at lower levels of weight gain.

Retinitis pigmentosa

2009-10-22T16:02:00.000-07:00

http://www.noah-health.org/en/eye/disorders/retinitispigment.html

r/o Usher Syndrome and Bardet-Biedl Syndrome

Usher: http://www.ushersyndrome.nih.gov/whatis/fulltext.html

Bardet-Biedl Syndrome http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=gene&part=bbs

Ophthalmology minutes

2009-10-22T15:45:00.001-07:00

http://telemedicine.orbis.org/bins/content_page.asp?cid=1-600

Strabismus Diagnosis - Comprehensive Evaluation

2009-10-22T11:21:00.001-07:00

http://telemedicine.orbis.org/bins/volume_page.asp?cid=1-3-4-7

Nystagmus

2009-10-22T11:18:00.001-07:00

http://telemedicine.orbis.org/bins/volume_page.asp?cid=1-3-4-34

Acquired strabismus

2009-10-22T11:14:00.000-07:00

Differential diagnoses:

* Thyroid ophthalmopathy
* Myasthenia
* Diabetic vasculopathy - stroke
* Aneurysm
* Tumor
* Multiple sclerosis (nystagmus - oscillopsia, internuclear ophthalmoplegia)
* Blowout fracture
* Decompensated congenital IV N palsy (head tilt - facial asymmetry)
* Convergence insufficiency
* Post retina or glaucoma surgery
* Myositis
* Etc.

http://telemedicine.orbis.org/bins/volume_page.asp?cid=1-3-4-25

Brown's syndrome

2009-10-22T11:06:00.000-07:00

"superior oblique tendon sheath syndrome".
The definition of the syndrome has since been expanded to limited elevation in adduction from mechanical causes around the superior oblique
also been called pseudo paresis of the inferior oblique
Left Brown - Limited Elevation in Adduction
Favored head posture with left Brown: head up and to right where eyes do not go! Eyes positioned down and left to look straight ahead.
1. Vision and stereo acuity usually normal
2. Chin up face points to opposite side
3. Deficient elevation in adduction
4. Usually some elevation limitation in straight upgaze and in abduction
5. Widened palpebral fissure on adduction
6. May or may not have downshoot of involved eye in adduction
7. May be acquired
8. May be intermittent with or without pain

Causes:

"Short" Superior Oblique Tendon -Including Anomalous, Broad Insertion
Fascial Restrictions
Intrasheath Septae
Trochlear Entrance Restriction
Inflammation of the Trochlea
Cyst of the Reflected Tendon
Trochlear Trauma* (Canine Tooth) * This causes superior oblique underaction and Brown syndrome
Tuck of the superior oblique tendon is usually done at or near the insertion on globe

http://telemedicine.orbis.org/bins/volume_page.asp?cid=1-3-4-18

White/yellow flat macular lesion/pigment change DD

2009-10-22T09:57:00.000-07:00

Posttraumatic - pigmentary disturbance; cysts or hole at macula
Postinflammatory - chorioretinal atrophy with pigment clumping at center and periphery of lesion
Coloboma of macula-atrophic area at macula often associated with coloboma of disc; sclera may be ectatic (see p. 450)
Radiation injuries-common after solar eclipse; punched-out appearance
Fuchs dark spot-pigmented spot associated with other signs of degenerative myopia
Drugs, including the following:
adrenal cortex injection, aldosteroneallopurinol (?), amodiaquine, betamethasone (?), chloroquinecortisone (?), desoxycorticosterone (?), dexamethasone (?), diiodohydroxyquin, fludrocortisonefluprednisolone (?), griseofulvinhydrocortisone (?), hydroxychloroquine, indomethacin (?), iodochlorhydroxyquin, methylprednisolone, oral contraceptives, paramethasone (?), prednisolone (?), prednisone (?), quininetriamcinolone
Stellate retinopathy - star-shaped exudates
Hard exudates and circinate retinopathy
Drusen – common, discrete yellow spots beneath the retina
Doyne honeycomb choroiditis-rare; honeycomb pattern of yellow patches at posterior pole; degenerative changes at macula
Heredomacular dystrophies:
Best disease (vitelliruptive macular dystrophy) up to 18 years of age; egg-yolk lesion at macula, later absorbed to leave atrophic scar
Fundus flavimaculatus - yellow patches at posterior pole; degenerative changes at macula
Stargardt disease (juvenile macular degeneration) to 10 years of age; variable appearance in different families; bilateral lesions showing some degree of symmetry
Behr disease (optic atrophy-ataxia syndrome) – adults, similar to Stargardt type
Presenile and senile-pigmentary changes followed by atrophy, bilateral and symmetric
Central choroidal sclerosis - rare, atrophic retina with sclerosed choroidal vessels showing clearly
Central areolar choroidal atrophy-rare, exudate and edema followed by sharply defined atrophic area with white strands of choroidal vessels
Pseudoinflammatory macular dystrophy-rare, initially edema and exudates followed by scarring with pigmentary disturbance and atrophic patches
Gaucher disease (glucocerebroside storage disease)-rare, ring-shaped macular lesions, lipid deposits in cornea and conjunctiva
Diffuse leukoencephalopathy - rare, white deposits in periphery and macular area
Sjögren-Larsson syndrome (oligophrenia-ichthyosis-spastic diplegia syndrome)
Angioid streaks
Multiple evanescent white-dot syndrome (MEWDS) usually unilateral, predominantly healthy women, vitreitis
Acute multifocal placoid pigment epitheliopathy – rare, map-like pigmentary disturbance of posterior pole or more widespread over posterior fundus

White Dot Syndromes

2009-10-22T09:15:00.000-07:00

http://emedicine.medscape.com/article/1227778-overview

group of idiopathic multifocal inflammatory conditions involving the retina and the choroid
characterized by the appearance of white dots in the fundus

Include:

acute posterior multifocal placoid pigment epitheliopathy (APMPPE),
serpiginous choroiditis,
multiple evanescent white dot syndrome (MEWDS),
multifocal choroiditis and panuveitis (MCP),
punctate inner choroidopathy (PIC),
diffuse subretinal fibrosis (DSF)
presumed ocular histoplasmosis syndrome (POHS)
birdshot retinochoroidopathy

Acute Posterior Multifocal Placoid Pigment Epitheliopathy (APMPPE)

occurs predominantly in young adults, with a mean age of onset of 27 years
presents with bilateral, acute, painless loss of vision
in approximately one third of patients, symptoms of fever, myalgia, headache, and malaise are noted prior to the onset of ocular symptoms.
vitreous cells and flat yellow-white placoid lesions in the posterior pole, ranging in size from 0.5 to several disc diameters. These lesions spontaneously become less opaque within 2-3 weeks and develop pigment changes at the level of the retinal pigment epithelium. During this time, a rapid improvement in the visual acuity may occur
most patients completely recover; however, in a small percentage of patients, atrophy and scarring of the retinal pigment epithelium develop with resultant poor visual acuity.
additional findings may include optic disc edema and episcleritis.
APMPPE has been associated with erythema nodosum, a vasculitic condition that consists of painful subcutaneous nodules in the axilla and lower extremities.
APMPPE with concomitant cerebral vasculitis also has been described.
Fluorescein angiography displays early hypofluorescence and late hyperfluorescence of the active lesions. Inactive lesions may show window defects as a result of depigmentation of retinal pigment epithelium. Indocyanine green angiography (ICG), with its ability to visualize the choroidal vascular structure, also has been used to diagnosis APMPPE. ICG angiography displays decreased visibility of the larger choroidal vessels in the early phase.
The differential diagnosis includes sarcoidosis, MEWDS, and birdshot retinochoroidopathy. Sarcoidosis has small yellow-white retinal pigment epithelial lesions that are usually in the peripheral fundus. Ocular sarcoidosis may present together with systemic findings of the disease, which include bilateral pulmonary hilar adenopathy, articular changes, and erythema nodosum. Patients with MEWDS have unilateral visual loss and have small lesions that usually are located in the midperiphery. MEWDS displays early hyperfluorescence on fluorescein angiography and less depigmentation overall. Birdshot retinochoroidopathy, which often has an association with the presence of the human leukocyte antigen A29 (HLA-A29), also is usually bilateral but presents subacutely with smaller lesions and is associated with significant vitreous reaction and retinal vasculitis. Fluorescein angiography may show retinal vascular leakage and macular edema.
The pathogenesis of APMPPE is unknown. Occasionally, a viral prodrome occurs, and speculation exists that APMPPE may have an infectious etiology. In fact, adenovirus 5 has been isolated in one patient with a concurrent viral infection. APMPPE also has been associated with human leukocyte antigen DR2 (HLA-DR2) and human leukocyte antigen B7 (HLA-B7), suggesting a genetic predisposition to the disease.
No treatment is required for most patients with APMPPE. The disease is self-limited with spontaneous recovery of vision in most cases. Of those eyes that are affected, 90% of them typically achieve a visual acuity of more than 20/25. In rare cases, recurrences may occur within 6 months of the initial episode, thereby giving a less favorable prognosis.
In cases of foveal involvement, corticosteroids may be considered, although their efficacy has not been proven in a controlled study. Corticosteroids may be beneficial in cases of associated cerebral vasculitis. Choroidal neovascularization is a rare complication of APMPPE.

Serpiginous Choroiditis

also known as geographic choroidopathy
rare condition that typically affects middle-aged males
patients present with unilateral or bilateral visual loss when the macula is involved, and they also may notice photopsias and scotomata
Gray-white lesions are noted at the level of the retinal pigment epithelium.
Active lesions usually are found at the border of inactive lesions and appear in an interlocking polygonal pattern that spreads out toward the periphery from the optic nerve.
Macular involvement is common.
Mild vitreous and anterior chamber inflammation is observed in one third of cases.
Branch vein occlusions, although not common, have been reported.\
On fluorescein angiography, hypofluorescence is present in the center of the lesions, and hyperfluorescence is present at the rim of the lesions in the early phase. Active lesions are hyperfluorescent in the late phase. Inactive lesions are hypofluorescent in the early phase and staining of the sclera is visible in the late phase. In addition, the choroidal vessels are easily seen on fluorescein angiography. ICG angiography does not contribute significantly toward the diagnosis.
Serpiginous choroiditis often is confused with APMPPE. Younger patients with APMPPE who may have a viral prodrome typically present with an acute loss of vision. The lesions in APMPPE do not emanate from around the optic nerve, and active lesions do not border inactive lesions. APMPPE causes less scarring than serpiginous choroiditis. APMPPE has an acute onset and typically has a rapid recovery, whereas serpiginous choroiditis has a subacute presentation and ultimately results in significant visual loss, especially if the macula is involved. In addition, patients with serpiginous choroiditis are more likely to develop choroidal neovascularization than patients with APMPPE. Other diseases to consider in the differential diagnosis include MCP, age-related macular degeneration, and sarcoidosis.
The etiology of serpiginous choroiditis is unknown. Speculation exists regarding an association with exposure to various toxic compounds.
The pathology of serpiginous choroiditis reveals lymphocytic infiltration in the affected choroid and the presence of fibroglial tissue surrounding the Bruch membrane.
Within a few weeks, the active lesions convert into inactive lesions with eventual retinal pigment epithelial atrophy.
If foveal involvement is absent, the visual prognosis is good, and no treatment is necessary. However, if the fovea is involved, treatment with anti-inflammatory medication is recommended.
A study involving long-term treatment with prednisone, cyclosporine, and azathioprine demonstrated a possible benefit. Additionally, the role of cyclosporine alone has been investigated.
Recurrences are common in serpiginous choroiditis.
A serious complication of serpiginous choroiditis is choroidal neovascularization.
Laser photocoagulation has been used for extrafoveal choroidal neovascularization; however, it is of limited benefit, likely due to the abnormalities of the Bruch membrane and the presence of lymphocytic infiltration.

Multiple Evanescent White Dot Syndrome

MEWDS occurs predominantly in young to middle-aged females, with a mean age of onset of 26.8 years.
In one half of patients, an associated viral prodrome is present.
Patients also present with acute, painless, unilateral loss of vision.
patients may notice photopsias and scotomata, particularly in the temporal visual field.
Examination of the fundus reveals flat, multifocal, gray-white lesions that appear to extend as deep as the retinal pigment epithelium layer. The lesions typically are found outside the macula in the posterior pole, ranging in size from 100-300 µm in diameter. The lesions can be subtle in appearance, and careful examination is essential for accurate diagnosis.
A characteristic finding of MEWDS is foveal granularity.
Additional findings that may be present include optic disc edema, mild vitritis (usually posterior vitreous cells), and a relative afferent pupillary defect.
A report described the appearance of brown areas after the resolution of the acute phase of
Fluorescein angiography demonstrates early punctate hyperfluorescence with late staining, in areas corresponding to the white dots. On closer examination, the early fluorescence of the lesions appears in a wreathlike pattern. Patients with MEWDS may have optic nerve staining and retinal vascular sheathing. ICG angiography demonstrates multiple hypofluorescent spots in the posterior pole and hypofluorescence around the optic nerve head, particularly in patients with enlarged blind spots. The hypofluorescent spots persist until the patient recovers.
Visual field testing usually shows considerable enlargement of the blind spot. The actual defect does not correlate with the distribution of white dots in the fundus, since the presence of white dots around the nerve are rare and the visual field defect persists even after the disappearance of the lesions.
Electroretinographic studies demonstrate reduction of the a-wave amplitude and early receptor potential with prolonged early receptor potential regeneration times, indicating photoreceptor dysfunction. These abnormalities resolve with resolution of the disease.
Differential diagnosis
The differential diagnosis includes APMPPE, birdshot retinochoroidopathy, acute retinal pigment epitheliitis, and diffuse unilateral subacute neuroretinitis. APMPPE causes bilateral visual loss. The lesions in APMPPE are larger than MEWDS, and they block fluorescence early on fluorescein angiography, whereas there is early hyperfluorescence in MEWDS.
Birdshot retinochoroidopathy differs from MEWDS because it presents as bilateral disease in older patients. Accompanied by a subacute presentation, it is associated with significantly greater vitreous inflammation when compared to MEWDS.
Acute retinal pigment epitheliitis, one of the very rare white dot syndromes, also presents with acute visual loss in young patients. However, it differs from MEWDS because the lesions are located in the macula and are dark in color with a halo of depigmentation.
Electroretinogram findings are normal in these patients.
Diffuse unilateral subacute neuroretinitis has been attributed to an intraocular nematode. Patients present with unilateral loss of vision and widespread retinal pigment epithelial atrophy and optic atrophy. It differs from MEWDS in that there is a prolonged clinical course and associated progressive loss of vision.
The pathogenesis of MEWDS is unknown. The frequent viral prodrome may indicate an infectious etiology. Since the disease has a strong female predominance, hormonal status as a possible contributing factor is being investigated.
MEWDS is a self-limited disease with almost all patients regaining good visual acuity within 3-9 weeks. Consequently, no treatment is recommended for patients with MEWDS. The lesions disappear without scarring, and photopsias and scotomata gradually resolve.
Occasionally, patients with MEWDS may have persistent blind spot enlargement.
Although uncommon, recurrences can occur. However, the prognosis is fairly good for these patients.
A rare complication of MEWDS is choroidal neovascularization that may require laser photocoagulation.

