Corneal Trauma: Evaluation and Management of Ocular Surface Injuries

Etiology

Corneal trauma arises from a broad spectrum of mechanical, chemical, thermal, infectious, and iatrogenic causes, each with distinct mechanisms of injury and clinical implications (see Table. Etiological Classification of Corneal Trauma). Understanding the underlying etiology of the injury is essential for accurate diagnosis, risk stratification, and selection of appropriate management strategies. The following sections categorize common causes of corneal injury and highlight key features that inform clinical evaluation and treatment.

Corneal Abrasions and Foreign Bodies

Corneal abrasions and foreign body injuries occur when objects strike or embed within the ocular surface. Common causative objects include fingernails, contact lenses, and plant branches. Certain activities, such as agricultural work, landscaping, and metalwork, also predispose patients to injury from particulate wood, vegetative matter, and metal. In the absence of eye protection, high-speed projectile objects may penetrate through the cornea and create additional serious damage past the initial corneal insult.[15]

Corneal Lacerations and Perforations

Corneal lacerations and perforations can occur under any of the same circumstances as corneal abrasions. However, these injuries more often involve equipment or activities that generate high-speed projectiles, such as saws, angle grinders, and metal-pounding tools. Clinicians should elicit from the history the type of causative object (eg, wood and metal) and its estimated projectile speed.[25]

Ocular Burns

Exposure to chemical substances, ultraviolet light, and excessive heat can alter the surface structure of the cornea and cause ocular burns. Alkali chemical injuries are more common than acidic chemical injuries due to the prevalence of household cleaning agents containing ammonia and lye. Acidic burns are typically work-related insults involving industrial processes, but such burns can also be intentional assaults.[26] Ultraviolet keratitis from radiation burns is associated with tanning beds, high-altitude environments, welding arcs, and the occasional solar eclipse. Thermal burns are distinctly uncommon but can occur with objects such as curling irons, hot liquids, and fire-related injuries.[27]

Infectious and Posttraumatic Etiologies

Trauma to the corneal epithelium significantly increases susceptibility to infectious keratitis by disrupting the natural barrier against microbial invasion. Bacterial pathogens such as Staphylococcus aureus and Pseudomonas aeruginosa are commonly implicated, particularly in contact lens wearers. Fungal infections, particularly those caused by Fusarium and Aspergillus spp, are more commonly associated with vegetative trauma. Protozoal infections, such as Acanthamoeba keratitis, may occur following exposure to contaminated water sources, especially among contact lens users. Emerging organisms such as P insidiosum have been increasingly recognized as significant causes of severe keratitis following trauma, often mimicking fungal infections but requiring distinct therapeutic approaches.[28][29][30]

Iatrogenic and Environmental Factors

Iatrogenic causes of corneal trauma include surgical procedures, improper use of ophthalmic instruments, and complications from refractive surgeries such as laser-assisted in situ keratomileusis (LASIK) or photorefractive keratectomy. Inadequate lubrication during surgery or postoperative epithelial defects can predispose to delayed healing and secondary infection. Environmental factors such as air pollution, occupational chemical exposure, and UV radiation can exacerbate corneal injury or delay healing. Chronic exposure to particulate matter may lead to repeated microtrauma and inflammation, further compromising ocular surface integrity.[31]

Table 1. Etiological Classification of Corneal Trauma

Abbreviations: FB, foreign body; IOFB, intraocular foreign body.

Epidemiology

Recent global studies estimate that nearly 60 million eye injuries occur annually (see Table. Global Epidemiologic Patterns of Corneal Trauma).[1][2] Over the past 3 decades, the number of incident cases increased by 24%.[1] Unintentional trauma was the leading cause of eye injuries worldwide, followed by self-harm, assault, and transportation accidents. According to the Global Burden of Diseases, Injuries, and Risk Factors Study, the most common causes of unintentional eye trauma were foreign bodies, mechanical forces, and falls. Males in each age group were more likely than females to experience ocular trauma. Both male and female adults aged 25 to 49 had the highest years lived with disability rates of any age group.[1]

The highest total number of eye injuries occurred in South Asia and East Asia, whereas the highest eye injury burden was found in Australasia. Increasing eye injuries from conflict and terrorism were found in Eastern Europe, the Middle East, and North Africa. Rates of foreign-body eye injuries increased in Southeast Asia, sub-Saharan Africa, and Europe. West sub-Saharan Africa and North America had higher rates of eye injury due to self-harm than in previous decades.[1]

Similar patterns exist in childhood eye injury. Most eye trauma is unintentional, with the highest incidence in India and the highest injury burden in Australasia. Male adolescents aged 15 to 19 had the highest risk of injury.[5] Timely intervention and treatment are especially important in children because of the ongoing development of visual processing pathways and the risk of amblyopia.[32]

In England and Wales, corneal trauma accompanies 6.6% of major trauma cases with ophthalmic findings.[3] In the United States, ocular trauma contributes to 2.4 million annual emergency department visits.[33] Superficial ocular injuries accounted for 44%, and external ocular foreign bodies accounted for 16% of the total ocular trauma emergency visits over 10 years.[34] Ophthalmic trauma was also slightly more common in emergency departments in the southern US.[34] 

Ocular chemical burns are an emergency, accounting for 11.5% to 22.1% of all ocular injuries.[35] Haring et al found that young children in the United States were the highest-risk individual group for ocular chemical burns, with ages 1 to 2 years at greatest risk.[36] Generally, ocular chemical injuries occur in individuals aged 18 to 64; they are the second most common cause of workplace ocular injuries after ocular foreign bodies.[37][38] Further epidemiologic information on ocular burns remains sparse. A recent study in the United States indicates that ocular burns may affect males and females at similar rates and at older ages than previously documented (mean ages of 45 and 52, respectively). The prevalence of ocular burn cases also increased by 20% during the study period.[39]

Beyond global estimates, regional epidemiologic variability in corneal trauma is strongly influenced by occupational exposure, socioeconomic factors, and access to eye care services. Low- and middle-income countries bear a disproportionately higher burden of ocular trauma due to increased involvement in high-risk occupations such as agriculture, construction, and manual labor. In these regions, delayed presentation and limited access to specialized ophthalmic care contribute significantly to poor visual outcomes.[40]

Occupational ocular trauma accounts for a substantial proportion of cases worldwide, with studies suggesting that up to 70% of eye injuries in certain populations are work-related. Lack of protective eyewear remains a critical modifiable risk factor, particularly in industrial and agricultural settings. In high-resource countries, although workplace safety regulations have reduced the incidence of severe injuries, recreational and sports-related trauma has emerged as a significant contributor.[15] Seasonal variation in ocular trauma has also been reported, with higher incidence rates during harvesting seasons and warmer months, particularly in agrarian societies. This pattern is attributed to increased outdoor activity and exposure to vegetative matter, which also correlates with a higher incidence of fungal keratitis following trauma.

Pediatric ocular trauma demonstrates distinct epidemiological trends compared to adults. In children, common causes include household injuries, school-related accidents, and sports activities, whereas occupational exposure is the predominant cause among adults. Boys are consistently reported to have a higher incidence of ocular trauma than girls, likely due to behavioral and activity-related differences. Importantly, visual outcomes in children are often worse due to delayed diagnosis and the risk of amblyopia development following corneal injury.[40]

Geriatric populations represent another at-risk group, with falls being a leading cause of ocular trauma. Age-related factors such as reduced visual acuity, impaired coordination, and systemic comorbidities contribute to increased susceptibility. Additionally, older patients may experience poorer healing responses due to reduced corneal regenerative capacity.

