bubble_chart Overview

A perforating injury to the eye wall caused by sharp objects or foreign bodies is referred to as an ocular perforation. Depending on the location of the perforation, it can be classified as corneal perforation, scleral perforation, or corneoscleral perforation involving the limbus. Since the cornea is exposed at the front, corneal perforations are the most common clinically. Ocular perforations can be divided into two categories: simple perforations with wounds smaller than 3mm and no incarcerated intraocular tissue, and those with wounds larger than 3mm containing incarcerated intraocular tissue.

bubble_chart Clinical Manifestations

1. Vision: The degree of visual impairment varies depending on the location of the perforation. For example, a small, simple perforation in the peripheral part of the cornea may not affect vision.

2. Anterior chamber: If the perforation is in the cornea or corneosclera, the aqueous humor continuously leaks out, causing the anterior chamber to become shallow. In cases of larger wounds, iris tissue may prolapse and become incarcerated in the wound, leading to pupil deformation. If the perforation is in the sclera, intraocular contents may prolapse toward the wound, and the depth of the anterior chamber may remain unchanged or even deepen. Both eyes should be compared carefully for accurate assessment.

3. Intraocular pressure: Due to perforation of the eyeball wall, leakage of aqueous humor, and prolapse of intraocular contents, intraocular pressure is significantly reduced. Caution is required during intraocular pressure examination to avoid exacerbating the prolapse of intraocular contents.

bubble_chart Diagnosis

The diagnosis can be confirmed based on clinical manifestations.

bubble_chart Treatment Measures

Close the wound to prevent infection. For simple perforating wounds, if the wound is clean, administer antibiotics both locally and systemically, and apply a light-pressure monocular bandage. The wound usually closes and the anterior chamber forms within 1–2 days. If the wound is larger than 3 mm, suturing is required. If intact iris tissue is incarcerated in the wound, and the injury occurred within a few hours with the wound being clean, carefully reposition the tissue into the eye after rinsing with an antibiotic solution and close the wound (typically using 10-0 nylon sutures). Otherwise, remove the incarcerated intraocular tissue before suturing. For scleral perforations larger than 7 mm at the corneoscleral limbus, perform scleral cryotherapy or diathermy on both sides of the wound after suturing to prevent retinal detachment. After wound management, administer antibiotics and corticosteroids locally and systemically, along with tetanus antitoxin.

bubble_chart Complications

1. Traumatic iridocyclitis: Inflammation caused by direct damage to the iris, incarceration of iris tissue in the wound, or retained intraocular foreign bodies. Management includes mydriasis, intensive topical corticosteroids, and often subconjunctival injection of dexamethasone.

2. Suppurative endophthalmitis: Often caused by bacterial infection entering through a perforating wound or introduced by the injuring object or foreign body. Symptoms include rapid vision loss, eye pain, and tearing. Examination reveals conjunctival congestion and edema, corneal edema with a hazy appearance, and highly turbid aqueous humor, possibly with hypopyon. Severe cases may show a yellow reflex in the pupillary area (indicating vitreous pus). Treatment involves systemic and local high-dose antibiotics, along with early vitrectomy and direct intravitreal antibiotic injection. The prognosis is poor, often leading to panophthalmitis or phthisis bulbi.

3. Panophthalmitis: A progression of endophthalmitis where inflammation spreads to the ocular wall and surrounding tissues. In addition to endophthalmitis symptoms, it presents with proptosis, severe conjunctival edema and congestion, restricted eye movement, complete vision loss, and even corneal abscess perforation with pus discharge. Without timely treatment, it may progress to orbital cellulitis, spread intracranially, and cause purulent meningitis, which is life-threatening. Treatment involves evisceration of the eye. Enucleation may risk spreading infection to the brain. Postoperative wound drainage and systemic/local antibiotics are essential.

4. Intraocular foreign body: Foreign bodies are classified as magnetic or non-magnetic and may be located anywhere in the eye, varying in size. Magnetic intraocular foreign bodies require precise localization and removal via the nearest scleral incision. Non-magnetic foreign bodies, if chemically stable and located in the posterior pole, may not require removal.

5. Sympathetic ophthalmia: When a perforating injury, especially with an intraocular foreign body, leads to persistent uveitis, the unaffected contralateral eye may later develop similar uveitis, termed sympathetic ophthalmia. The injured eye is the "exciting eye," and the unaffected eye is the "sympathizing eye." The latent period is typically 2–8 weeks post-injury, though rare cases may occur within days or decades. In China, the incidence is about 1.2% of perforating injuries, influenced by the wound location and incarceration of uveal tissue. Injuries to the ciliary body or with incarcerated uveal tissue have higher risks. Repeated intraocular surgeries shortly after injury may also trigger it. Rarely, it occurs after intraocular surgery, corneal ulcer perforation, or intraocular melanoma. The cause is believed to be a delayed autoimmune response.

Clinical manifestations include two types: ① Predominantly anterior uveitis—photophobia, tearing, eye pain, conjunctival mixed congestion, turbid aqueous humor, keratic precipitates, miosis, and posterior synechiae. ② Predominantly posterior uveitis—vision loss, optic disc congestion and edema, blurred margins, macular edema, loss of foveal reflex, retinal detachment. Chronic cases show scattered yellow-white exudates in the choroid and vitreous opacity, eventually progressing to panuveitis, possibly causing bilateral blindness.

Prevention is key, including proper wound management and early corticosteroid use to reduce incidence. Once sympathetic ophthalmia occurs, avoid hastily enucleating the injured eye, especially if residual vision remains. High-dose systemic and local corticosteroids, combined with immunosuppressants if necessary, along with adjunctive energy supplements, are required. Treatment must be thorough to prevent recurrence.