Multifocal Choroiditis and Panuveitis

characterized by multifocal chorioretinal lesions with significant anterior chamber and vitreous inflammation.
It occurs predominantly in myopic females between the second and sixth decades of life, with a mean age of onset of 33 years.
Patients usually present with an acute onset of blurred vision, photopsias, and scotomata.
Bilateral involvement is present in approximately 75% of patients.
Examination of the fundus reveals multiple yellow or gray lesions at the level of the choroid and retinal pigment epithelium.
These active lesions can range in size from 50-1000 µm and can be numerous (as many as several hundred at a time).
The lesions usually are concentrated in the midperiphery.
The active lesions can progress into chronic lesions, which are punched-out atrophic scars that develop pigmentation over time.
The optic disc is usually normal, although, in some cases, it may be edematous.
Peripapillary scarring and prominent linear chorioretinal streaks also may be present.
Choroidal neovascularization can be present, in addition to peripapillary fibrosis.
Almost all patients have vitreous inflammation, and many have anterior chamber inflammation.
The patient also may present with cystoid macular edema.
The diagnosis is based on clinical examination and can be confirmed by angiographic studies. Fluorescein angiography demonstrates that active lesions show early hypofluorescence and late hyperfluorescence. However, if patients present at a later stage, the active lesions usually have scarred or are in the process of scarring, thereby giving early hyperfluorescence and late staining. If choroidal neovascularization is present, it usually is observed as early hyperfluorescence with a lacy appearance and a late leakage of dye. ICG angiography shows both active and chronic lesions as hypofluorescent. ICG angiography of choroidal neovascularization reveals hyperfluorescence.
The major disease to consider in the differential diagnosis is POHS. POHS has similar ocular findings, including multiple atrophic chorioretinal spots, choroidal neovascularization, and peripapillary scarring. The lesions in POHS are less numerous and smaller. However, the key distinguishing feature is that POHS does not present with anterior segment and vitreous inflammation. Other diseases to consider in the differential diagnosis of MCP include sarcoidosis and birdshot retinochoroidopathy.
The pathogenesis of MCP is unknown. Controversy exists regarding the significance of a statistical association of the disease with the Epstein-Barr virus.
Patients with MCP have a chronic condition with recurrent bouts of active lesions and vitreous inflammation. These patients require long-term follow-up care.
Overall, visual prognosis is variable, with final visual acuity of 20/40 or better in 66% of eyes. With each bout of inflammation, patients with MCP develop more active lesions, which later become atrophic with significant scarring.
Visual loss usually results from inflammatory scars in the fovea, cystoid macular edema, choroidal neovascularization, and iatrogenic induced by long-term corticosteroid use.
The treatment of patients with MCP consists of corticosteroids. Oral steroids are helpful in patients with active posterior segment inflammation or with cystoid macular edema.
Topical corticosteroids are helpful if there is severe anterior segment inflammation.
However, cases in which corticosteroids have not improved the inflammation have been described.
The most common complication of MCP is choroidal neovascularization, which develops in 30% of patients. Laser photocoagulation may be indicated in these patients. Oral steroids also may be used for choroidal neovascularization since they have been shown to decrease the neurosensory detachments associated with choroidal neovascular membranes.
Two conditions are related to MCP. The first condition, PIC, affects young myopic females. It presents with an acute bilateral loss of vision, photopsias, and scotomata. However, PIC lesions are smaller and have a more cylindrical punched-out appearance. Unlike MCP, patients with PIC do not have anterior segment or vitreous inflammation. Also, patients with PIC rarely have recurrences of the lesions. The initial lesions become atrophic and scar; no new lesions erupt. In one third of patients, choroidal neovascularization develops at the site of the scar; thus, visual prognosis is variable.
Another related condition to MCP is DSF. In these cases, in addition to the presence of multifocal choroiditis, a prominent fibrosis exists. The fibrosis is predominantly at the area of previous inflammatory lesions, and a turbid, subretinal fluid that overlies the lesions also is present. This disease is rare, and the visual prognosis is poor.
Both PIC and DSF represent a spectrum of disease as it relates to MCP. PIC represents a milder form of disease, while DSF is a more severe form.

Birdshot Retinochoroidopathy

Also known as vitiliginous choroiditis
typically affects females in the fourth to fifth decade of life.
Patients present with a painless gradual blurring of vision, floaters, and loss of color vision.
More than 90% of patients with birdshot chorioretinopathy are HLA-A29 positive.
Ocular findings include multiple depigmented yellow-white patches scattered throughout the fundus.
These lesions radiate from the optic nerve and follow the larger choroidal vessels. The term "birdshot" is given because the pattern of the lesions in the fundus is similar to the shotgun scatter of a birdshot.
Vitritis, optic disc edema, and cystoid macular edema also may be present.
Diagnosis is by clinical examination, fluorescein angiography, and HLA-A29 status.
Fluorescein angiography demonstrates mild hyperfluorescence and staining in the late phase.
The pathogenesis is unknown at this time; however, speculation exists regarding an autoimmune etiology.
Ocular and systemic corticosteroids are generally the treatment of choice.
is a chronic disease with multiple recurrences, and, consequently, the long-term visual prognosis generally is guarded.

Presumed Ocular Histoplasmosis Syndrome

POHS usually occurs in endemic areas of Histoplasma capsulatum, which includes the Ohio and Mississippi River Valley.
Typically, adults in the fourth decade of life are affected.
No sexual predilection exists.
Patients may be asymptomatic or may present with visual decline and a central scotoma.
On ocular examination, the vitreous is clear with no evidence of inflammation.
Typically, peripapillary atrophy, atrophic chorioretinal lesions, and choroidal neovascularization are present.
The lesions, which are yellow in color and resemble punched-out lesions, also may be present in the macula. Linear streaks in the midperiphery are found in a minority of the patients.
The pathogenesis is presumed to be due to H capsulatum; however, the organism has never been isolated from the choroid.
Fluorescein angiography shows the typical features of choroidal neovascularization, ie, early lacy hyperfluorescence with late leakage. Management of this condition includes argon laser photocoagulation for extrafoveal choroidal neovascularization, while krypton laser photocoagulation is beneficial for juxtafoveal choroidal neovascularization.

Controversy exists involving the white dot syndromes; some have stated that because of the significant overlap among them, the various white dot syndromes may just represent a spectrum of the same disease. For example, women have a predilection for multifocal choroiditis, PIC, and MEWDS. Occasionally, patients have presented with findings consistent with a specific syndrome; then, they later developed findings that led to the diagnosis of a different white dot syndrome. Although controversy may exist in the artificial classification of these syndromes, it is clear that an accurate diagnosis needs to be attained in all cases to ensure appropriate management may be undertaken.

Dry eye/eczema

2009-10-15T10:40:00.000-07:00

http://www.athealth.com/consumer/disorders/eczema.html

Atopic dermatitis is often referred to as "eczema," which is a general term for the several types of dermatitis (inflammation of the skin. )
Is a chronic (long-lasting)
Not contagious
Emotional factors, such as stress, can make the condition worse, but they do not cause the disease

Types of Eczema (Dermatitis)

Allergic Contact Eczema (dermatitis): A red, itchy, weepy reaction where the skin has come into contact with a substance that the immune system recognizes as foreign, such as poison ivy or certain preservatives in creams and lotions.
Atopic Dermatitis: A chronic skin disease characterized by itchy, inflamed skin.
Contact Eczema: A localized reaction that includes redness, itching, and burning where the skin has come into contact with an allergen (an allergy-causing substance) or with an irritant such as an acid, a cleaning agent, or other chemical.
Dyshidrotic Eczema: Irritation of the skin on the palms of hands and soles of the feet characterized by clear, deep blisters that itch and burn.
Neurodermatitis: Scaly patches of the skin on the head, lower legs, wrists, or forearms caused by a localized itch (such as an insect bite) that become intensely irritated when scratched.
Nummular Eczema: Coin-shaped patches of irritated skin-most common on the arms, back, buttocks, and lower legs-that may be crusted, scaling, and extremely itchy.
Seborrheic Eczema: Yellowish, oily, scaly patches of skin on the scalp, face, and occasionally other parts of the body.
Stasis Dermatitis: A skin irritation on the lower legs, generally related to circulatory problems.

Skin Features of Atopic Dermatitis

Atopic Pleat (Dennie-Morgan fold): An extra fold of skin that develops under the eye.
Cheilitis: Inflammation of the skin on and around the lips.
Hyperlinear Palms: Increased number of skin creases on the palms.
Hyperpigmented Eyelids: Eyelids that have become darker in color from inflammation or hay fever.
Ichthyosis: Dry, rectangular scales on the skin.
Keratosis Pilaris: Small, rough bumps, generally on the face, upper arms, and thighs.
Lichenification: Thick, leathery skin resulting from constant scratching and rubbing.
Papules: Small raised bumps that may open when scratched and become crusty and infected.
Urticaria: Hives (red, raised bumps) that may occur after exposure to an allergen, at the beginning of flares, or after exercise or a hot bath.

Patient education:

Stop after shave, cologne, perfume or makeup on or near the face, (there are so many chemicals in those products it blends into an unidentifiable soup on your skin.
Switch to plain water to wash your face or a simple non-soap facial cleanser, shampoo, body wash.
If you shave, use witch hazel to close the pores and refresh your skin.
Switch to perfume-free products for anything that comes near your skin including laundry soap and dryer sheets.
Be careful with hair products near your eyes. (The skin around the eyes is extremely sensitive to soaps, conditioners, silicone hair sprays, and other hair products. )
When you wash and rinse your hair, let the soap and water run towards the back of the scalp rather than over your face.
DON'T RUB YOUR EYES!
Warm Compresses. Rinse a clean washcloth with warm water and wring out thoroughly. Place the folded washcloth over the eyes for about 3 minutes, twice a day, setting a timer helps. The warmth helps to loosen the oil glands that lubricate the eyeballs. This is essential if you have dry eye, meibomitis or blepharitis.
Eyelid cleansing. TheraTears SteriLid Eyelid Cleanser twice a day. Make sure your hands are clean before using it. Place it gently on the eyelids, massage very lightly to remove debris, and leave it on for a full minute. It takes away any pollens and debris that builds up. My eyes always feel freshened after using SteriLid.
Face Cream. e.g Aveeno (extra moisturizing non-scented skin relief formula). Use the cream every time after you wash your face.
Eye Drops.
Eye Ointments. Use as soon as any irritation is felt. Give it a good hour to two and the itching inevitably goes away. I never use it for more than a few days a time
Drink lots of water to keep hydrated and flush impurities out of your system.
Restasis

Supplements:

Vitamin A (Fish oil, yellow and green fruit and vegetables),
essential fatty acids (hemp seed, flax, pumpkin oil)
Vitamin B complex
Vitamin E topical oil

http://www.healthy.net/scr/article.asp?Id=2866

Antioxidants (vitamins A, C, E and selenium). Ensuring that your diet is rich with these well-known free-radical scavengers can help support the body’s defences against the daily chemical onslaught. Vitamin C strengthens the skin; vitamin E improves skin healing; and vitamin A helps to regulate the rapid turnover of skin cells seen in eczema. The trace mineral selenium plays a crucial role in the glutathione-peroxidase system (the body’s natural antioxidant process) and is effective for detoxing heavy metals. Suggested dosages: vitamin C, 1000 mg twice daily; vitamin E, 400 IU/day; vitamin A, 5000-10,000 IU/day; selenium, 50-200 mcg/day
B vitamins. B3 (niacin) and B6 (pyridoxine) are both integral to the process of new cell formation, and play a key role in the healthy function of body tissue - especially skin, which has a quick rate of turnover. A deficiency of these vitamins has been linked to various types of eczema and other skin disorders. Suggested dosages: B3, 100-500 mg/day; B6, 50-100 mg/day
Gamma-linolenic acid (GLA), an omega-6 fatty acid found naturally in borage (starflower), evening primrose and blackcurrant oils, could help to improve the roughened skin seen with eczema, as well as keep inflammation under control (Am J Clin Nutr, 2000; 71 [1 Suppl]: 367-72S). One study gave 3 g/day of GLA for 28 days to children with atopic eczema; although none were completely cured, all experienced improvement in their symptoms and a reduced need for medication (J Int Med Res, 1994; 22: 24-32). Suggested dosage: 2-3 g/day
Omega-3 fatty acids. These essential fatty acids have recognised anti-inflammatory properties. A double-blind study found that atopic eczema patients given 10 g of fish oil for 12 weeks all achieved a reduction in itching, scaling and other eczema symptoms (J Intern Med Suppl, 1989; 225: 233-6). Suggested dosage: 1000 mg three times daily
Zinc. A deficiency in this essential mineral is common among people with allergies, and may play a role in the development of recurring or chronic eczema (Br J Dermatol, 1984; 111: 597-601). One team of Hungarian researchers found that zinc supplementation reduced the severity of eczema symptoms in children (Orv Hetil, 1989; 130: 2465-9). Suggested dosage: 15 mg/day of zinc with 2 mg of copper (as zinc is known to deplete the body’s copper reserves)

Management tips of the week

2009-10-15T10:19:00.001-07:00

http://www.optometric.com/om_mtotw.aspx

Benign eyelid myokymia

2009-10-08T15:28:00.000-07:00

precipitating factors such as fatigue, stress and excessive caffeine/alcohol/nicotine intake may result in irritation of the orbicularis’ nerve fibers

Medical-ocular history should be comprehensive and should include such questioning as antipsychotic medication usage, past CN VII palsy and prior injection in or around the eye

Patients should be observed for overt eyelid twitching in isolation, associated with speaking or accompanying facial/neck/limb involvement.

Anterior segment biomicroscopy will demonstrate contributory conditions such as trichiasis, blepharitis, keratitis, dry eye syndrome, corneal abrasion, recurrent corneal erosion and foreign body. In some instances, BEM will not be observed during the course of examination.

In these instances, superior oblique myokymia (SOM) should be ruled out. (While viewing the suspect eye under the slit lamp, the patient is directed to look down and in toward his or her nose. SOM, if present, will demonstrate subtle ocular oscillations lasting less than 10 seconds.)

