9 Warning Signs of Corneal Edema That Affect Vision

Corneal edema is a condition in which the cornea—the clear, dome-shaped surface at the front of the eye—becomes swollen due to excess fluid accumulation. The cornea normally maintains precise transparency and thickness to focus light properly, but when fluid builds up, vision can become blurry, hazy, or distorted. Corneal edema may occur in one or both eyes and can develop suddenly or gradually depending on the underlying cause.

Understanding the warning signs of corneal edema is important because early recognition can prevent further damage and help preserve vision. The condition can result from a variety of factors, including eye surgery (like cataract surgery), trauma, infections, inflammation, glaucoma, or endothelial cell dysfunction. This article explains nine warning signs of corneal edema that can affect vision, along with potential causes, diagnosis, and treatment options.

What Is Corneal Edema?

Corneal edema is a condition in which the cornea—the clear, dome-shaped surface at the front of the eye—becomes swollen due to excess fluid accumulation. Normally, the cornea remains transparent and maintains a precise thickness, allowing light to pass clearly to the retina for sharp vision. When fluid builds up, it disrupts the cornea’s normal clarity and smoothness, leading to blurry or hazy vision and sometimes causing halos or glare around lights.

Corneal edema can develop in one or both eyes and may occur suddenly or gradually depending on the cause. Common triggers include eye surgery (like cataract or glaucoma procedures), trauma, infections, inflammation, increased intraocular pressure, or damage to the cornea’s endothelial cells, which help pump fluid out of the cornea.

Left untreated, persistent corneal edema can lead to discomfort, vision distortion, and in severe cases, permanent vision loss. Early diagnosis and treatment are essential to restore clarity and protect long-term eye health.

The 9 Visual and Physical Warning Signs

The direct consequence of structural swelling inside the eye manifests as nine specific warning signs:

• Blurry or Cloudy Vision: A foggy, indistinct obscuration of sight.

• Halos Around Lights: Diffracted rings or starbursts around point light sources.

• Eye Pain or Discomfort: Intense physical distress from advanced tissue changes.

• Light Sensitivity (Photophobia): Pain or discomfort triggered by bright environments.

• Watery Eyes (Epiphora): A reflexive profuse tearing response to surface irritation.

• Foreign Body Sensation: Gritty discomfort caused by an uneven corneal surface.

• Eye Redness: Persistent discoloration arising from ongoing tissue inflammation.

• Decreased Contrast Sensitivity: A visual shift where objects appear washed out.

• Visibly Hazy or Blue-Tinted Cornea: A noticeable cloudiness apparent to outside observers in advanced stages.

The Specific Nature of Blurry or Cloudy Vision

The earliest and most prevalent sign of this swelling is a distinct type of blurry vision. Patients report that this visual disturbance feels like looking through a heavy fog, thick steam, or a dirty window, leaving their sight hazy, indistinct, or smeared. This leaves individuals struggling to read text, see fine details, or identify faces. This obscuration is persistent and cannot be corrected by blinking or using standard eyeglasses, meaning it is entirely distinct from a simple refractive error.

This symptom presents a distinct diurnal pattern: it is most severe immediately upon waking in the morning. When a person sleeps, their eyes remain closed, which prevents the natural evaporation of tears from the corneal surface.

This closed environment allows fluid to pool and accumulate within the cornea overnight because there is no evaporation mechanism to pull it out, and the compromised endothelial pump cannot keep up with the influx. Once a person wakes and opens their eyes, exposure to the open air allows evaporation to resume. This evaporation helps pull the excess fluid out of the tissue, resulting in a gradual improvement in visual clarity as the day goes on.

In the initial stages of underlying conditions like Fuchs’ Dystrophy, this morning blurriness that improves later in the day serves as a classic diagnostic clue. However, as the overall endothelial cell count drops further and pump function deteriorates, this fluid accumulation becomes permanent. The blurriness transitions into a constant state that no longer clears up, severely disrupting daily activities at all hours of the day.

Why Halos and Glare Form Around Light Sources

The perception of halos around lights is an optical phenomenon caused directly by the excess fluid accumulated inside the swollen cornea, which bends and diffracts incoming light rays before they can reach a proper focus on the retina.

Individuals experience this as seeing rainbow-like rings, starbursts, or severe glare radiating from point sources of light, such as indoor lamps, streetlights, or oncoming car headlights. This visual distortion becomes highly noticeable and debilitating at night when the contrast between a bright light source and a dark background is most extreme.

