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MEDICINE

Continuing Medical Education

Acute Closed-Angle Glaucoma—


An Ophthalmological Emergency
Simone Nüßle, Thomas Reinhard, Jan Lübke
Department of
Ophthalmology,
University Hospital
Freiburg, Faculty of
Medicine, University Sumary
of Freiburg:
Dr. Simone Nüßle, Background: Acute closed-angle glaucoma has an incidence of 2.2–4.1 cases per 100 000 persons per year in Europe. It is an
Prof. Dr. Thomas ophthalmological emergency in which markedly elevated intraocular pressure can damage vision permanently. Because the
Reinhard, PD Dr.
Jan Lübke acute symptoms are not always clearly referable to the eyes, patients often present to physicians who are not ophthalmologists.

Methods: This review is based on pertinent articles retrieved by a selective search in PubMed.

Results: The diverse symptoms of acute closed-angle glaucoma include eye redness, worsening of vision and other visual dis-
turbances, headache, and nausea. Acute closed-angle glaucoma has multiple causes. Not all predisposing factors have been
definitively identified; above all, there are certain anatomical configurations of the eye that make it more likely to arise. The goals
of treatment are to reduce the elevated intraocular pressure rapidly, which usually leads to marked symptom relief, as well as to
eliminate the situation that led to closed-angle glaucoma. For proper treatment, the patient should be seen by an ophthalmol-
ogist without delay, on the day of symptom onset if possible.

Conclusion: Primary prevention of acute closed-angle glaucoma is not always possible. Even physicians who are not ophthal-
mologists can diagnose markedly elevated intraocular pressure by palpation of the globe. Proper, specific treatment can help
patients rapidly and lastingly.

Cite this as
Nüßle S, Reinhard T, Lübke J: Acute closed-angle glaucoma—an ophthalmological emergency.
Dtsch Arztebl Int 2021; 118: 771–80. DOI: 10.3238/arztebl.m2021.0264

A
cute angle closure represents an ophthalmic Learning goals
emergency. Without timely treatment, irreversible In view of the frequency of acute angle closure and the
blindness may result. Blockage of the flow of challenges of its management, readers of this article
aqueous fluid can greatly increase the intraocular pres- should:
sure. The ophthalmological signs such as red eye, impair- ● Be aware of the predisposing factors and the ana-
ment of vision, and pain may be accompanied by the tomical risk constellations
occurrence of general and neurological symptoms, e.g., ● Have internalized the warning signs
headache, nausea, vomiting, and fixed pupil. In a study ● Be familiar with the treatment options and be in a
carried out at our institution, we found that almost one position to carry out specific treatment themselves
third of persons with acute angle closure, like the patient or refer the patient to the appropriate specialist
whose case is described in this article, initially consult a
physician who is not an ophthalmologist, and that in one Description of the disease
third of such cases cranial imaging is performed (1). This Definition
shows clearly that physicians from other disciplines also Acute angle closure belongs to the group of narrow-
need to be familiar with the signs of this disease. angle ocular diseases. The outflow of aqueous fluid into

Definition Importance
Acute angle closure is one of the narrow-angle diseases. The Acute angle closure is a genuine ophthalmic emergency:
outflow of aqueous fluid into the trabecular meshwork in the without prompt treatment, blindness may ensue.
angle of the anterior chamber of the eye is completely blocked
by the iris, causing rapid elevation of intraocular pressure.

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Mechanism of pri- FIGURE 1 Closure of the anterior chamber angle is not always
mary angle closure acute, but can be intermittent or chronic. It may also
by pupillary block: Trabecular meshwork be primary (a disease in its own right) or secondary (a
a) The physiological Iris consequence of other diseases or alterations of the
flow of aqueous fluid
from the ciliary body
eye). Intermittent angle closure, in contrast to acute
into the trabecular angle closure, is self limiting; its symptoms are also
meshwork. usually milder. Chronic angle closure may be a conse-
b) Pupillary block quence of acute or intermittent angle closure or may
forces accumulation arise due to enduring contact between the iris and the
of the aqueous fluid trabecular meshwork in the form of adhesions.
behind the iris,
pressing it forward. a Lens Ciliary body Epidemiology
The trabecular
meshwork becomes
Acute angle closure is a rare emergency event in Cau-
obstructed, resulting casians. The annual incidence in Europe has been
in angle closure reported as 2.2–4.1 cases per 100 000 inhabitants (3–7).
Pupillary block Closed angle
In Singapore, however, the figure is higher, with 12.2
cases each year per 100 000 inhabitants over the age of
30 years (8).
Overall, glaucoma disease, consisting predomi-
nantly of different forms of open-angle glaucoma, is
the second most commonly occurring cause of blind-