Differential diagnosis of BEM includes blepharospasm, hemifacial spasm, Meige syndrome, aberrant regeneration of CN VII, trigeminal neuralgia, Tourette syndrome, spastic-paretic facial contracture and SOM.

antihistamine and antihistamine-combination products also proved successful in treating the condition.

severe cases of BEM, botulinum toxin A (Botox, Allergan) injection to the affected eyelid area has been used

http://www.pconsupersite.com/default.asp?ID=20040

Ophthalmic agents during pregnancy/lactation

2009-10-08T15:23:00.001-07:00

http://www.pconsupersite.com/default.asp?ID=20040

Optometric nutrition

2009-10-08T15:18:00.000-07:00

http://www.vindicomeded.com/cmelc/pcon_ce0809.asp

Unusual retinal vessels

2009-10-08T10:18:00.000-07:00

http://www.optometry.co.uk/articles/docs/8a09ee2c4a719fd88e90e28ce345ac0e_Swann1991119.pdf

Remnants of the hyaloid system

Mittendorf dot
Bergmeister’s papilla
Vogt’s arcuate line
very rarely, the whole vessel being preserved from disc to lens
associated with persistence of the primary vitreous, coloboma and ONH hypoplasia

Cilioretinal artery

present in 30-40% of eyes
arise from the temporal optic disc in a hook-like manner, often traversing the papillomacular area
more common in cases of optic disc pit, situs inversus, pre-papillary loops and optic disc drusen
in CRAO, the presence of a cilioretinal arteriole may enable some degree of central vision to be retained

Congenital tortuosity

more commonly involves retinal arterioles than veins
usually non-progressive with all other findings being normal
there is a progressive form which is inherited as an autosomal dominant trait and may be
associated with retinal haemorrhages
should bedifferentiated from that secondary to other problems, such as epiretinal membrane,
vein occlusion and diabetes

Situs invertus

retinal vessels emerge from the optic disc in an anomalous direction
typically seen in tilted disc syndrome and also in myopic eyes
a dragged disc and vessels can have a similar appearance and occurs in retinopathy of prematurity

Congenital retinal macrovessel

a retinal vessel, usually the inferio-temporal retinal vein, is enlarged and drains an area
superior to the macula
vision may be slightly reduced by the large vessel crossing the macula
macular cysts are more common in these patients

Pre-papillary loops

95% of these vessels are arterioles, and usually originate from and return to an arteriole on or near the disc
the loops may be small and simple or large and corkscrewed
many are surrounded by the white remnants of Bergmeister’s papilla
usually unilateral with associated cilioretinal arterioles
fill before or with other retinal arteries on fluorescein angiography and do not leak
vitreous haemorrhage and occlusion of the loop have been reported

AV malformations

arterioles and veins communicate without an intervening capillary bed
may be isolated to a small arteriole and venule or be widespread involving the entire vascular tree
intracranial and facial vascular malformations may be associated and constitute the Wyburn-Mason syndrome
similar vascular anomalies can involve the orbit, conjunctiva, sclera and iris, and
neovascular glaucoma can be a complication
should be differentiated from the phakomatosis von Hippel-Lindau’s disease
patients should be referred for neurological assessment

Collateral vessels

preformed capillaries connecting retinal, and retino-choroidal circulations
indicate a preceding vascular disorder which may point to a significant ocular and/or systemic disease
unlike new vessels, they do not leak on fluorescein angiography
potential causes include retinal vein thrombosis and glaucoma
if the patient, especially a middle-aged female, has a chronic, progressive vision loss, together with a pale, swollen optic disc and a disc collateral, then optic nerve sheath meningioma is a likely cause

New vessels

new vessels proliferate following ischaemia in conditions such as diabetic retinopathy and central retinal vein thrombosis
may form on the optic disc, elsewhere in the fundus and in the anterior segment
delicate feathery appearance and leak fluorescein

Dry eye

2009-09-26T18:34:00.001-07:00

http://www.lasvegasoptometrycare.com/2009/08/10/dry-eye-syndrome/

LASIK-induced neurotrophic epitheliopathy (LINK)

2009-09-26T18:16:00.000-07:00

(The most severe cases of post-Lasik dry eye.)
from: http://www.revoptom.com/index.asp?ArticleType=SiteSpec&Page=osc/105700/lesson.htm

Etiologies:

The “neural feedback loop theory.” Corneal nerve fibers are disrupted during creation of the LASIK flap and stromal ablation --> interferes with the cornea-central nervous system-lacrimal gland regulatory loop -->reduced corneal sensitivity causes a decreased blink rate and diminishes reflex tear production. The combination of these two factors increases the time the cornea is unprotected by the tear film.

Goblet cell damage. A normal lipid layer is necessary to prevent evaporation of the tear film.Likewise, a normal mucin layer is critical to a healthy ocular surface. However, prolonged microkeratome pressure can damage conjunctival goblet cells, disrupting the normal tear film composition. The resultant unstable mucin layer will decrease the tear film break-up time and increase dry eye symptoms.

Change in corneal curvature. While the change in curvature provides better vision, it also affects how the tear film overlays the cornea. The change in tear function is evident months after surgery. It presents as iron-stained epithelium.

Osmolarity changes and exposure keratopathy. Studies have also shown an incomplete blink in patients following LASIK, which results in osmolarity changes and potential exposure keratopathy.

Type of ablation. Hyperopic ablations affect the tear film more than myopic ablations. Specifically, the tear film has more trouble overlaying the steeper cornea following hyperopic surgery, thus causing an increase in dry eye symptoms.

Higher myopic prescriptions tend to cause greater dryness than lower myopic modifications (due to greater change in corneal curvature, possibly affecting more corneal nerve fibers.)

Patients who undergo photorefractive keratectomy (PRK) tend to have less dryness problems than LASIK patients.

Pre-existing dry eye is rarely an absolute contraindication for corneal refractive surgery; however, there are some cases when patients should not have surgery. Patients who have Sjögren’s or Stevens-Johnson syndrome should not undergo surgery because the extent of their pre-existing dryness is too great. Patients who have dryness secondary to other autoimmune diseases, such as rheumatoid arthritis or lupus, are also poor candidates. Patients who are in good health, but have chronic superficial punctate keratopathy (SPK) and moderate to severe dry eye disease should not have corneal refractive surgery.

Screening

To determine if a patient is at risk for developing significant dryness following LASIK, perform a thorough case history and carefully evaluate the tear film. The patient’s history should include age, gender, systemic health, medications and occupational environment.

Women past age 50 are affected by dryness almost twice as often as men over the age of 50.Post-menopausal women who take hormone replacement therapy are at higher risk for developing dryness after surgery. The pre-existing dryness they experience can be exacerbated by the creation of the LASIK flap and laser ablation.Men who take antihormonal or antiandrogen therapy for prostate cancer may also experience significant dry eye symptoms following surgery.

Other systemic diseases that are associated with dry eye include rheumatoid arthritis, acne rosacea, systemic lupus erythematosis, thyroid dysfunction and Sjögren’s syndrome. Numerous medications, such as antihistamines, certain antidepressants, beta-blockers and diuretics, can affect the ocular surface.

A history of either dryness or contact lens intolerance is a risk factor for post-LASIK dryness. These patients often pursue refractive surgery because they have problems with contact lens wear. Long-term contact lens wearers, particularly gas-permeable lens wearers, are prone to dryness. Their existing uncomfortable corneal sensation is exacerbated by the LASIK procedure, which can lead to postoperative dryness.

Evaluate a patient’s tear film before surgery:

Tear film testing to determine if there is a problem with tear quantity or quality. For instance, the tear film break-up time (TFBUT) is one of the simplest ways to measure tear film stability.

A Schirmer tear test with anesthetic to measure basal tear secretion. Realize that Schirmer testing may demonstrate variable results because of reflexive tearing and the presence of a residual tear lake in the fornix. Still, the Schirmer test remains the standard measurement of basal tear secretion.

Lissamine green staining to identify conjunctival or corneal staining, a risk factor for postoperative dryness that should be treated before LASIK.

Measurement of tear meniscus height, which can be done quickly and easily at the slit lamp. You can observe both tear meniscus and tear quality by looking for heavy debris in the tear film.

Phenol red thread tear test testing, which also measures tear secretion. You can perform this test in 15 seconds.

There are similar limitations to Schirmer’s testing; specifically, the test may measure the residual tear lake instead of tear secretion.

Fluorescein dye to stain areas of the cornea and conjunctiva where cell damage has occurred. Any number of conditions may cause cell damage, but dry eye is often the culprit.

Performing each test on every patient being screened for refractive surgery is unnecessary. However, performing the exact same test on all patients may also be inappropriate. To determine if a patient has a pre-existing dry eye problem, it is necessary to document any problems with tear quality and/or quantity. Schirmer tear testing, phenol red thread tear testing, and measuring the tear meniscus height are good ways to determine the tear quantity. TFBUT is a good measurement of tear quality. A breakdown of one or both of these components may necessitate lissamine green or fluorescein staining.

Also, carefully evaluate the eyelids and meibomian gland orifices during the preoperative examination, and aggressively treat any pre-existing blepharitis and meibomianitis. Treating blepharitis will improve tear quality and lessen the risk of infection and inflammation after surgery.

Patients are more likely to comply with a treatment regimen that is simple to follow and comes with written instructions. An informational sheet that describes blepharitis and provides instructions for using of hot compresses and lid hygiene reminds patients to treat their eyelids before surgery.

Cleansing pads are a better choice than baby shampoo for lid hygiene. Treat more advanced cases of blepharitis with topical or oral antibiotics, or combination antibiotic/steroid drops or ointments. Low-dose oral doxycycline b.i.d. for one to two months followed by q.d. dosing for an additional month or longer may be warranted.

Pre-op Treatment

Once you determine that a patient has a dryness problem, you must begin dry eye therapy prior to surgery. The treatment regimen depends on the severity of the condition. Options include:

Artificial tears. Patients who have mild corneal or conjunctival staining should be pretreated with artificial tears. This optimizes the ocular surface prior to surgery and lessens the chance for intraoperative complications.

Cyclosporine. Patients who have mild to moderate dryness may benefit from Restasis (cyclosporine 0.05%, Allergan). The typical preoperative regimen is twice a day for one month before surgery. Some doctors wait to see if patients have problems after surgery to begin cyclosporine eye drops. However, it is best to be proactive and start the drops before surgery to give the medication a chance to take effect.

A recent study found that using cyclosporine 0.05% prior to LASIK improved refractive predictability.¹¹In this study, researchers randomized 21 myopic patients with dry eye to receive unpreserved artificial tears or cyclosporine b.i.d. for one month before undergoing LASIK.

The study drops were discontinued for 48 hours after surgery, and then resumed for three months following surgery.

The patients who received cyclosporine had better uncorrected visual acuity following LASIK compared with patients who received artificial tears.¹⁵

As far as refractive stability, 69% of the cyclosporine group had a manifest refraction spherical equivalent (MRSE) within ±0.50D of emmetropia at six months vs. 26% of those patients using unpreserved artificial tears.¹⁶

Corticosteroids. Patients with moderate dry eye, particularly patients who manifest superficial punctate keratopathy (SPK), may benefit from topical corticosteroids. In one study, dry eye patients with staining scores higher than 10 or conjunctival chemosis greater than grade 2 were prescribed loteprednol 0.5% q.i.d. for four weeks. At examination, the results showed statistical improvements in corneal staining, hyperemia and chemosis, compared to the control group.¹⁷

Punctal occlusion. This is another treatment option for patients who have moderate preoperative dryness. Punctal plugs occlude the lacrimal drainage system and may reduce dependency on artificial tears after surgery.²Punctul occlusion is recommended for patients who have lower Schirmer scores or phenol red thread tear testing from decreased tear production.

There are several types of plugs to choose from, namely silicone plugs, intracanalicular plugs, collagen plugs and extended-duration dissolvable plugs. Extended-duration dissolvable collagen plugs that last one to four weeks work well for LASIK patients. The first four weeks after surgery is typically when patients experience the most problems with dryness.

Post-op Treatment

Even with the proper precautions, some patients may experience significant dryness following LASIK. These patients may or may not report symptoms. Frequently, patients present for post-op visits with a white conjunctiva and no signs of dryness, but they complain of blurry vision or halos and glare. The patients are unaware of the irritation to the corneal surface because of the temporary neurotrophic effect of LASIK. Remind patients to use artificial tears following LASIK even if their eyes do not feel dry.

Artificial tears. Preservative-free artificial tears should be used on all patients for the first month following surgery, regardless of their signs and symptoms. To increase the probability that patients will buy the type of artificial tear you recommend, give them samples and provide coupons for the eye drop in their postoperative kit.

Following the first month post-op, patients can decrease the volume of artificial tears they are using based upon their signs and symptoms. For example, if a patient presents for a one-month post-op visit with no signs or symptoms of dryness, you can lower their dose to b.i.d. and switch them to a bottled tear, such as Optive (Allergan), Systane (Alcon) or Genteal (Novartis Ophthalmics).

Questionnaires. Dry eye questionnaires are not needed for every patient who seeks refractive surgery. However, if a patient has significant postoperative dryness, the questionnaires may help identify an environmental factor that is exacerbating the dryness. For example, a questionnaire may reveal that the patient uses a table fan while working on the computer to keep cool. The questionnaire may also reveal problems with the patient’s diet or fluid intake. Treating the dry eye problem may be as simple as modifying the patient’s normal habits.

Cyclosporine. If a post-op patient presents with significant SPK and dryness symptoms, topical cyclosporine eye drops may be beneficial. Studies show topical cyclosporine 0.05% is helpful to patients after LASIK surgery.

Another study found that cyclosporine 0.05% increases goblet cell density.²³The researchers treated patients diagnosed with dry eye disease with artificial tears or cyclosporine 0.05% for 12 weeks, and found that mean goblet cell density increased by 17% in the cyclosporine group.²³

The artificial tear group exhibited no change in goblet cell density. This indicates that cyclosporine inhibits the pathologic mechanisms that lead to reduced conjunctival goblet cell density in chronic dry eye disease. These results are pertinent to post-LASIK patients, as the microkeratome pressure may damage goblet cells.

Punctal occlusion. A possible drawback of using topical cyclosporine 0.05% is that it can take from three weeks to three months before the medication takes effect. If a patient desires an immediate effect, punctal plugs are a viable option for treating postoperative dryness; 60-day, three-month and six-month duration punctal plugs are often ideal. Each punctal plug has a varying duration time, but every option works well in refractive surgery patients. If a patient continues to have problems after the initial plugs dissolve, permanent silicone plugs, form-fitting plugs or hydrophobic acrylic plugs may be warranted.

Topical corticosteroids. Another treatment option is concurrent use of corticosteroids. One hundred twenty patients with dry eye were enrolled in a prospective, multicenter, randomized, controlled, masked study, to evaluate the efficacy and safety of using Lotemax (loteprednol etabonate 0.5%, Bausch & Lomb) in conjunction with Restasis therapy.²⁴Patients received either Lotemax (test) or an artificial tear (control) in masked bottles q.i.d. for two weeks, and then received the masked test or control drop b.i.d. plus Restasis from days 15 to 60. At day 60, patients achieved an improvement in corneal and conjunctival staining and Schirmer test results. Additionally, patients randomized into the Lotemax group experienced decreased stinging with the start of Restasis.²⁴

At baseline, tear production in both treatment groups increased. When normalized to baseline, however, the Lotemax/Restasis treatment significantly increased tear production by 27%).²⁴The long-term treatment (60 days) with Lotemax reduced patients' use of artificial tears.

It is important to identify and treat keratitis sicca before the patient undergoes LASIK. The surgeon may recommend modifications to the surgical treatment plan to decrease the risk of significant dryness following surgery. After surgery, encourage patients to maintain their postoperative dry eye therapies to improve their odds of obtaining a favorable and comfortable outcome.