Contact lens–associated trauma has become increasingly relevant in modern epidemiology, particularly in urban populations. Improper hygiene practices, extended wear, and exposure to contaminated water sources significantly increase the risk of corneal abrasions and subsequent microbial keratitis. This category represents a preventable cause of vision-threatening complications with appropriate patient education.[41]

Emerging trends also highlight the increasing role of environmental and behavioral risk factors, including air pollution, UV exposure, and digital device–related eye strain, which may predispose individuals to ocular surface compromise and increase susceptibility to trauma. Climate change and increasing environmental hazards may further influence the epidemiology of ocular trauma, particularly in regions prone to extreme weather conditions.[42]

Table 2. Global Epidemiologic Patterns of Corneal Trauma

Abbreviations: LMICs, lower- and middle-income countries; PPE, personal protective equipment.

Pathophysiology

Corneal Injury

The corneal epithelium is avascular, fragile, and richly innervated. Therefore, any injury in an otherwise healthy cornea is very painful. In superficial injury, the epithelium regenerates quickly, with most abrasions healing within 24 to 48 hours.[43] For alcohol-related injuries, the de-epithelialization of the ocular surface typically heals without further sequelae.

In cases of chemical eye injuries, the extent of damage varies depending on the substance involved. Acids cause tissue proteins to bind and get neutralized, leading to coagulation and tissue necrosis. Theoretically, this coagulation acts as a barrier to further acid penetration and damage.[43] One notable anomaly is hydrofluoric acid, commonly used in glasswork and metal refinement. Here, dissociated fluoride ions can quickly traverse the cornea and enter deeper ocular structures.[44] 

Alkali ocular injuries are more prevalent and cause hydrophilic and lipophilic degeneration. The fatty acids of cellular membranes undergo saponification upon contact with alkalis. Unlike acid exposure, saponification allows rapid penetration of alkali into epithelial cells and eventual release of proteolytic enzymes, making the involved tissue more susceptible to enzymatic degradation and damage.[43] Rapid tissue damage to the trabecular meshwork and aqueous outflow in the early injury phase, and subsequent inflammation and adhesions in later phases, can all contribute to elevated intraocular pressure (IOP).[45]

Corneal Healing

Superficial corneal healing requires corneal epithelium regeneration via cellular migration, proliferation, and differentiation as well as extracellular matrix remodeling. Limbal stem cells migrate and differentiate to cover the defect with a single layer of epithelial cells. Proliferation from the basal layer restores the normal thickness of the epithelium. The healing response to a corneal abrasion depends on the size and depth of the defect. Larger abrasions require greater cellular migration and proliferation, and the restoration of normal adhesions can take up to 6 weeks.[43] Recurrent corneal erosion (RCE) can occur over time if the process is incomplete.

For deeper injuries involving the corneal stroma, healing requires keratocytes to transform into fibroblasts and myofibroblasts, which can lead to corneal opacification and scarring. Extensive chemical injuries initiate a similar cascade of inflammation, oxidative stress, and neovascularization, creating fibrosis.[45] These modifications compromise the cornea's optical clarity and can significantly affect vision.

Beyond the immediate structural disruption, corneal injury initiates a complex neuroinflammatory cascade mediated by corneal nerves and resident immune cells. Injury-induced release of neuropeptides such as substance P and calcitonin gene-related peptide amplifies local inflammation and modulates nociceptive signaling and epithelial healing. This neurogenic inflammation plays a critical role in both acute pain and subsequent tissue repair.

The innate immune response is rapidly activated following corneal trauma, with epithelial cells and keratocytes releasing cytokines such as interleukin-1 and tumor necrosis factor-alpha, as well as chemokines that recruit neutrophils and macrophages to the site of injury. While this response is essential for debris clearance and microbial defense, excessive or prolonged inflammation can result in stromal degradation and delayed epithelial healing.[46] 

Matrix metalloproteinases (MMPs), particularly MMP-9, are significantly upregulated after corneal injury and play a key role in extracellular matrix remodeling. Dysregulation of MMP activity may lead to corneal melting and ulceration, especially in severe trauma or secondary infections. Concurrently, oxidative stress induced by reactive oxygen species contributes to cellular apoptosis and further tissue damage.

Corneal nerve injury is another important component of pathophysiology, often resulting in reduced corneal sensitivity and impaired epithelial healing. Damage to the subbasal nerve plexus can lead to neurotrophic keratopathy, characterized by persistent epithelial defects and increased risk of ulceration. The regeneration of corneal nerves is a slow process and may be incomplete in severe injuries.[47]

In cases of limbal involvement, damage to limbal stem cells disrupts the normal homeostasis of the corneal epithelium, resulting in conjunctivalization of the corneal surface, vascular ingrowth, and chronic epithelial instability. The severity of limbal stem cell deficiency directly correlates with the extent of chemical or thermal injury. Endothelial cell injuries, although less common in superficial trauma, can have profound consequences due to the limited regenerative capacity of these cells. Loss of endothelial function leads to stromal edema and loss of corneal transparency, which may necessitate surgical intervention such as endothelial keratoplasty.[48]

Additionally, posttraumatic angiogenic signaling mediated by VEGF promotes corneal neovascularization. Neovascularization not only impairs corneal clarity but also increases the risk of graft rejection in future corneal transplantation. This effect is particularly pronounced in cases of chronic inflammation or hypoxia.

Finally, aberrant wound healing responses may lead to fibrosis and permanent stromal scarring through myofibroblast activation and disorganized collagen deposition. These structural alterations result in irregular astigmatism and reduced visual acuity, representing a major cause of long-term visual morbidity following corneal trauma.[49] Together, these pathophysiologic processes underscore the importance of timely and targeted intervention to preserve corneal integrity and visual function.

Histopathology

Corneal trauma induces distinct histopathological changes that vary according to the depth, mechanism, and chronicity of injury, affecting all layers of the cornea, including the epithelium, Bowman layer, stroma, Descemet membrane, and endothelium. The earliest microscopic changes are typically observed in the epithelium, where cellular loss, disruption of tight junctions, and intercellular edema occur following mechanical or chemical insult. In superficial injuries, epithelial cells demonstrate increased mitotic activity with migration of basal epithelial cells to cover the defect, often accompanied by loss of hemidesmosomal attachments and basement membrane irregularities. Electron microscopy studies have shown cytoplasmic vacuolization and microvillar disruption in damaged epithelial cells, reflecting impaired barrier function (see Image. Pathophysiology and Histopathologic Changes in Corneal Trauma).[43]

The Bowman layer, once disrupted, does not regenerate and is replaced by fibrous scar tissue, leading to permanent structural alteration and light scattering. This acellular layer acts as a critical barrier, and its damage contributes significantly to long-term corneal opacity. Stromal involvement is characterized by activation of quiescent keratocytes into fibroblasts and myofibroblasts, which produce a disorganized extracellular matrix, including type III collagen and fibronectin. These cells are responsible for stromal fibrosis and haze formation by depositing opaque scar tissue. Inflammatory cell infiltration, predominantly neutrophils and macrophages, is commonly observed during the acute phase, particularly in contaminated or infected trauma.[50]

In chemical injuries, histopathological examination reveals widespread stromal necrosis, collagen degradation, and loss of keratocytes, particularly in alkali burns, where rapid penetration leads to diffuse tissue destruction. Acid injuries, although more localized, demonstrate coagulative necrosis with preservation of deeper structures in early stages. Severe burns may also lead to limbal ischemia, resulting in depletion of limbal stem cells and subsequent conjunctivalization of the corneal surface.

