Traumatic Glaucoma

Types of traumatic glaucoma
Causes of traumatic glaucoma
Symptoms
Diagnostic tests
Non-Pharmacological Treatments (Therapies and Other Measures)
Drug Treatments
Dietary “Molecular” Supplements
Regenerative / stem cell” drugs or approaches
Surgeries
Preventions
When to See a Doctor Urgently
Diet: “What to Eat” and “What to Avoid”
Frequently Asked Questions

Traumatic glaucoma is high pressure inside the eye that happens after an eye injury. The injury can be a strong hit to the eye, a cut or puncture, a burn, or a foreign body that goes into the eye. The pressure rises because the normal drain of the eye stops working well after the trauma. The clear fluid inside the front of the eye is called aqueous humor. This fluid is made all the time by the ciliary body and it normally leaves the eye through a fine sieve called the trabecular meshwork and then out through the eye’s drainage canal. When an injury harms this drainage pathway, blocks it with blood cells or debris, narrows or closes the angle, or makes the eye inflamed and swollen, the fluid cannot leave easily. The fluid still keeps being made. Pressure builds up. When pressure stays high, it can slowly damage the optic nerve, which is the cable that carries visual signals from the eye to the brain. If not treated, this damage can lead to permanent loss of vision.

Traumatic glaucoma is high pressure inside the eye that happens after an injury to the eye. The injury can be blunt (like a ball, fist, or airbag), sharp (like a cut), chemical, explosive, or from surgery or medical procedures. The pressure is called intraocular pressure (IOP). When IOP is high for too long, it can damage the optic nerve, which is the cable that carries sight from the eye to the brain. If the optic nerve is damaged, vision can be lost permanently.

Traumatic glaucoma can happen right away after the injury, a few days later, or even months to years later. In some people, the pressure spikes come and go at first. In others, the pressure stays high. The condition is different from “regular” or primary open-angle glaucoma because the starting trigger is the trauma. But the final pathway is the same: harm to the optic nerve from pressure that the nerve cannot tolerate. The good news is that careful follow-up after eye injury, early recognition of pressure rise, and the right treatment can protect vision in many people.

How trauma raises eye pressure — the core mechanisms

Blockage of the drain by blood or debris: After blunt trauma or a cut, blood can leak into the front chamber (hyphema). Red blood cells, white blood cells, clot fragments, and pigment can collect in the trabecular meshwork and clog it like hair clogging a sink. Pressure rises until the blood clears and the meshwork starts working again.
Damage and scarring of the drain: A strong hit to the eye can split the muscle layer of the ciliary body and the angle. This is called angle recession. The trabecular meshwork can be bruised and later scarred. Scarred tissue does not pass fluid well, so pressure can be high months or years after the injury.
Swelling, inflammation, and synechiae: Trauma triggers inflammation. Inflammatory proteins and cells make the meshwork sticky and less porous. The iris can stick to the cornea in the angle (peripheral anterior synechiae) and close the angle, or stick to the lens (posterior synechiae) and block pupil flow. Both raise pressure.
Lens-related block: Trauma can dislocate the lens, rupture the capsule, or make the lens swell. A swollen or shifted lens can push the iris forward and narrow the angle (phacomorphic angle closure). Ruptured lens material can spill and block the meshwork (lens-particle glaucoma). A very leaky, old lens can shed proteins that clog the meshwork (phacolytic glaucoma).
Blood breakdown products: Weeks after a vitreous hemorrhage, old red cells turn into “ghost cells.” These stiff cells can drift forward and jam the trabecular meshwork (ghost-cell glaucoma). Macrophages loaded with hemoglobin (hemolytic glaucoma) can also plug the drain. Iron from a retained iron foreign body can poison tissues (siderosis) and lower outflow.
Treatment-related pressure rise: Strong steroid eye drops are often needed after trauma to calm inflammation. Some people are “steroid responders,” which means steroids cause their eye pressure to go up. This is not anyone’s fault, but it must be watched and managed.
Space-occupying bleeding or swelling around the eye: A big retrobulbar hemorrhage (bleeding behind the eye) can compress the eye from the outside and cause a dangerous, sudden pressure rise. This is an emergency because the optic nerve and blood flow can be squeezed.