Ocular motor dysfunction

2009-09-15T08:29:00.000-07:00

Poor saccadic, pursuit, and fixation difficulties
Children who have difficulties with reading, such as loss of place, skipping lines, skipping words and slow inefficient reading
Have tech do DEM (Developmental Eye Movement test) before patient is seen

Home activities to improve ocular motor function (do 3-5 of these daily):

put jigsaw puzzles together
solve simple mazes, crossword puzzles, or word searches
fill-in all of the "O's on a newspaper page
use highlighter or index card while reading to keep place
Hart Chart: read letters in first column then 10th column, then 2nd to 9th, etc.
have child sit at front of class so there are less distractions for copying off the board
http://homevisiontherapy.com or http://www.bernell.com

Amblyopia

2009-09-15T08:20:00.000-07:00

Six-week follow-up visits are the standard of care for amblyopia treatment
Children ages 3-7 with severe amblyopia (20/100-20/400) achieved as good results with 6 hours of patching a day vs. full-time patching
Children ages 3-7 with moderate amblyopia (20/10-20/80) achieved as good results with 2 hours of patching a day vs. 6 hours
1% atropine daily had same results as patching 6 hours/day
Similar outcomes with 1% atropine daily vs. only on weekends
If the patient's VA plateau's to an unacceptable enpoint, refer to pediatric optometrist for eccentric fixation treatment

Cotton wool spots

2009-09-14T15:45:00.000-07:00

DM and HTN are by far the most common cause of cotton-wool spots
Patients with diabetes mellitus might also harbor other typical retinal findings such as macular edema, retinal exudate, flame or dot/blot hemorrhages, microaneurysms, venous beading or microvascular abnormalities or proliferations
Patients with systemic hypertension would be expected to demonstrate generalized arteriolar narrowing, arteriolar/venous nicking and, in extreme cases, optic-disk swelling.

Etiologies of Cotton Wool Spots

1) Ischemic

Ocular ischemic syndrome
Retinal vascular occlusion
Anemia
Increased blood viscocity (e.g. multiple myeloma)

2) Embolic

Carotid emboli
Cardiac emboli
Deep venous emboli
White blood cell emboli (Purtcher’s Retinopathy)
Severe chest compression/long bone fractures
Foreign bodies (IVDA)

3) Infectious

HIV infection
Rocky Mountain Spotted Fever
Cat scratch fever (bartonela henslae)
Leptospirosis e. Onchocericiases
Bacteremia
Fungemic

4) Toxic

Interferon

5) Radiation

6) Neoplastic

Lymphoma/Leukemia
Metastatic carcinoma

7) Collagen Vascular Disease/Immune complex disease

Systemic lupus erythematosus
Dermatomyositis
Polyarteritis nordosa
Scleroderma
Giant cell arteritis

8) Tractional

Epiretinal membrane

9) Traumatic

Nerve fiber layer laceration

10) Idiopathic

Fuch's heterochromic iridocyclitis

2009-09-14T13:08:00.000-07:00

the affected eye presents as the lighter eye (90% of the time) due to iris atrophy due to chronic inflammation
10% of the time the darker iris is the affected eye due to progressive atrophy within the anterior iris and stroma, revealing the posterior iris pigment epithelium
4-5% of uveitis cases
chronic recurring mild A/C reaction, usually unilateral
small, round, grey-white keratic precipitates across entire endothelium (including superiorly, unlike other inflammatory conditions)
often with iris nodules and transillumination
synechiae are rare

assocated with mildly elevated occurrences of glaucoma, vitreous opacities and cataracts
Amsler's sign: a classic finding of hyphema occurring immediately after a paracentesis

Treatment

often do not require treatment
topical cycloplegic and corticosteroids if symptomatic, although true resolution of the inflammation may never be achieved
often have a low grade of A/C reaction that proves to be resistant to topical corticosteroids

Ganciclovir 0.15% (Virgan or Zirgan -- name not decided on yet)

2009-09-14T12:51:00.000-07:00

-new drug for acute herpetic keratitis treatment
-gel form
-has been available in Europe for >10 years
-inhibits viral DNA synthesis, but is less toxic than Viroptic
-may also work for EKC

Long-term oral antiviral dosing

2009-09-14T12:41:00.000-07:00

-Ask patients if they have kidney or liver disease
-Have patient see PCP for lab testing if they are on oral antivirals (Famvir/Acyclovir) for >12 months

PDF med guides

2009-09-14T12:24:00.000-07:00

Glaucoma meds: http://www.pconsupersite.com/pdfs/0904guide.pdf

Allergy meds: http://www.pconsupersite.com/pdfs/0902guide.pdf

Anti-infective meds: http://www.pconsupersite.com/pdfs/0809guide.pdf

Fabry’s disease

2009-09-14T12:12:00.000-07:00

inherited lysosomal storage disease in which the enzyme á-galactosidase (á-GAL), which breaks down the compound globotriaosylceramide, does not function properly or is absent --> globotriaosylceramide accumulates in the walls of blood vessels --> eventually decreasing blood flow to the kidneys, heart, skin and nervous system
progresses slowly
symptoms of kidney, heart or cerebrovascular involvement occur between the ages of 15 and 40
if left untreated, Fabry’s disease leads to renal failure, cardiovascular disease or cerebrovascular disease in these patients, leading to an early death.

Symptoms

discomfort and pain in the hands and feet
dark red skin rash known as angiokeratoma

Corneal signs manifest early

Optometrists play a pivotal role in diagnosing Fabry’s disease because several indications of this disorder are found in the cornea at an early age
corneal whorls (brownish or cream-colored wisps)
cataracts -- a propeller cataract and a Fabry cataract (whitish, spot-like deposits of fine granular material near the posterior capsule)
secular dilation of blood vessels on the conjunctiva
ischemic changes in the retina (vessel dilation)
many patients may be on amiodarone because Fabry’s disease is affecting their heart. A patient who is 75 years old and on amiodarone is a cardiac patient; certainly a 30-year-old on amiodarone should be suspected of Fabry’s disease

Refer to a geneticist + specialists

refer patients for confirmatory enzyme or DNA testing,” Dr. Desnick said in an interview
the disease can be treated by replacing the missing enzyme activity. Studies have shown that early intervention is the most effective, before irreversible pathology has occurred
because the patient may need to see many specialists — depending on how Fabry’s disease is expressed in that particular patient refer the patient to a Fabry’s disease expert at one of the larger universities who will take a team approach.

Enzyme replacement therapy

The only treatment for Fabry’s disease is an enzyme replacement therapy called Fabrazyme (agalsidase beta, Genzyme), which replaces the missing enzyme through a biweekly infusion.
Diagnosis is made by demonstrating the deficient activity of á-GAL in plasma or leukocytes from males and the presence of the family’s specific á-GAL gene mutation in females
Enzyme replacement therapy has been shown to be effective in double-blind, randomized placebo-controlled trials, even in older patients with advanced disease

Genetic links

Because Fabry’s disease is an X-linked disorder, the patient’s family should also be evaluated if this disease is suspected
Fabry’s is inherited as an X-linked trait — males are affected and female heterozygotes can be symptomatic

Newer antibiotics

2009-09-14T11:34:00.000-07:00

Besivance (besifloxacin ophthalmic suspension 0.6%, Bausch & Lomb),

has a long-lasting vehicle, DuraSite, which facilitates prolonged exposure
treats a wide spectrum of bacteria, particularly methicillin-resistant Staphylococcus aureus, with no apparent toxicity
dosing is listed as 4 to 12 hours on the labeling, (e.g. presurgical prophylaxis TID, keratitis q2h then QID, depending on severity, and for a conjunctivitis BID or TID).”

Iquix (levofloxacin ophthalmic solution 1.5%, Vistakon Pharmaceuticals),

approved for the treatment of susceptible gram-positive and gram-negative bacterial corneal ulcers (incl. Pseudomonas usually in CL infections)
dosage and administration: for days 1 through 3, instill one to two drops in the affected eye q30minutes to 2 hours while awake and about 4 and 6 hours after retiring. For day 4 through treatment completion, instill one to two drops in the affected eye every 1 to 4 hours while awake.

AzaSite (topical azithromycin solution 1%, Inspire Pharmaceuticals)

also formulated with DuraSite (prolonged exposure)
is approved for bacterial conjunctivitis; however off-label use for blepharitis is showing positive results
hot compresses, lid scrubs and omega-3 supplements are effective in maintaining blepharitis patients long-term after they stop initial therapy of topical azithromycin
blepharitis is a chronic disease, and doctors should consider additional courses of topical azithromycin throughout a year to improve patients’ symptoms
Restasis (0.05% cyclosporine ophthalmic emulsion, Allergan) may be a consideration long-term for the concurrent dry eye
Azithromycin as a molecule has significant penetration and residence time in tissue
for bacterial conjunctivitis, the recommended dosing of topical azithromycin is one drop BID for 2 days, and QD for five day
for blepharitis, dosing is extended to 1 month in moderate or severe cases and 2 weeks in mild cases
also effective in treating recurrent corneal erosion with its anti-inflammatory activity in reducing MMP9 mediators
has anti-inflammatory activity similar to doxycycline, which has been shown to be an effective treatment for recurrent corneal erosions
treating meibomian gland disease -- best to put the drop in the eye as opposed to the eyelids, then have the patient gently massage their eyelids; typically dosed BID for 2 days, then QD for 2 to 4 weeks depending on the severity

Staphylococcus is the most common pathogen on the lids and the likely pathogen in conditions such as preseptcal cellulitis and dacryocystitis

avoid using amoxicillin because of the resistance to it by staph
prescribe Augmentin (amoxicillin clavulanate, GlaxoSmithKline)
additional options would be dicloxacillin or a cephalosporin such as Ceclor (cefaclor, Eli Lilly)

E/M vs. Eye codes -- Part 3 choosing which to use

2009-04-06T18:24:00.000-07:00

http://www.optometricmanagement.com/article.aspx?article=102686

New Patients. If your level is 4 or higher, you should probably be using E/M codes. If your level is 3 or lower, you should be using Eye Codes unless you fail to initiate a diagnostic and treatment program at the comprehensive eye code level. Then you will have to drop to 99203.

• Consultations. If your adjective is moderate, level 4 or higher, the E/M consultation code should be used. If not, switch to the eye codes.

Return Office Visits:

92012 versus 99213. For return office visits for conditions requiring more frequent visits the choice is often between CPT codes 99213 and 92012. An error was made in the relative value units calculation in 1998, and the erroneous calculation has been pretty much maintained. This has resulted in significantly higher reimbursement for code in 2009 — $9.38 in 2009 on a national average. Given the choice, the eye code pays better than the E/M code and can be used in most instances.

• 92014 vs. 99214. Code 92014 basically should be used when coding for comprehensive eye examinations and not for follow-up visits for serious disease.

Use 92014 for your follow-ups in which medical necessity dictates a comprehensive examination — such as a return in one year for cataract follow-up. The code is not intended to be used for frequent follow-up visits for serious pathological conditions.

Use 99214 when following serious diseases as long as your medical decision-making is moderate and you have the medical necessity to perform nine of the elements. This code has been a target of OIG investigations and you should be confident of your coding skills and chart documentation when using it.

• 99212. Most Medicare local coverage determinations for the eye codes mandate that for minimal services code 99212 be used — not 99213 or 92012. Quick check ups for conjunctivitis or healing corneal abrasions would fall into this category.

E/M vs. Eye codes -- Part 2 Eye codes

2009-04-06T18:14:00.000-07:00

New Patient

► 92002 Ophthalmological services: medical examination and evaluation with initiation of diagnostic and treatment program; intermediate, new patient

► 92004 Ophthalmological services: medical examination and evaluation with initiation of diagnostic and treatment program; comprehensive, new patient, one or more visits

Established Patient

► 92012 Ophthalmological services: medical examination and evaluation, with initiation or continuation of diagnostic and treatment program; intermediate, established patient

► 92014 Ophthalmological services: medical examination and evaluation, with initiation or continuation of diagnostic and treatment program; comprehensive, established patient, one or more visits

"Intermediate ophthalmological services describes an evaluation of a new or existing condition complicated with a new diagnostic or management problem not necessarily relating to the primary diagnosis, including history, general medical observation, external ocular and adnexal examination and other diagnostic procedures as indicated; may include the use of mydriasis for ophthalmoscopy."

The narrative descriptions for the comprehensive eye codes contain the following excerpted information:

"Comprehensive ophthalmological services describes a general evaluation of the complete visual system. The comprehensive services constitute a single service entity but need not be performed at one session. The service includes history, general medical observation, external and ophthalmoscopic examination, gross visual fields and basic sensorimotor examination. It often includes, as indicated: biomicroscopy, examination with cycloplegia or mydriasis and tonometry. It always includes initiation of diagnostic and treatment programs.

"Intermediate and comprehensive ophthalmological services constitute integrated services in which medical decision making cannot be separated from the examining techniques used. Itemization of service components, such as slit lamp examination, keratometry, routine ophthalmoscopy, retinoscopy, tonometry, or motor evaluation is not applicable.

"Initiation of diagnostic and treatment program includes the prescription of medication, and arranging for special ophthalmological diagnostic or treatment services, consultations, laboratory procedures and radiological services.

"Special ophthalmological services describes services in which a special evaluation of part of the visual system is made, which goes beyond the services included under general ophthalmological services, or in which special treatment is given. Special ophthalmological services may be reported in addition to the general ophthalmological services or evaluation and management services."

E/M vs. Eye codes -- Part 1 E/M

2009-04-06T17:42:00.000-07:00

http://www.optometricmanagement.com/article.aspx?article=102510

http://www.optometricmanagement.com/article.aspx?article=102619

KEY COMPONENT 1: History

The First Key Component, the History, contains four component parts. They are:

► Chief Complaint

► History of the Present Illness (HPI): location, duration, timing, quality, context, severity, modifying factors, associated signs and symptoms.

► Review of Systems (ROS)

► Past History, Family History, and Social History (PFSH).

KEY COMPONENT 2: Examination

KEY COMPONENT 3: Medical Decision Making

A stable glaucoma would be low risk; a glaucoma that is not in control and requires change of medicine would be moderate risk. A patient presenting with acute glaucoma is considered high risk.

