Primary angle-closure glaucoma

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Presentation transcript:

Primary angle-closure glaucoma Sartaj Sandhu

Outline Case study: Mrs. LH Glaucoma: a sight-threatening condition Who is at risk? How can glaucoma present to ED? Diagnosis and treatment Outcomes and disposition

Case study: Mrs. LH Presenting complaint 52 years old female of Asian b/g p/w sudden onset RIGHT eyebrow pain/headache, blurred vision, nausea and vomiting Further history – halos around lights, symptoms began 2 hours ago after she watched a movie in a cinema NB. No trauma/flashes/floaters/diplopia/metamorphopsia/amaurosis fugax

Case study: Mrs. LH History POHx – no surgery, laser, injection or other treatment; wears glasses for reading PMHx – LBP, healthy otherwise, previous appendicectomy FHx – grandmother ?blind in one eye, otherwise nil Glauc/MD/RD/DM/IHD/HTN SHx – smoker (upto 15/day); EtOH on special occasions, Admin-worker Meds – Panadeine forte PRN, NKDA

Case study: Mrs. LH Examination RVA 6/60, NIPH, LVA 6/6 IOP RE = 56 mmHg, LE = 15 Pupils – RIGHT mid-dilated, sluggishly responsive to light, LEFT normal Visual fields NAD bilaterally Slit lamp exam – RE: injected conj, corneal oedema, shallow AC, ‘Iris bombe’, gonioscopy – closed angle on LE

Glaucoma “a group of disorders leading to optic neuropathy, often chronic and associated with a high intraocular pressure” Primary angle-closure glaucoma Accountable for up to 50% of all Glaucoma cases worldwide

Primary angle-closure glaucoma Who is at risk? Asian or Inuit descent Hyperopes Female Age (most common between 55 and 65) “Screening has a role, especially in adults > 40 years old and is done with a gonioscope”

Pathophysiology Occlusion of the trabecular meshwork by the peripheral iris Can be seconday/drug-induced Two types of closure  IOP rise Appositional Synechial Glaucomatous changes in optic nerve  visual field loss  blindness

Diagnosis Diagnosis based on clinical findings ?role for provocation testing Pen-light test Van Herick staging Gonioscopy findings (both eyes)

Treatment Guiding principles Reduce IOP Open the outflow tract for the aqueous humour Prevent/treat inflammation Treat any symptoms

Medical treatment I Urgent referral to Ophthalmology team Hospital admission Supine position IV Acetazolamide 500 mg +/- PO (if IOP >50) PO Acetazolamide 500 mg (if IOP <50) Anti-glaucoma drops e.g. timolol 0.5%

Medical treatment II Steroid drops e.g. prednisolone 1% +/- Pilocarpine 1-2% (beware of pupillary sphincter ischaemia) Analgesia and anti-emetic PRN Mannitol 20% 1-2g/kg IV over 1 hr; others incl glycerol and isosorbide

Surgical treatment Surgical treatment (Corneal indentation) Anterior chamber paracentesis Laser peripheral iridotomy or iridoplasty (need to clear corneal oedema first) Others include peripheral iridectomy, lens extraction, goniosynechialysis, trabeculectomy and cyclodiode laser

Differential diagnoses Other causes of headache/vomiting

Complications Fellow eye attack (can be up to 80% change within 5-10 years) Consider prophylactic laser PI Permanent decrease in VA Endothelial dysfunction in cornea ‘Decompression retinopathy’ Ischaemia of the optic nerve Loss of vision

Emergency pearls Acute, atraumatic eye pain or decreased visual acuity – need to r/o PACG Headache and vomiting – need to r/o PACG Always check the unaffected eye – will have a shallow AC Beware when dilating patient’s eyes – as iatrogenic PACG can occur in susceptible individuals Pilocarpine may be ineffective above IOP of 40-50 and after ‘hours’ have passed

Thank you