Retinal hemorrhages

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

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

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


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

Punctal plugs codes

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

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

• 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

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

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

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

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