Lasik calucations

2009-04-06T17:27:00.000-07:00

-ablation depth = 15 um per diapter
-lasik flap thickness = 160 um (Intralase 100)
-available tissue = pachy - flap - bed
-total treatment depth = flap + ablation
-residual tissue = available - ablation

Treatment of post-LASIK inflammatory keratitis

2009-04-06T17:17:00.000-07:00

-cycloplegic if painful (homatropine 5%bid, scopolamine 0.25% tid)
-zymar/vigamox q1h
-if there is a risk of MRSA, alternate with Vancomycin q1h
-after improvement on antibiotic, add pred-forte 1%/FML qid (epi-intact)
-preservative-free AT q1h (on 1/2 hour)
-follow-up daily

OCT RNFL thickness average analysis

2009-04-06T16:55:00.000-07:00

Imax/Smax 0.80-1.25 um
Smax/Imax 0.77-1.25
Smax/Tavg 1.70-3.06
Imax/Tavg 1.69-3.12
Smax/Navg 1.37-2.93

Min-Max 96-154
Smax 124-189
Imax 125-194
Savg 97-152
Iavg 98-156

Average thickness 82-118

http://www.meditec.zeiss.com/88256DE3007B916B/0/C26634D0CFF04511882571B1005DECFD/$file/stratusoct_en.pdf

Latisse

2009-04-06T16:47:00.001-07:00

-Latisse 0.03% is indicated to treat hypotrichosis of the eyelashes by increasing their growth including length, thickness, and darkness
-25% increase in eyelash growth length
-106% increase in fullness/thickness
-18% increase in darkness
-about 2 months to work
-adverse effects in 4% of patients: eye pruritis, conjunctiva hyperemia, skin hyperpigmentation, possible increased brown iris pigmentation (only seen in Lumigan)
-apply once nightly directly to the skin of the upper eyelid margin at the base of the eyelashes using the supplied, FDA-approved sterile applicators

Gonioscopy.org

2008-10-28T10:37:00.000-07:00

http://www.gonioscopy.org/

Glaucoma & Thyroid disease

2008-10-28T10:23:00.000-07:00

The prevalence of self-reported glaucoma was significantly higher among [respondents] who reported a history of thyroid problems [6.5%] compared with those who did not [4.4%]

Hypothyroidism "may lead to the deposition of mucopolysaccharides in the trabecular meshwork, which increases IOP as well as aqueous outflow resistance"

Work up for Optic Neuropathy

2008-10-14T21:07:00.000-07:00

Lab tests to r/o nfectious, inflammatory or nutritional problems:

CBC
C-reactive protein (GCA)
ESR (GCA)
Platelet count
Lyme titer (infectious)
ANA with reflex titer (rheumatologic)
ACE (sarcoid)
RPR (syphillis/infectious)
FTA-ABS (syphillis/infectious)
Vitamin B₁₂(nutritional)
Folic acid (nutritional)
Methylmalonic acid (occult vitamin B₁₂deficiency)

Neuroimaging:

MRI (preferred) or CT scan

Differentials:

a young patient complaining of sudden vision loss will more likely have an optic neuritis (ON)
a middle-aged person would more likely have nonarteritic anterior ischemic optic neuropathy (NAION).
an older patient with the same complaint would more likely have arteritic anterior ischemic optic neuropathy (AAION) associated with giant cell arteritis (GCA).
NAION: no pain, “disk-at-risk” appearance in the fellow eye (small, crowded optic disc with little or no cupping that is predisposed to the ischemic process of NAION), less pale nerve
AAION: pain with eye movements, optic nerve dema usually associated with hemorrhages during the acute phase, more pale nerve
AAION and GCA symptoms: jaw claudication, scalp tenderness, fatigue, loss of appetite and fever.
ON: pain on eye movement; you will see either a normal optic disc (retrobulbar optic neuritis) or disc swelling without hemorrhages (papillitis).
Multiple sclerosis (MS) symptoms: weakness, numbness, pares-thesias or any other neurologic symptoms.
Traumatic optic neuropathy: pallor of the neuroretinal rim suggests a longstanding or chronic process
Structural abnormality or mass: non-acute, nonglaucomatous optic neuropathy; patient is in need of neuro-imaging to look for either a structural abnormality such as a mass or abnormal enhancement indicating an inflammatory process, or some form of disruption of the blood-brain barrier.
GCA: A CBC, ESR, C-reactive protein and platelet count must be performed on patients over the age of 50

Ocular Side Effects Of Systemic Medications

2008-10-14T20:38:00.000-07:00

http://www.revoptom.com/index.asp?ArticleType=SiteSpec&page=osc/105682/lesson.htm

Sinusitis

2008-10-14T20:22:00.002-07:00

Clinical Features
- stuffy nose, followed by the slow onset of increased sinus pressure

- malaise, toxicity, headache, possibly a slightly elevated temperature, and usually a normal WBC count.

- as the disease progresses over two to three days, symptoms become more pronounced and severe.

- associated pain to the eye and orbit is a constant, dull ache with no throbbing. It may worsen if the patient bends over, coughs or strains.

- patients with chronic sinusitis usually have: allergic rhinitis, which is signaled by itchy/watery eyes, seasonal variation in symptoms and a family history of the disorder.

- acute sinusitis symptoms: facial pain or tenderness, colored nasal discharge, headache, decreased sense of smell, maxillary toothache, cough (usually daytime), fever, malodorous breath and occasional periorbital swelling.Less common findings include middle ear effusion, swelling of the face and nasal bleeding.²⁴

- ethmoid sinusitis: headache is a prominent symptom, located either behind or between the eyes with radiation to the temporal region.The eyes may be tender to pressure, and extreme tenderness on palpation of the medial and superior aspects of the orbit may be present.The patient may experience discomfort with eye movement.

- frontal sinusitis: may cause a frontal headache, which radiates behind the eyes to the vertex of the skull. The pain is generally constant and tends to feel like a pressure sensation. There is also point tenderness on the undersurface of the medial aspect of the superior orbital rim, which is the floor of the frontal sinus.Often, the pain is not present in the early morning after a night of rest. It usually appears one or two hours after waking, increases for three or four hours and becomes less severe in the late afternoon or evening. Apply finger pressure upward toward the floor of the sinus, where the sinus wall is thin, or perform palpation directly over the frontal sinus. Swelling caused by tumors or retained secretions (mucoceles) may cause a downward bulge in the floor of the frontal sinus. Transillumination of the frontal sinuses is done by placing a light source below the supraorbital rim, under the floor of the frontal sinus, at the upper inner angle of the orbit. This technique helps assess light transmission into the lower forehead.

- sphenoid sinusitis: causes pain at the occiput or vertex, yet frontotemporal, retro-orbital or facial pain is more common.It may also travel from the orbit to the mastoid area. The pain is described as constant, and if it occurs retrobulbarly, quite severe.This type of severe retro-orbital pain can cause photophobia and tearing.

- maxillary sinusitis: 10% of maxillary sinusitis is generally secondary to dental root infection. Simultaneous finger pressure over both maxillae exemplifies differences in tenderness.Perform transillumination by placing the light source over the middle of the infraorbital rim.

Examination and Testing
- thorough patient history and physical examination to establish either acute or chronic sinusitis
- an evaluation of vision, pupils, extraocular muscle function, exophthalmometry, slit lamp and funduscopy helps identify any secondary periorbital, orbital or ocular complications
- evaluation of the head and neck should be performed.

Amaurosis Fugax

2008-10-14T20:22:00.001-07:00

-Most commonly caused by emboli thrown from the carotid artery or the heart; this eventually causes occlusion of the retinal arteriole system and/or an occlusive event anywhere else in the body.

-Patients usually have a history of hypertension, diabetes or hypercholesterolemia; danger of cerebral vascular accident (CVA) in addition to ocular sequelae.

-patients must be referred to the emergency room to rule out emboli actively being thrown from the carotid artery, cardiac valves or aortic arch.

-If a patient with these symptoms is 56 or older, one must consider giant cell arteritis (GCA)

-Other conditions, such as antiphospholipid antibody syndrome and systemic lupus erythematous, may also result in arteriole occlusion

-A central artery occlusion of less than 24 hours might be aided by intervention, including lowering IOP, performing ocular massage and attempting vasodilation by increasing carbon dioxide levels in the blood (this is accomplished by having the patient breathe into a paper bag).

-r/o weakness, numbness, headache or speech difficulty

-lab w/u:

emergent complete blood count (CBC) with differential
prothrombin time (PT)
partial thromboplastin time (PTT) tests
platelets
carotid duplex
echocardiogram

-start on ASA

-educate to report immediately to the ER if any non-recovering vision loss or peripheral weakness or numbness

Oral medical therapies

2008-07-19T20:20:00.000-07:00

Oral Antibiotics

Penicillins

Augmentin (amoxocillin + clavulanic acid)

500mg, 875mg, or 1,000mg b.i.d. x 1 week (depending on severity)
The dosage is determined by the severity of the clinical condition.

Cephalosporins --5% to 10% cross-sensitivity with PCN

Keflex (Cephalexin)

500mg b.i.d. x 1 week

Macrolides -- only for pregnancy or chlamydia

erythromycin

500mg t.i.d. x 1 week
safe for pregnancy

azithromycin

250mg tablets, 500mg tablets, 1,000mg oral suspension
Zmax, a 2,000mg extended-release oral suspension
chlamydial infection: one dose of either 1,000mg or 2,000mg azithromycin

Fluoroquinolones (usually reserved for PCN allergies)

Levaquin (Levofloxacin)

500mg q.d. x 1 week

Oral Corticosteroids

best taken with meals to minimize the risk of GI upset
caution: diabetes or peptic ulcer disease
oral steroids exacerbating peptic ulcers

a proton (hydrogen) pump inhibitor (PPI) can be prescribed, which will either fully protect or greatly diminish any expression of gastric ulceration
PIs simply and safely reduce gastric acid secretion
Prilosec (OTC, 20mg capsules, swallowed whole before a meal once daily), Nexium, Prevacid for the duration of the steroid therapy and for one additional week.

patients with diabetes are prone to lose glycemic control while on oral steroids
type II may well have increased blood glucose levels for a few days, which is rarely a problem; glycemic control returns after cessation of the steroid
type I diabetes, they should be instructed to adjust their insulin dosagethe duration of their therapy

Acute optic neuritis and giant cell (cranial/temporal) arteritis

1,000mg of methylprednisolone (500mg q12 hours) IV daily for three days

Episcleritis

Lotemax or FML q.i.d. x 1 week, then b.i.d. x 1 week, and that’s it
For stubborn cases, add 40mg of p.o. prednisone x 2 days, then 30mg x 2 days, then 20mg x 2 days (up to six days), then 10mg x 2 to 4 more days
rarely are systematic laboratory studies indicated
if there are multiple recurrences or if the presentation is difficult to suppress. Lab work-up:

Rheumatoid arthritis: Rheumatoid factor (RF) and antinuclear antibody (ANA)
Systemic lupus erythematosus: Antinuclear antibody (ANA) and anti-DNA antibody
Gout: Serum uric acid
Syphilis: FTA-ABS, VDRL, MHA-TP or RPR
Wegener’s granulomatosis: Antineutrophil cytoplasmic antibody (ANCA).
Acne rosacea: None. This is a clinical diagnosis.

Orbital pseudotumor/orbitalmyositis/dacryoadenitis

idiopathic white blood cell infiltration resulting in chemosis (without itching, therefore not allergic), proptosis, eyelid edema, and occasionally diplopia (because of orbital congestion)
send patients for a CT scan to rule out any other orbital process, and to confirm our clinical diagnosis
unusual or atypical eyelid or orbital presentation, order a CT scan

if strongly feel the condition is infectious, start Augmentin 875mg b.i.d. or, if penicillin-allergic, Levaquin 500mg q.d.,

Orbital pseudotumor is treated with 60mg p.o. prednisone x 3 to 4 days, then 40mg x 3 to 4 days, then 20mg x 1 to 2 weeks, then 10mg x 1 to 2 weeks

Marked or stubborn iridocyclitis

If, after a few days of aggressive use of Pred Forte and a therapeutic cycloplegic (with perhaps FML ointment h.s.), the iritis appears unyielding (and the patient is compliant with the medications), try augmenting the topical medications with oral prednisone
consider starting at 40mg a day x 2 or 3 days, 30mg x 2 or 3 days, and then reevaluate the patient. Assuming good improvement, continue the topical assault and continue to reduce the p.o. prednisone to 20mg x 1 week and recheck the patient. Assuming continued progress, stay the course topically, and reduce the p.o. prednisone to 10mg q.d.x 1 week and recheck the patient. This iritis should be very well controlled.
Now the topical taper can begin. Reduce the Pred Forte to q2 hours x 1 week, and stop the FML ointment now, or after one more week. If the condition continues to improve, then continue q.i.d. x 1 week and recheck the patient. At this point, there should be little or no anterior chamber evidence of iritis. Keep this patient at b.i.d. for another 1 to 2 weeks.
Regarding the cycloplegic agent, stop it when the cells and flare are reduced to Grade I or less
If the IOP becomes elevated 10mm Hg or more from baseline, consider adding beta-blocker once daily if there are no contraindications, or brimonidine 0.2% q12 hours
Once the inflammation is controlled and the patient is a steroid responder, switch the medication to Lotemax to finish the corticosteroid component of the therapy.
If the iritis rebounds when the oral steroid is reduced below 20mg q.d., add a COX-2 inhibitor such as Celebrex (celecoxib, Pfizer) 100mg or 200mg b.i.d., or ibuprofen 400mg q.i.d. can be beneficial. In this scenario

add one of these non-steroidals to the 20mg of oral prednisone q.d. x 1 week and then begin tapering the oral prednisone to 10mg q.d. x 1 week (or two) while concurrently using the oral NSAID.
Many times, the use of NSAIDs in such instances enables the completion of the oral prednisone taper as planned. Once off the oral prednisone, continue the patient on the NSAID for a couple more weeks.

Bell's Palsy

prednisolone 60mg a day for a few days, then tapering to 40mg, 20mg, and 10mg, depending upon the clinical response
acyclovir 400mg five times a day for one week, or valacyclovir (Valtrex, GlaxoSmithKline) 500mg three times a day for one week, or famciclovir (Famvir, Novartis) 250mg three times daily for one week
there is indecision regarding the need for such oral antiviral therapy in the setting of Bell’s palsy, however
the current thinking is to prescribe an antiviral if the condition is severe or complete.
preserve and maintain ocular surface integrity with frequent lubrication with a preservativefree artificial tear such as TheraTears Liquid Gel, or a gel formulation such as GenTeal Gel
If more aggressive lubrication is required, an ointment such as Refresh P.M. can be employed
modypatients fully recover in three to nine months.

MGD/posterior blepharitis

no effective topical therapy to enhance meibomian gland function beyond warm soaks, lid scrubs and glandular massage.
Doxycycline can exert a beneficial effect on the secretory function of these glands
two 50mg capsules daily for two weeks (as a loading dose), then just one 50mg capsule daily x 3 to 6 months or longer, depending upon the clinical response. (read “Meibomian Gland Dysfunction,” by P.J. Driver, et al., in Survey of Ophthalmology, March-April 1996)
side effects: occasional vaginal candidiasis
OCuSOFT: ALODOX™ Convenience Kit

Allergic Blepharodermatitis

usually just cold compresses and/or 0.1% triamcinolone cream applied b.i.d. to q.i.d.
add oral prednisone p.r.n., or, depending upon your clinical judgment, prescribe oral prednisone as initial therapy, with or without concurrent topical steroid cream.
the more severe the blepharodermatitis (or greater surface area involvement), the more we lean toward oral therapy.
Fortunately, these conditions tend to resolve with only two to four days of therapy. We generally prescribe 40mg q.d. x 2 days, then 20mg q.d. x 2 to 4 more days, and then stop. There is no reason to taper such a low dose or short course of oral prednisone any further

Recurrent epithelial errosion

Tetracyclines and corticosteroids can improve tissue adhesion of the basal epithelium/Bowman’s membrane/anterior stromal complex
50mg tablets of doxycycline to be taken by mouth as one 50mg tablet p.o. b.i.d. x 2 weeks, then q.d. x 6 to 8 weeks
concurrently prescribe Lotemax q.i.d. x 1 month, then b.i.d. x 1 month

Oral Antivirals

Acyclovir is available in 200mg capsules, 400mg and 800mg tablets, and in a 200mg-per-teaspoon (5ml) banana-flavored oral suspension

Valtrex comes in 500mg and 1,000mg tablets
Famvir is available in 125mg, 250mg and 500mg tablets.
Acyclovir and Valtrex arePregnancy Category C; Famvir is Category B.
precautions: kidney function, as all of the antiviral drugs are eliminated via the urine; ask patients about any known renal disease.

