Glaucoma: Types, Signs, Diagnosis, Treatment and Emergency Management

Scope. Glaucoma is a group of progressive optic neuropathies that damage retinal ganglion cells and the optic nerve, producing characteristic visual-field loss. Raised intraocular pressure (IOP) is an important treatable risk factor, but glaucoma is not simply “high pressure”: optic-nerve injury can occur at statistically normal IOP, and many people with elevated IOP never develop glaucoma. This lesson covers the supplied 41-slide deck in full: definitions, risk factors, pathophysiology, primary and secondary disease, childhood glaucoma, clinical features, diagnostic tests, medicines, laser and surgical procedures, nursing care, complications and research on sustained-release treatment. Where the slide wording is inaccurate, dated or oversimplified, the correction is explained.

Learning objectives

• Define glaucoma as progressive optic-nerve damage, and explain why IOP is a risk factor rather than the definition.
• Describe aqueous humour circulation and distinguish open-angle from angle-closure mechanisms.
• Classify primary, secondary, congenital, infantile and juvenile glaucoma.
• Recognise silent chronic disease and acute angle-closure warning signs.
• Identify secondary glaucoma due to lenses, uveitis, neovascularisation, steroids, trauma, pigment or intraocular tumours.
• Explain the roles and limitations of tonometry, gonioscopy, optic-nerve assessment, perimetry, OCT and pachymetry.
• Summarise emergency and chronic management, including medicines, laser, surgery and patient education.
• Prioritise emergency-medicine and nursing actions that protect vision and prevent avoidable injury.

1. Definition, anatomy and aqueous humour flow

Glaucoma is a group of diseases in which retinal ganglion-cell axons and the optic nerve are progressively lost, causing characteristic structural change and corresponding visual-field damage. The central cup of the optic disc may enlarge as the neuroretinal rim thins or develops notches. Damage is irreversible: treatment aims to slow or stop further loss, not restore the field already lost.

The ciliary body produces aqueous humour. It passes from the posterior chamber through the pupil into the anterior chamber and leaves mainly through the trabecular meshwork, Schlemm canal and collector channels. A smaller portion exits by the uveoscleral pathway. The balance between production and drainage contributes to IOP. Outflow resistance, angle obstruction, inflammation, blood, pigment, lens material, abnormal vessels or scarring may raise pressure. The supplied slides correctly connect reduced outflow with pressure elevation but overstate aqueous overproduction as the usual cause of primary open-angle glaucoma (POAG); in POAG, increased resistance at the trabecular outflow pathway is the central teaching model.

IOP measurement is useful but cannot diagnose or exclude glaucoma alone. Some healthy people have pressure above the statistical reference range, while a person with normal-tension glaucoma (NTG) can have characteristic optic-nerve damage at measured pressures within that range. The optic nerve, anterior chamber angle and visual function must be assessed together.

2. Epidemiology and risk factors

Glaucoma becomes more common with age and can remain undetected until substantial peripheral field has been lost. It is a major cause of irreversible blindness worldwide. Because early POAG is usually painless and central acuity is often preserved, asking about symptoms alone will miss many cases. A person may only notice difficulty when navigating, reading across a page, driving or using one eye at a time.

The source slides give an older global estimate of “6 to 67 million,” state that normal IOP is “19–21 inches of mercury” in one place and “16–23 mmHg” elsewhere, and imply that IOP above 24 mmHg defines disease. These figures and units are unreliable as diagnostic rules. IOP is recorded in mmHg; pressure thresholds vary by device, corneal properties and context. Glaucoma is diagnosed from the whole clinical picture, and normal-tension disease exists.

3. Classification

3.1 Primary and secondary glaucoma

Primary glaucoma occurs without an identified secondary ocular cause. Its main adult patterns are primary open-angle glaucoma and primary angle-closure disease. Secondary glaucoma is raised IOP or optic-nerve damage associated with another ocular or systemic condition, a medication, trauma or altered anatomy. A secondary mechanism may be open-angle, angle-closure, or both.