Types of traumatic glaucoma

Post-hyphema glaucoma (early): Blood and clots in the front chamber block the meshwork in the first hours to days after injury. Pressure can swing up and down as the blood settles or re-bleeds.
Angle-recession glaucoma (late): A blunt hit splits the ciliary muscle and injures the meshwork. Months to years later, scarring reduces outflow and pressure rises. The angle looks “deep and torn” on gonioscopy.
Ghost-cell glaucoma: Weeks after a vitreous hemorrhage, old, rigid red cells float into the front and jam the drain. It often follows trauma with bleeding into the back of the eye.
Hemolytic glaucoma: Macrophages stuffed with hemoglobin circulate and clog the meshwork. It may occur after large intraocular hemorrhages.
Hemosiderotic (siderosis) glaucoma: Iron from a retained iron foreign body damages the trabecular meshwork and other tissues over time, reducing outflow.
Lens-particle glaucoma: Ruptured capsule leaks lens fragments into the front chamber. These particles block the meshwork and can also trigger inflammation.
Phacolytic glaucoma: A very leaky, overripe lens releases high-molecular proteins that obstruct the drain. Trauma can hasten lens breakdown.
Phacomorphic angle-closure: A swollen or dislocated lens crowds the angle and shuts it. Pressure rises quickly and the eye becomes painful and steamy.
Inflammatory/uveitic glaucoma after trauma: Inflammatory cells and proteins reduce outflow and synechiae form. Steroids help the inflammation but must be balanced against pressure rise.
Steroid-induced glaucoma (post-trauma treatment): Some eyes respond to steroid therapy with a big pressure increase due to changes in the meshwork.
Pupillary block with posterior synechiae: The iris sticks to the lens at the pupil, trapping fluid behind the iris. The iris bows forward and closes the angle.
Peripheral anterior synechiae angle closure: The iris sticks to the trabecular meshwork in the angle, sealing it. This can be patchy at first and then become more extensive.
Vitreous blocking the angle (anterior vitreous herniation): After lens loss or zonular rupture, vitreous can prolapse into the front and obstruct the meshwork.
Silicone-oil-related pressure rise (after repair of traumatic retinal detachment): Silicone oil can migrate forward and block the meshwork or pupillary flow.
Secondary neovascular glaucoma following traumatic carotid-cavernous fistula or ischemia: Abnormal vessels grow on the iris and angle and close the outflow. This is less common but important.
Angle closure from ciliary body swelling (traumatic choroidal effusion): Swelling behind the iris–lens diaphragm pushes the angle closed.

Causes of traumatic glaucoma

Blunt eye injury that bruises the trabecular meshwork and causes angle recession.
Penetrating or perforating injury that scars or blocks the eye’s drainage pathway.
Hyphema (blood in the front chamber) clogging the trabecular meshwork.
Re-bleeding after hyphema, which adds new clots and cells to the drain.
Vitreous hemorrhage that later produces ghost cells which jam the drain.
Macrophage-rich hemolysis after large intraocular bleeding.
Retained iron foreign body (siderosis) poisoning the outflow tissues.
Chemical burns causing inflammation and scarring of the angle.
Thermal burns or blast injuries damaging the meshwork and angle.
Lens capsule rupture spilling lens particles into the front chamber.
Swollen or dislocated lens narrowing or closing the angle (phacomorphic block).
Lens protein leakage in a very leaky lens (phacolytic blockage).
Inflammation (traumatic uveitis) making the drain sticky and swollen.
Posterior synechiae creating pupillary block and forward bowing of the iris.
Peripheral anterior synechiae sealing the angle directly.
Vitreous prolapse into the front chamber obstructing the meshwork.
Steroid-induced pressure rise during post-trauma anti-inflammatory treatment.
Retrobulbar hemorrhage compressing the globe and acutely elevating pressure.
Carotid-cavernous fistula after head/face trauma leading to venous congestion and secondary angle problems.
Post-operative changes after trauma repair (including silicone oil) that block the drain or pupil.