Neovascularization is a hallmark of chronic corneal injury and is characterized by the ingrowth of new blood vessels from the limbus into the normally avascular corneal stroma. Histologically, neovascularization is associated with increased expression of angiogenic factors such as VEGF and inflammatory mediators. These vessels disrupt corneal transparency and increase the risk of lipid deposition and graft rejection in future keratoplasty.[45]

The Descemet membrane may show folds, ruptures, or detachment in cases of blunt trauma or severe edema, often accompanied by endothelial cell loss. Endothelial damage is particularly significant because these cells have limited regenerative capacity, and their loss leads to stromal hydration and corneal edema. Persistent endothelial dysfunction may culminate in bullous keratopathy. Corneal nerve alterations are also evident histologically, with reduced density and fragmentation of the subbasal nerve plexus following trauma. These changes contribute to decreased corneal sensitivity and impaired epithelial healing, especially when it progresses to neurotrophic keratopathy.[51]

In cases complicated by infection, histopathology may reveal organism-specific features such as fungal hyphae within the stroma, bacterial colonies, or cyst forms in protozoal infections. In P insidiosum keratitis, characteristic sparsely septate hyphae-like structures with surrounding inflammatory infiltrates may be observed, often mimicking fungal morphology but lacking chitin in the cell wall. Chronic or poorly healed injuries may demonstrate epithelial hyperplasia, stromal thinning, and persistent inflammatory cell presence, reflecting ongoing tissue remodeling and failed resolution of injury. These histopathological changes correlate clinically with persistent epithelial defects, scarring, and visual impairment.[52]

Toxicokinetics

The toxicokinetics of ocular surface injuries primarily depend on the nature of the offending agent, namely its chemical properties, concentration, and duration of exposure, which determine the rate of penetration and extent of tissue damage. Lipophilic substances penetrate the corneal epithelium more rapidly due to disruption of cellular membranes, whereas hydrophilic agents tend to remain more superficial unless epithelial integrity is compromised. Alkali substances rapidly diffuse through the cornea by saponifying membrane lipids and denaturing stromal collagen, thereby penetrating the anterior chamber within minutes. This process facilitates the release of hydroxyl ions, which induce cellular necrosis, proteoglycan degradation, and activation of proteolytic enzymes.[27]

Acidic agents, in contrast, cause protein coagulation at the epithelial and stromal levels, forming a barrier that limits deeper penetration, although strong acids such as hydrofluoric acid can bypass this mechanism due to its lipophilic fluoride ions. UV radiation causes direct DNA damage in epithelial cells via the formation of pyrimidine dimers, leading to apoptosis and delayed epithelial desquamation. Thermal injuries induce protein denaturation and coagulative necrosis, primarily affecting the superficial layers, with the extent depending on the intensity of exposure. Toxic substances also disrupt tear film stability and alter ocular surface pH, further impairing epithelial barrier function and facilitating the progression of secondary inflammation and injury.[53]

History and Physical

A systematic history and a thorough physical examination are essential for accurately characterizing corneal trauma, identifying high-risk features, and guiding timely management. Particular attention should be given to the mechanism of injury, symptom onset and progression, and associated risk factors, as these elements help differentiate superficial injuries from vision-threatening pathology. The following subsections outline key components of the clinical evaluation.

History

A focused ocular history is critical for elucidating the mechanism of injury and identifying risk factors for complications (see Table. Key Historical Clues and Their Clinical Significance). Patients with small corneal abrasions are most likely to report eye pain or a foreign-body sensation. In these cases, presentation can be delayed for several hours after the inciting event. Healthcare practitioners should ask about the circumstances under which the injury occurred and specifically about the use of high-speed machinery and metalworking, as these injuries are more often associated with corneal laceration and globe perforation. A history of eye pain following metal-on-metal hammering suggests a metal projectile as the cause of the ocular injury, and the possibility of globe rupture should be thoroughly investigated. Patients with radiation and thermal corneal burns typically present with a history of exposure in a susceptible environment. For example, eye pain following welding without a welder's shield and eye pain following a house fire are suggestive of radiation burns and thermal burns, respectively.[54]

Patients with chemical ocular injuries are more likely to present immediately. For these ocular burns, identification of the chemical to which the eye was exposed is extremely important, as treatment and prognosis vary significantly depending on the offending agent. Clinicians should also ask if the patient ingested or inhaled any chemical substances, as respiratory passage edema can lead to asphyxiation. Unless an open globe injury is suspected, emergency treatment of potential chemical burns must begin immediately before proceeding with the typical ocular examination, including the deferral of visual acuity testing.[55]

A detailed history should also assess the interval between injury and presentation, as delayed presentation is associated with an increased risk of infection, stromal involvement, and poor visual outcomes. The nature of symptom progression, including worsening pain, decreased vision, or discharge, may indicate secondary complications such as infectious keratitis. Clinicians should inquire about contact lens use, including hygiene practices, overnight wear, and exposure to water sources, as these significantly increase the risk of microbial keratitis following trauma. A history of previous ocular surface disease, including dry eye, blepharitis, or prior trauma, may impair epithelial healing and predispose to recurrent erosions.[56]

Medication history is essential, particularly the use of topical corticosteroids or anesthetics, which may mask symptoms, delay healing, and increase the risk of corneal melting. Occupational history should be expanded to include the use or absence of protective eyewear, duration of exposure, and prior similar injuries. In pediatric and elderly populations, additional history should include the mechanism of injury (accidental versus non-accidental trauma) and functional status, as these groups may present atypically or with delayed symptoms.[57]

Physical Examination

A thorough physical examination is essential to confirm the diagnosis, assess injury severity, and identify associated ocular or adnexal involvement. A comprehensive ocular examination should begin with a visual acuity assessment unless contraindicated, as in chemical injuries requiring immediate irrigation. External inspection should evaluate for periocular edema, lid lacerations, and adnexal injuries, which may coexist with corneal trauma. Slit-lamp examination remains the cornerstone of evaluation (see Table. Slit-Lamp Findings and Diagnostic Correlation). Clinicians should assess for:

• Epithelial defects using fluorescein staining
• Depth of stromal involvement
• Presence of foreign bodies or rust rings
• Anterior chamber reaction (cells, flare, and hypopyon) [25]

Corneal staining patterns provide critical diagnostic clues, including linear abrasions, which suggest a foreign body under the lid, and diffuse punctate staining, which suggests a toxic or radiation injury. A positive Seidel test indicates aqueous leakage and confirms corneal perforation. IOP measurement should be performed cautiously and avoided in suspected open globe injuries. Pupillary examination may reveal afferent pupillary defects, suggesting deeper ocular involvement. Fundus examination, when feasible, helps identify posterior segment involvement, particularly in high-velocity injuries. If visualization is limited, B-scan ultrasonography may be considered, provided globe rupture is excluded.[53] 

Red Flag Features (Must Not Miss)

• Sudden decrease in vision → Possible globe rupture 
• Severe pain with minimal findings → Neurotrophic or early infection 
• History of metal-on-metal injury → Intraocular foreign body (IOFB)
• Chemical exposure → Immediate irrigation required 
• Contact lens use → Risk of Pseudomonas keratitis [12]

Table 3. Key Historical Clues and Their Clinical Significance

 Table 4. Slit-Lamp Findings and Diagnostic Correlation

Evaluation

Traumatic Corneal Abrasions

Gross examination may reveal conjunctival erythema, lid swelling, tearing, and blepharospasm. Visual acuity is considered the vital sign of the eye and should be determined in every patient with an ocular complaint. If the patient wears corrective lenses, acuity should be assessed with the lenses in place. Best corrected visual acuity is typically normal in the setting of corneal abrasions, except in the case of an associated iritis or corneal defect in the central visual axis. The corneal defect can often be visualized under magnification, even without fluorescein. In the event of severe pain, a topical anesthetic may be necessary to obtain a complete ocular examination. Pain relief with a topical anesthetic such as proparacaine strongly suggests a superficial (corneal) etiology of ocular pain. Fluorescein staining followed by examination under cobalt blue illumination highlights the corneal abrasion as a bright green, superficial defect of the cornea.[58][59][60][61]

Corneal Foreign Bodies

As with corneal abrasions, patients usually experience pain, foreign-body sensation, tearing, and blepharospasm. Likewise, application of a topical anesthetic often aids in slit lamp examination and diagnosis. Ocular foreign bodies may lodge beneath the upper eyelid and cause repeated corneal abrasions with each blink. The resulting corneal injury may appear as numerous vertical or curvilinear abrasions. The upper eyelid should be everted and examined for foreign bodies when a corneal or conjunctival foreign body is suspected. In the setting of a metallic foreign body, a rust ring generally forms in the surrounding cornea within several hours. 