Herpes Zoster

herpes zoster ophthalmicus 50% of the time

keratitis, inflammatory anterior uveitis (or both), and less commonly as episcleritis and trabeculitis (which can result in high IOP).

treated aggressively with topical corticosteroids such as Lotemax or Pred Forte.

Oral antivirals can be used to treat childhood chickenpox, if indicated. The FDA/CDC recommended dosage for treating chicken pox in children over age 2 weighing at least 40 pounds can be as much as acyclovir 800mg q.i.d. x 5 days (the dosage for shingles is 800mg 5 times a day for 7 days).
patient presenting with ophthalmic division shingles: standard dosage is acyclovir 800mg p.o. 5 times a day x 7 days, and potentially up to 10 to 14 days p.r.n. The clinically equivalent dosage for Valtrex is 1,000mg p.o. t.i.d. x 7 days. For Famvir, the dosage is 500mg p.o. t.i.d. x 7 days.

Herpes Simplex

primary herpetic dermatitis to the face and/or eyelids. The cornea is not usually involved, but can be. In either case,
400mg of acyclovir 5 times per day x 7 days, Valtrex 500mg t.i.d. x 7 days, or Famvir 250mg t.i.d. x 7 days.
HSV keratitis: supplement the oral antiviral with preservative-free artificial tears.
Concurrent topical trifluridine is rarely ever needed
Certainly, if in a few days the ocular dermatitis is resolved and the keratitis is unchanged, then adding topical Viroptic q2 hours x 4 days, then q.i.d. x 4 days may be needed, but this would be highly unusual.

Analgesics

eye-related pain, which can certainly be intense, is invariably short-lived
ask patients what they generally use for pain (extra-strength acetaminophen and ibuprofen)
Acetaminophen (Extra Strength Tylenol) is indeed an excellent analgesic, which also has antipyretic (fever-reducing) properties

is synergistic with oral narcotic analgesics

Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen are likewise very broadly used and are generically available.
Ibuprofen is available over-the-counter as 200mg tablets or capsules.
The optimum dosage of ibuprofen is 1,600mg per day. It is most often dosed as two 200mg tablets taken every four hours. This dosage is generally sufficient and approximates that of a Schedule III opioid.
Tylenol #3 (30mg of codeine and 300mg of acetaminophen.)

IL Society for the Prevention of Blindness

2008-07-19T20:05:00.001-07:00

Low Vision information and resources guide:

http://www.eyehealthillinois.org/visionloss.pdf

Fish oil

2008-07-19T16:55:00.000-07:00

Omega-3 fatty acids from fish oil:

support body's natural inflammatory response
support tear production
protect eyes from oxidative damage

450mg = minimum for healthy eyes
1g = advanced support for healthy eyes
2-3g = for high intesnity eye support/dry/red/itching/painful eye

CPR

2008-07-19T16:45:00.000-07:00

Office visit procedural codes

2008-06-24T07:40:00.000-07:00

Corneal dystrophies

2008-06-24T06:43:00.000-07:00

EPITHELIUM

Meesmann's corneal dystrophy

autosomal dominant
presents in 1st decade and progresses into adulthood
diffusely distributed intraepithelial cysts that are usually concentrated in the interpalpebral zone
in severe cases cysts can rupture on surface causing irritation and photophobia (use bandage CL)

EBMD (Map-Dot fingerprint dystrophy or Cogan's microcystic epithelial dystrophy)

autosomal dominant or due to trauma or surgery
geographic epithelial changes (maps), opaque irregularities (dots) or concentric irregular lines (fingerprints)
results from a thickened basement membrane
can result in recurrent corneal erosions (bandage CL)
Muro 128 during the day or ung at night may be necessary for up to 3 months (if this fails to prevent recurrent erosions, may need anterior stromal puncture or PTK

BOWMAN'S LAYER

Reis-Buckler's corneal dystrophy

autosomal dominant, presents 1st decade of life
subepithelial reticular changes that progress until middle age
may opacify or induce irregular astigmatism
may have erosions (bandage CL)

STROMA

Granular dystrophy

autosomal dominant, presents 1-2nd decade of life
grayish white opacities form in the central (almost never periphery) anterior stroma with clear intervening space
lesions can become larger and more numerous with stromal hazing

Macular dystrophy

rarest (autosomal recessive)
anterior stroma becomes hazy in 1st decade, progressing to opacified lesions
more likely to affect peripheral cornea
worse visual prognosis

Lattice dystrophy

autosomal dominant, 1st decade
refractile lines in the anterior stroma which eventually branch and develop deeper into stroma (lattice design)
prone to erosions (bandage CL)

ENDOTHELIUM

Posterior polymorphous dystrophy (PPD)

vesicles deep into the cornea that may be isolated, mutiple/coalesced, or broad bands/train tracks
may apear blister-like and have a gray white halo aroudn them
increased risk of glaucoma

Fuch's endothelial dystrophy

guttata (refractice excrescenses) on posterior cornea due to abnormal functioning endothelial cells (from aging, trauma or inflammation)
Fuch's is diagnosed when nonfunctioning endo causes corneal edema
vision worse upon awakening
muro 128 gtts and ung
extreme epithelial edema may cause bulae with pain and photophobia (bandage CL)
usually have cataracts
cataract surgery may cause a dramatic worsening of Fuch's

BANDAGE CL

use steeper curve (unless there is no mvmt then use flatter one)

Cross-cylinder calculators

2008-06-23T10:47:00.000-07:00

http://www.aoa.org/x4783.xml
procare.cibavision.com
coopervision.com
ecp.acuvue.com
eyedock.com

Online learning center

2008-05-22T11:34:00.000-07:00

Designed to help employees new to eye care gain a basic understasnding of the vision system while improving overall practice efficiency and productivity.

http://learning.coopervision.com/

Acuvue2 colors: https://www.jnjvision.com/imakeover/

Freshlook contacts: http://www.freshlookcontacts.com/

Resolving dry eye in RGP wearers

2008-05-22T09:45:00.000-07:00

3/9 stain

when the corneal surface isn't adequately resurfaced with tears after the blink
edge of GP lens holds lid away from corneal surface during blink
incomplete blinking
may see vascularized limbal keratitis

Adjusting the fit to minimize excessive edge lift and inferior position

Strive for superior lens position by:

decreasing diameter
reduce CT
+/- lenticulars
reduce edge clearance
steepen PC radius
narrow PC width
reduce edge thickness

Patient CL compliance handout from AOA

2008-05-22T09:43:00.000-07:00

What You Need to Know About Contact Lens Hygiene & Compliance
http://www.aoa.org/x8024.xml

Vogt-Koyanagi-Haraa (VKH) syndrome

2008-04-10T10:08:00.000-07:00

bilateral granulomatous panuveitis associated with serous retinal detachments, optic disc edema, neurologic abnormalities and skin pigment changes
systemic manifestations: tinnitus, vitiligo, alopecia, headache and meningismus
T cell-mediated autoimmune process directed against melanocyte antigens
more prevalent in Asians, Latinos and American Indians
women slightly > men
any age but usually 4th-6h decades of life

4 phases

prodromal
acute uveitic (poor VA, severe AC inflammation w/ or w/o posterior synchiae)
convalescent
chronic recurrent (RPE alterations, widespread loss of choroidal melanocytes producing a sunset-glow fundus and choroidal Dalen-Fuchs-like nodules, cutaneous vitiligo, poliosis and alopecia)

Complications

catarct, glaucoma, CNV, subretinal fibrosis, ERM, macular atrophy

Treatment

prompt initiation of high-dose systemic corticosteroid therapy (1 to 1.5 mg/kg/day) concurrent with a corticosteroid-sparing immunosuppresive agent) , tapering patients off within 2-3 months
rapid and aggressive treatment is important to minimize disease duration and lessen the risk of progression into a chronic recurrent form of disease and reduce the incidence of systemic and ocular complications

Lagophthalmos evaluation/treatment

2008-04-10T09:20:00.000-07:00

May lead to corneal exposure --> keratopathy --> ulceration/infections keratitis

Taking the history
recent trauma or surgery involving the head/face/eye
past infections e.g. herpes zoster
past symptoms suggestive of thyroid disease or obstructive sleep apnea

Testing the lids and globe
ask patient to look down and gently close both eyes
lagophthalmos is present when a space remains b/w the upper and lower eyelid margins in extreme downgaze
measure this space with a ruler
record the blink rate an the completeness of blink
test cranial nerve function (pay attention to ocular motility and the strength of the orbicularis oculi muscle by evaluating the force generated on attempted eyelid closure)
presence and quality of Bell's phenomenon should be noted (cornea is better protected when the eye rolls upward on attempted closure of the eyelids)

Testing the cornea
test corneal sensitivity by applying soft cotton to the unanesthetized cornea and comparing the blink reaction with that of the fellow eye
describe presence of PEE with NaFl
record TBUT

Etiology

Facial nerve (VII)

innervates frontalis muscle (raises the eyebrow) and the orbicularis oculi muscle (closes the eyelid)
loss of function of the VII nihibits eyelid closure, blink reflex, and lacrimal pumping mechanism
also innervates the muscles of facial expression including the zygomaticus (elevate the cheeks) and corrugator supercilii and procerus (depress the eyebrow) which help facial symmetry

Trauma

VII is susceptible to blunt trauma or laceration along it's bony course
fractures to the skull base or mandible can damage the nerve or one of its branches
neurosurgical procedures

Cerebrovascular accidents

VII receives its blood supply from the anterior inferior cerebellar artery (susceptible to ischemic damage)

Bell's Palsy

idiopathic VII palsy thought to be associated with an acute viral infection or reactivation of herpes simplex virus

Tumors

acoustic neuromas in the cerebellopontine angle and metastatic lesions are most commonly associated with lagophthalmos
need MRI with gadolinium

Infections, immune-mediated causes

less common causes: Lyme disease, chickenpox, mumps, polio, Guillain-Barre syndrome, leprosy, diphtheria and botulism

Mobius' syndrome

rare, congenital condition with CN palsies (esp. VI and VII), motility disturbances, limb anomalies and orofacial defects

Eyelids

damage or degeneration of any of the eyelid tissue structures (skin/subcutaneous tissue, orbicularis oculi muscle, orbital septum, orbital fat, muscles of retraction, tarsus, conjunctiva) may inhibit good eyelid closure

Cicatrices

chemical or thermal burns
ocular cicatricial pemphigoid
Stevens-Johnson syndrome
mechanical trauma
above may cause scarring of the soft tissues or retractor muscles

Eyelid surgery

excessive removal of eyelid skin or muscle (blepharoplsty, tumor excision)
overcorrection in ptosis repair

Proptosis

exophthalmos in thyroid ophthalmopathy

Enophthalmos

aquired causes (orbital blowout fractures, orbital fat atrophy from trauma, infection, inflammation, aging or wasting disease such as linear scleroderma or HIV-AIDS)
phthisical or prephthisical eye
scirrhous carcinomas leading to contraction of orbital fat

Floppy eyelid syndrome

result of severe laxity and flexibility of the superior and inferior tarsal plates
may be associated with obstructive sleep apnea

Symptoms

FBS and tearing
pain in AM from increased corneal exposure and dryness during sleep
blurry vision from unstable TF

Work-up and treatment

Medical treatment and supportive care for the cornea (non-preserved artifical tears at least QID, ointments QHS/PRN, moisture gogles, methylcellulose)
Tarsorrhaphy (suturing lateral 1/3 of eyelids, temporary or permanent)
Gold weight implantation (gold is inert and doesn't show through thin skin of eyelid)
Uper eyelid retraction and levator recession (for lagophthalmos due to thyroid ophthalmopathy)
Lower eyelid tightening and elevation (tightenting procedure will improve apposition fo the lower eyelid to teh globe and decrease tearing)
Ancillary surgical procedures (facial surgery)

Myasthenia Gravis

2008-03-25T13:21:00.000-07:00

autoimmune disorder in which antibodies prevent the neurotransmitter acetylcholine from attaching to muscle receptors, thereby interfering with muscle contractions
characterized by fatigability of voluntary eye movements (diplopia worsens as day progresses, improves with sleep)
can present with diplopia, ptosis or both

Tests

sustained upgaze: patients will show a gradual worsening as the levator muscle fatigues
ice pack test: apply a cold pack to the eyelid for 5 minutes (cold temp allows Ach to have more time to react with the muscle receptors), check for improvement in ptosis
sleep test: have the patietn take a nap in the exam chair for 30-45 minutes, check for improvement in ptosis
Tensilon is an IV cholinergic drug that typically shows improvement in muscle function within seconds

Treatment

Mestinon (cholinergic drug) and immunosuppresive therapy (neurophthalmology)
if medications don't eliminate ptosis/diplopia, may try prismatic corrections and ptosis crutches

Differentials

3rd nerve palsy: has vertical and horizontal component
skew deviation: usually appears with concomitant hypertropia and other abnormal eye movements such as nystagmus
disease of the orbit: neoplastic, inflammatory, infectious, traumatic can cause proptosis, lid retraction, periorbital edema, conjunctival hyperemia, disc edema

Determining Prism

2008-03-06T13:19:00.000-08:00

Sheard's criterion

Prism needed = 2/3 (phoria) - 1/3 (compinsating fusional vergence)
eg: pt has 6 XP and BO to blur is 6, the prism needed is 2/3 (6) - 1/3 (6) = 2 BI

Percival's criterion

Prism needed = 1/3 (greater limit of BI or BO range) - 2/3 (lesser limit of BI or BO range)
eg: pt has 6 XP and BO ranges of 6/10/8 and BI range of 21/26/22, prism needed = 1/3 (21) - 2/3 (6) = 3 BI

Parks-Bielschowsky Three Step Test (for head tilts "torticollis")

Which eye is hyper in primay gaze?
In which horizontal gaze does hyperdeviation increase?
In which direction of head tilt does the hyperdeviation increase?
right hyper --> right gaze --> right tilt = LIO
right hyper --> right gaze --> left tilt = RIR
right hyper --> left gaze --> right tilt = RSO (most common cause of vertical dipl.)
right hyper --> left gaze --> left tilt = LSR
right hyper --> right gaze --> right tilt = RSR
right hyper --> right gaze --> left tilt = LSO (most common cause of vertical dipl.)
right hyper --> left gaze --> right tilt = RIR
right hyper --> left gaze --> left tilt = RIO

Postures and Treatments

Left head turn --> Right gaze preferred --> LLR or RMR paresis --> give yoked prism base left
Right head turn --> Left gaze preferred --> RLR or LMR paresis --> give yoked prism base right
Left head tilt --> Right hyperdeviation --> RSO paresis (most common cause of vertical diplopia)--> BD over right eye if longstanding
Right head tilt --> Left hyperdeviation --> LSO paresis (most common cause of vertical diplopia)--> BU over left eye if longstanding
Head tip back --> Downgaze preferred --> V-pattern exotropia or A-pattern esotropia --> BU yoked prism
Chin depressed --> Upgaze preferred --> A-pattern exotropia or V-pattern esotropia --> BD yoked prism