Symptoms

Eye pain: Pressure stretches pain-sensitive tissues and causes a deep, aching pain.
Headache or brow ache: Pressure and eye strain can radiate into the forehead and temple.
Blurred or hazy vision: Corneal swelling from high pressure makes vision foggy.
Halos around lights: A swollen cornea scatters light and creates colored rings.
Eye redness: Surface blood vessels dilate with pressure and inflammation.
Light sensitivity (photophobia): An inflamed or pressure-stressed eye hurts in bright light.
Nausea and vomiting: Very high or sudden pressure spikes can trigger these symptoms.
Seeing a blood level or brownish tinge in the eye: This suggests hyphema after trauma.
Sudden drop in vision after a delay: Late pressure rise from angle recession or ghost cells can reduce vision weeks to months later.
Peripheral vision loss: Glaucoma damages side vision first; this is often subtle at the start.
Floaters or dark spots: Vitreous hemorrhage from trauma can cause drifting spots and shadows.
Eye feels “hard” to touch: The globe can feel firm with very high pressure (do not press on an injured eye).
Head throbbing when bending over: Pressure symptoms can worsen with position.
Unequal pupils or poor pupil reaction: Suggests nerve stress or iris damage.
Pain that gets worse with eye movement: Can occur with retrobulbar bleeding or severe inflammation.

Symptoms vary by type and timing. Some people have few symptoms even with high pressure. Regular checks after an eye injury are essential.

Diagnostic tests

A) Physical exam

Focused history and timeline of the injury
The doctor asks how the injury happened, what hit the eye, whether there was a cut, burn, or foreign body, and whether vision changed right away or later. This timeline points to likely mechanisms, such as early hyphema blockage or delayed angle-recession glaucoma.
Visual acuity test (reading chart)
Measuring how clearly you can see is the baseline for all later comparisons. Loss of clarity can come from corneal swelling, hyphema, lens problems, or optic nerve damage.
Pupil exam and swinging-flashlight test
The doctor checks pupil size, shape, and reaction to light. A slow or unequal reaction, or a relative afferent pupillary defect, can indicate optic nerve stress from high pressure or direct nerve trauma.
External inspection and eye movement check
Bruising, swelling, cuts, and restricted movements may show orbital fractures or retrobulbar hemorrhage. These findings guide urgent steps and imaging.

B) Manual / office-based clinical tests

Intraocular pressure measurement (Goldmann applanation)
This is the standard method to measure eye pressure. The doctor touches the cornea gently with a small tip after numbing drops and a dye. Accurate pressure numbers guide decisions and show response to treatment.
Indentation or handheld tonometry (Tono-Pen or iCare)
If the cornea is irregular, swollen, or if a slit lamp is not available, handheld devices give a reliable pressure reading. They are useful in the emergency room and for follow-up at the bedside.
Gonioscopy (viewing the drainage angle)
A special contact lens with mirrors allows the doctor to see the angle where fluid drains. The doctor looks for angle recession (a widened ciliary body band), blood, inflammatory debris, peripheral anterior synechiae, neovascularization, and other angle changes that explain the pressure rise.
Slit-lamp biomicroscopy of the anterior segment
The microscope exam shows hyphema, micro-hyphema, corneal swelling, anterior chamber inflammation, lens dislocation, lens capsule rupture, or lens particles. These signs point to specific types of traumatic glaucoma.
Dilated fundus exam (contact or non-contact lens; indirect ophthalmoscopy)
With the pupil dilated, the doctor checks for vitreous hemorrhage, retinal tears or detachment, optic nerve cupping, and silicone oil. These findings can trigger or accompany traumatic glaucoma.
Standard automated perimetry (visual field test)
This test maps side vision by showing faint lights in different spots. It detects early optic nerve damage from glaucoma over time and monitors whether treatment is protecting vision.