If the patient's history suggests a high-velocity projectile, special attention should be given to rule out a possible globe rupture with an IOFB.[62] Signs on examination of an IOFB include a positive Seidel test (described below), iris transillumination defects, anterior chamber inflammation, and the presence of a traumatic cataract. In the presence of these indicators, a hard shield should be placed over the eye, an orbital computed tomography (CT) scan should be obtained, and a referral to ophthalmology should be made for further evaluation.

Corneal Laceration or Perforation

Clinicians must evaluate the entire cornea with a slit lamp. Signs that suggest a full-thickness corneal laceration or perforation include a misshapen iris or irregular pupil, hyphema, microhyphema, decreased visual acuity, and a shallow anterior chamber compared to the fellow eye. Aqueous humor leaking from the anterior chamber during fluorescein examination indicates a corneal perforation (Seidel test). For small lacerations, the Seidel test can be negative with grossly normal-appearing ocular anatomy. Therefore, a high index of suspicion for globe penetration should be maintained, and a CT of the orbit should be obtained when the history or physical examination suggests the possibility of such an injury. While fairly accurate, CT is an imperfect diagnostic test. Consequently, an ophthalmology consultation is recommended in situations with a very high index of suspicion, even when the orbital CT is unremarkable.[16]

If a full-thickness traumatic corneal laceration or perforation is suspected, the eye should be treated as a potential ruptured globe. Further manipulation of the eye at the slit lamp should be avoided to prevent additional extrusion of ocular contents. Instead, a hard shield should be placed over the eye, and further physical examination can be performed in the operating room. If not treated promptly, the long-term sequelae of a full-thickness corneal laceration or perforation include permanent hypotony, ciliary body shutdown, and phthisis bulbi.[40]

Ocular Burns

Chemical burns to the eye are ocular emergencies due to the risk of scarring and permanent vision loss. Irrigation of the eyes and removal of any chemical substances must be performed immediately, before any evaluation or examination, including visual acuity testing. Once neutral pH is achieved, bilateral visual acuity and IOP should be documented. IOP may be measured more effectively with a Tonopen than with applanation tonometry, especially in cases of corneal distortion. Clinicians must also ascertain whether the patient has inhaled or ingested any chemical substance and assess for signs of respiratory compromise.[63]

Mild to moderate chemical burns may present with superficial punctate keratopathy on fluorescein staining, sloughing of the corneal epithelium, chemosis (mild to moderate), hyperemia, subconjunctival hemorrhage, anterior chamber reaction (mild to moderate), and first- or second-degree burns to the eyelids and surrounding skin. Significant perilimbal ischemia, defined by blanching of the surrounding conjunctival and episcleral vessels, should be absent.[64]

In contrast, severe chemical burns present with conjunctival blanching, significant chemosis, and an edematous, often opaque cornea. A significant anterior chamber reaction may be present, but it may be difficult to appreciate if the cornea is cloudy. IOP may be elevated, and necrotic retinopathy may be present if chemicals have penetrated the sclera. Second- or third-degree burns are often accompanied by damage to the surrounding tissue. Grading systems can be used to assess ocular ischemic damage and visual prognosis.[65]

Patients with radiation burns and photokeratitis are typically in severe pain and discomfort. On examination, superficial punctate keratopathy, decreased vision, tearing, and chemosis are often present. In all cases of chemical ocular burn, once the pH has been neutralized, prompt ophthalmologic follow-up is essential for further care and management.

Advanced Diagnostic Modalities

Beyond slit-lamp examination, AS-OCT provides high-resolution cross-sectional imaging of the cornea and is particularly useful in assessing the depth of corneal lacerations, detecting Descemet membrane detachment, and identifying occult perforations. AS-OCT is especially valuable in cases where corneal edema or opacity limits direct visualization.

IVCM enables cellular-level evaluation of the cornea and is particularly useful for identifying infectious etiologies (eg, fungal filaments and Acanthamoeba cysts) in posttraumatic keratitis. IVCM also aids in assessing corneal nerve damage and inflammatory cell infiltration. This modality may facilitate earlier diagnosis and targeted therapy in cases where conventional diagnostic methods are inconclusive.

Ultrasound biomicroscopy can be employed when anterior segment structures are obscured, allowing evaluation of anterior chamber depth, angle structures, and intraocular foreign bodies.[66] This modality is particularly useful when direct visualization is limited or contraindicated and intraocular extension of the injury is suspected. Together, these advanced imaging modalities complement clinical examination by refining diagnostic accuracy and guiding management decisions in complex cases of corneal trauma (see Table. Diagnostic Modalities in Corneal Trauma).

Microbiological and Laboratory Evaluation

In cases of suspected infectious keratitis following trauma, corneal scraping for microbiological analysis is essential (see Table. Microbiological Workup in Posttraumatic Keratitis). Samples should be examined using:

• Gram stain for bacterial pathogens
• Potassium hydroxide mount for fungal elements
• Giemsa stain for cellular morphology

Culture media, including blood agar, chocolate agar, and Sabouraud dextrose agar, are used to isolate causative organisms. Advanced diagnostic techniques such as polymerase chain reaction and next-generation sequencing have improved the detection of atypical organisms, including P insidiosum. Tear film analysis and inflammatory markers may be considered in chronic or non-healing cases to evaluate underlying ocular surface dysfunction.[67]

Radiologic Evaluation

Orbital CT remains the imaging modality of choice in suspected IOFBs or orbital fractures, particularly for detecting metallic foreign bodies. CT has high sensitivity for radiopaque objects but may miss small or non-metallic foreign bodies. Magnetic resonance imaging is contraindicated in suspected metallic foreign bodies due to the risk of migration and further tissue damage. However, magnetic resonance imaging may be considered in select cases of non-metallic foreign bodies when CT findings are inconclusive.[68] 

Functional and Adjunctive Testing

• Corneal sensitivity testing: Useful in identifying neurotrophic keratopathy following trauma; performed with a cotton wisp or esthesiometer. Reduced corneal sensation is associated with delayed epithelial healing and increased risk of ulceration.
• Tear film assessment (including tear breakup time and Schirmer testing): May be helpful in patients with persistent epithelial defects or chronic ocular surface instability
• Specular microscopy: Can evaluate endothelial cell density and morphology, particularly in cases with suspected endothelial damage or corneal edema.[69]

Guideline-Based Evaluation (National and International)

• American Academy of Ophthalmology: Recommends immediate assessment of visual acuity, a slit-lamp examination, and prompt imaging in cases of suspected open-globe injuries.
• Royal College of Ophthalmologists: Emphasizes urgent irrigation for chemical injuries before any diagnostic evaluation and the use of early grading systems such as the Roper-Hall or Dua classification.
• World Health Organization: Highlights early identification and referral of ocular trauma cases as critical in preventing long-term visual impairment, particularly in low-resource settings.[70]

Table 5. Diagnostic Modalities in Corneal Trauma

Abbreviations: AS-OCT, anterior segment optical coherence tomography; CT, computed tomography; DM, Descemet membrane; FB, foreign body; IOFB, intraocular foreign body; IVCM, in vivo confocal microscopy; UBM, ultrasound biomicroscopy.

