Sudden Vision Loss Flashcards
MOA of digitalis
NAK blocker
Increased CA2+ in heart
Can block PR NAK channels-entopic phenomenon
Can block NAK on NPCE-decreased IOP
LASIX MOA
Looses K+
Hypokalemia
CRVO
The CRV drains blood from the retina, on occlusion in this vessel results in a build up of blood within the retinal veins, resulting in extensive intraretinal hemorrhages extending towards the periphery in all 4 quadrants
CRVO stats
Prevalence of 0.1-0.4% in the general population (mostly 60-80s); they are the 3rd most commonly vascular cause of vision loss (1. DR, 2.BRVO). Appx 7% of patients will eventually have a CRVO in the fellow eye
Risk factors for CRVO
HTN
DM
Cardio disease
Open angle glaucoma
Open angle glaucoma and CRVO
POAG is the ocualr disease that is most commonly associated with CRVOs; 40-60% of patients with CRVO also have a diagnosis of POAG
Etiology of CRVOs
Compression of an artery on a vein; this causes turbulent blood flow, with subsequent venous vessel wall damage and thrombus formation
- thrombus formation results in eternal ischemia and the release of VEGF, leading to the classic retinal signs of retinal hemorrhages in all quadrants, collaterals, dilated tortuous retinal veins, CWS, and optic disc edema
Vision threatening complications of CRVO
Macular disease and complications from neo. VEGF stimulates neo of the anterior and posterior segment, and has also been proven to cause capillary leakage leading to macular edema
Treatment for neo in CRVO
PRP
Treatment of mac edema in CRVO
AntoVEGF
Macular diseases from CRVO includes
Macular ischemia
Macular edema
Intramacular hemorrhages
What is the leading cause of vision loss in CRVOs
Mac edema
Neo complications in CRVO
Results in NVG, pre-retinal or vitreous hemorrhage, and TRD
NVG
Significant concern in patients with CRVOs. It is most likely to develop within the first 3 months of Dx (90 day glaucoma), but may develop anywhere from 2 weeks to 6 months after the inital diagnosis. 60% of ischemic CRVOs develop iris neo, and 33% develop NVG. 6% of nonischemic CRVOs develop iris rubeosis or angle neo
Ischemic CRVO
10DD or more of capillary non perfusion on FA. 90% of cases present with 20/200 vision or worse, and the prognosis is poor (final BCVA of CF or worse)
Non-ischemic CRVO
Assocaited with a better prognosis compared to patietns with ischemic CRVOs; 16% of non ischemic progress to ischemic
Papillophlebitis
Described as a 3rd category of CRVOs; characterized by marked optic disc edema in an otherwise healthy young patient
FU for CRVO patients
Q1 month for 6 months, do gonio every time
Risk factors for BRVO
HTN DM Heart disease POAG And increased BMI (diff from CRVO)
Main culprit in BRVO and CRVO
Thrombus
Main culprit in CRAO and BRAO
Embolus
FU for CRAO
Refer to MD ASAP to check heart and carotid. Acute CRAO=MRI, possible stroke
BRVO stats
Most common retinal vascular occlusive disease; pts have a similar health histroy compared to CRVOs.
Etiology of BRVO
Thrombus at an AV crossing; 60% occur at AV crossing within the ST quadrant
BRVOs that do not occur at AV crossing
Should be evaluated for vasculitis, retinal arteries and veins share a common adventitia at AV crossings, allowing thickened arteries to compress the veins, resulting in occlusion
Signs of BRVO
Occur in the area of distribution of the occluded vessel and include dilated tortuous veins,CWS, collateral vessels, an intraretinal hemorrhages (confined to one quadrant).
Vision threatening complications of BRVOs
Mac disease (ischemia, edema, hemorrhages) Neo (pre-retinal or vitreous hem)
BRVO prognosis
Better compared to CRVO; 55% of pts with BRVO will have 20/40 vision or better at 1 year after the inital diagnosis
Presentation of artery occlusion
Ischemic and edematous white retina due to lack of blood supply to the retina
CRAOs prestn with retinal infarction in all 4 quads
BRAO present with retinal infarction in the area of distribution of the occluded retinal vessel
Retinal edema eventually resolves and the retina gradually returns to its normal color (within weeks to months); however, the retina is still permanently damaged
CRAO stats
Elderly patients, there is a 10% risk of a CRAO occurring in the fellow eye, risk factors include HTN, DM, carotid occlusive disease, cardiac valve disease
Symptoms of CRAO
Visual blackout and/or blur (amaurosis fugax) and transient ischemic attacks (TIAs) prior to the CRAO. They typically present with painless loss of vision to 20/400, unless a cilioretinal artery is present.