3.2 Open-angle and angle-closure mechanisms

Angle-closure disease is not synonymous with an acute attack. A person may have a narrow or occludable angle without raised IOP or optic-nerve damage. Classification distinguishes an angle-closure suspect from pressure elevation and from established optic neuropathy; the distinction affects counselling, follow-up and preventive treatment.

3.3 Childhood glaucoma

Primary congenital glaucoma results from abnormal development of the anterior chamber angle, impairing aqueous outflow. Age labels vary across references, but teaching commonly distinguishes disease present at birth, early-onset disease in infancy, and juvenile-onset glaucoma later in childhood or adolescence. The slide deck divides congenital disease into “true congenital,” infantile and juvenile forms, but its percentages and exact age cutoffs should not be memorized as universal statistics.

Childhood glaucoma may also be secondary to congenital anomalies or systemic syndromes, prior surgery, trauma, inflammation, steroid treatment, aphakia or other structural disorders. Childhood glaucoma is uncommon, but delay can quickly impair visual development and permanently damage the optic nerve. A suspicious child needs urgent assessment by a paediatric ophthalmologist; examination under anaesthesia may be required to measure IOP and inspect the angle accurately.

4. Primary open-angle glaucoma

POAG is a chronic, usually bilateral but often asymmetric optic neuropathy with an open anterior chamber angle and no other identifiable cause. Elevated IOP is common, but the level varies. In NTG the optic nerve and field show glaucomatous damage despite IOP readings that are not elevated by conventional thresholds. Pressure lowering can still slow progression in NTG.

4.1 Symptoms and signs

• Most people have no symptoms early. Peripheral visual-field defects develop gradually and may go unnoticed because the other eye compensates.
• Late disease can cause tunnel-like vision, difficulty navigating, bumping into objects, impaired mobility or marked functional visual loss.
• Central visual acuity is often retained until disease is advanced; reading acuity alone does not rule out glaucoma.
• Optic-disc signs include focal neuroretinal rim thinning or notching, vertical cup enlargement, asymmetry between eyes, disc haemorrhage and retinal nerve-fibre-layer defects.
• Visual-field defects may include a nasal step, arcuate scotoma or defects respecting the horizontal meridian; structural and functional changes should correspond.

The slide deck lists mild ache, headache, night acuity loss and corneal oedema as clinical features of POAG. These are not reliable defining features of uncomplicated chronic POAG. A quiet, painless eye is typical; pain, red eye or corneal haze suggests acute pressure elevation or another diagnosis and requires urgent evaluation.

5. Primary angle-closure glaucoma

5.1 Acute angle-closure crisis

In a predisposed eye, the iris blocks the trabecular meshwork and aqueous outflow. Pupillary block is a common mechanism: pressure differential bows the iris forward and closes the angle. An acute crisis causes a rapid IOP rise and is an ophthalmic emergency. Delay can cause permanent optic-nerve injury within hours. The deck’s claim that blindness predictably follows within three to five days is not a safe waiting period; treat immediately.

Symptoms can be mistaken for migraine, gastrointestinal illness or a neurologic problem. Ask about new unilateral visual blur, halos and ocular pain whenever headache and vomiting are unexplained. Assess the fellow eye because it may have a narrow angle and be at risk of a future attack.

5.2 Chronic or intermittent angle closure

Partial or intermittent angle closure may produce transient episodes of blur, halos, brow ache or headache, especially in dim light, then improve when the angle reopens. Repeated closure can form peripheral anterior synechiae and cause chronic IOP elevation, optic-nerve damage and field loss. A patient may have few or no symptoms despite progressive disease. Gonioscopy, not symptom pattern alone, establishes the angle anatomy.