Artwork: Dr. Simone Nüßle


ness in Western Europe after age-related macular
degeneration (9). In Europe in the year 2013, an esti-
b mated 1.41 million persons between the ages of 40
and 80 years had primary narrow-angle glaucoma and
5.36 million had primary open-angle glaucoma. This
corresponds to a 0.42% prevalence of narrow-angle
the trabecular meshwork at the angle of the anterior glaucoma in this population. Worldwide, the esti-
chamber of the eye is completely blocked by the iris, mated number of persons in this age group with
causing a rapid increase in intraocular pressure. This is narrow-angle glaucoma was 20.17 million (10).
often wrongly referred to as “glaucoma attack” or
“acute closed-angle glaucoma,” although formally the Risk factors
criteria of glaucoma are not fulfilled. Glaucoma is char- Although many different risk factors for a narrow ante-
acterized by increasing excavation of the optic nerve rior chamber angle have been described, it has not been
head owing to the death of retinal ganglion cells or their completely clarified which of them apply to acute pri-
nerve fibers. An acute augmentation of pressure is not mary angle closure.
necessarily associated with glaucomatous injury, The risk factors for narrow-angle disease include
although the risk of such damage exists with persistent biometric factors such as short eyeball, which is often
pressure elevation. The classification of the American associated with longsightedness, i.e., spectacle pre-
Academy of Ophthalmology takes this into account. scriptions beginning with a “+”. Furthermore, the risk
Suspicion of primary angle closure (“primary angle for narrow-angle disease is increased by a shallow
closure suspect,” PACS) is defined as a narrow anterior anterior chamber and a thick lens. Anterior chamber
chamber angle with ≥ 180° iridotrabecular contact. depth is viewed as the most easily measured index for
Should elevation of intraocular pressure or formation of the risk of chamber angle obstruction. However, these
anterior chamber adhesions ensue, these stages are risk factors explain only a certain proportion of the
termed “primary angle closure” (PAC) and “primary cases of acute primary angle closure (11).
angle-closure glaucoma” (PACG), respectively (2). In The principal demographic risk factors are ethnic-
the German-language literature the terms used for dis- ity, increasing age, and female sex. With regard to
eases involving narrowing of the anterior chamber incidences, Asians are three times more likely to ex-
angle have still not been clearly defined and are used perience acute primary angle closure than Caucasians
inconsistently. (3–8). The higher prevalence of acute primary angle

Incidence Risk factors


The incidence in Europe is reported as 2.2–4.1 cases per The principal risk factors are a short eyeball (often associated
100 000 inhabitants. with longsightedness) and a shallow anterior chamber of the
eye.

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closure in the Chinese cannot be entirely explained in


terms of simple biometric parameters (12). Differ-
ences in the anatomy of the iris and ciliary body are
thought to play a role (13). The increase in incidence
with advancing age may be attributable to the grow-
ing thickness of the native lens and the associated
decrease in anterior chamber depth (6, 14). Lens/cata-
ract surgery abolishes this risk constellation, as the
inserted artificial lenses are much thinner. Finally,
women are at greater risk of acute angle closure than
men (6, 8).

Pathophysiology
In the acute form of angle closure, the blockage of
aqueous fluid outflow into the trabecular meshwork a
leads to a rapid, excessive, and non-self-resolving
increase in intraocular pressure. The mechanisms
responsible for closure of the anterior chamber angle can
be divided into primary causes, secondary causes, and an
iatrogenic effect. Angle closure is described as primary
when it occurs in isolation, for example due to pupillary
block (see below), with no other causative disease. Situ-
ations of blockage in the anterior chamber angle that
arise as a consequence of other diseases are referred to as
secondary angle closure. Examples of such diseases are
tumors that force the iris forward in the direction of the
chamber angle and adhesions in the anterior chamber
following inflammation. A classification drawn up by
Ritch et al. divides the causes into four anatomical
levels: iris, ciliary body, lens, and behind the lens (15). b
Mixed forms are common. Many of the mechanisms
leading to angle closure occur quite rarely and it is pri-
marily ophthalmologists that need to be aware of them,
so they will be not described in detail here. The predomi-
nant primary mechanism and the commonly used medi-
cations that may act as triggering factors are discussed in
Source: Department of Ophthalmology, University Hospital Freiburg

the next two sections.

Pupillary block
Pupillary block is considered the most common cause
of primary angle closure in Caucasians (16). In the
Chinese population, 54% of cases of narrow-angle
glaucoma are caused by combined mechanisms and
only 38% are attributable to pupillary block alone
(17). In pupillary block the flow of aqueous fluid
from the posterior to the anterior chamber is disrupt- c
ed, with the result that the accumulated fluid forces
Figure 2a–c: The correct procedure for palpation of the eyeball.
the peripheral iris forward so that it comes into con- Downward gaze with eyes open (a). Fingers of both hands resting on
tact with the trabecular meshwork. In the event of temple and forehead, index fingers on eyelid, alternating gentle pres-
complete trabecular obstruction, acute angle closure sure (b). Palpation of other eye—also by less experienced examiners,
ensues (Figure 1). Both physiological and pharmaco- for comparison (c).

