Glaucoma- Primary Angle Closure Flashcards
Mechanisms of PACG
Pupillary block where the lens contacts the iris at pupillary margin
Plateau iris as an anatomical defect
General information about PACG
Normal/high IOP with no subacute attacks or normal/high IOP with infrequent AACC
Characteristics of AACC
Wild IOP fluctuations (≤80mmHg), rapid vision damage, typically unilateral
Prodrome of AACC
Can be caused by rapid mydriasis
Halo around light, edematous cornea, pain, headache, N/V
Risk factors for PACG
Shallow anterior chamber depth, Eastern Asian ethnicity, family history, far-sightedness, age
Subacute attacks characteristics
Usually self-limiting, vary by the patient’s pain threshold and awareness and relieved by sleep or miosis (bright light or induced)
What happens if a patient has AACC?
TELL THEM TO GO TO THE ER
Goals of PACG treatment
Medically break the attack quickly to preserve vision and prep the eye for laser peripheral iridotomy
Which eyes should you treat in AACC?
BOTH EYES
First-line treatment for AACC
Carbonic anhydrase inhibitor, topical beta-blocker, topical alpha agonist, pilocarpine
Carbonic anhydrase inhibitor used in AACC treatment
500mg acetazolamide IV* or PO
IV decreases IOP in ~2 minutes with peak effect in 10-15 mins; PO has 2 hour onset
Topical alpha agonist used in AACC treatment
Topical apraclonidine
Pilocarpine ADEs
Spasm, headache, brow ache, lid twitch
Second-line therapies for AACC
Hyperosmotics and ophthalmic steroids
Hyperosmotics used in AACC
PO glycerin or isosorbide 1-2g/kg
IV mannitol 1.5-2g/kg (works the fastest)