6. Secondary glaucoma: causes and mechanisms

The supplied slides include lens-induced, uveitic, neovascular, tumour-associated, steroid-induced and pigmentary glaucoma. They also list inflammation, intraocular haemorrhage, prior operations and diabetes as broad secondary causes. The table preserves each of those categories and shows why finding the mechanism matters: treating pressure alone may fail if the underlying cause is not addressed.

7. Congenital glaucoma: recognition in infants and children

Infants cannot describe blurred vision or pain. Caregivers may instead report constant tearing, light sensitivity, frequent blinking or forceful eyelid closure. The classic triad is epiphora, photophobia and blepharospasm. Corneal clouding from oedema, a large corneal diameter, enlarged globe (buphthalmos), Haab striae, high IOP, optic-disc cupping or increasing myopia may be found. The source slides specifically note lacrimation, photophobia, corneal oedema, raised IOP, myopia and a large cornea; the clinical meaning is an urgent childhood eye assessment, not watchful waiting.

In older children, the only clue may be reduced school performance, squint, abnormal head posture, enlarged eyes, progressive myopia or unexplained visual difficulty. Check both eyes and assess visual behaviour. Paediatric glaucoma is generally managed surgically by a specialist; medication may be used as a bridge or adjunct. Delay risks amblyopia as well as irreversible optic-nerve damage.

8. Diagnostic assessment

8.1 History

• Establish onset, duration, laterality, progression, pain, redness, halos, headache, nausea, vomiting, transient episodes, field loss and functional impact.
• Ask about family history, ancestry, previous eye pressure treatment, previous eye surgery, trauma, hyphema, uveitis, retinal disease and cataract.
• Review all medications and routes, especially topical or systemic corticosteroids, inhalers, periocular injections, anticholinergics, mydriatics and recently started topiramate.
• Ask about diabetes, vascular disease and systemic conditions; identify barriers to follow-up, medication access or correct drop administration.
• For a child: ask when symptoms began, developmental progress, family history, congenital anomalies and caregiver observations of tearing, photophobia or enlarged/cloudy eyes.

8.2 Examination

1. Visual acuity: test each eye separately, with correction and pinhole when appropriate. A normal central acuity does not exclude early field loss.
2. Pupils and eye movements: compare pupils, reactivity and relative afferent pupillary defect; inspect for anisocoria, abnormal response or ocular misalignment.
3. External and slit-lamp examination: look for injection, corneal oedema, shallow anterior chamber, inflammation, pseudoexfoliation, pigment, hyphema, lens changes, iris neovascularisation and other secondary signs.
4. Tonometry: measure IOP using an available calibrated method. Repeat a surprising measurement when safe. Do not apply pressure or perform tonometry if open-globe injury is suspected.
5. Gonioscopy: an ophthalmic examination using a mirrored contact lens to inspect the drainage angle. It is essential to distinguish open-angle from angle-closure and to identify secondary material, synechiae, recession or neovascularisation. Do not dilate an eye with a potentially occludable angle unless an eye clinician has judged it safe.
6. Optic nerve examination: assess disc size, cup-to-disc ratio, rim thickness, notching, haemorrhage and nerve-fibre-layer defects. Compare both eyes and correlate with visual function.
7. Visual-field testing: automated perimetry detects and follows functional loss. A reliable baseline helps determine severity and progression; early disease may require repeat testing.
8. Optical coherence tomography (OCT): measures retinal nerve-fibre-layer and ganglion-cell complex thickness and helps document structural loss. It supports, but does not replace, clinical examination and field testing.
9. Pachymetry: measures central corneal thickness and informs risk interpretation of IOP. It does not diagnose glaucoma in isolation.
10. Photography: optic-disc or fundus photographs can document change over time. Slit-lamp biomicroscopy and fundus imaging complement each other.

