• It is a true medical emergency !!!
  • acute presentation
  • requires immediate Tx
• Pt outcome and morbidity depends on what you do and how fast you do it:
  • Rapid Dx, immediate intervention; follow up and referral

• At least 2 of the following symptoms:  unilateral
  • Ocular pain
  • Nausea / vomiting
  • Intermittent blurry vision w/ halos
• At least 3 of the following signs:
  • IOP > 21 mmHg
  • Conjunctival injection
  • Corneal epithelial edema
  • Mid-dilated nonreactive pupil
  • Shallow ant. chamber in the presence of occlusion

• Classic presentation w/ sudden onset: periorbital pain, visual defects --- "halo’s around objects"
• Extraocular or Systemic complains:
• Headache: migranes; subarachnoid hemorrhage
• Nausea and / or vomiting: +/- abd. pain; gastroenteritis

• Basic Eye Exam: visual acuity, external eye inspection, visual fields, a funduscopic exam, pupils, ocular motility; and IOP
• Findings:
• Blurred vision: inability to identify numbers and letters; peripheral vision decresed
• Cornea and sclera injections
• Edematous and cloudy “steamy” cornea --- obscured funduscopic exam
• Globe is firm to palpation
• Tonometry reveals an ↑-ed IOP !!!!     NML = 15  !!!!

Potential causes of

Acute Angle-Closure Glaucoma:

• Sympathomimetics: ephedrine; cocaine
• Anticholinergics: Atropine; Scopolamine
• Mydratic and Cycloplegic agents: Tropicamide (Mydriacyl), Cyclopentolate (Cyclogyl)
• Walking into a dark room: already narrowed Ant. chamber w/ sudden papillary dilation
• Antidepressant meds:
• SNRI (Serotonin-Norepinephrine Reuptake Inhibitor): Duloxetine (Cymbalta); Venlafaxine (Efflexor)
• Tricyclic antidepressants: Amitriptyline (Elavil)

Describe

Open-Angle Glaucoma (Chronic Glaucoma)

• Gradual and progressive loss of bilateral peripheral vision
• can lead to complete blindness if uncorrected  
• secondary to decreased arterial flow to the retina
• Decreased drainage of aqueous thru the trabecular network creating an increased IOP

Describe 2 types of

Chronic Glaucoma (Open-Angle Galucoma)

• Primary Open-Angle Glaucoma (usually bilateral, but unilateral occurs)--- increased risk:
• Family History in 1^st degree relatives; DM; African American pop-n has ↑ risk at earlier age w/ more sever damage
• Secondary Open-Angle Glaucoma – causes: Uveitis, Trauma; Corticosteroids

Presentation of a patient with

Chronic Glaucoma (Open-Angle Glaucoma)

• Pts are asymptomatic and identified during a routine eye exams
• Maintain a high degree of suspicion:
  • Pt > 40 yo;  DM, Afr. –Amer. pop-n; vision changes

• Acetazolamide PO
• Topical beta-blockers (timolol) to lower IOP
• Osmotic diuretic (Mannitol)
• Topical Pilocarpine - for miosis, drainage of aqueous humor to lower IOP
• Laser iridotomy

Tx for Chronic Glaucoma

(Open-Angle Glaucoma)

Obtain a decrease in IOP thru the use of :

Medications:

-          Prostaglandin analogs: increase aqueous drainage

-          Β-blockers: reduce production of aqueous humor

Surgery

-          Laser trabeculoplasty --- adjunct therapy w/ meds

-          Trabeculectomy --- std surgery of choice

• Gradual painless changes “cloudiness” of the lens
• Cataracts block and distort light passing thru the lens, causing visual symptoms and complaints.
• A common process involved during aging --- commonly occur bilaterally but unilateral presentations also occur

What is Retinal Detachment?

separation of the inner layers of the retina from the underlying retinal pigment epithelium

• Rhegmatogenous RD - most common; a hole/tear/break in the neuronal layer allowing fluid from the vitreous cavity to seep in bw and separate sensory and RPE layers (ie. Spontaneous or traumatic)
• Tractional RD – traction from inflammatory or vascular fibrous membrane on the surface of the retina, which tether to the vitreous (ie. SCD, Retinopathy)
• Exudative or Serous Rd – exudation of material into the subretinal space from retinal vessels such as a HTN, central retinal venous occlusion, vasculitis or papilledema (ie. Tumor or inflammation)

Sensation of a flashing light (photopsia) – related to retinal

                   traction and separationof the post.erior vitreous

Shower of floaters

Vision loss (late onset)

- Over time, the pt may report a shadow in the peripheral visual field

          (may spread rapidly (days) to involve the entire visual field)

- Vision loss may be filmy, cloudy, irregular, or “curtain-like”

Visual acuity

External exams: puillary findings, visual field eval

Funduscopic exam

Slit –Lamp Exam

IOP assessment

• Laboratory - not generally helpful unless for confirmation of Dx
• Radiologic:
• CAT Scan/MRI - helpful in the eval of foreign bodies /tumors; not necessary for Dx
• Ultrasound:
• Helpful if the retina cannot be visualized bc of corneal changes, cataracts or hemorrhage
• Has the ability to detect an differentiate multiple etiologies

