Acute Glaukoma

Introduction and Facts

Acute glaucoma (Acute Angle Closure - AAC) is a condition where there is blockage of the trabecular meshwork by the peripheral iris at the corner of the eye, which is an eye emergency that requires immediate treatment to prevent damage to the optic nerve that can lead to blindness. Medical treatment should be initiated as soon as possible to reduce intraocular pressure, before definitive laser or surgical iridectomy is initiated.

A study by Qugley and Broman (2006) shows that 21 million people will experience Chronic Angle Closure Glaucoma (CACG), and 5.2 million of them will experience bilateral blindness due to this disease by 2020. Most cases are asymptomatic. until it reaches an advanced stage, but not infrequently also with a history of an acute attack (AAC). The incidence of angle-closure glaucoma is more common in Asian races than Caucasian or African races.

Pathophysiology

The pathophysiology of increased intraocular pressure is influenced by the balance between secretion of aqueous humor by the ciliary body and drainage through the trabecular meshwork and uveoscleral. Therefore, it is divided into 2 mechanisms, namely in angle-closure glaucoma and open-angle glaucoma. In patients with open-angle glaucoma, there is increased obstruction to the flow of aqueous humor in the trabecular meshwork pathway. While there is an obstruction in the pathway to drainage, it is known as angle-closure glaucoma.

The main mechanism of decreased visual function in glaucoma is retinal ganglion cell apoptosis which causes thinning of the nerve fiber layer and this layer of the retina. It also causes atrophic reduction in the axons of the optic nerve and optic disc, as well as enlargement of the optic cup. In general, until now there are 2 known theories that underlie the mechanism of visual impairment, namely the mechanical theory (increased intraocular pressure causes damage to the optic nerve papillae) and the vascular theory (decreased blood flow/perfusion causes damage to the optic nerve papillae). In the mechanical theory, increased intraocular pressure causes pressure on nerve fibers, especially in the Elschnig's ring and the lamina cribrosa. Then there is a break in the axoplasmic transport pathway, both anterograde and retrograde.

Clinical Symptoms and Complications

Symptoms of acute glaucoma are:

- Pain, is a typical sign of an acute attack that occurs suddenly and is very painful in the eye around the area of ​​innervation of the fifth cranial nerve branch.

- Nausea, vomiting and weakness, this is often associated with pain.

- Decreased vision rapidly and progressively, hyperemia, photophobia.

- Past medical history.

Diagnosis

a. History obtained complaints related to acute glaucoma.

b. Slit-lamp biomicroscopy

- Ciliary hyperemia due to injection of limbal and conjunctival vessels.

- Corneal edema

- Shallow anterior chamber with peripheral iridocorneal contact

- Flares and aqueous cells

- Pupils mid-dilated and unresponsive to light

- Significantly elevated intra-ocular pressure (50-100 mmHg)

c. Gonioscopy

Gonioscopy examination was postponed until the corneal edema subsided, and peripheral irido-corneal contact was demonstrated. Contra-lateral gonioscopy examination is also important to do, generally in cases of acute primary angle-closure glaucoma found a latent angle-closure image in the other eye.

d. Ophthalmoscopy

Disc-optic abnormalities can be evaluated using a direct ophthalmoscope, slit-lamp biomicroscopy using a +78 D lens, or Goldmann contact lenses and an indirect ophthalmoscope. Fundus in acute glaucoma may reveal optic-disc edema and hyperemia due to disturbances in axoplasmic transport/flow.

Management and Care

1. Medical therapy:

a. Carbonic anhydrase inhibitor

Acetazolamide, is a very appropriate choice for emergency treatment in acute glaucoma. The effect can lower the pressure by inhibiting the production of aqueous humor, so it is very useful to reduce intraocular pressure rapidly. Acetazolamide with an initial dose of 2x250 mg orally, can be given to patients who have normal kidney function and no gastric abnormalities. Increasing the maximum dose of acetazolamide can be given after 4-6 hours to lower the intraocular pressure. Topical carbonic anhydrase inhibitors can be used as initial therapy in acute glaucoma patients with emesis.

b. Beta blocker

It is an effective adjunct therapy to treat angle-closure attacks. Beta blockers can reduce intraocular pressure by reducing the production of aqueous humor. Timolol is a nonselective beta blocker with the highest activity and concentration in the posterior chamber achieved within 30-60 minutes after topical administration. Nonselective beta blocker eye drops as initial therapy can be given 2 times with an interval of every 20 minutes and can be repeated 4, 8, and 12 hours later.

c. Strong Miotic

Pilocarpine 2% or 4% 4 x 1 drop given as initial therapy. Its use is not effective on attacks that have been more than 1-2 hours. This is because the sphincter pupillary muscle is ischemic and cannot respond to pilocarpine.

d. Osmotic agent

This agent is very effective in reducing intraocular pressure rapidly, its administration is recommended to patients who do not have emesis.

- Glycerin, effective dose 1 - 1.5 g/kg body weight in 50% fluids. Can lower intraocular pressure within 30-90 minutes after administration, and duration of effect is 5-6 hours. During its use, glycerin can cause hyperglycemia and dehydration. Contraindicated in DM patients and patients with renal failure.

- Mannitol, intravenous administration in 20% fluids at a dose of 2 g / kg for 30 minutes. Mannitol with a high molecular weight, will penetrate the eye more slowly so it is more effective in lowering intraocular pressure. A pressure-lowering effect was observed within 1 hour after intravenous mannitol administration.

e. Topical steroids

2. Laser Peripheral Iridotomy (LPI)

Iridotomy is indicated in the setting of angle-closure glaucoma with pupillary block, iridotomy is also indicated to prevent pupillary block in the eye at risk, which is determined by gonioscopic evaluation. LPI cannot be performed on eyes with rubeosis iridis, because it can cause bleeding. The risk of bleeding is also increased in patients taking systemic anti-coagulants, such as aspirin.

Argon lasers and Nd:YAG lasers can both be used for iridectomy. Complications that can occur after laser surgery are corneal burn, tearing of the anterior lens capsule, bleeding (usually not for long), increased intraocular pressure after surgery and inflammation.

3. Iridectomy Surgery

Incisional iridectomy was performed in patients who were unsuccessful with laser iridotomy. As;

- In situations where the iris cannot be seen clearly due to corneal edema, this often occurs in patients with severe acute glaucoma lasting 4-8 weeks.

- Shallow anterior chamber angle, with extensive irido-corneal contact.

- Uncooperative patient.

- No laser equipment available

4. Lens extraction

There are several studies that prove the effectiveness of lens extraction in reducing and controlling intraocular pressure in patients with Primary Angle Closure Glaucoma (PACG). Lens extraction should be considered in PACG cases, especially those with hyperopia or anteriorly vaulted lens conditions.

Reference:

1. Ratna Suryaningrum, I Gusti Ayu. Penatalaksanaan Glaukoma Akut. Internet [Cited 28/8/2021]. Availabole from: http://erepo.unud.ac.id/id/eprint/22893/1/08ebe93020bfa58e031336852a308d3c.pdf

2. - Glaukoma. Internet [Cited 28/8/2021]. Availabole from: http://eprints.undip.ac.id/72082/3/LAPORAN_KTI_JOHANES_JETHRO_NUGROHO_S._22010115130125_BAB_II.pdf