Pathophysiology Pupillary block


The aqueous fluid outflow is blocked by the obstruction of the A common cause is the so-called pupillary block, which may
trabecular meshwork and a pronounced increase in intraocular induce a pressure difference between the spaces behind and
pressure ensues. in front of the iris.

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α1-receptors of the dilator muscle of the pupil, while


anticholinergics such as atropine, tropicamide, and
cyclopentolate inhibit the muscarinic receptors of the
sphincter muscle of the pupil. Both of these mecha-
nisms result in pupillary dilation, and together they pro-
duce a synergistic effect (20). The general population
risk of acute angle closure being induced in this way is
low, reported as 0.03% (2 of 6 679 unselected persons
aged over 55 years) in a large study conducted in the
Netherlands (21). However, other medications outside
the ophthalmological indication spectrum whose
a effects include parasympatholytic or sympathomimetic
actions are also thought to be potential triggers of acute
angle closure in at-risk patients. This rare adverse effect
has been described principally in case reports (22).

Source: Department of Ophthalmology, University Hospital Freiburg


Patients for whom these substances are prescribed
should be informed about the symptoms of acute angle
closure. It must be emphasized that acute angle closure
following administration of medication is a very rare
event that occurs mainly in at-risk patients. The classic
open-angle glaucoma is generally not involved in this
instance. Routine ophthalmological monitoring, e.g.,
before commencement of treatment with antidepres-
sants, is indicated only in exceptional cases. The poten-
b tial risk of occurrence of acute angle closure should,
Figure 3: Clinical findings on slit-lamp examination: however, be mentioned. The medications reported to
a) In acute angle closure: clear reddening with ciliary injection (*); have triggered acute angle closure, by virtue of either
pupil moderately widened and no longer exactly circular (distorted local or systemic actions, are listed in Table 1. Local
area shown by +++); clouding of iris structures by corneal edema (#) exposure has been described, for example, with nebu-
b) In a normal eye: no irritation of conjunctiva (*); pupil round, con-
lized bronchodilators. Since some of the substances
stricted on illumination (+++); clearly discernible iris structures (#)
may also be used perioperatively, care must be taken to
avoid overlooking or misinterpreting symptoms of
acute angle closure in sedated or comatose patients.

Diagnosis
logical stimuli can trigger acute angle closure in per- Symptoms
sons with predisposing factors. In 1964, Lowe postu- The clinical findings in acute angle closure are striking.
lated that coactivation of the two pupillary muscles, The ophthalmic symptoms may be accompanied by se-
the sphincter muscle and the dilator muscle, could be vere vegetative general symptoms and intense pain that
a cause of the disrupted transpupillary flow, because cannot be precisely localized (Table 2).
in the presence of moderate pupillary dilation the cen- The classic combination of symptoms in acute
tral posterior surface of the iris approaches the anter- angle closure is rapidly worsening visual loss, red
ior surface of the lens (18, 19). A physiological scen- eye, and periocular pain.
ario in which this could occur is sudden stimulation in The visual symptoms comprise reduction of visual
conditions of reduced lighting, e.g., getting a fright acuity and, in some cases, multicolored halos around
while reading in poor light. light sources. Pain, if present, may be periocular or
may also present as frontal headache on the affected
Medication as causative factor side. The further non-ocular symptoms include severe
Mydriatic eyedrops are one of the typical pharmaco- vegetative general symptoms such as nausea and vo-
logical stimuli that may trigger acute angle closure. miting, less commonly stomach cramps or tachycar-
α1-Agonists like phenylephrine stimulate the dia. The oculocardiac reflex, by which the general

Causative medications Diagnosis


A large number of medications are potential triggering factors The usual ophthalmological findings are distinct reddening, vi-
for acute angle closure. sion loss, a pupil that does not react normally to light, and in
some cases periocular pain.

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symptoms can be explained, was first described in TABLE 1