C) Lab and pathological tests

Sickle cell screening and hemoglobin electrophoresis (when appropriate)
In people at risk for sickle cell disease or trait, testing is important because sickled cells worsen pressure problems after hyphema and change treatment choices. The doctor avoids certain pressure-lowering drugs and tends to treat earlier if sickling is present.
Complete blood count and coagulation profile
These tests look for anemia, platelet issues, or clotting problems that increase the chance of re-bleeding in the eye. They help plan safe care if surgery or procedures are needed.
Aqueous or vitreous cytology (rare, selected cases)
In unusual or unclear cases, sampling the eye fluid can show ghost cells, hemoglobin-laden macrophages, or lens material. This confirms the specific blockage but is seldom required in routine care.

D) Electrodiagnostic tests

Visual evoked potential (VEP)
This test records the brain’s electrical response to visual signals. It helps when the optic nerve function is uncertain and the media are cloudy, or when the exam is hard to perform after trauma.
Electroretinography (ERG), including photopic negative response (PhNR) or pattern ERG
ERG measures retinal cell function. The PhNR or pattern ERG components are sensitive to ganglion-cell health, which is the cell layer harmed by glaucoma. This can complement visual fields in complex trauma.

E) Imaging tests

Anterior-segment optical coherence tomography (AS-OCT)
This light-based scan shows the angle and front structures in cross-section. It can document angle narrowing, iris bowing, or membrane formation without touching the eye.
Ultrasound biomicroscopy (UBM)
UBM uses high-frequency ultrasound to view the ciliary body, angle recession, cyclodialysis clefts, and lens zonules. It is very helpful when the cornea is cloudy and the angle cannot be seen with gonioscopy.
B-scan ocular ultrasound
This shows the back of the eye when the view is blocked by blood. It detects vitreous hemorrhage, retinal tears, or choroidal effusions that can shift the iris–lens diaphragm forward and raise pressure.
Optical coherence tomography of the optic nerve and retinal nerve fiber layer (OCT RNFL/GCC)
This measures the thickness of nerve layers. Thinning over time suggests glaucoma damage and helps judge whether treatment is working.
CT orbit (and MRI when safe and indicated)
CT detects fractures and metallic foreign bodies after trauma. MRI (not used when metal is suspected) shows soft-tissue injury. These scans guide urgent management that can influence pressure control and vision outcomes.

Non-Pharmacological Treatments (Therapies and Other Measures)

These measures support healing and help control pressure. They don’t replace medical or surgical care.