The supplied deck lists ocular and medical history, tonometry, ophthalmoscopy, gonioscopy, perimetry, slit-lamp examination, fundus photography, pachymetry and nerve-fibre analysis. Each is represented above. In a resource-limited emergency department, do not delay urgent referral because OCT, perimetry or pachymetry is unavailable; measure visual acuity, recognize the danger pattern and contact the eye service.

8.3 Differential diagnosis in the emergency department

9. Emergency management of acute angle closure

Acute angle closure is a time-critical diagnosis and should be co-managed with an ophthalmologist. The aim is to lower IOP promptly, relieve pain and nausea, reopen the angle where possible and prevent optic-nerve damage. Pressure-lowering medicines are a bridge to definitive treatment; they do not remove the anatomical predisposition.

1. Recognise and call early. Contact ophthalmology or the emergency eye service immediately. State the visual acuity, pupil appearance, corneal clarity, symptom onset, measured IOP if safely obtained, relevant comorbidities and medicines.
2. Assess both eyes. Document acuity in each eye, pupils, pain, redness and systemic symptoms. The fellow eye may also have a narrow angle and can need prompt preventive treatment.
3. Provide supportive care. Keep the patient in a monitored setting, manage pain and vomiting, and avoid unnecessary delay. Use a calm environment and prepare for urgent specialist review or transfer.
4. Lower IOP under protocol. Ophthalmology-directed treatment may combine topical aqueous suppressants such as a beta blocker, alpha-2 agonist and carbonic anhydrase inhibitor with systemic acetazolamide when appropriate. A hyperosmotic agent such as mannitol may be considered for a severe or refractory attack after renal, cardiac and volume status are reviewed.
5. Use pilocarpine at the right time. A very high IOP can make the iris sphincter ischaemic and unresponsive to pilocarpine. A specialist may introduce a miotic after pressure begins to fall and the pupil responds. Giving it reflexively at the start can be ineffective and is not suitable for every mechanism of angle closure.
6. Check contraindications. Topical timolol may be unsafe with asthma or significant obstructive lung disease, bradycardia, heart block or decompensated heart failure. Acetazolamide and mannitol have important renal, electrolyte, cardiac, hepatic, allergy and volume-status considerations. The eye team should select medicines and doses using the current Uganda Clinical Guidelines and local hospital protocol.
7. Definitive treatment. Laser peripheral iridotomy relieves pupillary block when that is the mechanism, and the fellow eye is often treated because it is at risk. Lens extraction or another procedure may be needed when lens anatomy, persistent closure or inadequate pressure control is central. Recheck IOP and angle after treatment and arrange follow-up.

Current ophthalmology guidance describes acute angle-closure initial treatment as urgent IOP lowering followed by treatment of the angle mechanism. Pilocarpine may be ineffective while pressure is extremely high because the iris sphincter is ischaemic. This is why sequencing and specialist input matter; the detailed regimen depends on pressure, mechanism, comorbidities and local availability.

10. Long-term management of chronic glaucoma

10.1 Treatment goals

The goals are to preserve useful vision and quality of life by slowing progression, lowering IOP to an individualized target, monitoring optic-nerve structure and visual fields, treating secondary causes, and supporting long-term adherence. Established glaucomatous loss does not return with drops, laser or surgery. Target pressure and follow-up frequency depend on baseline IOP, disease severity, rate of change, age, life expectancy, fellow-eye status and the patient’s ability to use treatment.

10.2 Medicines used to lower IOP

In chronic POAG, a prostaglandin analogue or laser trabeculoplasty may be selected as initial therapy depending on disease, patient preferences, access, cost and current guidance. Beta blockers, carbonic anhydrase inhibitors, alpha agonists and miotics can be used as alternatives or additions. The slide list includes timolol, betaxolol, pilocarpine, carbachol, carbonic anhydrase inhibitors, prostaglandin analogues and osmotic agents; the distinction above clarifies which are commonly used long term and which belong mainly to acute care.