General Care: Protect the globe; Cover w/ goggles or ocular shield; Treat underlying emergent conditions

Definite Tx: surgical repair dependent upon type, location, and size of the detachment:

Laser, intraocular gas, intraocular surgical repair

• The progressive deterioration of bilateral central vision
• Leading cause of permanent vision loss in the pts >50
• Most common pt profile: caucation female w/ a previous or current Hx of cigarette smoking
• Age-related Maculopathy – develops prior to the onset of age related macular degeneration --- retinal drusen (hard, soft)

• Atrophic degeneration “dry” -  
  • gradual progressive loss of bilateral vision
  • Increasing blurriness of printed words , dfficulty recognizing faces
• Exudative degeneration “wet” – a more abrupt onset and severe onset of vision loss:
• Visual  distortion; straight lines appearing crooked
• Decrease of loss of central vision

Hx and PE      

Amster grid ocular eval

Fluorescein angiography

Photocoagulation;

PDT (photodynamic therapy);

Macular translocation Tx ,

anti-vascular endothelial growth factor

*****************************************************

***  no definitive treatment identified ***

Current treatments are directed at stopping further degeneration

difficulty  correcting what has already been affected

Describe Central Retinal Vein Occlusion

what are the 2 categories?

occlusion of the final retinal vwin at the optic nerves

sudden, painless, non-erythemic loss of monocular (unilateral) vision

Nonischemic RVO (venous stasis retinopathy)

              potentially benign and self-limited; usually a good visual outcome  

              presents w/ a more gradual onset

Ischemic RVO (hemorrhagic retinopathy) carries a poor visual prognosis  Account for a quarter of RVO cases overall 

              Acute (sudden) presentation

Describe Virchow's Triad

(Central Retinal Vein Occlusion)

-          Venus stasis – external compression, hypotension, immobility

-          Endothelial damage – inflammatory processes

-          Hypercoagulable state – deficiencies dysfunction

HTN,

DM,

Glaucoma,

Anemia,

Hyperviscosity syndrome (neoplasms, SCD anemia)

Central Retinal Vein Occlusion

PE

• Retinal hemorrhages – peripheral hemorrhages appear 1^st
• Cotton wool spots – deep focal retinal ischemia
• Decreased visual acuity – more common in ischemic presentation
• Dilated, tortuous retinal veins
• Edematous optic disk

What are S/S and Tx for

Branch Retinal Vein Occlusion

(blockage of the portion of the circulation that drains the retina of blood)

• Sx/SnS – blurred vision; loss of visual fields
  • (corresponding to the distribution of the obstructed vein)
• Tx:     
  • Systemic corticosteroids -  reduction of macular edema   
  • Laser Photocoagulation

Describe Retinal Artery Occlusion

"Ocular Stroke"

is it an emergency?

painless loss of monocular (unilateral) vision.

It is a true emergency  !!!

only 20% of pts having a return of NML vision

Retinal Artery Occlusion

Funduscopic findings:

• Pale retina --- 2’ to lack of perfusion
• “Cherry-red” macula -- thinnest part of the choroid is still perfused w/increased blood supply from the ciliary artery

• Supine osition to maintain optimal perfusion
• High flow supplemental oxygen
• Acetazolamide (Diamox) IV --- decreased IOP
• Thrombolytic drug administration --- mixed results

Describe Amaurosis Furax

• brief, acute attack of partial or total vision loss lasting from seconds to minutes.
• Pt may describe the “attack” as the gradual pulling of a curtain (transient, not permanent), blurring, fogginess, or a dimming vision
• Ischemia is the most common mechanism of acute visual dysfunction and it can affect any aspect of the visual system

Amaurosis Fugax

PE

• Visual acuity, external eye exam, funduscopic eye exam
• Slit-lamp exam, fluorescein staining, IOP determination
• Complete Cardiovascular exam
• Complete pulmonary exam
• Complete neurovascular exam

• Risk reduction
• Antiplatelet drugs: Daily ASA; Clopidogrel (Plavix), eptifibatide (Integrelin)
• Surgical approach to stenoic vessels

• leading cause of blindness in adults and present in 40% of diagnosed diabetics
• Poorly controlled BS = ↑ retinopathy
• Type I Diabetes (IDDM) – not detectable until 3 yrs s/p initial Dx
• Type II Diabetes (NIDDM) – present in 20% of pts upon initial Dx

• Non-proliferative (easier to treat) – clinical findings of venus dilation, microaneurysms, retinal hemorrhages and edema, and hard exudates
• Proliferative (worse) – neovascularization arising from the optic disk w/ the presence of vitreous hemorrhage (more significant type w/ a worse prognosis)

Diabetic Retinopathy

PE Findings

• Microaneurysms
  • Ealiest clinical sign of diabetic retinopathy – 2’ to capillary wall out pouching d/t pericyte loss
  • Appear as small red dots in the superficial retinal layers
• Cotton Wool spots – capillary infarction
• Macular edema: Leading cause of visual impairment in pts w/DM;  D/t functional damage and necrosis of retinal capillaries