1908 by Aschner and Dagnini (23, 24). This reflex
can be induced by manipulation of the extraocular Medications with the potential to induce acute angle closure*1
muscles in the course of interventions or by pressure Class Active substance Indications (examples)
on the eyeball. Such stimulation of the trigeminal (examples)
nerves leads to secondary stimulation of the vagus α1-Agonists – Phenylephrine – Mydriatic
nerve, which can result in bradycardia (25). The – Decongestant nasal spray
abdominal symptoms have also been attributed to the – Ephedrine – Vasopressor
oculocardiac reflex (26). However, other authors have
β2-Agonists – Albuterol – Bronchodilator
postulated a direct oculoemetic reflex: the massive – Salbutamol
pressure increase leads to corneoscleral expansion,
Anticholinergics – Atropine – Mydriatic
triggering the reflex (27, 28). – Bradycardia
All in all, the symptoms can be extremely variable
– Glycopyrrolate – Antidote to non-depolarizing
and may overlap. Nevertheless, precisely this combi- muscle relaxants
nation of symptoms should prompt consideration of – Reduction of respiratory secre-
acute angle closure as a differential diagnosis. tions
– Oxybutynine – Urge incontinence
Clinical and technical examination – Scopolamine – Antiemetic
Clinical examination reveals marked elevation of
– (Ipratropium) – Bronchodilator
intraocular pressure (normally between 10 and
21 mm Hg) to levels as high as 50–80 mm Hg. The – Botulinum toxin – Blepharospasm
gold standard for diagnosis is applanation tonometry, – Headache
but massively increased intraocular pressure can also Antihistamines – Cetirizine – Antiallergic
be detected without using a tonometer—namely by (anticholinergic ac- – Loratadine
tion)
transpalpebral palpation, an important examination
technique for estimation of excessively elevated Sulfonamines – Topiramate – Anticonvulsive
– Migraine
intraocular pressure. With the patient’s gaze directed
downward, the examiner palpates the eyeball con- – Acetazolamide – Diuretic
– Antiglaucomatous agent
cerned with both fingers through the upper lid. The – Altitude sickness
eyeball feels rock hard (Figure 2). – Meniere disease
As a rule, the patient’s visual acuity is reduced. – Methylsulfonylmethane – Nutritional supplement
During the episode of acute angle closure or there- (MSM)
after, the pupil may be moderately widened and no Serotonergic – SSRI – Antidepressant
longer exactly circular. Moreover, the reaction to light substances – SNRI
may be directly or indirectly restricted or even absent. – Triptan – Migraine
A fixed pupil that does not react to light represents an
– Aripiprazole – Antipsychotic
expression of ischemia-related sphincter muscle
paralysis. * From Yang and Lin (22)
The eye may also be strikingly reddened, due to SSRI, Selective serotonin reuptake inhibitors; SNRI, serotonin–norepinephrine reuptake inhibitors
ciliary injection and venous congestion of the con-
junctival and episcleral blood vessels.
A further, albeit primarily ophthalmological means
of diagnosis is slit-lamp microscopy. This usually
shows corneal edema, which may present as small
epithelial vesicles with stromal swelling. Exami- Examination of the anterior chamber angle helps to
nation of the anterior chamber shows that it is shallow differentiate between primary and secondary disease.
with forward protrusion of the peripheral iris. If the Because the angle usually cannot be visualized during
iris and trabecular meshwork are in direct contact, the an episode of acute angle closure, examination of the
anterior chamber angle cannot be visualized. For fellow eye may be informative. Furthermore, the
comparison, Figure 3 shows one example each of an presence of masses behind the iris should be ruled out
affected and an unaffected eye. by means of sonography.

General symptoms Examination


Headache and nausea may occur as general symptoms. Assessment of intraocular pressure by palpating the eyeball
with the fingers can also be performed by non-
ophthalmologists.

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TABLE 2 be given either topically or, in the form of acetazol-


amide, systemically. For intravenous administration of
Symptoms and findings of acute angle closure* acetazolamide, the recommended dosage is 5–10 mg/
Incidence Incidence (1) kg bodyweight (16). The conventional hyperosmotic
(4) (at least) substances include intravenous mannitol (no more than
Symptoms 1–1.5 g/kg bodyweight). With regard to the choice of
medication, attention must be paid to the contraindi-
Visual symptoms – Reduction in visual acuity – 82%
– Blurred vision 86% – cations and potential adverse effects, particularly in the
– Prodromal halos 22% – case of acetazolamide and hyperosmotic agents, which
Periocular pain 83% 47% in patients with renal insufficiency can lead to meta-
bolic disorders or to acute cardiac, hepatic, or renal fail-
Headache – 34%
ure owing to increased blood volume (16).
Nausea/vomiting 44% 24% Invasive drainage of the anterior chamber is avail-
Stomach cramps – – able as an alternative emergency procedure for short-
Tachycardia – –
term reduction of intraocular pressure (29). This is
more difficult with a shallow or completely flattened
Findings
anterior chamber, and decompression via posterior
Elevated intraocular pressure 100% – sclerotomy may be a better solution.
Red eye 75% 23% Furthermore, in an acute situation, but also in the
event of persistently elevated intraocular pressure, the
Corneal edema 80% –
pressure can be lowered by means of peripheral laser
Shallow anterior chamber – – iridoplasty with the argon laser. In an acute case, this
Anisocoria/fixed pupil 100% 14% may be more difficult in the presence of pronounced
Bradycardia/arrhythmia – – corneal edema. A recent Cochrane Review (evidence
level Ia) showed that this treatment was equivalent to
* Modified from(16), incidence data from Chua et al. 2017 (4) and Nuessle et al. 2021 (1) the described alternatives in narrow-angle glaucoma
(30).