Rigid eye shield
Purpose: Protects from re-injury after trauma.
Mechanism: Physical barrier; prevents accidental rubbing or pressure.
Head elevation (30–45°) when resting
Purpose: Reduces pressure spikes and helps blood settle with hyphema.
Mechanism: Gravity lowers venous pressure and improves outflow.
Relative rest and activity restriction
Purpose: Lowers the chance of re-bleeding and pressure surges.
Mechanism: Avoids Valsalva strain that spikes IOP.
Avoid heavy lifting, bending, and straining
Purpose: Prevents IOP and venous pressure spikes.
Mechanism: Reduces thoracic pressure → less episcleral venous pressure.
Avoid rubbing the eye
Purpose: Prevents further internal bleeding or lens shift.
Mechanism: Mechanical trauma avoidance.
Cold compress in the first 24–48 hours
Purpose: Decreases pain and swelling.
Mechanism: Vasoconstriction reduces inflammation and leakage.
Dark glasses / photophobia control
Purpose: Comfort and reduced pupil movement.
Mechanism: Less light → smaller pupil → less iris chafing on damaged tissues.
Stool softeners and hydration
Purpose: Prevents straining on the toilet.
Mechanism: Less Valsalva → steadier IOP.
Sleep hygiene and regular schedule
Purpose: Blunts nocturnal pressure peaks.
Mechanism: Stable circadian rhythm may modulate aqueous production.
Caffeine moderation
Purpose: Avoids transient IOP spikes in sensitive persons.
Mechanism: Caffeine can raise IOP briefly; moderating intake evens it out.
Smoking cessation
Purpose: Improves wound healing and ocular blood flow.
Mechanism: Less vasoconstriction and oxidative stress.
Protective polycarbonate eyewear
Purpose: Prevents second injuries during recovery and future sports/work.
Mechanism: Impact-resistant shield.
Medication adherence coaching
Purpose: Ensures drops and pills are used correctly.
Mechanism: Technique training, alarms, written plans → steady IOP control.
Home BP and blood sugar control (if hypertensive/diabetic)
Purpose: Optimizes ocular perfusion and healing.
Mechanism: Stable systemic status supports optic nerve health.
Nausea control (per clinician)
Purpose: Prevents Valsalva from vomiting.
Mechanism: Antiemetics reduce spikes.
Sickle cell–specific precautions (if trait/disease)
Purpose: Lowers re-bleed and ischemia risks in hyphema.
Mechanism: Avoid dehydration, hypoxia, and acidosis; prompt care if pain rises.
Allergy avoidance and lubricants
Purpose: Less eye rubbing and inflammation.
Mechanism: Stabilizes ocular surface.
Regular follow-up and gonioscopy schedule
Purpose: Early detection of angle recession or PAS.
Mechanism: Direct inspection of the drainage angle guides timing of treatment.
Written “return-now” plan
Purpose: Fast action for red flags.
Mechanism: Patients know exactly when to seek urgent care.
Workplace and sports safety training
Purpose: Long-term prevention of repeat trauma.
Mechanism: Helmets, face shields, tool guards, and rules.

Drug Treatments

Doses are examples for adults; real prescriptions differ by age, kidney/liver status, comorbidities, and the exact traumatic mechanism. Your eye specialist decides the regimen and taper.

Topical β-blocker – Timolol 0.25–0.5%
Dose: 1 drop BID
Purpose: First-line IOP lowering.
Mechanism: Decreases aqueous humor production.
Side effects: Low pulse/BP, fatigue, bronchospasm (avoid in asthma/COPD), depression, masking hypoglycemia.
Topical α2-agonist – Brimonidine 0.1–0.2%
Dose: 1 drop BID–TID
Purpose: Additional IOP lowering; some neuroprotective signals.
Mechanism: Lowers production and increases uveoscleral outflow.
Side effects: Dry mouth, fatigue, allergic conjunctivitis; avoid in infants.
Topical Carbonic Anhydrase Inhibitor (CAI) – Dorzolamide 2% or Brinzolamide 1%
Dose: 1 drop TID (often BID if combined)
Purpose: Add-on IOP reduction.
Mechanism: Lowers aqueous production by blocking CA in ciliary body.
Side effects: Bitter taste, stinging; caution in sulfa allergy.
Prostaglandin analog – Latanoprost 0.005% (or travoprost, bimatoprost)
Dose: 1 drop QHS
Purpose: Potent nightly IOP control (once inflammation is quiet).
Mechanism: Increases uveoscleral outflow.
Caution: May worsen active inflammation; side effects include redness, lash growth, iris/skin darkening.
Rho-kinase inhibitor – Netarsudil 0.02%
Dose: 1 drop QHS
Purpose: Improves outflow through trabecular meshwork; helpful in damaged drains.
Mechanism: Cytoskeletal relaxation of outflow pathway; lowers episcleral venous pressure.
Side effects: Conjunctival redness, corneal verticillata, mild irritation.
Oral CAI – Acetazolamide
Dose: 250 mg QID or 500 mg BID (extended-release), short term
Purpose: Rapid IOP reduction in acute rises.
Mechanism: Systemic CA inhibition → less fluid production.
Side effects: Tingling, frequent urination, fatigue, kidney stones, metabolic acidosis; avoid in sickle cell disease/trait for hyphema, severe kidney disease, sulfa allergy, pregnancy (relative).
Hyperosmotic agent – Mannitol 20% IV
Dose: 1–2 g/kg IV over 30–60 min (hospital use)
Purpose: Emergency IOP drop when very high.
Mechanism: Draws water out of eye via osmotic gradient.
Side effects: Fluid shifts, headache, nausea; avoid in heart or renal failure unless closely monitored.
Topical corticosteroid – Prednisolone acetate 1%
Dose: 1 drop q1–4h, then taper per inflammation
Purpose: Calms post-traumatic inflammation; helps unblock the drain.
Mechanism: Suppresses inflammatory pathways.
Side effects: Steroid IOP rise, cataract progression, delayed healing; must be monitored.
Cycloplegic/mydriatic – Cyclopentolate 1% TID or Atropine 1% BID
Purpose: Pain relief from ciliary spasm; stabilizes iris–lens relationship; prevents synechiae.
Mechanism: Temporarily paralyzes ciliary muscle and dilates pupil.
Side effects: Light sensitivity, dry mouth, confusion in elderly with strong anticholinergics; do not use if angle is acutely narrow without supervision.
Antifibrinolytic (selected cases of hyphema) – Aminocaproic acid or Tranexamic acid (off-label in some regions)
Dosing: Specialist-directed; oral regimens vary.
Purpose: Lowers re-bleeding risk in significant hyphema.
Mechanism: Stabilizes blood clots by blocking fibrin breakdown.
Side effects: Nausea, thrombosis risk; use only when benefits outweigh risks and alternatives are limited.