10.3 Drop technique and adherence

• Wash hands; check the bottle label, eye and expiry; avoid touching the tip to the lashes, eye or fingers.
• Instil the prescribed single drop into the lower conjunctival sac; close the eye gently rather than blinking hard.
• Press gently over the inner corner of the closed eye for one to three minutes when taught, especially with beta blockers, to limit systemic absorption.
• Leave about five minutes between different drops unless the clinician gives different instructions.
• Use the medicine every day as prescribed, even when the eye feels normal. Patients usually cannot feel whether chronic glaucoma drops are working.
• Ask the patient to demonstrate the technique. Consider caregiver support, reminder routines, simpler dosing, affordability and access to refills.
• Discuss adverse effects and what to do if a dose is missed; do not double a dose or stop therapy without advice.

The source slides appropriately emphasize patient understanding and emotional response. Glaucoma can be frightening because loss is permanent, yet early disease may feel invisible. Explain the purpose of treatment in plain language: drops do not sharpen vision immediately; they aim to protect remaining vision over time.

11. Laser and surgical treatment

Surgery lowers pressure and can reduce the rate of further damage, but it does not reverse optic-nerve loss and does not guarantee freedom from drops or follow-up. Potential complications include transient or persistent hypotony, shallow anterior chamber, choroidal detachment or effusion, retinal detachment, cataract, bleb leak or infection, endophthalmitis, scarring and failure to meet target IOP. The deck’s list of complete vision loss, choroidal or retinal detachment, chronic hypotony and anterior-segment necrosis is preserved here as serious complications; risk depends on the procedure and patient.

12. Sustained-release treatment and ongoing research

The final research slide in the supplied deck mentions safety and efficacy of sustained-release bimatoprost for open-angle glaucoma or ocular hypertension. Sustained-release intracameral implants and other long-acting delivery systems are being used or studied in some jurisdictions to reduce dependence on daily drops. They are not automatically suitable for every patient, and regulatory approval, repeat dosing, cost and availability differ between countries. For Ugandan practice, follow the locally approved formulary and specialist guidance rather than assuming that a product discussed in a research slide is routinely available.

13. Complications, prognosis and follow-up

13.1 Disease complications

• Progressive peripheral field constriction, reduced contrast and impaired mobility.
• Advanced tunnel vision and irreversible blindness if untreated or inadequately controlled.
• Acute angle-closure crisis with rapid pressure rise and risk of optic-nerve injury.
• Secondary ocular damage from inflammation, trauma, tumour, neovascularisation or lens-related obstruction.
• In children, amblyopia and loss of visual development in addition to optic-nerve damage.

13.2 Treatment-related complications

Eye drops can cause surface irritation, allergy, redness, pigment change or systemic effects depending on class. Laser can cause a transient pressure spike, inflammation or inadequate angle response. Filtering and drainage surgery may cause hypotony, choroidal detachment, shallow chamber, cataract, bleb leak, infection, retinal detachment or failure. Cyclodestructive procedures can reduce pressure but carry risk of inflammation, hypotony and loss of useful vision. Report sudden postoperative pain, reduced vision, redness, discharge, flashes, floaters or a curtain urgently.

13.3 Long-term monitoring

Follow-up is lifelong for established glaucoma. The treating eye team checks IOP against the individualized target, adherence and side effects, optic-disc appearance, OCT or nerve-fibre layer, and visual fields. A single “normal” pressure reading does not prove that the disease is stable; progression can occur at apparently acceptable IOP and may require a lower target or a different treatment. Bring all drops to appointments and tell the team about new medicines, pregnancy, breathing problems, slow pulse, cost barriers or missed doses.