In a healthy and compact cornea, highly organized collagen fibers are arranged in a precise structure that allows light rays to pass directly through to the retina with minimal scattering, generating crisp, clear images. When cornea edema develops, the tissue becomes waterlogged. This excess fluid separates the organized collagen fibers, creating microscopic fluid-filled spaces or small droplets within the stroma, which is the main layer of the cornea.

When incoming light enters the eye, it strikes these trapped fluid droplets, which behave like tiny, irregular prisms. Instead of traveling straight through the cornea, the light rays are bent and scattered in multiple directions.

This widespread dispersion causes light rays to land on areas of the retina surrounding the true focal point, creating the visual perception of halos and glare. Beyond producing these distracting visual artifacts, the internal light scatter degrades the overall quality of vision, reducing contrast sensitivity and rendering tasks like night driving highly dangerous and difficult.

Advanced Structural Swelling, Severe Pain, and Discomfort

Physical eye pain and discomfort are definitive signs that the tissue swelling has reached an advanced or severe stage, which is clinically referred to as bullous keratopathy. While mild to moderate swelling causes painless visual changes, severe and chronic fluid buildup forces the development of bullae, which are small, fluid-filled blisters that form on the epithelium, the outermost layer of the cornea.

The epithelium is one of the most sensitive tissues in the human body because it is densely packed with nerve endings. When fluid pressure building within the swollen stroma becomes too intense, it pushes forward and forces the epithelial layers to separate, creating these painful blisters. These bullae can rupture spontaneously on their own or from the simple friction of a blink.

When a blister ruptures, it leaves behind a raw, open sore on the eye, exposing the highly sensitive corneal nerves directly to the air and the rubbing motion of the eyelid. This exposure triggers an intense, sharp pain that patients frequently describe as a severe foreign body sensation, feeling exactly as though sand, glass, or a stray eyelash is trapped in the eye. This severe pain is regularly accompanied by profuse tearing, significant eye redness, and extreme light sensitivity.

Over time, the continuous cycle of blister formation and rupture can become chronic, causing persistent discomfort, recurrent corneal erosions, and a significantly higher risk of secondary infections, marking it as a highly debilitating complication of late-stage swelling.

The Underlying Mechanics of Light Sensitivity (Photophobia)

Pronounced light sensitivity, or photophobia, is caused by the internal scattering of light within the hazy, fluid-filled layers of the cornea. This scattering overstimulates the retina, making exposure to bright light highly uncomfortable or physically painful. A healthy, clear cornea transmits light in a focused, highly controlled path directly to the retina at the back of the eye. However, when the tissue is swollen, its structural clarity and integrity are broken.

The trapped fluid disrupts the uniform arrangement of the tissue, turning the cornea into an optically hazy medium. When light—especially bright sunlight or intense artificial light—enters the eye, it can no longer pass through cleanly. Instead, the light is scattered in countless directions by the microscopic fluid pockets trapped within the stroma. This uncontrolled internal dispersion, known as straylight, floods the retina with non-uniform, completely unfocused light, which completely overwhelms the photoreceptor cells (the rods and cones).

The brain interprets this chaotic overstimulation of the retina as glare, physical discomfort, and pain. This triggers a reflexive physical response to limit light exposure, such as intense squinting, closing the eyes, or seeking dimmer environments. Therefore, light sensitivity from a swollen cornea is a direct physiological response to the eye’s inability to manage and focus incoming light properly, forcing individuals to wear dark sunglasses even when indoors and avoid well-lit situations entirely to avoid pain.

Identifying the Underlying Triggers

When examining what causes corneal edema and looking at what causes fluid on the cornea, the condition is rooted in factors that disrupt the delicate fluid balance maintained by the corneal endothelium. The underlying processes driving corneal edema causes generally involve:

• Endothelial Dysfunction: Inherited diseases like Fuchs’ Dystrophy that cause a progressive loss of the vital endothelial pump cells.

• Surgical Trauma: Mechanical damage or cell loss occurring during intraocular procedures, such as cataract extraction or glaucoma surgery.

• Inflammatory and Infectious Processes: Deep ocular infections, corneal ulcers, or internal inflammation (uveitis) that compromise cell function.

• Elevated Intraocular Pressure: Severe spikes in eye pressure, such as in acute glaucoma, which mechanically force fluid into the corneal layers faster than the pumps can clear it.