Other drops like fixed combinations (e.g., timolol/dorzolamide, brimonidine/timolol) reduce bottle burden. Laser trabeculoplasty medications (pre-/post-) may be used selectively, but laser efficacy is limited in angle-recession glaucoma.

Dietary “Molecular” Supplements

Supplements do not replace medical or surgical care. Discuss with your clinician, especially after trauma or if you are pregnant, on blood thinners, or have kidney/liver disease.

Nicotinamide (Vitamin B3)
Typical dose used in studies: 1–3 g/day divided (start low; GI tolerance limits)
Function/Mechanism: Supports mitochondrial energy in retinal ganglion cells; potential neuroprotection.
Citicoline
Dose: 500–1000 mg/day (oral)
Function: May support neuronal membrane repair and visual pathway signaling.
Coenzyme Q10
Dose: 100–300 mg/day
Function: Antioxidant; mitochondrial support; sometimes used with vitamin E.
Omega-3 fatty acids (EPA/DHA)
Dose: 1–2 g/day combined EPA+DHA
Function: Vascular/anti-inflammatory support; ocular surface benefits.
Magnesium
Dose: 200–400 mg elemental/day
Function: Smooth muscle relaxation and vasoregulation; may help blood flow stability.
Ginkgo biloba extract (EGb 761)
Dose: 120–240 mg/day
Function: Microcirculation and antioxidant effects; evidence mixed.
Alpha-lipoic acid
Dose: 300–600 mg/day
Function: Antioxidant; supports mitochondrial enzyme complexes.
Resveratrol (from polygonum or grape skins)
Dose: 100–250 mg/day
Function: Antioxidant; SIRT1 pathway activation (theoretical neuroprotection).
Green tea catechins
Dose: As tea or standardized extract (e.g., EGCG 150–300 mg/day)
Function: Antioxidant support; general vascular health.
Vitamin D3
Dose: Individualized (commonly 1000–2000 IU/day; confirm level)
Function: Immune modulation and tissue health; correct deficiency.

Important: Some supplements can thin blood or interact with medications—avoid unapproved use in hyphema or before surgery.

Regenerative / stem cell” drugs or approaches

There are no approved “immunity booster” or stem-cell drugs that treat traumatic glaucoma in routine care. Below are research or adjunct concepts; they are not standard treatment and usually lack approved dosing for glaucoma.