Table 6. Microbiological Workup in Posttraumatic Keratitis

Abbreviations: KOH, potassium hydroxide; NGS, next-generation sequencing; PCR, polymerase chain reaction.

Treatment / Management

Management of corneal trauma is guided by the type, depth, and severity of injury, with priorities focused on preserving ocular integrity, preventing infection, and promoting epithelial healing. Early recognition of vision-threatening conditions, such as globe perforation and severe chemical burns, is critical, as these require immediate intervention and specialist involvement. Treatment strategies range from supportive care for minor injuries to advanced medical and surgical therapies for more complex presentations, often necessitating coordinated care across an interprofessional team (see Table. Stepwise Management Approach in Corneal Trauma).

Traumatic Corneal Abrasions

The majority of corneal abrasions heal spontaneously; thus, treatment consists primarily of pain control and infection prevention. Loose or hanging epithelium can be debrided at the slit lamp to aid in healing. Large epithelial defects should be measured on initial examination and monitored for improvement. For abrasions greater than 2 mm, or for those that are very painful, a cycloplegic agent such as cyclopentolate 1% or homatropine 5% can help control discomfort by relaxing the ciliary body and relieving pain from ciliary spasm. The cycloplegia of both these agents lasts approximately 24 hours, so a single administration at the time of care should be adequate. In the event of coexisting traumatic iritis, cyclopentolate can be prescribed for several days.

Although topical anesthetics are useful for patient examination, they should not be prescribed for corneal abrasion treatment, even as a temporary measure.[71] First, the efficacy of topical anesthetics in long-term outcomes (eg, epithelial healing) is unclear.[72] Second, the adverse effects of topical anesthetic use can be severe. Continual use of topical ocular anesthetics can inhibit corneal healing, impair the protective blinking reflex, and obscure the identification of pathological progression or additional complications. Miller et al describe the persistence of ocular complications following the use of prescribed topical anesthetics in the days after the initial evaluation.[73] Symptoms of prolonged anesthetic use include increased vision loss, ring infiltrates, eye redness, and corneal ulceration.[74] Some patients can also develop topical anesthetic abuse syndrome, which can lead to corneal perforation and phthisis bulbi.[75](A1)

Although 2 recent reviews have challenged the routine use of antibiotics in corneal abrasions, antibiotic prophylaxis remains widely practiced.[76][77] In cases unrelated to contact lens wear, fingernails, or vegetative matter, erythromycin ophthalmic ointment or polymyxin B sulfate/trimethoprim drops are suitable choices. Corneal abrasions involving organic matter (eg, wood, fingernails, plant material, and animal material) carry a higher risk of infection and complications.[78] In these cases, broader coverage with fluoroquinolones is appropriate [Gervasio KA, Peck TJ, Fathy CA, et al. The Wills Eye Manual. 8th ed. Wolters Kluwer; 2022]. Similarly, contact lens–related abrasions require antipseudomonal coverage, as contact lens use is associated with increased risk of infectious keratitis [Gervasio KA, Peck TJ, Fathy CA, et al. The Wills Eye Manual. 8th ed. Wolters Kluwer; 2022]. Patients should be counseled not to wear contact lenses until the abrasion has completely healed. If necessary, tetanus prophylaxis should also be administered. Corneal abrasions should be reevaluated within 24 to 48 hours of presentation to ensure complete resolution.(A1)

Corneal Foreign Bodies

Nonperforating superficial corneal foreign bodies should be removed at the time of diagnosis. Removal is preferably performed under slit-lamp magnification once anesthesia has been achieved with a topical anesthetic such as proparacaine 0.5%. Occasionally, a cotton applicator may be effective in removing a foreign body. Often, a sterile needle or an ophthalmic corneal burr is necessary.[79] Following foreign body removal, the remaining corneal defect should be managed as a corneal abrasion. In these cases, antibiotic prophylaxis is prudent given the higher likelihood of microbial contamination.[80] (B3)

Inert foreign bodies, such as glass or plastic, can be closely observed. Metallic foreign bodies should be removed to minimize oxidative damage. If a residual rust ring remains after removal of a metallic foreign body, rust removal can either be attempted at the initial visit or deferred to an ophthalmologist for removal the following day. Small rust rings outside the visual axis can be eliminated in stages.

Corneal scarring may follow removal of a foreign body and rust. Therefore, referral to an ophthalmologist should be considered, especially in cases involving the central visual axis. Similarly, deeper corneal foreign bodies, or those with signs of inflammation or infection, should be referred to an ophthalmologist for further evaluation and management.

Complex corneal foreign bodies may benefit from AS-OCT to determine the depth and extent of injury.[81] If the clinician has any suspicion that the foreign body traveled through the full thickness of the cornea, foreign body removal at the slit lamp should not be performed, and the injury should be treated as a globe perforation. Ophthalmology should be consulted immediately.(B3)

Corneal Laceration or Perforation

Partial-thickness corneal lacerations with gaping wound edges should be sutured in the operating room to minimize scarring and optimize restoration of corneal curvature. However, partial-thickness corneal lacerations associated with a shallower anterior chamber compared to the contralateral eye may actually represent full-thickness corneal lacerations that have self-sealed. [Gervasio KA, Peck TJ, Fathy CA, et al. The Wills Eye Manual. 8th ed. Wolters Kluwer; 2022]. Unrecognized corneal perforations and full-thickness corneal lacerations can quickly result in endophthalmitis or traumatic cataract. Therefore, both conditions should be treated as globe ruptures with the placement of a protective eye shield to prevent accidental pressure on the globe, and broad-spectrum intravenous antibiotics should be administered to cover common organisms that cause posttraumatic endophthalmitis. Vancomycin and ceftazadime, or a second- or fourth-generation fluoroquinolone, are appropriate.[82] Moderate evidence suggests that oral antibiotics are noninferior to intravenous antibiotics.[82] Antiemetics are commonly administered to prevent increases in IOP. In the context of traumatic injury, a CT orbit may be indicated to rule out other orbital injuries or retained IOFBs. Ruptured globes and the potential complication of endophthalmitis are ophthalmic emergencies and require intraoperative surgical management by an ophthalmologist. The priorities in ruptured globe repair are to close the globe and address potential infection. Many ruptured globes require subsequent surgeries to address any additional conditions or complications that may exist, such as traumatic cataracts, retinal detachments, or secondary glaucoma.(A1)

Ocular Burns

Treatment of radiation burns (UV keratitis) is supportive and consists of pain control and topical antibiotics, although evidence is limited for the latter. While UV keratitis is generally a self-limiting condition, ophthalmology follow-up in 24 hours is needed if symptoms have not resolved. Patients should be counseled on the adverse effects of UV radiation, including cataract formation, pterygium, and skin cancer, as well as the importance of protective eyewear, such as welder's shields and sunglasses, for future prevention.

