Glaukoma Akut Sudut Tertutup

Glaucoma is a nonspecific term used for several ocular diseases that ultimately result in increased
intraocular pressure (IOP) and decreased visual acuity. Acute angle-closure glaucoma (AACG) is an
ocular emergency and receives distinction due to its acute presentation, need for immediate treatment,
and well-established anatomic pathology.[1] Rapid diagnosis, immediate intervention, and referral can have
profound effects on patient outcome and morbidity.
The acute angle closure literature has been plagued by the lack of a uniform definition and specific
diagnostic criteria. Only in recent years has there been a strong push to standardize the definitions of the
various forms of angle closure disease. Primary angle closure, primary angle-closure glaucoma, acute
angle closure, and acute angle-closure glaucoma were previously used interchangeable. Now, acute
angle closure is defined as at least 2 of the following symptoms: ocular pain, nausea/vomiting, and a
history of intermittent blurring of vision with halos; and at least 3 of the following signs: IOP greater than
21 mm Hg, conjunctival injection, corneal epithelial edema, mid-dilated nonreactive pupil, and shallower
chamber in the presence of occlusion.
Primary angle closure is defined as an occludable drainage angle and features indicating that trabecular
obstruction by the peripheral iris has occurred (ie, peripheral anterior synechiae, increased IOP, distortion
of iris fibers [iris whorling], lens opacities, excessive trabecular pigmentation deposits). An eye in which
contact between the peripheral iris and the posterior trabecular meshwork is considered possible based
on ocular anatomy is termed primary angle closure suspect. The term glaucoma is added if glaucomatous
optic neuropathy is present.
AACG represents the end stage of processes resulting in the compromised egress of aqueous humor
circulation and the subsequent increase in IOP. Aqueous humor is produced by the ciliary body in the
posterior chamber of the eye. It diffuses from the posterior chamber, through the pupil, and into the
anterior chamber. From the anterior chamber, the fluid is drained into the vascular system via the
trabecular meshwork and Schlemm canal contained within the angle.
Several anatomic abnormalities lead to anterior chamber crowding and predispose individuals to AACG.
These include shallower anterior chambers, thinner ciliary bodies, a thinner iris, anteriorly situated thicker
lens,[2] and a shorter axial eye length. Recent studies have suggested that increased iris thickness and
cross-sectional area are associated with increased risk. [3] Of the many predisposing anatomical variations,
a narrow angle has the most devastating consequences.
In the traditional model of AACG, the eye's natural response of dilation to environmental or chemical
stimuli results in a pathologic iris-lens apposition. The apposition and contact between the lens and the
iris is called pupillary block. Furthermore, pupillary block describes a state in which the forward-most
surface of the lens is anterior to the plane of the iris insertion into the ciliary body. As a result, aqueous
flow from the posterior chamber to the anterior chamber is obstructed or altogether blocked. When
pupillary block occurs in conjunction with the iris, the increasing pressure in the posterior chamber causes
the pliable iris, particularly the peripheral region, to bow forward in a process termed iris bomb. Iris
bomb further closes the already narrow angle and compromises aqueous drainage, thus increasing IOP.
Recent research has suggested an alternative pathophysiologic pathway for AACG. Cronemberger et al
propose that acute events can be traced to an autonomic imbalance in individuals with AACG, specifically
increased sympathetic tone. Furthermore, the iris dilator muscles in these individuals have been found to

be more developed and stronger. In instances of increased ocular sympathetic tone, including emotional
distress, low light conditions, or after sympathomimetic drug use, contraction of the iris dilator muscles
leads to pupil dilatation and thickening of the middle-peripheral iris. This thickening can lead to angle
closure, thereby obstructing the outflow of aqueous humor.[4]
Other proposed mechanisms of AACG include plateau iris, lens swelling, and ciliary block. Plateau iris is
less common than pupillary block and is due to anterior insertion of the iris. The superfluous and crowded
iris tissue blocks the trabecular meshwork and again leads to increased IOP.
Lens swelling and ciliary block are extremely rare. Lens swelling occurs in cases of cataracts in which
hydration forces cause enlargement of the lens and subsequent crowding of the anterior chamber. Forces
posterior to the lens can push the lens and iris forward causing ciliary block or vitreous pressure. This can
be seen in panretinal photocoagulation, scleral buckles, and uveitis

