Glaucoma E2 Flashcards
Normal IOP Range/Elevated IOP
Normal: 13-21 mmHg
Elevated: 21 mmHg
Dx?
Glaucomataeous Changes + Normal IOP
Normal-Tension Glaucoma
Dx?
Glaucomatous Changes + Elevated IOP
Glaucoma
Dx?
No Glaucomatous Changes, but elevated IOP
Ocular Hypertension
What are the two outflow pathways for aqueous humor? Which one is IOP dependent?
- Trabecular/Schlemm’s Canal (90% of outflow) –> IOP Dependent
- Uveoscleral (10% of Outflow) –> IOP Independent
In what three situations should we treat patients with the therapies covered in this section?
- Glaucoma Diagnosis (GC and Elevated IOP)
- Ocular Hypertension and Risk Factors
- N-T Glaucoma and documentation of progression of visual field loss.
Goals of Glaucoma Treatment ( how much do we want to reduce IOP by in ALL patients).
- Preserve the Nerve “Stabilize the visial fields”
- Lower IOP (at least 25% pretreatment value) –> Reassess based on clinical progress or if the goal is not achieved.
Primary Open-Angle Glaucoma Risk Factors
- Elevated IOP
- Age >60 (40 if black)
- Family Hx
- Ethnicity (black/Hispanic)
- Increased cup to disc ratio
- Thin Central Cornea Thickness
- Low Ocular Perfusion Pressure (SBP/DBP minus IOP)
- TIIDM
- Myopia
Risk Factors of POAG Progression
- High IOP at baseline or increased at follow-up.
- Older age
- Disc hemorrhage
- Large Cup to Disc Ratio
- Thin Central Cornea
- Low Ocular Perfusion Pressure
- Low Adherence to meds
- Progression in fellow eye.
Benefits/Risks of Surgery for POAG
Benefits: More effective, few complications
Risk: Increased cataract risk, and increased risk of loss of visual acuity.
Benefits/Risks of Medical Treatment for Glaucoma
Benefits: Less invasive, Low cataract risk, better visual acuity stability.
Negatives: Daily for life.
Mechanism of Prostaglandin Analogs
Increase Scleral Permeability –> Reduces IOP by 25-35 %.
Prostaglandin Analog Contraindication
Existing Ocular Inflammation
Omnidepag Mechanism; How does it increase outflow?
EP2 receptor Agonist–> increases trabecular and scleral outflow.
non-inferior IOP reduction compared to latanoprost or timolol.
Similar ADE to Prostaglandin analogs but less ocular irritation.**
Prostaglandin Analog ADEs
Hyperemia
Hypertrichosis (eyelash growth)
Iris Pigmentation
Preferred Prostaglandins
Bimatoprost
OR
Latanoprost Bunod
Prostaglandins with the least ADEs
- Omnedepag
- Latanoprost Bunod
- Latnoprost
Ocular Beta-Blocker Mechanism
Decrease production of AH –> 20-25 % reduction in IOP.
All equally efficacious
- Preferred Beta-Blockers
- BB w/ least ADE
Preferred = Timolol or Levobunolol
Least ADEs = Betaxolol or Cartelol
BB ADE
- Local Irritation
- Systemic Symptoms ( Cardiac/Pulmonary/CNS)–> Minimized w/ proper administration.
- Tachyphylaxis (diminishing effect)
Ocular BB Contraindications
- Sinus Bradycardia
- Heart Block
- Heart Failure
- Pulmonary Disease
Brimonidine Mechanism; How does this lead to a reduction of IOP.
Alpha-2-agonist
*Decreases AH production –> Leads to 20-25% IOP reduction.
*May have a neuroprotective effect
Brimonidine ADEs
- Local Irritation
- Systemic (Drowsiness, Xerostomia)
- Tachyphylaxis
Precaution = CVD
Which is preferred and why:
Brimonidine/Timolol or Latanoprost
Latanoprost Preferred due to price
Carbonic Anhydrase Inhibitor Mechanism
How are topical agents different
Inhibit Carbonic Anhydrase leading to a decrease in AH production by the ciliary body by decreasing bicarbonate secretion.
Topical Agents = Specific for CA-2
CAI Oral vs Topical Efficacy
Oral Agents = 20-30% IOP reduction
Topical = 15-20% reduction
Oral CAIs
Acetazolamide
Metazolamide
Topical CAIs
Brinzolamide
Dorzolamide
Preferred CAI combination product
Preferred = Dorzolamide/Timolol (similar efficacy to latanoprost, better diurnal control than brimonidine)
Alternatives = Brinzolamide/Brimonidine
Rhopressa [Netarsudil] Mechanism. Explain how this reduces IOP.