Miotics
Pilocarpine in the form of eyedrops acts as a miotic and
can draw the peripheral iris tissue out of the anterior
Treatment chamber angle. As long as the sphincter muscle re-
The two principles of treatment for acute angle closure mains ischemic or paralyzed due to the elevated in-
are swift lowering of intraocular pressure followed by traocular pressure, however, pilocarpine has no effect
elimination of the pupillary block, if present. Symp- and should not be used, because there is also the danger
tomatic treatment with analgesics and antiemetics of rotation of the ciliary body and thus enhancement of
should be considered. the outflow obstruction (16). Pilocarpine should there-
fore be given only if the pupil is mobile. Only one con-
Pressure reduction trolled prospective (but not blind) study has compared
The goal of rapid lowering of the intraocular pressure is different dosages of pilocarpine. Two doses of pilocar-
first to prevent complications and swiftly relieve the pine 2% one hour apart seem to suffice (31). No sys-
symptoms. However, the pressure decrease also temic adverse effects of local treatment occurred in any
reduces the corneal edema, facilitating treatment of the treatment groups.
measures to eliminate the pupillary block. Topical and
systemic pressure-lowering agents usually suffice. In Elimination of pupillary block components
addition, hyperosmotically acting substances can be As soon as the acute attack has been managed, the pu-
used to lower the volume of the vitreous body. Miotics pillary block should be eliminated to reduce the risk
can then be given to release the pupillary block. Medi- of recurring attacks or conversion to chronic disease.
cations that can be used to reduce the production of Laser peripheral iridotomy (LPI), surgical iridectomy
aqueous fluid include topical β-blockers, topical (SI), which creates an additional outflow pathway
α-agonists, and carboanhydrase inhibitors, which can from the posterior to the anterior chamber, and

Etiology Pressure lowering


Examination of the anterior chamber angle is helpful in distin- Complications must be avoided and the symptoms relieved by
guishing between primary and secondary disease. prompt lowering of intraocular pressure. This also has the
effect of decreasing corneal edema, which facilitates treatment
measures to eliminate the pupillary block.

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primary lens surgery comprising phacoemulsification focal necrosis of the lens epithelium and ischemic in-
with intraocular lens implantation (Phaco/IOL) have jury of the iris musculature, may occur.
been shown to be the most effective means of However, the most dreaded complication is conver-
achieving this goal. sion to irreversible chronic glaucoma. Both the
SI and LPI are efficacious methods for elimination formation of adhesions and persisting appositional
of pupillary block. Randomized clinical trials have obstruction can damage the trabecular meshwork and
been conducted on both interventions (evidence level permanently disrupt the outflow of aqueous fluid
Ib). In Caucasians, adequate control of intraocular (16).
pressure is achieved in 65–76% of cases by this The rate of conversion to manifest glaucoma in
means alone, and in 84–99% with additional medi- Caucasians has been the subject of only a small
cation (32–36). LPI is performed with a Nd:YAG number of studies. Andreatta et al. described develop-
(neodymium–yttrium aluminum garnet) laser and ment of closed-angle glaucoma in 15% of patients
requires sufficient translucency of the cornea. SI can with acute angle closure after a mean follow-up of
also be carried out in patients with an opaque cornea 27 ± 14 months. These patients showed greater
and is thus often necessary in acute angle closure damage to the optic nerve at the 6-month and
(16). 12-month visits. Vision was impaired in 10% of the
A review conducted by Chan et al. revealed that eyes. The duration of symptoms and the time taken to
primary lens surgery is superior to LPI and SI with re- resolve the attack were found to be risk factors for
gard to further treatment or secondary interventions conversion to primary closed-angle glaucoma (39).
(29). It must nevertheless be pointed out that the oper- In a comparable study with similar duration of
ation may be technically challenging. The shallow an- follow-up in an Asian population, Tan et al. reported
terior chamber, the poor visibility in the presence of that 21% of eyes had elevated intraocular pressure
corneal edema, the narrow pupil, the elevated in- around 12 months after acute angle closure. Glau-
traocular pressure, and instability of the lens may in- comatous optic neuropathy was present in 17% and
crease the risk of surgical complications. The advan- visual field deficits typical for glaucoma in 12%. Two
tages of the operation must therefore be weighed thirds of eyes with acute angle closure went on to
against the danger of complications in each individual develop adhesions of the anterior chamber angle.
case. Again, the duration of symptoms and the time taken
On the basis of the available evidence, the Euro- to resolve the attack were revealed to be risk factors
pean Glaucoma Society recommends first carrying for conversion. In this regard, patients who subse-
out LPI or SI. Phaco/IOL can be considered later in quently developed primary closed-angle glaucoma
the disease course or in the event of development of consulted a physician after a mean 56.3 hours of
chronic narrow-angle glaucoma. symptoms, while the corresponding figure for those
If goniosynechiae are present (particularly in who did not develop primary closed-angle glaucoma
chronic disease), surgical release of these adhesions was 20.5 hours (40).
in the chamber angle can be performed to open up the
angle and enable resumption of aqueous fluid outflow Prevention
(37). If this should prove impossible or the results are Approximately half of the patients with acute primary
not good enough, pressure-reducing surgery to create angle closure go on to experience the same event in the
an artificial channel for outflow of aqueous fluid can be fellow eye within 5 years (2). Because of the elevated
considered. Because an operation of this kind may risk, prophylactic LPI should be performed at an early
delay recovery and lead to further complications, the stage in fellow eyes that have a shallow anterior
treatment options described above should be ex- chamber (2).
hausted first (38). Due to the results of the EAGLE study, the recom-
mendations of the European Glaucoma Society have
Complications been adapted to add clear lens extraction to LPI as
The goals of prompt initiation of treatment are to re- first-line treatment for primary angle closure or pri-
lieve the symptoms and avoid long-term damage. En- mary closed-angle glaucoma in persons over 50 years
dothelial cells in the cornea may die off due to excess- of age (evidence level Ib). In that age group, lens
ive pressure, potentially leading to subsequent cor- extraction was significantly superior to LPI in terms
neal decompensation. Glaucoma blind spots, a sign of of lowering of intraocular pressure, pressure-reducing