Neuroprotection strategies (concept)
What it is: Using agents (e.g., brimonidine’s potential, citicoline, nicotinamide) to protect retinal ganglion cells.
Status: Adjunct/experimental; used mainly as supportive care, not a cure.
Rho-kinase pathway modulation beyond drops
What it is: Drugs that biologically “relax” the outflow tissue; netarsudil is approved as a drop; other modalities are investigational.
Status: Standard as eye drop; advanced regenerative angles are research.
Trabecular meshwork cell therapy
What it is: Lab-grown or stem-cell-derived TM cells to repopulate damaged drain.
Status: Preclinical/early research; no approved dose.
Retinal ganglion cell (RGC) neuroregeneration
What it is: Stem cells or gene therapy to repair/replace damaged RGCs.
Status: Research-stage; no clinical dosing.
Gene therapy to correct outflow tissue defects
What it is: Viral vectors to deliver genes that improve drainage function.
Status: Early studies only.
Biologic anti-scar approaches
What it is: Agents that precisely limit scarring (e.g., targeted anti-TGF-β) to keep the angle open or protect filtering surgery.
Status: Experimental outside standard mitomycin-C use in surgery.

Bottom line: For traumatic glaucoma, proven tools are pressure-lowering drops, short-course systemic meds, and surgery when needed. “Immune boosters” are not a treatment.

Surgeries

Anterior chamber washout (with/without clot evacuation)
Procedure: A tiny incision lets the surgeon flush out blood/clots from the front chamber.
Why: Used for large or non-resorbing hyphemas or when IOP stays high despite meds, especially in sickle cell disease/trait.
Lens surgery (lensectomy or cataract extraction; sometimes with vitrectomy)
Procedure: Removes a swollen, leaking, ruptured, or dislocated lens; may add intraocular lens if safe.
Why: Relieves lens-induced blockage (phacomorphic, phacolytic, lens-particle) and reopens the angle.
Trabeculectomy with antimetabolite (e.g., mitomycin-C)
Procedure: Creates a new drainage pathway (filtering bleb) under the upper eyelid.
Why: Lowers IOP when drops and laser fail; scarring risk is higher in trauma → antimetabolite helps keep it open.
Glaucoma drainage device (tube shunt; e.g., Ahmed, Baerveldt)
Procedure: A soft tube drains fluid to a plate implanted on the eye wall.
Why: Useful when angle is damaged (angle recession/PAS) or prior surgeries failed.
Cyclophotocoagulation (CPC – transscleral diode or endoscopic)
Procedure: Laser reduces ciliary body fluid production.
Why: For eyes with severe damage or when other surgeries are risky; can be repeated; careful dosing to avoid hypotony.

Other selective procedures: Laser peripheral iridotomy for pupillary block; goniosynechialysis to strip recent PAS; selective laser trabeculoplasty (SLT) has limited benefit in classic angle-recession glaucoma but may be tried case-by-case.

Preventions

Wear impact-rated protective eyewear for sports and high-risk work.
Use helmets/face shields for cycling, motorbikes, construction, and grinding tools.
Follow firework and explosive safety; keep distance and eye protection.
Store and handle chemicals (acids/alkalis/solvents) with goggles and training.
Use seatbelts and airbags; keep kids in proper restraints.
Keep home and workshop free of projectile hazards; secure elastic bands and bungees.
Educate children about toy guns and sticks—no pointing at faces.
Maintain diabetes/BP control; healthier tissues recover better after trauma.
Early eye exam after any head or orbital injury—even if vision seems okay.
Keep a spare pair of protective glasses; replace scratched or cracked lenses.