14. Emergency-medicine and nursing care

14.1 Immediate priorities in a painful red eye

• Record onset, laterality, visual acuity in each eye, pain, halos, headache, vomiting, trauma, previous surgery and medication history.
• Inspect pupils and cornea; assess for haziness, a shallow chamber, mid-dilated pupil and ciliary injection.
• Measure IOP only if globe integrity is secure and the examiner is trained. If open-globe injury is possible, place a rigid shield and avoid tonometry, pressure or manipulation.
• Recognize acute angle closure as an emergency, contact ophthalmology immediately and arrange transfer if needed.
• Give analgesia and antiemetic treatment as clinically appropriate. Do not let symptom relief substitute for IOP control and definitive eye care.
• Check the fellow eye and communicate comorbidities that affect medication choice, including asthma, COPD, bradycardia, heart block, heart failure, renal disease and relevant allergies.
• Document the medicines and times administered, response, visual findings and exact referral discussions.

14.2 Ongoing nursing and patient-support priorities

The deck lists acute pain, self-care deficit, fear/anxiety and risk for injury as nursing diagnoses. These remain relevant, especially for a patient with sudden pain, advanced field loss or a new diagnosis. Nursing care includes symptom and vision assessment, prescribed medication administration, observing for adverse effects, protecting a postoperative eye as instructed, supporting safe mobility and checking the patient’s understanding.

• Assess pain, visual function, IOP when ordered, medication response and emotional distress; escalate deterioration promptly.
• Administer prescribed eye drops in the correct eye and at the correct time; check the medication chart and contraindications.
• Teach drop technique, punctal occlusion when appropriate, spacing between drops, storage and refill planning.
• Use fall-risk measures and orientation support for people with field loss. Keep pathways clear, improve lighting and involve caregivers with consent.
• After glaucoma surgery, follow the surgeon’s positioning, shield, activity and drop instructions. A head-up position or shield may be prescribed in selected postoperative plans; they are not universal treatment for untreated glaucoma.
• Assess the patient’s understanding, beliefs, cost/access barriers and concerns about lifelong therapy. Use teach-back and provide a clear route for urgent help.
• Do not advise a patient to stop steroid or glaucoma treatment without contacting the prescriber or ophthalmologist.

15. Applied cases

Case 1: Silent peripheral field loss

A 58-year-old with a first-degree relative who went blind has no eye pain and reads the acuity chart well. Fundus examination suggests vertical cup enlargement and inferior rim thinning; IOP is 19 mmHg. This does not exclude glaucoma. The patient needs comprehensive ophthalmology evaluation including gonioscopy, optic-nerve assessment, repeat IOP, OCT and visual fields. NTG is one possible diagnosis after other causes are assessed.

Case 2: Pain, halos and vomiting

A 63-year-old develops sudden unilateral eye pain, blurred vision and coloured halos, followed by headache and vomiting. The eye is red, the cornea hazy and the pupil mid-dilated and sluggish. Suspect acute angle closure. Call ophthalmology immediately, document vision and examination, check medication contraindications and start protocol-directed pressure reduction without delaying definitive assessment.

Case 3: Diabetes, rubeosis and high pressure

A 66-year-old with proliferative diabetic retinopathy presents with a painful eye and raised IOP. New vessels are visible on the iris. Neovascular glaucoma is likely. Pressure control alone is insufficient; urgent glaucoma and retinal input is needed to address the ischaemic retina and angle mechanism.

Case 4: Infant with tearing and photophobia

A 4-month-old has persistent tearing, photophobia and forceful eyelid closure. The cornea looks cloudy and the eyes appear unusually large. Congenital glaucoma is a concern. Arrange urgent paediatric ophthalmology assessment; do not wait for the child to develop measurable behavioural visual loss.

Case 5: Pressure rise after steroid drops

A patient treated for uveitis with frequent steroid drops develops raised IOP. Steroid response is possible, but active uveitis, trabeculitis, synechial closure and other causes must also be considered. The clinician should reassess the inflammation and pressure with ophthalmology; the patient should not abruptly discontinue the steroid independently.