Elimination of pupillary block components Consequences


As soon as the acute episode has been dealt with, the pupil- There is a risk of conversion to a chronic condition, namely
lary block should be eliminated, thus reducing both the risk of narrow-angle glaucoma.
recurring attacks and the danger of conversion to chronic dis-
ease.

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Europe in 2015: magnitude, temporal trends and projections. Br J
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eugs.org/eng/guidelines.asp (last accessed on 25 October 2021).
treat in order to prevent one case of angle closure was
17. Wang N, Wu H, Fan Z: Primary angle closure glaucoma in Chinese
44 (e3). It is unknown whether these findings would and Western populations. Chin Med J (Engl) 2002; 115: 1706–15.
apply to a non-Chinese population. 18. Mapstone R: Provocative tests in closed-angle glaucoma. Br J
Altogether, then, although prophylactic treatment Ophthalmol 1976; 60: 115–9.
is possible, the risk constellation for acute angle clo- 19. Lowe RF: Primary creeping angle-closure glaucoma. Br J Ophthalmol
1964; 48: 544–50.
sure cannot always be clearly defined, so the decision 20. Park J-H, Lee Y-C, Lee S-Y: The comparison of mydriatic effect
has to be made in each individual case. between two drugs of different mechanism. Korean J Ophthalmol
2009; 23: 40–2.
Conflict of interest statement 21. Wolfs RC, Grobbee DE, Hofman A, de Jong PT: Risk of acute
The authors declare that they have no conflict of interest. angle-closure glaucoma after diagnostic mydriasis in nonselected
subjects: the Rotterdam study. Invest Ophthalmol Vis Sci 1997; 38:
Manuscript received on 10 February 2021, revised version accepted on 8 2683–7.
June 2021
22. Yang MC, Lin KY: Drug-induced acute angle-closure glaucoma: a
Translated from the original German by David Roseveare. review. J Curr Glaucoma Pract 2019; 13: 104–9.
23. Aschner B: Über einen bisher noch nicht beschriebenen
References Reflex vom Auge auf Kreislauf und Atmung. Verschwinden des
Radialispulses bei Druck auf das Auge. Wien Klin Wochenschr
1. Nuessle S, Luebke J, Boehringer D, Reinhard T, Anton A: [Acute angle
closure: an ophthalmological emergency in the emergency room]. Med 1908; 108: 1529.
Klin Intensivmed Notfmed 2021. Epub ahead of print. 24. Dagnini G: Interno ad un riflesso provocato in alcuni emiplegici collo
2. Prum BE, Herndon LW, Moroi SE, et al.: Primary angle closure pre- stimolo del la corne e co11a pressione sul bulbo oculare. Societa
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ferred practice pattern . Guidelines. Ophthalmology 2016; 123: 1–40. Medico-Chirurgica Di Bologna 1908; 8: 380–3.
3. Ramesh S, Maw C, Sutton CJ, Gandhewar JR, Kelly SP: Ethnic as- 25. Apt L, Isenberg S, Gaffney WL: The oculocardiac reflex in strabismus
pects of acute primary angle closure in a UK mulicultural conurbation. surgery. Am J Ophthalmol 1973; 76: 533–6.
Eye (Lond) 2005; 19: 1271–5. 26. Allen LE, Sudesh S, Sandramouli S, Cooper G, McFarlane D,
4. Chua PY, Day AC, Lai KL, et al.: The incidence of acute angle closure Willshaw HE: The association between the oculocardiac reflex and
in Scotland: a prospective surveillance study. Br J Ophthalmol. 2018; post-operative vomiting in children undergoing strabismus surgery.
102: 539–43. Eye (Lond) 1998; 12: 193–6.
5. David R, Tessler Z, Yassur Y: Epidemiology of acute angle-closure 27. van den Berg AA, Lambourne A, Clyburn PA: The oculo-emetic
glaucoma: incidence and seasonal variations. Ophthalmologica 1985; reflex. A rationalisation of postophthalmic anaesthesia vomiting. An-
191: 4–7. aesthesia 1989; 44: 110–7.