Coding Dry Eye

2008-03-06T12:02:00.000-08:00

Ocular findings:

Tear film insufficiency (375.15) -- test show decreased TF; for punctal plugs diagnosis
Keratoconjunctivitis sicca, not specified as Sjogren's (370.33) -- observation of "inflammation of the conjunctiva and cornea, characterized by "horny"-looking tissue and excess blood in these areas"
Punctate keratitis (370.21)
Exposure keratitis (370.34)
Sjogren's syndrome (710.2)

Patient symptoms:

Eye pain (379.91) -- may be used for all levels of eye discomfort, e.g. burning/stinging
Redness of eyes (379.93) -- r/o episcleritis (379.01) and scleritis (379.00)
Epiphora (375.20) -- dry eye due to reflex tearing

Procedure diagnastic codes:

External ocular photography (92285) -- photos need to document the efficacy of treatment or the progression of the disease, and not just enhance the medical record or billable procedures
Bandage contact lenses (92070) -- covers fitting and supply of lens

Flaxseed oil/Dry eye supplements

2008-02-25T13:30:00.000-08:00

- AT
- MGD/blepharitis
warm compresses/lid scrubs bid
Zylet qid x 1 week, bid x 1 week
- oral antibiotics
- nutritional supplements
- dry mouth therapies
Hydrate (OcuSoft)
BioTears fish oil supplements
Lovaza (omega-3)

1,000-1,500mg per day of each
4-6 weeks before response (including better skin and hair)

TheraTears nutrition supplements for patients with intestinal sensitivities

Alodox convenience kit (doxy 20mg + ocusoft lid scrubs), take with water, don't take with calcium (negates drug)

Sjogren's syndrome

2008-02-25T13:02:00.000-08:00

most age >40
women 9x > men
dry eye, dry mouth, autoimmune disorder
lid hygiene/massage for MGD, AT, Restasis, steroids
oral Minocycline 50mg bid x 2 weeks then 50mg qd x 1 month, then taper (usually 8 weeks to work); side effects: stained teeth, vaginitis, photosensitivity
or Doxycycline 50mg bid x 1-2 months then qd x 1 month (side effects: photosensivitiy, sensitivity to dair products/antacids)
or Periostat (20mg doxy) bid x 1-2 months then qd x 1 month
Salagen and Evoxac (30mg tid) drugs that stimulate the salivary glands to produce saliva

Classification system:

1. Ocular symptoms:

daily, persistent, troublesome dry eyes >3 months
recurrent sensation of sand or gravel in the eyes
use AT more than tid

2. Oral symptoms:

daily feeling of dry mouth for >3 months
recurrent or persistently swollen salivery glands
need to drink liquids to aid in swallowing dry food

3. Ocular signs:

Schirmer's test w/o anesthesia (<5>
Rose bengal or other dry eye findings

4. Histopathology:

focal lymphocytic sialoadentitis in minor salivary glands, evaluated by histopathologist

5. Salivary gland involvement (send to rheumatologist):

unstimulated whole salivary flow (<1.5>
parotid sialography showing diffuse sialectasias without evidence of major duct obstruction
salivary scintigraphy showing delayed uptake, reduced concentration and/or delayed excretion of tracer

6. Autoantibodies

presence of antibodies to Ro(SSA) or La(SSB) antigens or both

For primary Sjogren's:

any 4 of the 6 items as long as item 4 or 6 is positive
presence of any 3 of 4 objective criteria items (3 thru 6)

For secondary Sjogern's:

in patients with a potentially associated disease (e.g. connective tissue disease, RA, lupus) with the presence of item 1 or 2 plus any two from items 3-5

Ocular/Oculodermal melanocytosis (Nevus of Ota)

2008-02-25T12:44:00.000-08:00

most common in Asians/Blacks
women>men
10% have POAG

Posner-Schlossman sydrome (glaucomatocyclitic crisis)

2008-02-25T11:48:00.000-08:00

repeated attacks of a mild cyclitis with significantly elevated IOP, usually unilateral
asymptomatic or may have symptoms of sudden onset of blurred vision, mild pain and haloes around lights
signs: mild anterior uveitis and high IOP (40-60), may have KPs w/ corneal edema, gonio open angle, mild degree of iris heterochromia and anisocoria (involved pupil larger)
usually occurs b/w age of 20-50
unknown etiology (possible allergy, viral infection such as CMV or herpes simplex, stress-induced)
inflammatory material or precipitates on the TM reduce aqueous outflow or trabeculitis causes decreased outflow
acute and self-limiting (resolves or without treatment), lasting hours to weeks
associated with POAG and NAION in patients with small, crowded optic nerves
treatment: control inflammation -- topical corticosteroid may be used alone or with IOP med (e.g. PF 1% qid qid with alphagan tid); don't use miotics or prostaglandins; no need for medication b/w episodes
medical work-up: Chest x-ray, bilateral plain radiographs of ankles, feet and sacroiliac joints (to check for joint abnormalities), CBC with differential, ESR, TSH, HLA-B27, CRP, RF, ANA, Chorionic gonadotropin, RPR, Lupus

Reis-Buckler's dystrophy

2008-02-25T11:23:00.000-08:00

bilateral
causes photophobia, corneal erosions and subepithelial and anterior stromal scarring
multiple subepithelial ring-shaped opacities (honeycomb apperance) in the centre of the cornea corneal surface is irregular with ferritin deposition

EBMD

2008-02-25T11:11:00.000-08:00

10% of patients will have painful recurrent epithelial errosions
moderate presentations may require hypertonic drops and ointments (NaCl 5%), Q3H to QID, for a minimum of six months

ICD-9 codes website

2008-02-25T11:06:00.001-08:00

http://icd9data.com/

http://icd9cm.chrisendres.com/index.php?action=child&recordid=3125

Band keratopathy

2008-02-25T10:51:00.000-08:00

Precipitation of calcium salts, subepithelial

Due to:

hypercalcemia 2^ hyperparathyroidism, excessive vitamin D intake,
renal failure, hypophosphatasia, milk-alkali syndrome, Paget disease,
sarcoidosis
topical medications that contain phosphates (steroid phosphates,
pilocarpine)
chronic ocular inflammation (uveitis, end stage glaucoma) causes elevation
of the surface pH out of the physiologic range which changes the solubility
product and favors precipitation
compromised endothelial function and corneal edema (2^ silicone oil from RD surgery)

Lab studies:

serum calcium and phosphate level
if sarcoid is suspected, an angiotensin-converting enzyme (ACE) should be obtained
parathyroid hormone levels

Salzman's Nodular Degeneration

2008-02-25T10:03:00.000-08:00

peripheral elevated subephithelial nodules and irregular astigmatism
needs smaller diameter GPs to try to keep the leses away from the peripheral nodules

Terrien's Marginal Degeneration

2008-02-25T10:01:00.000-08:00

progressive thinning of the peripheral corneal (usually S/T)
increases regular and irregular against-the-rule astigmatism
needs larger GP lens diameters to prevent decentration

Nutrition in AMD

2008-02-25T08:28:00.000-08:00

Pharmacologic treatments for wet AMD

verteporfin(Visudyne)
pegaptanib (Macugen)
Lucentis
Avastin

Natural history of AMD progression

10% rate of conversion from dry to wet AMD
nutritional supplementation decreases risk
oxidation hypothesis: breakdown of antioxidant systems and generation of free radicals damages lipid membranes; antioxidant deficiency may predispose patient to disease

AMD and cardiovascular disease

shared risk factors: elevated lipids, cholesterol, CRP, arteriosclerosis, cigarette smoking, inflammatin, HTN

AREDS

category 1 or 2 (little-to-no AMD or few small drusen): risk of developing wet AMD at 5 years = 1.5%
category 3 (large intermediate-size drusen or nonvoeal geographic atrophy): risk of developing wet AMD at 5 years = 20%
category 4 (at least 1 eye with wet AMD or foveal geographic atrophy)
if wet AMD present in one eye, risk to the fellow eye is 45%
risk for vision loss at 5 years: antioxidant + zinc = 20% reduction in risk
risk for progression to wet AMD at 5 years: antioxidant + zinc or zinc alone = 25% reduction in risk
recommendations: patients with intermediate to advanced AMD (category 3 or 4) should take daily supplemental theraphy
people who smoke should avoid beta carotene due to increased risk of lung cancer

AREDS II

study of lutein, zeaxanthin, omega-3 fatty acids
lutein and zeaxanthin are natural carotenoids found in macula; antioxidants; filters of UV light; play role in structural signal transduction; macular pigment decreases with age; decrease predisposes patient to increased rsik for AMD
zeaxanthin can increase macular pigment
6m lutein associated with reduced risk for develping AMD by up to 43%

Dietary fat

higher body mass index associated with greater AMD risk
high intake of fat in prcessed baked gods increases odds for developing wet AMD by 2.4
other sources of fat (nuts) protective

Omega-3 fatty acids

lutein, zeaxanthin, and omega-3 fatty acids not produced by body
high intake of omega-3 fatty acids protects against wet AMD (dose-dependent)
omega-3 fatty acids in broiled or baked fish: dose-dependent decrease in risk for AMD progression

Side-effects/interactions

high levels of beta-carotene linked to increased incidence of lung cancer among heavy smokers
high volumes of zinc linked with genitourinary and GI disorders

Dosing guides

2008-02-19T11:30:00.000-08:00

Topical anti-infective medications:
http://pconsupersite.com/pdfs/0709guide.pdf

Topical allergy medications:
http://pconsupersite.com/pdfs/0802guide.pdf

Topical glaucoma medications:
http://pconsupersite.com/pdfs/0705guide.pdf

Pellucid marginal degeneration

2008-02-12T10:53:00.000-08:00

bilateral asymmetric focal ectasia of the corneal stroma 1-2mm above the inferior limbus b/w 5 & 7 o'clock w/o evidence of scarring, vascularization or lipid infiltration
progressive ectasia results in the development of ATR astigmatism
can lead to corneal hydrops
advanced cases show "kissing doves" or "crab claw" topography with superior flattening and a small island of inferior central flattening

Keratoconus

2008-02-12T10:49:00.000-08:00

Munson's sign (lower lid bulge on downgaze)
Rizzuti's sign (loss of normal corneal reflectance in the slit lamp)
retinoscopy scissors reflex
Charleaux oil droplet sign (retroillumination)
Vogt's striae (folds in Descemet's membrane)
Fleischer's ring (iron in corneal epithelium)
stromal thinning
stromal scarring
prominent corneal nerves
swirl SPK staining
pseudo-reduced IOP
loss of BCVA
asymmetric (>1D) astigmatism
elevated total higher-order aberrations
elevated vertical coma (> 0.53 um)
elevated topography I/S values (>1.4)
apical elevation over best fit sphere on anterior and posterior elevation maps
corneal thinning
corneal irregularity

Cornea ectasia

2008-02-12T10:46:00.000-08:00

two theories:

certain patietns have a genetically different type of collage composition of their cornea that predisposes them to ectasia (external factors such as eye rubbing, RGP wear and refractive surgery may trigger the process of thinning)
insult to collagen corneal fibrils via surgery, trauma, RGP wear or eye rubbing causes the corneal matrix to lose structural integrity

Rosacea treatment

2008-02-12T10:21:00.000-08:00

Periostat (2mg doxycycline) QD

Oracea (30mg immediate release, 10mg of slow release doxycycline) -- QAM on empty stomach or at least 1 hour prior or 2 hours after meals

MetroCream 0.75%

-use sunscreen to prevent sunburns

-can cause GI distress

My Love Remix (Glaucoma Suspect)

2008-02-11T13:45:00.000-08:00

http://www.youtube.com/watch?v=OJMEfGFbFMI

AzaSite "pink eye" drop

2008-02-11T10:17:00.000-08:00

AzaSite 1% ophth soln (azithromycin)

recommended dosage: BID x 2 days, QD x 5 days (total of 9 drops vs. 21 other brands)

demonstrated prolonged high levels in ocular tissue

good for bleph/bacterial conjunctivitis/dry eye patients (exerts anti-inflammatory activity along with antibacterial activity)

Acetaminophen dosages

2008-02-11T10:09:00.000-08:00

Age:
>2 mo. (5kg): 80mg per dose
>4 mo. (6.5 kg): 100mg per dose
>6mo. (8kg): 120mg per dose
>12mo. (10kg): 160 mg per dose
>2 years (13kg): 200mg per dose
>3 years (15kg): 240mg per dose
>5 years (19kg): 280mg per dose

well-hydrated child: 15 mg/kg q4-6hrs
dehydration risk: 10 mg/kg q4-6hrs
maximum: 90 mg/kg/day (up to 4 grams daily)

Pyogenic granuloma

2008-02-07T14:14:00.000-08:00

benign vascular lesion of the skin and mucosa
appear as a fleshy red mass with relatively rapid growth
Histology: mixed acute and chronic inflammatory cells, with capillary proliferation in a lobular pattern (capillary hemangioma)
occurs most often in children and pregnant women and may occur close to the site of a minor injury
causes: usually associated with some inflammatory process such as a chalazion, severe blepharitis and meibomianitis, as a foreign body reaction or trauma such as surgery (pterygium excision, chalazia incision and drainage, placement of orbital implants, nasolacrimal duct probing with silicone tube placement, insertion of silicone punctal plugs, blepharoplasty, and eye muscle surgery).
in most cases, these lesions will resolve with topical steroid administration x2-3 weeks
surgical excision may be required for those lesions that fail to resolve after topical treatment
in rare cases malignant neoplasms such as Kaposi’s sarcoma may mimic pyogenic granuloma
recurrence following excision is extremely rare

CRAO

2008-02-07T12:30:00.000-08:00

Symptoms:

abrubt, painless vision loss (pain = OIS)
amaurosis fugax precedes visual loss in 10% of patients
men:woman = 2:1; mean age = 60; bilateral involvement = 1-2%

Findings:

VA 20/800 to LP (NLP = ophthalmic artery obstruction or temporal arteritis)
+APD
anterior segment normal (except if OIS, can have NVI)
ischemic whitening of the retina
cherry red spot at macula
ONH pallor with splinter retinal hemorrhages
20-25% demonstrate visible emboli

Differential diagnoses:

mild, nonischemic CRVO
neuroretinitis
hypertensive retinoathy

Sequelae:

after 4-6 weeks, retinal whitening dissipates, leaving optic nerve pallor
arterial collaterals
absent foveal reflex
RPE hyperplasia from stress to the RPE
NVI/NVG = 18% (make referal for panretinal laser photocoagulation)
after >100 minutes, complete irreversible loss

Causes:

Blood conditions: coagulopathies or poor blood flow, antiphospholipid antibody syndrome, protein S deficiency, protein C deficiency, antithrombin III deficiency
Systemic disease: 60% of patients have HTN, 25% have DM, 50% no cause identified
Heart disease: 30% have carotid artery disease; Refer patients (especially those <50> 50 y/o
Optic neuritis
Local trauma producing damage to the optic nerve
Radiation exposure
Behcet disease
Migraine
Syphilis
Optic disc drusen
Prepapillary arterial loops

