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ACUTE ANGLE CLOSURE CRISIS
Acute angle closure crisis is an ophthalmic emergency caused by sudden rise in intraocular pressure due to blockage of aqueous outflow. It presents with severe eye pain, blurred vision, nausea and elevated eye pressure. Immediate treatment involves intravenous acetazolamide and topical eye drops to lower pressure. If pressure is not controlled, further interventions like laser iridotomy or surgery may be needed to relieve the block and prevent permanent vision loss from optic nerve damage. Long term management involves treatment of the underlying primary angle closure glaucoma with pressure lowering eye drops or surgery and monitoring for glaucoma progression.
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ACUTE ANGLE CLOSURE CRISIS
- 1. Acute Angle Closure Crisis BY DRSAFAA REFAAT FRCSG, M.Sc., MBBS
- 2. Glaucoma Definition: Glaucoma isa progressive optic neuropathy with characteristic changes in the optic nerve head and corresponding loss of VF. It represents a final common pathway for a number of conditions, for most of which raised IOP is the most important risk factor. Increased IOP VF Defect ON Cupping
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- 4. Classifications: Etiology Primary Secondary Anatomical Open Angle Closed Angle Ageof onset infantile juvenile Adult onse Clinical Acute Chronic
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- 8. Primary angle-closure glaucoma PACG is a significant cause of blindness worldwide. It is present in about 0.1% of the general population over 40y old. Acute angle closure crisis (AACC) is an ophthalmic emergency.
- 9. Risk factors Epidemiological Age:>40y old; mean age of diagnosis ± 60y. Female sex. Ethnicity: Chinese, South East Asians. Anatomical Pupil block mechanism Plateau iris mechanism
- 10. Pupil block mechanism Narrow angle, shallow AC, relatively anterior iris–lens diaphragm, large lens (older, cataract), short axial length (usually hypermetropic); risk increases with increasing lens thickness to axial length ratio.
- 11. In pupillary block, appositionof the iris to the lens impedes aqueous flow from PC to AC, causing relative build-up of pressure behind the iris, anterior bowing of the peripheral iris, and subsequent angle closure.
- 12. Plateau iris mechanism Plateau iris configuration : relatively anterior ciliary body that apposes the peripheral iris to the trabeculum meshwork; AC depth normal centrally, shallow peripherally with flat iris plane.
- 13. Important Terminology: Acuteangle closure Crisis (AACC): Irido-trabecular contact ITC with acute symptomatic elevated IOP. Primary angle closure glaucoma (PACG): Primary angle closure PAC with glaucomatous damage (changes in the optic disc and VF).
- 14. Acute angle closurecrisis Acute angle closure (AACC) is an ophthalmic emergency requiring urgent treatment to prevent irreversible optic nerve damage. Severe, permanent damage may occur within several hours. If visual acuity is hand motions or worse, IOP reduction is usually urgent Recurrent episodes of acute/subacute angle closure may lead to synechial angle closure, and eventually to Primary angle closure glaucoma (PACG)
- 15. Acute angle closureCrisis (AACC) Clinical Picture; symptoms: Pain (periocular pain , headache, abdominal colic), Blurred vision, Haloes around the light. Nausea, vomiting.
- 16. Clinical Picture; Signs: Redeye, Ciliary Congestion. Pupil; fixed semi-dilated, Visual Acuity may be as worse as HM Raised IOP (usually 50–80mmHg), Corneal oedema, Angle closed, Glaucomflecken; Contralateral angle narrow; Bilateral shallow AC.
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- 18. Raised IOP(usually 50–80mmHg), Very important to learn how to check IOP in ER: Tonopen: simple portable contact instrument for IOP Check ?? Digital Assessment: stony hard eye globe Ophthalmologist use Goldman Aplanation Tonometer
- 19. Differential diagnosis Consider: secondryangle closure Glaucoma (e.g.: phacomorphic, inflammatory, neovascular) acute glaucoma Open Angle Glaucoma syndromes (e.g.: Posner–Schlossman syndrome or Pigment Dispersion Syndrome)
- 20. Approach to thetreatment of APAC Immediate Systemic: Acetazolamide 500mg IV stat (then 250mg PO 4×/d). β-blocker (e.g. Timolol 0.5% Eye Drops stat, then every 12 hours). Sympathomimetic (e.g. Apraclonidine 1% ED stat). Steroid (e.g. Prednisolone 1% ED stat, then every 30 to 60 min.) Pilocarpine 2%ED (once IOP <50mmHg, e.g. twice in first hour, then eye 6 hours).
- 21. Consider: Indentation Gonioscopywith a 4-mirror goniolens may help relieve pupil block; lying the patient supine may allow the lens to fall back away from the iris; Analgesics and Anti-emetics may be necessary. Pilocarpine 1% is often given to the contralateral eye while awaiting Nd-YAG PI.
- 22. Intermediate Check IOPhourly until adequate control. If IOP not improving: consider systemic Hyperosmotics (e.g. Glycerol PO Mannitol 20% 1g/kg of 50% solution in lemon juice or solution IV 1–1.5g/kg). If IOP still not improving: consider acute Nd-YAG PI (YAG Laser Peripheral Iridectomy)
- 23. If IOPstill not improving: Review the diagnosis Review the patency of PI or proceed to surgical PI, argon laser iridoplasty, paracentesis, cyclodiode photocoagulation, or emergency cataract extraction/trabeculectomy.
- 24. Definitive Treatment BilateralNd-YAG or surgical Peripheral Iridectomy.
- 25. Follow-Up After definitivetreatment, patients are reevaluated in weeks to months initially, and then less frequently. Visual fields and stereo disc photo- graphs are obtained for baseline purposes. Follow Up: IOP, Optic Disc, Visual Field. Some eyes may develop chronic elevated IOP, and will require long-term medical ± surgical treatment.
- 26. Refrences: Oxoford HandBook Of Ophthalmology, third edition, 2014 Will’s Eye Manual, fifth edition 2008 Preferred Practice Pattern, AAO, 2015. Photos copied from internet open sources.
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