Prevention
Approximately half of the patients with acute primary angle
closure goes on to experience the same event in the fellow
eye within 5 years. Because of the elevated risk, prophylactic
LPI should be performed at an early stage in fellow eyes that
have a shallow anterior chamber.

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28. Waterman H, Slater R, Leatherbarrow B, Waterman C, Hillier V: Corresponding author


Post-operative nausea and vomiting following orbital hydroxyapatite PD Dr. med. Jan Lübke
implant surgery. Eur J Anaesthesiol 1998; 15: 590–4. Klinik für Augenheilkunde
29. Chan PP, Pang JC, Tham CC: Acute primary angle closure-treatment Killianstr. 5, 79106 Freiburg, Germany
strategies, evidences and economical considerations. Eye (Lond) jan.luebke@uniklinik-freiburg.de
2019; 33: 110–9.
Cite this as
30. Bayliss JM, Ng WS, Waugh N, Azuara-Blanco A: Laser peripheral Nüßle S, Reinhard T, Lübke J: Acute closed-angle glaucoma—
iridoplasty for chronic angle closure. Cochrane Database Syst Rev an ophthalmological emergency. Dtsch Arztebl Int 2021; 118: 771–80.
2021; 3: CD006746. DOI: 10.3238/arztebl.m2021.0264
®
31. Edwards RS: A comparative study of Ocuserta Pilo 40, intensive
pilocarpine and low-dose pilocarpine in the initial treatment of
primary acute angle-closure glaucoma. Curr Med Res Opin 1997; ►Supplementary material
13: 501–9. eReferences and Case Report:
32. Krupin T, Mitchell KB, Johnson MF, Becker B: The long-term effects www.aerzteblatt-international.de/m2021.0264
of iridectomy for primary acute angle-closure glaucoma. Am J
Ophthalmol 1978; 86: 506–9.
33. Playfair TJ, Watson PG: Management of acute primary angle-
closure glaucoma: a long-term follow-up of the results of peripheral
iridectomy used as an initial procedure. Br J Ophthalmol 1979; 63:
17–22. Further information on CME
34. Saunders DC: Acute closed-angle glaucoma and Nd-YAG laser
iridotomy. Br J Ophthalmol 1990; 74: 523–5. ● Participation in the CME certification program is possible only
35. Buckley SA, Reeves B, Burdon M, et al.: Acute angle closure via the Internet: cme.aerzteblatt.de. This unit can be
glaucoma: relative failure of YAG iridotomy in affected eyes and accessed until 11 November 2022. Submissions by letter,
factors influencing outcome. Br J Ophthalmol 1994; 78: 529–33.
e-mail, or fax cannot be considered.
36. Fleck BW, Wright E, Fairley EA: A randomised prospective
comparison of operative peripheral iridectomy and Nd:YAG laser ● The completion time for all newly started CME units is 12
iridotomy treatment of acute angle closure glaucoma: 3 year visual months. Theresults can be accessed 4 weeks following the
acuity and intraocular pressure control outcome. Br J Ophthalmol
1997; 81: 884–8. start of the CME unit. Please note the respective submission
37. Avar M, Jordan JF, Neuburger M, et al.: Long-term follow-up of deadline at: cme.aerzteblatt.de.
intraocular pressure and pressure-lowering medication in patients ● This article has been certified by the North Rhine Academy
after ab-interno trabeculectomy with the trabectome. Graefes Arch
Clin Exp Ophthalmol 2019; 257: 997–1003. for Continuing Medical Education. CME points can be man-
38. Luebke J, Neuburger M, Jordan JF, et al.: Bleb-related infections and aged using the “uniform CME number” (einheitliche Fortbil-
long-term follow-up after trabeculectomy. Int Ophthalmol 2019; 39: 571–7. dungsnummer, EFN). The EFN must be stated during regis-
39. Andreatta W, Elaroud I, Nightingale P, Nessim M: Long-term outcomes tration on www.aerzteblatt.de (“Mein DÄ”) or entered in
after acute primary angle closure in a white Caucasian population. “Meine Daten”, and consent must be given for results to be
BMC Ophthalmol 2015; 15: 108. communicated. The 15-digit EFN can be found on the CME
40. Tan AM, Loon SC, Chew PTK: Outcomes following acute primary card (8027XXXXXXXXXXX).
angle closure in an Asian population. Clin Experiment Ophthalmol
2009; 37: 467–72.

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MEDICINE

CME credit for this unit can be obtained via cme.aerzteblatt.de until 11 November 2022.
Only one answer is possible per question. Please select the answer that is most appropriate.