Cioloretinal artery
Branches from the SPCA of the choroid to supply the macula, allowing the macula to remain functional in a CRAO
If you suspect a CRAO in someone who’s VA is light perception or worse, what should you consider
Ophthalmic artery occlusion (results to ischemia to the retina AND the choroid)
Signs of CRAO
Superficial whitening of the inner retinal layers due to ischemia, acute CRAOs also present with narrowed retinal arteries, a cherry red macula (visibility of the underlying choroid), and an APD (optic nerve pallor due to orthograde degeneration of retinal ganglion cell axons). Hollenhurst plaques or other emboli are visible in 20-40% of cases
NVG and CRAO
Rare, only 5% of pts develop iris neo and NVG
TIAs
Always less than 24 hours, usually less than 15 minutes. Temporary pauses of brain activity due to inadequate perfusion; as perfusion is restored, patietns are left with no symptoms
What type of plaques cause CRAOs
Calcific
What type of plaques case BRAO
Hollenhurst
There is a ___risk of a BRAO occurring the fellow eye
10%
Symptoms of BRAO
Asymptomatic or a VF defect if the area of the occlusion is close to or involving the macula. 90% of cases involve the temporal retinal arteries, and hollenhurst plaques or other emboli are visible withi nthe area of occlusion in 62% of cases
AAION
Due to occlusion of the SPCA, resulting in infarction to the anterior optic nerve and optic disc edema. It classically presents in patients older than 55 years of age. Swollen unilateral nerve in older patients
Symptoms of AAION
Sudden unilateral vision loss with associated systemic sotptoms including jaw claudication, neck pain, anorexia, temporal headaches, scalp tenderness, a tender nodular temporal artery, and malaise/myalgia
Where is the thrombus formation in a CRVO usually located
Lamina cribrosa
CRVOs in young patients etiology
Oral contraceptives Protein s/c/antithrombin III deficiency Factor 12 deficiency Antiphospholipid Ab syndrome Collagen vascular disorders Papillophelbitis AIDS
If an emboli is not noted on exam, what are some other causes of CRAO
GCA Acute elevation in IOP Collagen vascular disease IV drug use Oral contraceptives Sickle cell disease Syphilis
The most common cause of AAION is
Giant cell arteritis
-systemic vasculitis that affects the medium and large sized blood vessels. Remember that AAION secondary to GCA is an ocular emergency. Vision loss can occur quickly in the fellow eye
Final VA in someone with CRVO
Typically similar to VA on initial presentation.
What are collaterals
Part of the normal fetal vasculature that is present at birth they connect retinal veins to one another. They are usually clear (and invisible) because there is no blood flowing through them, but they become visible in retinal vein occlusions as blood is shunted from the retina veins through the collateral vessels and into the choroidal circulation. Collaterals are visible in 50% of patients with CRVO (often months after initial diagnosis)
Why do we get retinal neo
In response to the release of VEGF by the ischemic nerve fiber layer of the retina. It grows in the preretinal space between the ILM and the posterior hyaloid face. Neo lacks right junctions between the endothelial cells, leading to rpe-retinal and/or virtuous hemorrhages. Neo traction on the retina may also result in a TRD
Causes of preretinal neo
DRVOS
- DR
- ROP
- retinal vein occlusions
- OIS
- sickle cell
FU for CRVO patients
Followed every month for 6 months, with gonio at each visit. Patients should be evaluated for underlying medical conditions, such as HRN, DM, and CHF. Blood tests may hep to determine the etiology; patients should also be referred for treatment of any underlying systemic conditions.
Treatment of neo from CRVO
The Central Retinal Vein Occlusion Study (CRVOS) demonstrated the following
- if rubeosis (>2 clock hours of iris involved), angle neo, NVG, or any posterior segment neo develops, PRP is indicated
- prophylactic PRP in the absence of neo is NOT beneficial
Treatment of ME in CRVO
The Central Retinal Vein Occlusion Study (CVOS), Standard Care vs Corticosteroids for Retinal VEin Occlusions (SCORE) study, CRUISE study, and COPERNICUS study provide evidence for how to treat ME secondary to CRVO
CVOS study
Demonstrated that focal laser photocoagulation of the macula does NOT improve VA in patietns with ME secondary to CRVO
SCORE study
Demonstrated that 1mb intravitreal triamcinolone improves CA in patietns with ME secondary to CRVOs. Triamcinolone injections were given every 4 months unless treatment was deemed a success (flat macula, VA20/25 or better, or OCT central retinal thickness <225um)
- 27% of patients who received 1mg triamcinolone injection experienced an improvement in VA by 15 letters or more after 12 months, compared to only 7% who received sham injection
- the Abel sure rusk reduction is 20% and the number needed to treat is 5.