When to See a Doctor Urgently

Sudden eye pain, severe headache, or nausea/vomiting after injury
Blurred vision, halos around lights, or a shadow/curtain in vision
Red eye with light sensitivity, unequal pupils, or a new white/red layer in the lower eye (possible hyphema)
IOP readings at home (if you have a device) that spike or stay high
New floaters or flashes of light
Trauma in people with sickle cell trait/disease—seek care immediately
Any vision change after a previous eye trauma, even years later

Diet: “What to Eat” and “What to Avoid”

Eat (support ocular and vascular health):

Leafy greens (spinach, kale) – dietary nitrates may support blood flow
Fatty fish (salmon, sardines) – omega-3s for vessels and surface
Citrus and berries – vitamin C and polyphenols
Nuts and seeds – vitamin E, healthy fats, magnesium
Legumes and whole grains – steady energy, micronutrients
Colorful vegetables (peppers, carrots) – carotenoids, antioxidants
Green tea – catechins as antioxidants
Olive oil – heart-healthy monounsaturated fat
Adequate water spread through the day – avoid dehydration
Foods rich in B-vitamins (eggs, fortified cereals) – support nerve health

Avoid or limit (especially during recovery):

Very salty meals – can raise BP/ocular perfusion issues
Excess caffeine shots – may cause short IOP spikes
Binge alcohol – dehydration and poor healing
Large rapid fluid loads – quick 1–2 L chugs can transiently raise IOP
Trans fats/ultra-processed foods – vascular/oxidative stress
Smoking/vaping – vasoconstriction and oxidative damage
Unapproved herbal blood thinners (e.g., high-dose ginkgo) during hyphema risk
Energy drinks with high caffeine/taurine after surgery/bleed
Crash dieting – poor tissue repair
High-dose vitamin A/retinoids without guidance – potential ocular side effects

Frequently Asked Questions

Is traumatic glaucoma always permanent?
Not always. Some causes (like short-lived blockage from blood) resolve. But any long-term pressure rise can damage the optic nerve. Early control protects vision.
Can glaucoma appear years after a sports injury?
Yes. Angle-recession glaucoma can show up months to years later. That’s why periodic eye exams with gonioscopy are important after blunt trauma.
Do prostaglandin drops worsen inflammation?
They can in active uveitis phases. Many doctors delay them until inflammation is quiet, then use them if needed.
I have sickle cell trait. Are there special rules?
Yes. Hyphema plus sickle cell needs aggressive monitoring. Avoid dehydration and acidosis; systemic CAIs (like acetazolamide) are often avoided. Pressure thresholds for surgery are lower.
Does SLT (selective laser trabeculoplasty) work for angle recession?
Often less effective because the outflow tissue is structurally damaged. It may be tried case-by-case but surgery (tube shunt) is commonly needed if meds fail.
Can steroids cause high pressure?
Yes. Some people are steroid responders. Doctors balance the need to calm inflammation with IOP safety and will taper or switch when possible.
What signs mean my optic nerve is being harmed?
You usually won’t feel it. Doctors track optic nerve scans, visual fields, and IOP trends. Keep appointments even when you feel fine.
Can I fly after hyphema or surgery?
Usually yes after the eye is stable, but only after your surgeon clears you. Altitude changes can affect gas bubbles or fragile wounds.
Will I need surgery?
Many cases are controlled with drops and time. Surgery is considered if IOP remains high, the angle is scarred, or the lens causes blockage.
Can I return to sports?
With your doctor’s clearance, protective eyewear, and sport-specific shields. High-impact sports may be restricted longer.
Are supplements enough to protect my vision?
No. Supplements are adjuncts only. The essentials are proper diagnosis, prescribed therapy, and monitoring.
What if my other (uninjured) eye’s pressure rises?
Doctors will check both eyes; some mechanisms and steroid response can affect either eye.
How long do I need drops?
It varies—days to lifelong—depending on the mechanism (temporary blockage vs permanent drain damage).
Can traumatic glaucoma happen after surgery or injections?
Yes. Post-operative inflammation, silicone oil, or steroid response can raise IOP. It’s monitored and treated promptly.
What’s the outlook?
With early care, many people keep good vision. Delays, repeated bleeds, and uncontrolled pressure worsen outcomes.

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 28, 2025.

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