Recognizing these specific corneal edema symptoms and identifying what causes corneal edema allows individuals to seek prompt clinical evaluation before chronic swelling leads to permanent visual scarring.

Causes and Treatments of Corneal Edema

To fully understand what causes corneal edema, the underlying trigger is almost universally linked to the condition and function of the corneal endothelium. This single layer of highly specialized cells lines the inner surface of the cornea and is responsible for continuously pumping fluid out of the tissue to preserve its clarity.

When these cells experience damage, decrease in overall number, or become dysfunctional, they can no longer execute this vital pumping mechanism. This failure leads directly to an accumulation of fluid on cornea tissue. Pinpointing the exact cause is the essential first step toward designing a successful treatment plan.

The pathways leading to tissue swelling vary significantly, ranging from medically induced (iatrogenic) damage during common ocular procedures to the gradual, progressive loss of cells caused by inherited conditions.

Consequently, medical interventions must be carefully customized based on the overall severity of the swelling, the degree of vision loss, and the inherent capacity of the cornea to heal on its own. Conservative, non-surgical management aims to offer temporary relief from symptoms, whereas surgical options provide a definitive, long-term cure by replacing the diseased tissue.

The Link Between Eye Surgery and Corneal Swelling

The underlying connection between intraocular operations and subsequent swelling centers on the potential for intraoperative trauma to the delicate endothelial cell layer, which can ultimately impair the eye’s ability to remain clear. The endothelium is a single, non-regenerating layer of cells, meaning these cells cannot multiply to replace dead tissue.

During intraocular procedures—most notably cataract surgery—the physical instruments, the fluid used for irrigation, and the ultrasonic energy generated to break up the cataract (a process known as phacoemulsification) can inadvertently damage or destroy a fraction of these crucial cells. A minor degree of endothelial cell loss is considered an expected, unavoidable consequence of most anterior segment surgeries.

In a healthy eye with a high initial cell density, this minor loss is well-tolerated because the surrounding, healthy cells can stretch to cover the empty spaces, resulting in only mild, temporary post-operative swelling that clears within days or weeks. However, if a patient enters surgery with a pre-existing low endothelial cell count (due to advanced age or an underlying disorder like Fuchs’ Dystrophy), or if the surgical procedure is unusually complex and prolonged, the cell destruction can be extensive.

When the overall endothelial cell density falls below a critical threshold—typically around 500 cells/mm²—the remaining cells lose the capacity to drain fluid effectively. This pump failure results in chronic, persistent swelling. When this occurs following cataract surgery, the condition is clinically referred to as pseudophakic bullous keratopathy (or aphakic bullous keratopathy if no lens implant is present), and it frequently requires a corneal transplant to recover visual clarity.

How Fuchs’ Dystrophy Triggers Fluid Accumulation

Fuchs’ Dystrophy causes severe tissue swelling by driving a progressive, genetically programmed death of the corneal endothelial cells. This inherited disease is characterized by the premature, slow deterioration of the inner cell layer over time. As the disease advances, two primary pathological changes take place:

Accelerated Cell Death and Polymegathism: The endothelial cells die off at an accelerated rate. Because they cannot regenerate, the surviving cells are forced to stretch out and enlarge to cover the developing gaps on the back surface of the cornea. Although this cell enlargement (polymegathism) temporarily keeps the surface covered, these irregular, oversized cells are metabolically less efficient at pumping fluid out of the stroma.

Guttae Formation: The disease forces the formation of tiny, abnormal bumps called guttae on Descemet’s membrane, which is the thin basement membrane that supports the endothelial cells. These microscopic bumps disrupt the uniform cellular architecture and further degrade endothelial pump performance.

In the initial stages of Fuchs’ Dystrophy, this cellular breakdown is mild, resulting in the classic diurnal pattern of hazy vision upon waking that gradually improves as the day progresses. However, as the cell count continues to drop and the pumping mechanism reaches a state of critical failure, the cornea loses its ability to regulate its internal fluid balance.

This leads to persistent, all-day swelling, major vision loss, and eventually, the painful formation of epithelial blisters (bullous keratopathy), which represents the definitive end stage of the disease.