History
Classically, patients are elderly, suffer from hyperopia, and have no history of glaucoma. Most commonly,
they present with periorbital pain and visual deficits. [8]The pain is boring in nature and associated with an
ipsilateral headache. Patients note blurry vision and describe the phenomenon of "seeing halos around
objects."
Careful investigation may elucidate a precipitating factor, such as dim light or medications (eg,
anticholinergics, sympathomimetics).
In a large percentage of patients, extraocular symptoms and systemic manifestations are the chief
complaint. Patients present with headache and may receive medications for migraines or an evaluation
for a subarachnoid hemorrhage. Several case reports discuss patients presenting with vomiting and
abdominal pain that were misdiagnosed with gastroenteritis.[9]

Physical
The emergency department evaluation of the eye includes visual acuity, the external eye, visual fields, a
funduscopic examination, pupils, ocular motility, and IOP. All of which tend to be affected in AACG.
Slit-lamp evaluation may reveal corneal edema, synechiae, irregular pupil shape or function, or segmental
iris atrophy.
Patients complain of blurred vision, and testing reveals the ability only to detect hand movements. They
are unable to identify numbers and letters on distance charts or near cards.
Cornea and scleral injection and ciliary flush are present. The obviously edematous and cloudy cornea
obscures the funduscopic examination.
Increased IOP (normal limit, 10-20 mm Hg) and ischemia result in pain on eye movement, a mid-dilated
nonreactive pupil, and a firm globe. Clinicians must take a comprehensive history and perform a thorough
physical examination to ensure that this time-sensitive diagnosis is not missed.

Causes
Shallower anterior chambers; anteriorly situated lens; shorter axial eye length; thick iris; overdeveloped
iris dilator muscles; and a narrow angle lead to a higher propensity for development of AACG.
Precipitating factors include drugs (ie, sympathomimetics, anticholinergics, antidepressants [SSRIs],
anticonvulsants, sulfonamides, cocaine, botulinum toxin), [10, 11, 12, 13, 14] dim light, and rapid correction of
hyperglycemia.

Case reports have identified AACG associated with carotid-cavernous sinus fistula, trauma, prone
surgical positioning, and giant cell arteritis.
DD

Acute Orbital Compartment Syndrome

Conjunctivitis
Corneal Abrasion
Corneal Laceration
Corneal Ulceration and Ulcerative Keratitis
Endophthalmitis
Glaucoma, Malignant
Glaucoma, Neovascular
Herpes Zoster Ophthalmicus
Iritis and Uveitis
Orbital Infections
Periorbital Infections
Ultraviolet Keratitis
Vitreous Hemorrhage

Complications
Complications may include the following:

Permanent decrease in visual acuity

Repeat episode
Malignant glaucoma
Fellow eye attack
Central retinal artery occlusion
Central retinal vein occlusion

Prognosis
Several studies evaluated patients after treatment for AACG and demonstrated favorable outcomes. With
adequate treatment, most patients recover their lost vision. In whites, IOP was controlled with LPI alone in
65-76%. Asians more often have medically refractory initial attacks and require medications after LPI.
[5]
They also have higher rates of visual field loss and subsequent increases in IOP.[5] It has been
hypothesized that the initial attack is often more severe in Asians resulting in greater trabecular damage.
Another possibility is the formation of peripheral synechiae (adhesions) causing a creeping angle
reclosure.

Emergency Department Care

The treatment of acute angle-closure glaucoma (AACG)
consists of IOP reduction, suppression of inflammation, and
the reversal of angle closure. Once diagnosed, the initial

intervention includes acetazolamide, a topical beta-blocker,

and a topical steroid.
Acetazolamide should be given as a stat dose of 500 mg IV
followed by 500 mg PO. A dose of a topical beta-blocker (ie,
carteolol, timolol) will also aid in lowering IOP. Studies have
not conclusively demonstrated the superior neuronal or

visual field protectiveness of one beta-blocker over another.

