Acute Angle Closure Crisis

BYDR SAFAA REFAAT

FRCSG, M.Sc., MBBS

GlaucomaDefinition:

Glaucoma is a 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

Increased IOP

VF DefectON Cupping

Classifications:

EtiologyPrimary

Secondary

Anatomical

Open Angle

Closed Angle

Age of onset

infantile

juvenile

Adult onse

ClinicalAcute

Chronic

Anatomical Review

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.

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

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.

In pupillary block, apposition of 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.

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.

Important Terminology:

Acute angle 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).

Acute angle closure crisis

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)

Acute angle closure Crisis (AACC)

Clinical Picture;symptoms:  Pain (periocular pain , headache, abdominal

colic), Blurred vision, Haloes around the light. Nausea, vomiting.

Clinical Picture;Signs: Red eye, 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.

Glaucomflecken

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

Differential diagnosis

Consider: secondry angle closure Glaucoma

(e.g.: phacomorphic, inflammatory, neovascular)

acute glaucoma Open Angle Glaucoma syndromes (e.g.:Posner–Schlossman syndrome or Pigment Dispersion Syndrome)

Approach to the treatment 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).

Consider: Indentation Gonioscopy with 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.

Intermediate  Check IOP hourly 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)

 If IOP still 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.

Definitive Treatment

Bilateral Nd-YAG or surgical Peripheral Iridectomy.

Follow-Up

After definitive treatment, 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.

Refrences:

Oxoford Hand Book 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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