Question 1 Question 6
What are the characteristic symptoms of acute angle Which of the following helps to differentiate between
closure? primary and secondary acute angle closure?
a) Sooty rain and agitation a) Measurement of intraocular pressure
b) Flashes of light and dizzy spells b) Measurement of visual acuity
c) Somnolence and photophobia c) Examination of the anterior chamber angle
d) Periocular pain and rapid deterioration of vision d) Optical coherence tomography
e) Disorientation and disturbance of color vision e) Retinal examination

Question 2 Question 7
Which of the following is the most easily Which of the following is an evidence-based method for
assessed index for the risk of anterior chamber angle elimination of pupillary block after resolution of the acute
obstruction? attack?
a) Severity of cataract a) Puncture of the vitreous body
b) Vitreous body diameter b) Corneal transplantation
c) Posterior chamber depth c) Surgical iridectomy
d) Zonular fiber length d) Laser puncture of the retina
e) Anterior chamber depth e) Immobilization of both eyes

Question 3 Question 8
Which of the following combinations of findings is Which of the following is a severe complication that
common in acute primary angle closure? may occur in the wake of acute angle closure?
a) Elevated intraocular pressure and fixed pupil a) Gradual corneal opacification
b) Nystagmus and postural vertigo b) Development of halos in dim light
c) Ptosis und vestibular vertigo c) Increased likelihood of glare sensitivity
d) Nystagmus and hypotension d) Conversion to irreversible chronic glaucoma
e) Blepharitis and fever > 38.5 °C e) Acute development of cataract

Question 4 Question 9
Which of the following epidemiological statements is true Which of the following hyperosmotically acting
for acute angle closure? substances can be used to lower the pressure in acute
a) Men are more commonly affected than women. angle closure?
b) Asians are more commonly affected than Caucasians. a) Acetylsalicylic acid
c) Younger persons are more commonly affected than older b) Mannitol
persons. c) Simvastatin
d) Acute angle closure occurs more frequently in Europe than d) Physostigmine
on other continents. e) Low-molecular heparin
e) Angle-closure glaucoma is the most commonly occurring
form of glaucoma in Europe.
Question 10
Medications of which class can trigger acute angle
closure?
Question 5
a) Antimycotics
Which of the following is an important examination
b) Immunosuppressants
technique for assessment of excessively elevated
c) Diuretics
intraocular pressure that can be performed anywhere
d) Anticholinergics
at any time?
e) Laxatives
a) Transpalpebral palpation
b) Retinal examination
c) Measurement of visual acuity
d) Examination of the optic nerve
e) Measurement of corneal thickness ►Participation is possible only via the Internet: cme.aerzteblatt.de

780 Deutsches Ärzteblatt International | Dtsch Arztebl Int 2021; 118: 771– 80
MEDICINE

Supplementary material to:

Acute Closed-Angle Glaucoma—An Ophthalmological Emergency


by Simone Nüßle, Thomas Reinhard, and Jan Lübke
Dtsch Arztebl Int 2021; 118: 771–80. DOI: 10.3238/arztebl.m2021.0264

eReferences
e1. Azuara-Blanco A, Burr J, Ramsay C, et al.: Effectiveness of early
lens extraction for the treatment of primary angle-closure glaucoma
(EAGLE): a randomised controlled trial. Lancet 2016; 388: 1389–97.
e2. Pakravan M, Sharifipour F, Yazdani S, Koohestani N, Yaseri M:
Scheimpflug imaging criteria for identifying eyes at high risk of acute
angle closure. J Ophthalmic Vis Res 2012; 7: 111–7.
e3. He M, Jiang Y, Huang S, et al.: Laser peripheral iridotomy for the
prevention of angle closure: a single-centre, randomised controlled
trial. Lancet 2019; 393: 1609–18.

Deutsches Ärzteblatt International | Dtsch Arztebl Int 2021; 118: 771– 80 | Supplementary material I
MEDICINE

CASE REPORT

O
ne evening a 49-year-old woman presents to a hos-
pital emergency room. She states that for the sec-
ond time in 6 weeks she is experiencing an
extremely strong headache with nausea; in the morning of
the same day, she vomited. She is also having problems
with her sight; in particular, light from any source is
unpleasant. The vision in her right eye is blurred.
Migraine was the only known pre-existing illness. Physi-
cal examination revealed little in the way of abnormal-
ities, but the pupil of her right eye seemed not to react to
light. Blood test results were normal. Because of the
severity of the patient’s pain, she was admitted to a gen-
eral medical ward. However, administration of analgesics
and antiemetics brought no improvement. Further diag-
nostic work-up was planned for the next day, including
ophthalmological consultation. The patient’s symptoms
remained just as intense the next morning despite maxi-
mal conservative treatment, so cranial computed
tomography was performed. However, no reason for the
symptoms was detected. Ophthalmological examination
finally showed that the intraocular pressure in the right
eye was increased to 62 mm Hg, and acute angle closure
was diagnosed. The symptoms subsided swiftly after
administration of pressure-lowering medication. On the
next day, the patient was treated with surgical iridectomy
of the right eye and prophylactic laser iridotomy of the
left eye.

II Deutsches Ärzteblatt International | Dtsch Arztebl Int 2021; 118: 771– 80 | Supplementary material

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