Management:

350mg ASA, agressive digital ocular massage, topical beta blocker, oral Diamox 2 x 250mg (attempt to lower IOP to decrease resistance to nerve and retinal blood flow), breath into brown paper bag (stimulate rtinal arterials)
Labs:
CBC w/ differential and platelets
blood pressure
fasting BS
lipid panel
cholesterol
ESR (if yes, requires high-dose corticosteroid treatment)
CRP
HLA-B27
FTA-Abs
HIV
electrocardiogram with 2-D echo
transesophageal electrocardiogram
carotid doppler
MRI

msd Mini-Scleral Design (from Blanchard CL company)

2008-02-05T08:07:00.000-08:00

designed to vault the cornea and fit on the sclera/conjunctiva, reducing the net-vault of the contact lens over the cornea
reduction in the chance of irritation and better centering
keratoconus fits that dont center or dislodge with eye mvmt
irregular cornea fits
GP-intollerant patients (chronic awareness)
sagital depth of the CL
trial fit progressively deeper vaults until corneal clearance achieved
compression ring on conjunctiva after full day wear is ok
if mid-peripheral or limpal touch exists, increase the mid-peripheral zone of the lens to move the surface of the lens off the cornea
if mid-peripheral space b/w lens and cornea is too great (causing an air bubble), which may cause epithelial desiccation, decreasing the mid-peripheral zone will minimize these issues
small air bubbles in periphery that move during lens wear don't interfere with vision or cause epithelial surface drying

Tears Again Hydrate

2008-02-05T08:00:00.000-08:00

for dry eye, blepharitis, MGD
Rx only
omega-3 fatty acid, flaxseed oil, evening primrose oil, omega-6, bilberry extract
anti-inflammatory properties
4 soft gels daily, directly or during meals/snacks
avoid taking at the same time with other medications or supplements, or if pregnant/nursing
possible side effects: intestinal blockage, thyroid problems, may reduce blood vessel platelet aggregation (if you're taking ASA or blood thinners have your clotting time checked, may lower the seizure threshold in patients taking seizure meds

Visual Fields - documenting progression

2008-02-02T20:25:00.000-08:00

Glaucoma Progression Analysis (GPA)

change in the total deviation values over time may be due to factors other than glaucoma such as advancing cataract or decreased pupillary size.
by using the pattern deviation values, the GPA software specifically targets the localized change associated with glaucoma
If there were a diffuse component to the glaucomatous change, it would not be reflected in the GPA result, but the more likely localized component due to the formation of new glaucomatous defects or the expansion and deepening of existing defects would be characterized
change needs to be present in 3 consecutive visual fields before progression can be confirmed
if progression has occurred and there is a resultant change in therapy, the clinician should
establish a new baseline so that any additional progression can be found
if the patient undergoes ocular surgery or develops another ocular condition, new baseline
tests after he stabilizes should be selected for use in evaluating subsequent examinations

Mean deviation plot

gives the slope associated with change in the mean deviation
this change will include anything that affects the subject’s visual sensitivity, including advancing cataract, and that it may not reflect change due to glaucoma.

The GPA software will automatically assess the next visual field (and the next) to determine if that change is repeatable.
If it is present on two consecutive tests, a half-filled triangle will appear at the location
For repeatable change on three consecutive tests, a closed triangle will appear.
The GPA software then assesses the repeatability of three or more points and gives a plain-language report of “possible progression” if two consecutive fields show that
the same three or more points changed from baseline or “likely progression” if three consecutive fields show change at the same three or more points.

Retinal hemorrhages

2008-01-31T12:21:00.000-08:00

Subhyaloid and preretinal hemorrhages

located on retinal surface
subhyaloid hemorrhage is located b/w the posterior vitreous base and the internal limiting membrane (ILM)
preretinal hemorrhage is located posterior to the ILM and anterior to the NFL
"boat-shaped" with sharp demarcation line
obscure retinal features
tend to clear quickly without any sequelae
associated with pathology affecting the major retinal vessels or superficial beds
most common etiology: retinal neovascularization
other etiologies: PVD, retinal breaks, associated with the tearing of a mjor retinal vessel
less common etiologies: Terson's syndrome, retinal trauma, valsava retinopathy

Flame-shaped hemorrhages (NFL hemorrhages)

located within the NFL
flame shape is the result of the structure of the NFL
typically located in the posterior pole
tend to resolve within a 6 weeks
associated with retinal vasculature pathology affecting the superficial and peripapillary capillary beds
etiology: hypertensive retinopathy (AV nicking present), retinal vein occlusions, optic neuropathy (papilledema, NTG, anterior ischemic optic neuropathy)
Roth spot = flame-shaped hemorrhage that has a white or pale center; represent non-specific signs of blood dyscrasias (anemia/thrombocytopenia, anoxia, AV malformation, bacterial endocarditis, collagen vascular disease, diabetic retinopathy, HIV, HTN retinopathy, leukemia, multiple myeloma, trauma)

Dot-and-blot hemorrhages

located in the retina's inner nuclear and outer plexiform layers
configuration is due to intraretinal compression
take longer to resolve because they're deeper than flame-shaped hemorrhages
commonly associated with microvascular signs of edema
etiology: pathology affecting the prevenular capillaries -- diabetic retinopathy, idiopathic juxtafoveal retinal telangiectassis, vein occlusion and OIS
OIS: vascular insufficiency associated with carotid artery disease leads to ocular hypoperfusion --> not enough pressure to push blood from retinal arterioles to the venules --> increased capillary congestion results in a breakdown of the capilary walls with subsquent hemorrhage and edema --> venules attempt to compensate for the decreased blood flow by distending, giving them a dilated, but non-tortuous appearance

Subretina and subretinal pigment epithelium (RPE) hemorrhages:

located beneath the neurosensory retina and the RPE
sub-RPE hemorrhages are located b/w the RPE and Bruch's
exhibit a dark coloration with the retinal vessels clearly visible above
tend to have an amorphous shape, due to the absence of firm attachments b/w the neursensory retina and RPE, allowing the blood to spread
sub-RPE hemorrhages have well-defined borders attributed to the tight cell junctions among RPE
may be associated with neurosensory or RPE detachments in the posterior pole
tend to resolve slowly
may be associated with the functional and/or structural changes at the level of the photoreceptors (therefore, unfavorable prognosis)
most common etiology: CNV
other etiologies: choroidal tumors, trauma, retinal angiomatous proliferation
referal to a retinologist

Management

referral if needed
patients without systemic history need medical work-up (most common etiologies: HTN, DM; other: clotting disorders such as hemophilia or patients on warfarin)
fasting plasma glucose test (<100> 126 is indicative for diabetes)
HbA1c (normal <5%)
CBC with white cell differential (test for anemias, polycythemias, bleeding disorders, leukemias, infections)
prothrombin time (PT) and international normalized ratio (INR) -- evaluates clotting factors
OIS: work-up of above plus heart echo, carotid USG and/or Doppler color imaging to rule-out carotid or heart disease
in older patients (>60) -- ESR & C-reactive protein & temporal artery biopsy to confirm
in younger patients (18-40) -- at risk for blood dyscrasias, diabetes, HTN, hyperlipidemia -- obtain a serum lipid profile, consider antiphospholipid and anticardiolipin enzymes to determine whether they have antiphospholipid syndrome; ANA or double-stranded DNA testing to r/o Lupus; ANA & ESR screening test for autoimmune diseases and inflammatory conditions
other tests: HLA-B51, HLA-B27, HLA-B5, ELISA, Western-blot specific testing for HIV, Lyme disease, toxoplasmosis, tuberculosis
other tests: FTA-Abs and RpR to r/o syphilis
other tests: blood cultures to identify widespread infection (speticemia)

Retinal vasculature anatomy

2008-01-31T12:16:00.000-08:00

Retina blood supply from 1) retinal vasculature 2) choroidal vasculature

Carotid artery --> ophthalmic artery branch --> branches into the CRA (blood supply of the inner retina) --> branches in NFL to all quadrants except the foveal avascular zone
choroidal vasculature supplies nutrients and oxygen to the macula

Dry Eye -- Ocular Surface Disease Index

2008-01-31T08:29:00.000-08:00

http://www.agape1.com/Questionnaires/Ocular%20Surface%20Disease.pdf

http://www.restasisprofessional.com/documents/OSDI_PAD.pdf

Punctal plugs codes

2008-01-31T08:19:00.000-08:00

from: http://www.ocusoft.com/OcclusionTherapyRateCharts/CaiforniaRestofState.pdf

Diagnostic Codes used to characterize Lacrimal System Dysfunction:

Tear Film Insufficiency 375.15
Keratoconjuctivitis Sicca 370.33
Redness or Discharge 379.93
Pain in or around eye 379.91

1st VISIT (LO1) - Lacrimal EfficiencyTesttm with dissolvable Collagen / CollaSyn™ test plugs in upper and lower puncta

Occlude left upper punctum with test plug 68761-E1
Occlude left lower punctum with test plug 68761-E2
Occlude right upper punctum with test plug 68761-E3
Occlude right lower punctum with test plug 68761-E4
10 Day Post-Operative Period

2nd VISIT (LO2) - Non-Dissolvable or 6 Month Dissolvable VisiPlug™ Lacrimal Plugs in upper puncta, re-test lower puncta

Occlude left upper punctum 68761-E1
Occlude right upper punctum 68761-E3
Occlude left lower punctum with test plug 68761-E2
Occlude right lower punctum with test plug 68761-E4
10 Day Post-Operative Period

3rd VISIT (LO3) - 6 Month Dissolvable VisiPlug™ Lacrimal Plugs® in lower puncta

Occlude left lower punctum 68761-E2 3
Occlude right lower punctum 68761-E4 3

RELATED CPT CODES

Probing of canaliculi, with / without irrigation,Plug Repositioning or Removal (L04, L05) 68840
Dilation of punctum, with / without irrigation, Plug Removal (LO5) 68801
Probing of nasolacrimal duct, with / without irrigation, Plug Removal (LO5) 68810

Combigan

2008-01-29T08:31:00.000-08:00

brimonidine tartrate/timolol maleate 0.2%/0.5% (Allergan)

dual mechanism of action to lower IOP by reducing aqueous-humor production and enhancing aqueous-humor drainage/outflow
BID dosing
mean decrease from baseline IOP 4.4-7.6mm HG with Combigan (vs. 2.7-5.5 with brimonidine tartrate, vs. 3.9-6.3 with timolol)
maintained mean IOP throughout day better than individual gtts
mean daytime IOP was consistently <18>
systemic absorption helps to control for crossover effects of the drugs and controls for asymmetric fluctuations of IOP b/w right and left eyes
mean daytime decrease from baseline IOP was >20% in 42% of Combigan patients, 13% brimonidine, 27% timolol
lower incidence of conjunctival follicles compared to brimonidine (but higher than timolol group)
rate of discontinuation for adverse effects was 14% with Combigan (vs. 30.6 with brimonidine vs. 5.1% with timolol)
rate of allergic conjunctivitis was 5.2% with Combigan (vs. 9.4% brimonidine vs. 0.3% timolol)
contraindications: patients with bronchial asthma, sinus bradycardia, severe COPD, overt cardiac failure, cardiogenic shock, atrioventricular block

DLK after LASIK

2008-01-28T10:51:00.000-08:00

inflammatory cells (eosinophils, neutrophils, lymphocytes) that migrated underneath the LASIK flap
leads to collagenolytic activity that weakens the corneal structure and leads to stromal melting and ectasia
0.2%-5.3% incidence
occurs in both mechanical microkeratome and IntraLase procedures
usually due to bacterial endotoxins released from sterilizer reservoirs
can occur as soon as 24 hours after surgery or as a late-onset problem, occuring many months after surgery
increased risk: epithelial defects after surgery or patients who have atopic disease

Signs/symptoms:

symptoms may mimic dry eye
grainy appearance b/w the flap and underlying stromal bed
only mildly hyperemic conjunctiva
no ciliary flush like infectious keratitis
as severity increases, may cause decrease in VA, irregular astigmatism, ectasia, hyperopia

Treatment:

Pred Forte q1-2hour, follow-up every day until improves
topical fluoroquinolone tid prophylaxis if needed
cyclopentolate for pain
severe cases need referral back to surgeon to lift flap and irrigate the area with sterile balanced salt solution to remove inflammatory cells
severe cases oral prednisolone 40-80mg per day for at least one week

Corneal transplant examinations

2008-01-28T10:42:00.000-08:00

Signs/symptoms of graft rejection

redness
irritation,
light sensitivity
FBS
blurred vision
general inflammatory response (vascular dilation and transudation)
cellular infiltration -- sub-epithelial infiltrates ~0.5 mm scattered throughout the donor tissue only (respond to topical steroids)
tissue edema
stromal rejection -- neovascularization and stromal infiltrates
endothelial rejection -- KPs scattered across the endothelium or in a linear form advancing in from the peripheral cornea; causes edema of stroma and epithelium

GP fittings

2008-01-28T10:33:00.000-08:00

Diameter:

intermediate (8.6-9.2) --> Flat K
large (9.3-10.2) --> 0.50 flatter than flat K
small (8.0-8.5) --> 0.50 steeper than flat K

Adjust for corneal toricity:

steepen slightly if toricity is between 1.25D and 2.ooD
consider toric design if >2.00 corneal toricity

Misc

steepen the GP if the lens rides nasally or temporally
flatten the GP if it rides inferiorly
increase the optical zone and overall diameter if the GP rides superiorly

Piggyback fittings:

observe for excessive apical bearing or superior alignment with seal off of a GP (results in a "swirl staining")
select high-DK silicone hydrogels

OHTS findings

2008-01-27T16:28:00.000-08:00

OcHTN patients:

At 5 years: observation group = 9.5%, treatment group = 4.4% developed glaucoma
At 7 years, observation group = 13%, treatment group = 4.4% developed glaucoma

Risk factors for developing POAG identified:

advanced age
race (the prevalence of glaucoma is higher in blacks than in whites)
sex (male)
larger vertical cup-to-disc ratios
greater pattern standard deviation on Humphrey visual fields
thinner central cornea measurements.

Other risks factors:

IOP fluctuation and Diurnal curves -- peak IOP at night
systemic disease
optic nerve hemorrhages
PPA
zone alpha -- further from the disc; chorioretinal/pigment crescent
zone beta -- adjacent to disc; scleral crescent (more associated with glaucoma)
sleep apnea
high myopia (structural changes make it hard to evaluate nerve shape)

Glaucoma risk calculators

2008-01-27T16:18:00.000-08:00

Devers:
http://www.discoveriesinsight.org/grc_web/grc.cfm

WashU:
http://ohts.wustl.edu/risk/calculator.html

American Academy of Ophthalmology definition of glaucoma:
"A multi-factorial optic neuropathy in which there is characteristic acquired loss of retinal ganglion cells and atrophy of the optic nerve."(This definition allows for the presence of glaucoma in the absence of visual field loss, and does not even address IOP. )

NTG = 1 out of 6 POAG patients