Non-Surgical Solutions for Mild Cases

When managing mild swelling, non-surgical approaches focus on hypertonic saline eye drops and ointments. These topical therapies utilize osmosis to draw excess fluid out of the waterlogged tissue. These hypertonic drops and ointments serve as the primary line of defense for controlling corneal edema symptoms and improving visual acuity in the early stages of Fuchs’ Dystrophy or during temporary post-operative recovery.

Hypertonic saline formulations contain a significantly higher concentration of salt (typically 2% or 5% sodium chloride) than the natural fluid balance inside the cornea. Applying these agents to the surface of the eye establishes a strict concentration gradient. This gradient creates an osmotic pull that draws trapped water out of the swollen epithelial and stromal layers, moving it onto the external tear film where it can be naturally cleared by evaporation.

[Hypertonic Saline (2% or 5% Salt)] Applied to Eye Surface ──► Creates Osmotic Gradient ──► Pulls Water Out of Stroma/Epithelium ──► Tear Film Evaporation

Topical Drops (e.g., Muro 128 5%): These are typically administered multiple times throughout the daytime to help maintain functional corneal clarity while the individual is active.

Topical Ointment: This formulation is much thicker and offers a prolonged, long-lasting therapeutic effect. It is most effective when applied right at bedtime, as it actively combats the heavy fluid accumulation that occurs overnight when the eyelids are closed, thereby reducing the severity of morning blurriness.

Bandage Contact Lenses: In cases of advanced swelling where the fluid blisters (bullae) have actually ruptured, a soft bandage contact lens can be utilized. This option does not treat or reduce the swelling itself; instead, it is used purely for pain management. The soft lens serves as a physical, protective shield over the raw, exposed corneal nerves, reducing the friction generated by the closing eyelid and providing profound pain relief while the underlying epithelium attempts to heal.

When Surgical Intervention is Required

A corneal transplant becomes the recommended course of treatment once the swelling has reached an advanced, permanent state and has caused vision loss severe enough to disrupt an individual’s basic daily activities, such as reading, driving, or recognizing faces.

Surgery is pursued only when conservative, non-surgical treatments fail to provide adequate relief. This stage typically indicates that the endothelial cell pump has suffered irreversible failure, a common outcome in late-stage Fuchs’ Dystrophy or following severe surgical trauma.

The definitive, modern surgical solution is a partial-thickness transplant known as endothelial keratoplasty (EK). This specialized technique isolates and replaces only the diseased, non-functioning inner layer of the cornea, leaving the healthy outer tissue untouched. The two primary types of endothelial keratoplasty are:

In both surgical procedures, the ophthalmologist removes the patient’s worn-out, dysfunctional endothelial layer and replaces it with a thin disc of healthy donor tissue containing a brand-new, fully functional layer of endothelial cells. By implanting these healthy cells, the transplant successfully restores the eye’s biological capacity to pump out fluid, allowing the waterlogged tissue to clear up and restoring functional vision.

In rare instances where chronic swelling has caused widespread, permanent scarring throughout the entire tissue structure, a traditional, full-thickness corneal transplant—known as a penetrating keratoplasty (PKP)—may be required to replace the entire cornea.

Understanding what is cornea edema, identifying what causes fluid on the cornea, and recognizing how these underlying mechanisms operate allows patients to navigate these advanced medical options effectively.

Broader Aspects of Diagnosing and Managing Corneal Conditions

Diagnosing and managing corneal conditions involve a multi-faceted approach that extends beyond identifying symptoms, incorporating advanced imaging, precise differentiation from similar diseases, and tailored management strategies based on the condition’s origin and patient age.

Furthermore, a comprehensive understanding requires looking at preventative measures for secondary causes and recognizing the distinct pathways of congenital versus adult-onset corneal pathologies. This broader perspective ensures accurate diagnosis, effective treatment, and better patient.

Ophthalmic Diagnosis of Corneal Edema

Ophthalmologists diagnose corneal edema by employing a series of highly specialized clinical examinations designed to evaluate the physical architecture of the cornea, quantify its thickness, and analyze the health of its individual cellular layers.

Slit-Lamp Examination

This high-magnification microscope utilizes a focused beam of light to act as the cornerstone of ophthalmic diagnostics. It allows the physician to inspect each individual layer of the cornea in microscopic detail, moving systematically from the outer epithelium down to the inner endothelium. During this evaluation, the clinician searches for classic clinical indicators of fluid retention, including:

• A distinct loss of tissue transparency (haziness).

• The formation of microcysts or larger fluid blisters (bullae) on the external surface.

