acute angle closure.pptx

glaucoma

1. Acute Angle Closure Glaucoma By: Dr. Ruthra Devi Supervisor: Dr. Nanthini

2. Patient R 64 years old, Malay, Lady Underlying Diabetes Mellitus and Hypertension No known food or drug allergy Case was referred from Hospital Gerik for RE Acute Glaucoma Complaint of RE blurry of vision for past 2-3 Days +RE redness for past 2-3 days +RE pain for past 2-3 days + headache for past 2-3 days + nauseated but no vomiting for past 2-3 days

3. History No floaters No flashes of lights No scotoma No metamorphosis No trauma history No surgery history No fever No URTI/UTI/AGE symptoms Denies family history of gllaucoma

4. Examination RE LE Reverse RAPD Negative RAPD 6/60, PH 6/24 VA 6/9 normal Lids normal + injected Conjunctiva white + mild hazy Cornea Clear Shallow AC Shalow +mid dilated, 5mm in size, sluggish Pupil/iris Round and reactive, 3mm insize NS 2+, no phacodenesis Lens NS+ 62 IOP 14 OD pink, CDR 0.4, Macula normal, Retina flat, No DR changes Fundus OD pink, CDR 0.4, Macula normal, Retina flat, No DR changes

5. Management Diagnosis: RE Acute Angle Closure Glaucoma LE Primary Angle Closure Glaucoma Suspect BE Immature Cataract BE DM No DR changes Treatment: IV Diamox 500mg STAT, to review IOP in 1 Hour Tab Diamox 250mg QID Tab Slow K 11/11 OD Gt. Maxidex QID RE Gt. Alphagan TDS RE Gt. Xalatan ON RE Gt. Timocomad RE

6. Investigations FBC (Normal) WBC 9.8 x 10 9 /L Hb 13.0 g/dL Plt 371 x 10 9 /L RP (Normal) Urea 5.9 mmol/L Na 130 mmol/L K 4.4 mmol/L Creatinine 65 umol /L RBS (Normal) : 7.6 mmol/L

7. Progress in ward (D1 of admissions) RE LE Reverse RAPD Negative RAPD 6/60, PH 6/24 VA 6/9 normal Lids normal + injected Conjunctiva white + mild hazy Cornea Clear Shallow AC Shalow +mid dilated, 5mm in size, sluggish Pupil/iris Round and reactive, 3mm insize NS 2+, no phacodenesis Lens NS+ 32 IOP 1 OD pink, CDR 0.4, Macula normal, Retina flat, No DR changes Fundus OD pink, CDR 0.4, Macula normal, Retina flat, No DR changes

8. Management Treatment: Tab Diamox 250mg QID Tab Slow K 1/1 OD Gt. Maxidex QID RE Gt. Alphagan TDS RE Gt. Xalatan ON RE Gt. Timolol RE For RE Peripheral Iridiotomy laser today For RE PHACO/PCIOL once patient keen. For LE Peripheral Iridiotomy laser later

9. RE Day 1 post Peripheral Iridiotomy laser

10. Progress in ward (D2 of admissions) RE LE Reverse RAPD Negative RAPD 6/60, PH 6/24 VA 6/9 normal Lids normal + injected Conjunctiva white + mild hazy Cornea Clear Shallow temporally/ cells 1+, PI patent at 11 o’clock AC Shalow peripherally, deep centrally +mid dilated, 5mm in size, sluggish Pupil/iris Round and reactive, 3mm insize NS 2+, no phacodenesis Lens NS+ 18 IOP 16

11. Management Treatment: Continue Tab Diamox 250mg QID Tab Slow K 1/1 OD Gt. Maxidex QID RE Gt. Alphagan TDS RE Gt. Xalatan ON RE Gt. Timolol RE For LE Peripheral Iridiotomy laser today For RE PHACO/PCIOL once patient keen.

12. LE Day 1 post Peripheral Iridiotomy laser

13. Progress in ward (D3 of admissions) RE LE Reverse RAPD Negative RAPD 6/60, PH 6/24 VA 6/9 normal Lids normal + injected Conjunctiva white + mild hazy Cornea Clear Deep/cells 1+, PI patent at 11 o’clock AC Deep/quiet, PI patent at 11 o’clock +mid dilated, 5mm in size, sluggish Pupil/iris Round and reactive, 3mm insize NS 2+, no phacodenesis Lens NS+ 16 IOP 14

14. Management Treatment: Off Tab Diamox 250mg QID Off Tab Slow K 1/1 OD Continue Gt. Maxidex QID RE Gt. Alphagan TDS RE Gt. Xalatan ON RE Gt. Timolol RE TCA PC upon discharge for RE KPE/PCIOL

15. Progress in ward (D4 of admissions) RE LE Reverse RAPD Negative RAPD 6/60, PH 6/24 VA 6/9 normal Lids normal + injected Conjunctiva white + mild hazy Cornea Clear Deep/cells 1+, PI patent at 11 o’clock AC Deep/quiet, PI patent at 11 o’clock +mid dilated, 4mm in size, sluggish Pupil/iris Round and reactive, 3mm insize NS 2+, no phacodenesis Lens NS+ 20 IOP 16

16. Management Treatment: Continue Gt. Maxidex QID RE Gt. Alphagan TDS RE Gt. Xalatan ON RE Gt. Timolol RE TCA PC upon discharge for RE KPE/PCIOL

17. Acute Angle Closure Glaucoma

18. Acute Angle Closure Glaucoma Angle closure glaucoma is an ophthalmic emergency Acute angle closure glaucoma results from appositional or synechial closure of the anterior chamber angle leading to reduction in aqueous outflow facility. Intraocular pressure elevation, and subsequent damage to the optic nerve associated visual field loss. In primary angle closure , the mechanism causing disease is primarily pupillary block In secondary angle closure, the mechanisme causing is underlying causes.