Rho Kinase Inhibitor –> Decrease actin-myosin contractions which leads to an increase in trabecular outflow.
*20% IOP reduction if <27 mmHg. However, more pronounced effect at higher IOPs.
Rhopressa ADEs
HIGH INCIDENCE
*53% hyperemia
*20% Conjunctival Hemorrhage
Open-Angle Glaucoma First Line Agents
Preferred = Prostaglandins
Alternative = Beta-Blocker
Use as few drugs as possible at the lowest effective dose
educate on lacrimal occlusion to prevent systemic side effects
Open-Angle Glaucoma Second Line Agents
- Brimonidine
- Dorzolamide/Timolol
- CAIs
- Netarsudil/Omnidenepag
How frequent should you schedule follow up for open-angle glaucoma patients under the following situations:
- Disease Progression?
- No progression, IOP met for 6 + months
- No progression, IOP met <6 months
- No progression, IOP goal not met.
- 1-2 months
- 6-12 months
- 6 months
- 3-6 months
When should you treat Ocular Hypertension?
If they have risk factors including:
ethnicity, family history, thin central cornea, large cup to disc ratio, IOP >25.
When should you treat a patient with normal-tension glaucoma?
If they have documented the progression of visual field loss.
What is the main pathophysiology of Primary-Angle Closure Glaucoma
- Pupillary Block –> Lens contact iris at the pupillary margin. or “Iris bombe” where the iris bows and contacts the trabecular meshwork.
- Plateau Iris –> “Less Common”
*Anatomical Defect of the ciliary body
*Typically Unilateral
Primary Angle-Closure Glaucoma Clinical Presentation
*Unilateral
*Rapid IOP Fluctuations (up to 80 mmHg)
*Rapid Vision Damage
PACG RF
- Shallow Anterior Chamber Depth
- Eastern Asian Ancestry
- Family History
- Hyperopia
- Age
Subacute vs Acute PACG Attacks
- Subacute–> Self Limiting (vary by pain threshold of the patient. Relieved by sleep or miosis.
- Acute “AACC”
Signaled by prodrome
Caused by rapid mydriasis
Halo around light
Edematous Cornea
Pain, HA, N/V
Ophthalmic Emergency
PACG Treatment Goals
- Preserve Vision (Decrease optic nerve damage)
- Prep Eye for Laser Peripheral Iridotomy (decrease IOP, inflammation, and open the angle)
Agents used to reduce IOP in PACG
- Carbonic Anhydrase Inhibitors (IV Preferred) –> Acetazolamide 500 mg IR
- Topical Beta-Blocker
- Topical Alpha Agonist –> Apraclonidine Preferred
No prostaglandins–> Take too long
What CAI is preferred in PACG?
Acetazolamide 500 mg IR IV
What alpha agonist is preferred in PACG to reduce IOP?
Apraclonidine
What agent is used in acute PACG to open the angle?
Pilocarpine
How does Pilocarpine work?
It induces myosis, pulling the iris away from the trabecular network.
This prevents ciliary body thickening.
It also can cause vascular congestion, cholinergic crisis, spasm, brow ache, headache, and lid twitch.
What agent is used in acute PACG to address inflammation?
Ophthalmic Steroids.
In acute PACG, when are hyperosmotics used?
When anti-secretagogues and pilocarpine have no effect after 1 hour.
These cause the quickest and largest reduction in IOP.
How do hyperosmotics work?
They reduce vitreous volume significantly leading to a quick and large IOP decrease.
What are the oral hyperosmotics?
- Glycerin (1-2 g/kg)
- Isosorbide (1-2g/kg)
What is a risk of using glycerin?
Ketoacidosis in TIIDM
What is an IV hyperosmotic?
Mannitol (1.5-2 g/kg)
What is the risk of using mannitol?
Circulatory overload risk
What is the goal of PACG treatment? What three things are we targetting?
Lower IOP, Open the Angle, Maintain a miotic Pupil.
After initial treatment for PACG, when should clinicians follow up on the patient?
- Check IOP q 15-30 minutes
- Check angle when IOP drops into normal range.
In the management of acute PACG, what should be done 1 hour after initial treatment?
- Give hyperosmotic if needed for high IOP
- Repeat First Line Medications
- Add steroid as needed for inflammation
How is chronic PACG managed?
Keep the angle open to reduce the risk of attack
Managed similar to Primary Open-Angle Glaucoma.
First Line = Prostaglandin Analogs or Beta-Blockers
May also perform Iridotomy