Treatment of ocular chemical burns begins at the scene of the injury with copious irrigation with water for at least 30 minutes and continues upon arrival to the hospital. Contact lenses worn at the time of exposure should be removed. In the event of unilateral injury, irrigating fluid should be directed away from the unaffected eye. The use of irrigation devices, such as a Morgan Lens, helps deliver continuous irrigation. The amount of irrigating solution needed varies widely depending on the duration and extent of exposure. If available, buffered eyewash solutions may be better than standard normal saline for irrigating the eyes after caustic exposure. Sterile hypertonic solutions are also helpful, as they use osmotic pressure to draw water and unwanted compounds out of the cornea.[83] Irrigation should continue until the pH remains neutral (pH 7-7.2) for 5 to 10 minutes after the last irrigation in both eyes. Fresh litmus paper should be used for each pH testing, and the conjunctiva and fornices should be checked for any particulate matter.

Ophthalmology consultation should be obtained for all but minor burns. Any patient with corneal clouding or an epithelial defect should be promptly referred to an ophthalmologist. The principles of acute management include:

• Removal of inciting chemical agents
• Promotion of ocular surface epithelial healing (ascorbate and citrate)
• Control of inflammation (topical steroids, citrate, and acetylcysteine)
• Prevention of infection (topical antibiotics)
• Control of pain (cycloplegia and systemic oral analgesia)
• Control of IOP

AMT is often performed in the acute phase to accelerate corneal re-epithelialization and decrease complications, such as corneal neovascularization. However, a recent review of AMT efficacy in treating moderate and severe burns found no significant benefit over standard medical therapy alone.[84] Overall, management should be individualized based on burn severity, with close follow-up to monitor for complications such as limbal stem cell deficiency, scarring, and elevated IOP.(A1)

Advanced Medical Therapies

Beyond conventional antibiotic prophylaxis and lubrication, preservative-free artificial tears play a crucial role in maintaining ocular surface hydration and promoting epithelial healing by reducing mechanical friction. Topical nonsteroidal anti-inflammatory drugs such as ketorolac may be used selectively for pain control; however, prolonged use should be avoided due to the risk of corneal toxicity and delayed epithelial healing. Autologous serum eye drops have emerged as an effective therapy in persistent epithelial defects by providing essential growth factors, vitamins, and fibronectin that support epithelial regeneration. Recombinant human nerve growth factor, such as cenegermin, is increasingly used for neurotrophic keratitis following trauma to promote corneal nerve regeneration and epithelial healing (see Table. Drug Classes and Their Role).[85](B3)

Biologic and Anticollagenolytic Therapy

In moderate to severe corneal injuries, especially chemical burns, anticollagenolytic agents such as oral doxycycline and topical citrate are used to inhibit MMPs and prevent stromal melting. Vitamin C (ascorbate) supplementation is recommended to promote collagen synthesis and reduce the risk of corneal ulceration and perforation. Emerging therapies targeting inflammatory pathways, including anti-VEGF agents, have shown promise in reducing corneal neovascularization and improving long-term visual outcomes.[86]

Surgical and Interventional Management

Bandage contact lenses (BCLs) are widely used to promote epithelial healing, reduce pain, and protect the corneal surface from mechanical trauma. Tissue adhesives (cyanoacrylate glue) may be used in small corneal perforations to provide tectonic support and prevent aqueous leakage. AMT serves as a biological scaffold with anti-inflammatory and antifibrotic properties, facilitating epithelial healing and reducing scarring. In severe cases, therapeutic keratoplasty (penetrating or lamellar) may be required to restore structural integrity and remove necrotic or infected tissue (see Image. Corneal Trauma: Clinical Presentations and Surgical Management). LSCT is indicated in cases of limbal stem cell deficiency following severe chemical burns or trauma.[87] 

Management of Special Situations

• Neurotrophic cornea: Management includes lubrication, BCLs, autologous serum, and nerve growth factor therapy to restore epithelial integrity. 
• Posttraumatic infectious keratitis: Empirical broad-spectrum antimicrobial therapy should be initiated promptly and tailored based on microbiological results.
• Pythium keratitis (posttraumatic): Requires early recognition and treatment with antibacterial agents, such as linezolid or azithromycin, rather than antifungals due to intrinsic resistance.[88]

Guideline-Based Management

• American Academy of Ophthalmology guidelines: Emphasize early antibiotic prophylaxis, avoid misuse of topical anesthetics, and make urgent referral for suspected globe injury. 
• Royal College of Ophthalmologists guidelines: Recommend immediate irrigation in chemical burns and early use of anti-inflammatory and anticollagenolytic therapy. 
• World Health Organization recommendations: Highlight prevention strategies and early intervention to reduce blindness from ocular trauma [12] 

Table 7. Stepwise Management Approach in Corneal Trauma

Abbreviations: AMT, amniotic membrane transplantation; BCL, bandage contact lenses; LSCT, limbal stem cell transplantation; VA, visual acuity.

Table 8. Drug Classes and Their Role

Abbreviations: Anti-VEGF, anti-vascular endothelial growth factor; FB, foreign body; MMP, matrix metalloproteinase; NGF, nerve growth factor; NSAIDs, nonsteroidal anti-inflammatory drugs.

Differential Diagnosis

Although patients with corneal injuries typically present with a clear history of trauma or toxic exposure, several ocular conditions may mimic the presentation of corneal injury; commonly overlapping symptoms include pain, photophobia, tearing, and decreased vision (see Table. Differential Diagnosis of Ocular Findings in Corneal Trauma). In cases where the history is unclear or atypical, careful differentiation is essential to avoid misdiagnosis and inappropriate management (see Table. Red Flag Differentiation). Non-traumatic conditions often lack a clear inciting event and may demonstrate bilateral involvement, chronicity, or systemic associations, which help distinguish them from acute traumatic insults (see Table. Advanced Comparative Differentiation). Additionally, certain conditions may present with similar fluorescein staining patterns or epithelial defects, necessitating detailed slit-lamp evaluation and adjunctive testing.[18] If the source of the injury cannot be confirmed in the patient history, the following alternative diagnoses with corneal findings should be considered:

• Acute angle-closure glaucoma
• Corneal ulcer
• RCE
• Epithelial basement membrane dystrophy or map-dot-fingerprint dystrophy
• Acute conjunctivitis and epidemic keratoconjunctivitis
• Blepharitis, entropion, and trichiasis
• Non-traumatic iritis and uveitis

Table 9. Differential Diagnosis of Ocular Findings in Corneal Trauma

Abbreviations: AC, anterior chamber; EBMD, epithelial basement membrane dystrophy; IOP, intraocular pressure; LN, lymph node.

Table 10. Red Flag Differentiation

Abbreviations: IOP, intraocular pressure; RCE, recurrent corneal erosion.

Table 11. Advanced Comparative Differentiation

Abbreviations: CL, contact lens; IOP, intraocular pressure.

Pertinent Studies and Ongoing Trials

The current management strategies for corneal trauma and ocular surface injuries are supported by randomized controlled trials (RCTs), prospective cohort studies, and systematic reviews evaluating biologic scaffolds, anti-inflammatory therapies, and regenerative interventions (see Table. Evidence Hierarchy).