CRUISE trial
Demonstrated that 0.3mg or 0.5mg intravitreal lucentis dosed every 6 months improved VA in patients with ME secondary to CRVOS
- after 12 months of follow up, an improvement of 3 or more lines in VA was observed in 46% of patietns receiving 0.3mg lucentis, 48% of patients receiving 0.5mg lucentis, and 17% of patients in the sham injection group
- the ARR is appx 30% and the NNT is appx 3
COPERNICUS trial
Demonstrated that 3mg Eyelea dosed every month for 3 months, then PRN, improves VA in patients with ME due to CRVOs
- after 12 months of FU, an improvement of 15 ore more letters in VA occurred in 59% of patietns who received 2mg eyelea, compared to only 23% of patietns in sham injection
- the ARR is 36% and the NNT is appx 3
CRVO studies condensed
CVOS -focal laser doesnt help ME -prophylactic PRP does not prevent neo -PRP indicated for presence of neo SCORE -steroids CRUISE -CRVO, AntiVEGF COPERNICUS -variation of VEGF dosage
Fu for BRVO patients
Patients should initially be followed very 1-2 months and then ever 3-12 months thereafter; patients should be carefully evaluated for the development of ME and neo. Similar to pts with CRVO, pts with BRVOs should be evaluated for any underlying systemic etiologies. Remember the check BP in office
BVOS
BRVO
Sector laser photocoagulation in area of neo
Did not evaluate benefit of prophylactic laser
BRVO studies condensed
BVOS -sectoral laser for neo SCORE -steroids BRaVO -antivegf VIBRANT/MARVEL -antivegf dosing
BVOS for ME
Pts with persistent ME (>3 months) secondary to BRVO and a VA of 20/40 or worse benefit from focal laser photocoagulation to the macual
Score study for BRVO
Simialr benfits in the reduction of macular edema and the improvement of VA with intravitreoual triamcinolone injections compared to focal laser photocoagulation; however, the side effects of triamcinolone led the authors to conclude that focal laser photocoagulation of the macula is the best treatment for ME secondary to BRVO
BRAVO trial
- 3mg and 0,5mg lucentis, dosed every month for 6 months improved VA in patietns with ME secondary to BRVO
- after 12 months, an improvemebt of 3 or more lines of VA was observed in 55% of patietns who relieved 0.3mg lucentis, 61% of patients who received 0.5mg lucentis, and 29% sham
VIBRANT study
BRVO
- 2mg eyelea dosed monthly for 24 months, then every 8 weeks for an additional 24 weeks is superior to laser photocoagulation for the treatment of ME secondary toBRVO
- after 52 weeks, an improvement of 15 or more letters (3 or more lines of VA) was observed in 57% of pts in the eyelea group, compared to 41% of pts in the laser group
MARVEL study
BRVO
-lucentis and avastin monthly injections result in a similar improvement in the VA and decrease in macular thickness after 12 months
Treatment of CRAO and BRAO
Controversial and ineffective, but might provide some benefit if the macula is involved and hte pt presents within 24 hours of the onset of vision loss (best case scenario is within 90m). The overall goal of tax is to remove the embolus as far distially as possible in other to restore retinal arterial blood flow. Options include
- digital ocular massage
- admission to hospital for carbogen therapy
- hyperbaric oxygen chamber therapy
- IOP lowering drugs in order to improve retinal perfusion pressure
In older patietns with CRAO without acutely elevated IOP or visible embolus, strongly consider ordering an ESR and CRP to r/o GCA. Oral contraceptives should be DCed in younger patients
What should be done with patients with retinal emboli and/or retinalartery occlusions or ophthalmic artery occlusions?
Evaluated with an urgent CT or MRI, a carotid Doppler and cardiac studies (EKG and echo) to r/o an acute cerebral infarction, carotid artery disease, and cardiac disease. Studies say that appx 24% of patients with an acute retinal ischemia secondary to a CRAO or BRAO also have an acute cerebral infarction
Treatment of AAION
Evaluated immediately with an STAT CBC, ESR, and CRP; high dose oral prednisone should also be initiated