19. Chronic Angle Closure Glaucoma Chronic angle-closure glaucoma is diagnosed by noting peripheral anterior synechiae on gonioscopy, as well as progressive damage to the optic nerve and characteristic visual field loss.

20. History Presence of risk factors (eg, hyperopia, thick cataractous lens) Halos around lights Aching eye or brow pain Headache Nausea, vomiting Reduced acuity Eye redness Closed angle on gonioscopy Extremely elevated IOP Corneal edema Engorged conjunctival vessels Fixed dilated pupil

21. Investigations Gonioscopy examination of anterior chamber angle Slit-lamp examination Automatic static perimetry Ultrasound biomicroscopy Anterior segment optical coherence tomography (OCT) of angle Evaluation of the optic nerve head by fundoscopy Retinal OCT

22. Diagnostic Criteria Acute Angle Closure Presence of at least 2 of the following symptoms: Ocular or periocular pain Nausea or vomiting Antecedent history of intermittent blurring of vision with haloes Presenting IOP > 21 mm Hg Presence of at least 3 of the following signs: Conjunctival injection Corneal epithelial edema Mid-dilated unreactive pupil Shallow anterior chamber

23. Diagnostic Criteria Chronic Angle Closure 3 stages in the natural history of angle closure: Primary angle-closure suspect: an "occludable angle" with normal IOP, optic disc, and visual field, without evidence of peripheral anterior synechiae (PAS) Primary angle closure: an "occludable angle" with either raised IOP and/or primary PAS; optic disc and field normal Primary angle-closure glaucoma: primary angle closure with evidence of glaucomatous damage to optic disc and visual field

24. Medical Treatment Goal of treatment is to relieve the acute symptoms and decrease IOP Oral or topical carbonic anhydrase inhibitors, topical beta-blockers, and topical alpha-2 adrenergic agonists lower IOP through suppression of aqueous humor production. Beta-blockers reduce IOP by around 20% to 30% within 1 hour of instillation. Alpha-agonists reduce IOP by around 26% within 2 hours post-dose. Carbonic anhydrase inhibitors, topical beta-blockers, or alpha-2 adrenergic agents may be used as first-line therapies either alone or more typically in combination.

25. Medical Treatment Acetazolamide: 125-250 mg orally (immediate-release) up to four times daily, maximum 1000 mg/day; 250-500 mg intravenously every 2-4 hours, maximum 1000 mg/day Betaxolol ophthalmic: (0.5%) 1-2 drops into the affected eye(s) twice daily Brinzolamide ophthalmic: (1%) 1 drop into the affected eye(s) 2 or 3 times daily Dorzolamide ophthalmic: (2%) 1 drop into the affected eye(s) twice or three times daily Levobunolol ophthalmic: (0.25%) 1-2 drops into the affected eye(s) twice daily; (0.5%) 1-2 drops into the affected eye(s) once daily Methazolamide: 50-100 mg orally twice or three times daily Brimonidine ophthalmic: (0.1 to 0.2%) 1 drop into the affected eye(s) 3 times daily Timolol ophthalmic: (0.25% or 0.5%) 1 drop into the affected eye(s) twice daily; (0.5% gel) 1 drop into the affected eye(s) once daily

26. Surgical Treatment Laser peripheral iridotomy (LPI), where a laser is used to make an opening in the iris, is usually successful for acute angle-closure glaucoma. LPI alleviates pupillary block by allowing aqueous to bypass the pupil. The pressure differential between anterior and posterior chambers is eliminated, and the iris loses its convex configuration and falls away from the TM, resulting in opening or widening of the angle. LPI is indicated in all eyes with primary angle closure and usually in fellow eyes as well, since the majority of fellow eyes will also develop glaucomatous changes. Laser iridoplasty or gonioplasty can be considered in the presence of a patent LPI with a residual appositional angle. An argon laser is used to place contraction burns in the peripheral iris over its entire circumference in order to pull the peripheral iris away from the TM.

27. Prognosis If the disease is recognized and treated early, most patients recover without long-term sequelae. If untreated, about 25% of patients have one or more relapses in their lifetime. Most of these patients remain in the latent stage; however, about one-third go on to develop tertiary syphilis.

28. 1. Ocular syphilis is a rare manifestation of syphilis (6-9%) and was reported to have a prevalence rate of 0.6% in HIV-infected patients. 2. As syphilis is the most common bacterial eye infection in HIV-positive patients, all HIV- positive patients with uveitis should be tested for syphilis and vice versa. 3. RPR and Venereal Disease Research Laboratory test (VDRL), however, are more useful to obtain information on disease activity and therefore for therapeutic monitoring. 4. Ocular syphilis is not correlated with CD 4 counts. 

29. 1. Non-treponemal tests are used to monitor the disease and detect reinfection. 2. Seroconversion with non-treponemal tests may take 3–6 weeks. 3. Poor sensitivity (70%) in primary and late syphilis, false positive tests due to cross reactivity with other antigens false negativity due to prozone phenomenon, previous treatment, HIV coinfection and long latency especially late neurosyphilis 4. Syphilitic uveitis is considered equivalent to neurosyphilis.