AMT represents one of the most extensively studied interventions in ocular surface reconstruction. Early clinical evidence demonstrated successful restoration of corneal epithelial integrity and improved visual outcomes in chemical and thermal injuries. Subsequent randomized clinical trials have shown that early AMT, when combined with antimicrobial therapy in infectious keratitis, significantly enhances epithelial healing and reduces corneal vascularization compared to medical therapy alone.[89] 

Further comparative trials evaluating AMT versus lamellar corneal transplantation have demonstrated that while AMT provides rapid epithelialization and anti-inflammatory benefits, lamellar keratoplasty may offer superior restoration of corneal thickness in advanced stromal disease. Recent systematic reviews and meta-analyses that include multiple RCTs and prospective studies have confirmed that AMT accelerates epithelial healing, reduces pain, and improves functional visual outcomes, particularly in cases of moderate to severe corneal injury. Additionally, pooled data suggest that AMT reduces corneal neovascularization and improves ocular surface stability in refractory ulcers.[90] 

In the setting of corneal perforations and severe stromal thinning, prospective and retrospective clinical studies have demonstrated that multilayer AMT provides effective tectonic support, with successful closure rates in small perforations and avoidance of emergent keratoplasty in selected cases. More recent clinical studies have further supported its role in maintaining globe integrity and facilitating stromal remodeling in infectious and inflammatory corneal melts.[91]

Systematic evaluations of AMT as an adjunct to antimicrobial therapy in infectious keratitis have shown improved visual acuity outcomes and faster resolution of inflammation. However, the overall quality of evidence remains moderate due to heterogeneity among trials. Emerging clinical studies are also evaluating sutureless amniotic membrane devices and cryopreserved membrane systems, which aim to improve patient comfort, reduce surgical time, and enhance epithelial healing kinetics. These approaches represent a shift toward minimally invasive ocular surface reconstruction strategies.[92]

In neurotrophic keratopathy, RCTs have demonstrated the efficacy of recombinant human nerve growth factor (cenegermin) in promoting corneal healing and restoring nerve integrity, with significantly higher rates of complete epithelial healing compared to placebo. Despite these advances, large, multicenter randomized trials specifically addressing severe ocular trauma and rare posttraumatic infections such as P insidiosum remain limited. Current literature highlights the need for standardized treatment protocols and well-designed clinical trials to optimize therapeutic timing and long-term outcomes.[69]

Table 12. Evidence Hierarchy

Abbreviations: AM, amniotic membrane; AMT, amniotic membrane transplantation; NGF, nerve growth factor; RCT, randomized controlled trial.

Treatment Planning

After acute management, most superficial corneal abrasions and foreign bodies require no further intervention.[16] However, severe corneal trauma such as chemical burns and globe rupture require intermediate and long-term care. Long-term management of chemical ocular burns focuses on 3 areas: encouraging re-epithelialization, treating symptomatic LSCD, and diagnosing and managing secondary glaucoma. A heightened immune response and fibrovascular pannus formation can make intermediate and long-term treatment especially challenging.

After the acute phase of AMT, treatment options for chronic phase ocular burns include limbal cell transplantation and various reconstructive surgeries.[4] For bilateral cases, allogeneic stem cell transplants may be considered but carry the risks associated with systemic immunosuppression.[93] Cultivated oral mucosal epithelial transplantation is an alternative therapy that reduces inflammation and promotes re-epithelialization, using autologous buccal mucosal cells.[94] Management of globe rupture focuses first on closing the open globe and preventing infection, then on addressing other ocular injuries and complications.[95]

Management of corneal trauma requires a structured, stepwise approach that integrates rapid triage, targeted evaluation, mechanism-based therapy, and timely intervention to preserve vision and ocular integrity (see Table. Clinical Decision Framework). The following clinical decision framework outlines an approach to triage, evaluation, investigation, treatment, and follow-up across the continuum of corneal injury management.

Step 1: Immediate Triage

Principle: Stabilize before you analyze.[12]

• Rule out open globe injury
• Shield eye (no pressure) and avoid manipulation

• Chemical injury → Irrigate immediately
• Do not delay the examination

• Assess vision quickly (if safe)
• Identify red flags:
• Severe vision loss
• Hypopyon or infiltrate
• Positive Seidel
• High-velocity injury

Step 2: Focused Clinical Evaluation

Goal: Define depth, contamination, and risk.[18]

• Establish the mechanism of injury (mechanical, chemical, thermal, or radiation)
• Perform slit-lamp biomicroscopy to assess:
• Epithelial defect (fluorescein)
• Stromal involvement
• Foreign body/rust ring

• Evaluate:
• Anterior chamber reaction
• Corneal sensation
• IOP (only if globe is intact)

Step 3: Targeted Investigations

Principle: Investigate only that will change management.[16]

• Suspected infection → Corneal scraping
• High-velocity injury → CT orbit
• Opaque cornea → AS-OCT or UBM
• Non-healing defect → Tear film + neurotrophic evaluation

Step 4: Mechanism-Based Treatment

Principle: Treat the mechanism, not just the defect.[40]

Superficial injury (abrasions/FB):

• Topical antibiotics
• Lubricants ± bandage contact lens
• Cycloplegics for pain

Chemical burns:

• Copious irrigation → pH normalization
• Steroids (short-term), ascorbate, doxycycline
• Early AMT in moderate to severe cases

Infectious/contaminated trauma:

• Empirical broad-spectrum therapy
• Tailor based on microbiology
• Consider fungal or Pythium in vegetative injuries

Structural damage (laceration or perforation):

• Tissue adhesive or BCL (small defects)
• Surgical repair or keratoplasty (large defects)

Step 5: Healing Optimization:

• Lubrication (preservative-free)
• Autologous serum (non-healing defects)
• Control inflammation (judicious steroids)
• Address:
• Lid abnormalities
• Tear film dysfunction
• LSCD [96]

Step 6: Follow-Up Strategy

• Daily review in the acute phase
• Monitor:
• Epithelial closure
• Infection signs
• Stromal thinning

• Escalate early in the case of:
• Non-healing defect
• Increasing infiltrate
• Risk of perforation [97]

 Table 13. Clinical Decision Framework

Abbreviations: AMT, amniotic membrane transplantation; BCL, bandage contact lenses; IOFB, intraocular foreign body; PK, penetrating keratoplasty.

Principles

• Urgent management is prioritized over diagnostic perfection.Infection is presumed in all doubtful cases.In chemical injuries, time is considered equivalent to tissue loss.
• Neurotrophic or stem cell dysfunction is considered in non-healing epithelial defects.Prevention of late surgical burden is achieved through early intervention.

Toxicity and Adverse Effect Management

Management of corneal trauma must balance therapeutic efficacy with the prevention of treatment-related ocular surface toxicity, which can delay epithelial healing and worsen outcomes.

Topical Medication Toxicity

Prolonged or inappropriate use of topical anesthetics is a well-recognized cause of corneal toxicity, leading to epithelial breakdown, stromal infiltration, ring ulcers, and even corneal perforation. Close follow-up is essential to monitor for progression and to ensure timely intervention if complications such as stromal thinning or ulceration develop. Management involves immediate discontinuation, aggressive lubrication, and treatment of any secondary infection.[98]

Topical antibiotics, particularly aminoglycosides and fluoroquinolones, may induce epithelial toxicity and delay healing when used excessively. Preservative-free formulations and appropriate dosing schedules are recommended to minimize toxicity.[99] Therapy should be reassessed regularly and de-escalated when clinically appropriate to reduce unnecessary exposure and promote epithelial recovery.

Topical corticosteroids, while effective in controlling inflammation, can impair epithelial regeneration, increase susceptibility to infection, and exacerbate corneal melting if used indiscriminately. The use of corticosteroids should be carefully timed and closely monitored, especially in infectious or epithelial-defective states.[100] Topical steroids are generally reserved for cases with controlled infection and intact epithelium.