• A generalized increase in overall corneal thickness.

Pachymetry

To provide an exact objective measurement of the tissue swelling, a diagnostic test known as pachymetry is performed. This procedure calculates the precise thickness of the cornea. It can be executed via an ultrasound probe that makes gentle contact with the eye, or through non-contact optical imaging modalities.

A cornea that measures thicker than normal parameters serves as a definitive confirmation of edema. Ophthalmologists routinely gather serial pachymetry measurements over time to monitor the structural progression of the condition or evaluate how well the tissue is responding to medical therapy.

Specular Microscopy

To isolate the specific underlying cause of the fluid retention—particularly when suspecting endothelial pump failure like Fuchs’ dystrophy—physicians utilize specular microscopy. This non-invasive imaging modality provides a highly detailed view of the inner endothelial cell layer.

This allows specialists to calculate exact cell density and closely observe changes in cellular size and shape. Finding a low overall cell count or irregular variations in cell structure—known clinically as polymegathism and pleomorphism—confirms that the endothelial pump function is structurally compromised, causing fluid on cornea layers.

Differentiating Corneal Edema from Keratitis

While both conditions impact the same structural area of the eye and impair visual acuity, they are fundamentally different diseases characterized by distinct underlying mechanisms, origins, and clinical presentations.

[Corneal Edema] ──► Dysfunction of the Endothelial Pump ──► Passive Fluid Buildup in Stroma (Non-Inflammatory)
[Keratitis]     ──► Infection, Injury, or Autoimmunity   ──► Active Inflammatory Response (Cellular Infiltration)

Preventability and Risk Mitigation Strategies

The potential to prevent cornea edema depends heavily on its primary origin. When evaluating what causes corneal edema, cases are categorized as primary or secondary, each carrying a different outlook for prevention:

Primary Cases (Non-Preventable)

Primary edema stemming from inherited genetic conditions cannot be prevented. The classic example is Fuchs’ Endothelial Corneal Dystrophy, a progressive disorder hardwired into a patient’s DNA that causes endothelial cells to die prematurely. There are no lifestyle modifications or medical therapies available to halt its development. Individuals with a known family history can only undergo close monitoring with an eye specialist to track corneal edema symptoms and manage them as they present.

Secondary Cases (Preventable)

Conversely, many cases of secondary swelling resulting from external factors or separate eye conditions can be actively prevented or minimized through targeted protective measures:

Preventing Traumatic Injury: Wearing appropriate safety goggles or protective glasses during sports, construction work, or yard maintenance shields the eye from traumatic injuries that physically destroy the endothelial layer.

Controlling Intraocular Pressure: High eye pressure associated with glaucoma can permanently damage endothelial cells over time. Strictly adhering to prescribed glaucoma medications and attending regular pressure checks keeps intraocular pressure controlled, preserving long-term corneal health.

Refining Surgical Protocols: During intraocular operations like cataract extraction, surgeons can prevent post-operative swelling by employing gentle techniques, utilizing high-quality viscoelastic solutions to physically shield the endothelium, and minimizing total surgical duration.

Practicing Strict Lens Hygiene: Diligent cleaning, handling, and replacement of contact lenses prevents severe ocular infections that cause the deep tissue inflammation responsible for secondary swelling.

Congenital Versus Adult-Onset Pathologies

The clinical distinction between congenital and adult-onset variations of this condition spans across their root causes, physical presentation, timing, and urgency of treatment.

[Congenital Edema] ──► Birth Onset ──► Global Cloudiness (CHED) ──► High Amblyopia Risk ──► Urgent Full-Thickness Transplant (PKP)
[Adult-Onset]      ──► Later Life  ──► Degenerative/Slow Slopes ──► Daytime Clearing    ──► Selective Layer Transplant (DMEK/DSEK)

Congenital Corneal Edema

This form is present at birth or manifests shortly thereafter, driven by genetic mutations that disrupt normal embryonic development of the eye. A primary example is Congenital Hereditary Endothelial Dystrophy (CHED), a condition where the endothelial pump layer is dysfunctional from birth. This results in a distinct cloudy, blue-gray appearance in one or both of the infant’s corneas.

The onset is immediate and often presents alongside light sensitivity and rapid, involuntary eye movements (nystagmus). Management is highly urgent because clear vision is mandatory for the brain’s visual pathways to mature properly during early childhood. If left untreated, the infant faces permanent vision loss from amblyopia (lazy eye). Consequently, a full-thickness corneal transplant—known as a penetrating keratoplasty—is frequently required within the first few months of life.