16. Self-test

1. What tissue is primarily damaged in glaucoma, and is the loss reversible?
2. Can glaucoma occur with a measured IOP in the normal range?
3. Why does a normal visual-acuity chart not exclude early POAG?
4. Which examination is essential for separating open-angle from angle-closure disease?
5. Name four secondary glaucoma mechanisms represented in the supplied slides.
6. What symptoms and signs should make an emergency clinician suspect acute angle closure?
7. Why may pilocarpine be ineffective at the beginning of an attack with very high pressure?
8. What is the purpose of laser peripheral iridotomy?
9. Which medicines need particular caution in a patient with asthma, bradycardia or renal/cardiac disease?
10. What are the three classic symptoms caregivers may notice in congenital glaucoma?
11. Why is lifelong adherence and follow-up important even when the patient feels well?
12. Which operations in the deck are now historical, uncommon or selected rather than routine?

Answers

1. Retinal ganglion cells and optic-nerve axons are progressively lost; established visual-field damage is permanent.
2. Yes. Normal-tension glaucoma has characteristic optic-nerve and field damage despite measured IOP in the conventional normal range.
3. POAG first affects peripheral fields; central acuity can remain good until advanced disease.
4. Gonioscopy.
5. Lens-induced, uveitic, neovascular, tumour-associated, steroid-induced or pigmentary glaucoma; trauma-related and pseudoexfoliative mechanisms are also important.
6. Sudden eye pain and redness, blur/halos, headache, nausea/vomiting, hazy cornea, shallow chamber and a mid-dilated poorly reactive pupil.
7. Very high pressure can make the iris sphincter ischaemic and unresponsive; a specialist may wait until pressure falls and the pupil responds.
8. It creates a small opening in the peripheral iris to relieve pupillary block in appropriate angle-closure disease.
9. Timolol requires caution with asthma/COPD, bradycardia, heart block or heart failure; acetazolamide and mannitol require renal, electrolyte, cardiac and volume-status review.
10. Epiphora (tearing), photophobia and blepharospasm.
11. Early glaucoma is usually silent, treatment prevents further loss but does not restore existing damage, and progression can continue unless pressure and function are monitored.
12. Cyclodialysis is not routine modern glaucoma surgery; cyclocryotherapy/cyclodestructive procedures are generally reserved for selected refractory cases. Trabeculotomy has an important role in congenital glaucoma, not as universal adult surgery.

Key takeaways

• Glaucoma is progressive optic neuropathy, not simply an IOP above a fixed threshold.
• POAG is usually silent until peripheral field loss is advanced; a normal acuity chart does not rule it out.
• Acute angle closure causes a painful red eye, blur/halos, headache and nausea/vomiting: call ophthalmology immediately.
• Gonioscopy classifies the drainage angle. Tonometry, optic-nerve assessment, perimetry, OCT and pachymetry answer different questions.
• Secondary causes include lens disease, uveitis, neovascularisation, steroids, trauma, pigment and tumours; treat the cause as well as the pressure.
• Lowering IOP with drops, laser or surgery slows further damage, but cannot restore lost vision; clear counselling and lifelong follow-up matter.
• For suspected acute angle closure, use the local protocol and specialist direction, check contraindications and arrange definitive treatment.

References and further reading

• Supplied teaching slides: Glaucoma.
• Uganda Ministry of Health: Uganda Clinical Guidelines 2023 (specialist ophthalmology section; use current local hospital protocols).
• Uganda Ministry of Health MediGuide: current clinical guidance.
• American Academy of Ophthalmology: Primary Open-Angle Glaucoma Preferred Practice Pattern, 2026.
• American Academy of Ophthalmology: Primary Angle-Closure Disease Preferred Practice Pattern, 2025.
• AAO EyeWiki: Primary open-angle glaucoma.
• AAO EyeWiki: Primary versus secondary angle-closure glaucoma.
• AAO EyeWiki: Review of topical glaucoma medications.
• World Health Organization: Blindness and vision impairment.