Drug-Induced Corneal Toxicity

Nonsteroidal anti-inflammatory drugs have been associated with corneal epithelial defects, thinning, and rare cases of corneal melt, particularly with prolonged use.[101] Discontinuation and supportive therapy are required if toxicity is suspected. Preservatives such as benzalkonium chloride can disrupt tear film stability and epithelial integrity, especially in patients requiring frequent dosing.[13] Switching to preservative-free alternatives is recommended in such cases.[102]

Procedure-Related Complications

Use of bandage contact lenses may predispose to microbial keratitis if hygiene is inadequate or follow-up is poor. Regular monitoring and prophylactic antibiotics are essential. AMT is generally safe but may rarely be associated with membrane displacement, infection, or delayed epithelialization. Proper surgical technique and follow-up minimize these risks.[15]

Systemic Therapy–Related Effects

Systemic agents such as oral doxycycline, used for their anticollagenolytic properties, may cause gastrointestinal intolerance and photosensitivity. Dose adjustment and patient counseling are advised. High-dose ascorbate therapy, used in chemical burns, may lead to gastrointestinal upset but is generally well tolerated and beneficial for collagen synthesis.[103]

Clinical Monitoring and Prevention Strategy

• Use the minimum effective dose of topical medications.
• Prefer preservative-free formulations in prolonged therapy.
• Avoid unsupervised use of anesthetics or steroids.
• Monitor for:
• Persistent epithelial defect
• Stromal thinning
• New infiltrates

• Early identification of toxicity allows reversal before structural damage occurs.

Key Clinical Pearls

• Non-healing corneal defect → Always rule out drug toxicity
• Topical anesthetic misuse → Vision-threatening emergency
• Steroids without infection control → Corneal melt risk
• Preservatives → Silent contributors to chronic epithelial damage [104]

Staging

Staging of ocular surface burns is essential for clinical assessment and visual prognosis. The Dua classification is the most widely used grading system for this purpose (see Table. Dua Classification of Ocular Surface Burns).[45][65] Limbal ischemia is quantified in clock hours, whereas conjunctival involvement is expressed as a percentage. The analog scale correlates the extent of limbal ischemia (measured in clock hours) with the percentage of involved bulbar and forniceal conjunctiva. Staging of ocular surface burns is essential not only for prognostication but also for guiding timing and intensity of therapeutic interventions, particularly decisions regarding early surgical procedures such as AMT and LSCT.

Dua Classification

The Dua classification is a comprehensive grading system based on 2 critical parameters:

• Extent of limbal ischemia (clock hours: 0-12)
• Extent of conjunctival involvement (percentage: 0%-100%) [55]

The analog relationship between limbal involvement and conjunctival damage reflects the extent of limbal stem cell loss, which is the key determinant of epithelial healing potential (see Table. Grades of Dua Classification).

Table 14. Grades of Dua Classification

Pathophysiologic Correlation of Staging

Higher grades are associated with:

• LSCD → Persistent epithelial defects
• Stromal ischemia and necrosis
• Increased inflammatory cytokine load
• Neovascularization and conjunctivalization

The severity of limbal ischemia directly correlates with the loss of regenerative capacity of the corneal epithelium, making it the most critical prognostic indicator.[105]

Comparison with the Roper-Hall Classification 

The Roper-Hall classification is an older grading system based on corneal haze and limbal ischemia. However, this classification system is less precise because it does not quantify conjunctival involvement and tends to underestimate injury severity (see Table. Roper-Hall Classification).[106] As such, the Dua classification is preferred due to better prognostic accuracy and reproducibility.

Table 15. Roper-Hall Classification

Clinical Utility of Staging

Staging directly influences management decisions (see Table. Staging-Based Management Approach):

• Grades I to II
• Conservative management sufficient
• Rapid epithelial healing expected

• Grades III to IV
• Require aggressive medical therapy
• Early consideration of AMT

• Grades V to VI
• High risk of LSCD and corneal melt
• Require early surgical intervention (AMT and LSCT) [19]

Table 16. Staging-Based Management Approach

Abbreviations: AMT, amniotic membrane transplantation; LSCD, limbal stem cell deficiency; LSCT, limbal stem cell transplantation.

Prognosis

Superficial corneal abrasions and superficial corneal foreign body injuries generally have an excellent prognosis, particularly when the visual axis is not involved. For anterior stromal scarring involving the visual axis, long-term visual rehabilitation may include excimer laser correction or lamellar corneal transplantation. In ocular chemical burns, greater than 50% conjunctival involvement or greater than 6 clock hours of limbal involvement indicate a poor visual prognosis. For these severe cases, corneal transplants are more frequently rejected, and keratoprosthesis surgery may be required.[107] The prognosis for perforating corneal injuries is also more guarded and dependent on the individual circumstances of each case.

Early intervention, particularly timely irrigation in cases of chemical injury, is one of the most critical determinants of visual outcomes and can significantly reduce long-term ocular surface damage. The extent of limbal stem cell damage remains the single most important predictor of epithelial healing and long-term ocular surface stability, with total limbal ischemia often resulting in persistent epithelial defects and conjunctivalization.[55]

The presence of a secondary infection, especially fungal or atypical organisms such as P insidiosum, is associated with poorer outcomes due to delayed diagnosis and limited therapeutic options. Corneal nerve damage and subsequent neurotrophic keratopathy may adversely affect prognosis by impairing epithelial regeneration and increasing the risk of chronic ulceration. Depth of stromal involvement is another key factor, as deeper injuries are more likely to result in fibrosis, irregular astigmatism, and permanent visual impairment. Posttraumatic corneal neovascularization further worsens prognosis by compromising corneal transparency and increasing the risk of graft rejection in future keratoplasty. Patient-related factors such as age, comorbid ocular surface disease, and delayed presentation also influence healing outcomes and visual recovery.[108]

Key Prognostic Indicators

• Limbal ischemia extent → Strongest predictor
• Time to treatment → Critical in burns
• Infection → Worsens outcome significantly
• Stromal depth → Determines scarring
• Neovascularization → Predicts graft failure

Complications

Complications of corneal trauma include scarring affecting the visual axis, recurrent corneal erosion due to weak adhesions between the healed corneal epithelium and underlying corneal layers, reduced limbal stem cell function and failure, secondary glaucoma due to trabecular meshwork damage, traumatic cataract, retinal detachment, endophthalmitis, and loss of vision or the eye.[109][110] In chemical ocular injuries, pseudomembranes, symblepharon, and cicatricial entropion or ectropion can also occur.

Persistent epithelial defects are a common sequela following corneal trauma, particularly in cases associated with LSCD or neurotrophic keratopathy, leading to delayed healing and increased risk of infection. Corneal thinning and stromal melt may result from an excessive inflammatory response and MMP activity, potentially progressing to perforation if not managed promptly. Posttraumatic corneal neovascularization can develop secondary to chronic inflammation and hypoxia, compromising corneal transparency and increasing the likelihood of graft rejection in future keratoplasty.[111]

Irregular astigmatism resulting from stromal scarring and surface irregularity is a frequent cause of long-term visual impairment even after structural healing. Neurotrophic keratopathy may develop following damage to corneal nerves, resulting in reduced corneal sensitivity, impaired epithelial healing, and recurrent ulceration. Anterior segment complications such as peripheral anterior synechiae and chronic angle damage may contribute to long-term IOP elevation and secondary glaucoma. In severe ocular surface burns, chronic cicatrization may lead to dry eye disease, ocular surface keratinization, and ankyloblepharon, significantly affecting ocular function and cosmesis. The negative psychosocial impact, including reduced quality of life and functional disability, is also increasingly recognized as an important long-term consequence of vision-threatening ocular trauma.[69]

Table 17. Comprehensive Classification of Complications in Corneal Trauma

Abbreviations: IOP, intraocular pressure; LSCD, limbal stem cell deficiency; MMP, matrix metalloproteinase; QOL, quality of life; TM, trabecular meshwork; VEGF, vascular endothelial growth factor.

Key Clinical Pearls

• Persistent epithelial defect → LSCD or neurotrophic cause
• Corneal melt → Vision-threatening emergency
• Neovascularization → Future graft failure risk
• Chemical burns → Chronic cicatricial complications [111]