Adult-Onset Corneal Edema

In sharp contrast, adult-onset types—such as swelling caused by progressive Fuchs’ dystrophy or post-surgical complications like pseudophakic bullous keratopathy—are degenerative conditions that advance slowly over years or decades. These patients are born with completely healthy corneas, but the endothelial cells gradually break down later in life due to aging, genetics, or surgical trauma.

Symptoms, such as morning blurriness that clears up during the daytime, emerge subtly and worsen gradually over time. Initial management is highly conservative, relying on hypertonic saline drops or ointments to osmotically drain fluid from the tissue. Surgical intervention is delayed until vision becomes persistently impaired and disrupts daily living.

Furthermore, the preferred surgical approach is an endothelial keratoplasty (such as DMEK or DSEK), which is a less invasive procedure that replaces only the damaged inner endothelial layer, allowing for a much faster visual recovery than the full-thickness transplants required in congenital cases.

By analyzing what causes fluid on the cornea through this comprehensive framework, clinicians can implement the exact diagnostic and therapeutic pathways required for long-term visual stability.

Conclusion

Corneal edema can significantly affect vision and eye comfort if left untreated. Symptoms such as blurred or cloudy vision, halos around lights, eye pain, sensitivity to light, or swelling of the cornea should not be ignored. Treatment depends on the cause and may include eye drops, medications, contact lenses, or in severe cases, surgical procedures such as corneal transplantation. Early detection and prompt management can help protect vision and improve quality of life for those affected by corneal edema.

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Frequently Asked Questions

1. What is corneal edema?

Corneal edema is swelling of the cornea caused by fluid buildup. This disrupts the cornea’s normal clarity and shape, leading to blurred vision, light sensitivity, and sometimes discomfort. The condition can be acute or chronic and may affect one or both eyes depending on the underlying cause.

2. What are the common causes of corneal edema?

Corneal edema can result from trauma, eye surgery (such as cataract or glaucoma procedures), infections, inflammation, elevated eye pressure, or endothelial cell damage. Certain hereditary conditions, contact lens overuse, or exposure to toxins may also contribute. Identifying the underlying cause is crucial for effective treatment.

3. How does corneal edema affect vision?

Corneal edema affects vision by disrupting the smooth, transparent surface of the cornea. This can cause blurred or hazy vision, halos around lights, glare, and difficulty seeing in bright conditions. In severe cases, vision may fluctuate or become significantly impaired, making daily tasks challenging.

4. What are the warning signs of corneal edema?

The warning signs of corneal edema include blurry or cloudy vision, halos around lights, eye pain or pressure, sensitivity to light, watery eyes, a feeling of grittiness, redness, swelling of the cornea, and temporary vision changes upon waking. Noticing these symptoms early and seeking evaluation can prevent complications.

5. How is corneal edema diagnosed?

Doctors diagnose corneal edema through a comprehensive eye exam, which may include slit-lamp microscopy, measurement of corneal thickness, and assessment of visual acuity. Additional tests, such as endothelial cell counts or imaging, can help determine the severity and underlying cause. Prompt diagnosis guides the appropriate treatment.

6. How is corneal edema treated?

Treatment for corneal edema depends on its cause. Mild cases may respond to hypertonic saline eye drops or ointments to draw out excess fluid. Managing underlying conditions, such as elevated eye pressure or infection, is also essential. Severe or persistent edema may require surgical options like endothelial keratoplasty or corneal transplant to restore vision and corneal clarity.

7. Can corneal edema be prevented?

While not all cases of corneal edema can be prevented, certain measures may reduce risk. These include proper contact lens hygiene, regular eye exams, prompt treatment of eye infections, careful monitoring after eye surgery, and controlling conditions like glaucoma. Protecting the eyes from trauma and following post-surgical instructions also help minimize the risk.

Sources

American Academy of Ophthalmology. Corneal Edema. 
Mayo Clinic. Corneal Edema: Causes, Symptoms, and Treatment. 
Cleveland Clinic. Corneal Edema. 
National Eye Institute. Cornea and Corneal Disorders. 
MedlinePlus. Corneal Edema. 
Johns Hopkins Medicine. Corneal Edema Overview. 
American Optometric Association. Corneal Swelling and Eye Health.