Both beta-blockers and acetazolamide are thought to
decrease aqueous humor production and to enhance
opening of the angle. An alpha-agonist can be added for a
further decrease in IOP.
Inflammation is an important part of the pathophysiology and
presenting symptomology. Topical steroids decrease the
inflammatory reaction and reduce optic nerve damage. The
current recommendation is for 1-2 doses of topical steroids.
Addressing the extraocular manifestations of the disease is
critical. This includes analgesics for pain and antiemetics for
nausea and vomiting, which can drastically increase IOP
beyond its already elevated level. Placing the patient in the
supine position may aid in comfort and reduce IOP. It is also
believed that, while supine, the lens falls away from the iris
decreasing pupillary block.
After the initial intervention, the patient should be
reassessed. Reassessment includes evaluating IOP,
evaluating adjunct drops, and considering the need for
further intervention, such as osmotic agents and immediate
iridotomy.
Approximately 1 hour after beginning treatment, pilocarpine,
a miotic that leads to opening of the angle, should be
administered every 15 minutes for 2 doses. In the initial
attack, the elevated pressure in the anterior chamber causes
a pressure-induced ischemic paralysis of the iris. At this
time, pilocarpine would be ineffective. During the second
evaluation, the initial agents have decreased the elevated
IOP and hopefully have reduced the ischemic paralysis so
pilocarpine becomes beneficial in relieving pupillary block.
Pilocarpine must be used with caution. Theoretical concerns
exist about its mechanism of action. By constricting the
ciliary muscle, it has been shown to increase the axial
thickness of the lens and to induce anterior lens movement.
This could result in reducing the depth of the anterior
chamber and worsening the clinical situation in a paradoxical
reaction. Despite this, pilocarpine is recommended to be
used as an additional agent.[17]
No standard rate of reduction for IOP exists; however,
Choong et el identified a satisfactory reduction as IOP less
than 35 mm Hg or a reduction greater than 25% of
presenting IOP.[16] If the IOP is not reduced 30 minutes after
the second dose of pilocarpine, an osmotic agent must be
considered. An oral agent like glycerol can be administered
in nondiabetics. In diabetics, oral isosorbide is used to avoid
the risk of hyperglycemia associated with glycerol. Patients
who are unable to tolerate oral intake or do not experience a
decrease in IOP despite oral therapy are candidates for IV
mannitol.
Hyperosmotic agents are useful for several reasons. They
reduce vitreous volume, which, in turn, decreases IOP. The
decreased IOP reverses iris ischemia and improves its

responsiveness to pilocarpine and other drugs. Osmotic

agents cause an osmotic diuresis and total body fluid
reduction. They should not be administered in cardiovascular
and renal patients. Choong et el demonstrated that 44% of
patients required the addition of an osmotic agent to
decrease IOP.[18]Repeat doses may be necessary if no effect
is seen and if tolerated by the patient.
When medical therapy proves to be ineffective, corneal
indentation (CI) can be used as a temporizing measure to
reduce IOP until definitive treatment is available. As the
cornea is indented, aqueous humor is displaced to the
periphery of the anterior chamber, which serves to
temporarily open the angle. This leads to immediate
reduction of IOP and occasionally may completely abort the
attack. After applying topical anesthetic, any smooth
instrument can be used to perform this procedure, including
a gonioprism (ideal, if available), or a cotton-tipped
applicator. Obviously, a concern with performing CI is the
possibility for damage to the corneal epithelium, which may
complicate the patients course.[19]
Laser peripheral iridotomy (LPI), performed 24-48 hours
after IOP is controlled, is considered the definitive treatment
for AACG. Furthermore, LPI may be offered prophylactically
to individuals anatomically predisposed to AACG if identified
before the first acute attack. While LPI is the current
definitive treatment, evidence suggests that argon laser
peripheral iridoplasty (ALPI) and anterior chamber
paracentesis (ACP) may have increasing roles in the
management of AACG.
In ALPI, burns are made in the peripheral iris resulting in iris
contraction and opening of the angle. Some studies suggest
ALPI causes a more immediate decrease in IOP, resulting in
better outcomes with fewer side effects than systemic
therapy.[20] However, a recent randomized-controlled trial
comparing LPI plus ALPI compared with ALI alone failed to
show improved outcomes with ALPI as an adjunctive
therapy.[21] Systemic therapy must still be used with ACP, but
ACP appears to instantaneously relieve symptoms.
An additional alternative is lens extraction. Although its role
in AACG has not been completely established, it has been
proven to effectively reduce IOP without the need for
medication postoperatively. Furthermore, it offers a
therapeutic advantage for individuals with coexisting
cataracts.[22]
The choice of which therapy to use will be made by an
ophthalmologist who will evaluate all patients via gonioscopy
with complete inspection of the angle. At institutions where
an ophthalmologist is immediately available on staff, initial
treatment should be performed in conjunction with the
specialist.
If there is a delayed interval between the initial presentation
and definitive ophthalmic care, the emergency department
physician should begin treatment as described above. After

an appropriate reduction in IOP, immediate ophthalmic

evaluation must be ensured. If the IOP is unchanged or
increased from the time of treatment, further treatment
should be discontinued and the attack most likely will

terminate only with LPI. Ocular massage through a closed

eyelid may be preformed while waiting for ophthalmology if
no other treatment reduces IOP.