Anterior Segment Trauma
Blunt and penetrating facial trauma may result in eyelid laceration. The laceration may be extramarginal, may involve the eyelid margin, or may cause tissue loss. Eyelid trauma is often associated with vehicle accidents, falls, sport-related traumas, and assaults. Eyelid laceration is more common in young males due to occupational and recreational preferences. Proper management is necessary to preserve correct lid dynamics and cosmetic appearance.
Patients usually complain of mild pain and epiphora. Displacement or abnormalities of the canthal angles may indicate canthal ligament injury. Lacerations of the deep head of the medial canthal ligament may cause telecanthus. Hyphema, other ocular adnexa traumas, and orbital fractures may be present (Fig. 1.1).
The mechanism of injury should be investigated first, followed by a complete ocular examination to rule out injuries to the globe. If no globe rupture is present, lids should be everted, palpated, and examined for foreign bodies. The laceration should be carefully examined to determine depth, extension, and margin involvement. Photography of the lesions is recommended. Canalicular involvement and injury to the levator and the supraorbital nerve should be excluded. A computed tomographic scan should be obtained when globe rupture and foreign bodies are suspected. Tetanus prophylaxis and baseline serology for human immunodeficiency virus (HIV) and hepatotropic viruses should be considered. Surgical repair should be performed under local anesthesia, with good lighting and magnification. After adequate anesthesia, wound cleaning, and decontamination, the laceration should be repaired using Vicryl (Ethicon, Inc., Somerville, NJ) or silk 6–0 suture. Posterior tendon repair and canalicular repair should precede lid suturing. Eyelid margin laceration should be sutured with a vertical mattress technique. Finally, antibiotic ointment should be applied to the wound, and systemic antibiotic therapy should be considered if contamination is suspected. Possible complications include posttraumatic upper lid ptosis and corneal ulceration due to corneal exposure or an exposed suture.
Lacrimal System Trauma
The lacrimal drainage apparatus consists of the lacrimal puncta on the upper lid and the lower lid, the canaliculi, the common canaliculus, the lacrimal sac, and the nasolacrimal duct. From their origin at the puncta, the canaliculi run medially toward the internal angulus of the eye, where they join to form the common lacrimal canaliculus that opens in the lacrimal sac. Canalicular lacerations are the most frequent cause of injury to the lacrimal system and occur in up to 16% of all eyelid injuries. Common causes of canalicular laceration include vehicle accidents, falls, assaults, sharp trauma, and animal bites. Successful management of these injuries depends on prompt intervention and good surgical technique to minimize the incidence of posttraumatic epiphora due to scarring and stenosis in any tract of the lacrimal drainage system.
Patients usually present with a history of trauma and mild pain. The lacrimal drainage system lesion may be obvious or occult. The use of methylene blue or fluorescein-tinged water irrigation through the puncta and subsequent visualization of the dye in the wound may be helpful in identifying the cut end (Fig. 1.2A,B).
Lid laceration not involving the lacrimal drainage system, preexisting epiphora
The mechanism of injury should be investigated, and a complete ophthalmic examination should be performed. The injury to the lacrimal drainage system can be proven with Bowman probe insertion in the puncta or by irrigation with fluorescein-stained saline solution. Tetanus prophylaxis should be considered. Surgical repair should provide accurate approximation of the severed ends to promote mucosal healing. Most surgeons use silicone intubations of the system, followed by apposition of the pericanalicular tissues with microscopically assisted 7–0 suture. The medial canthal ligament is often injured from the trauma and must be repaired to restore lid function and anatomy. The success rate with silicone intubation and microscopic reanastomosis ranges from 86 to 95%.
Subconjunctival hemorrhage follows the bleeding of conjunctival and episcleral blood vessels into the subconjunctival space. It is usually associated with minor trauma or arises spontaneously with increased venous pressure due to violent Valsalva maneuvers. Less frequently subconjunctival hemorrhage can be associated with severe hypertension and coagulopathies. Various drugs, such as warfarin, nonsteroidal antiinflammatory drugs (NSAIDs), and steroids can make conjunctival vessels more susceptible. It is also a normal sequela of ocular surgery.
A bright red and flat collection of blood is seen underneath the conjunctiva; it is usually sharply demarcated at the limbus and surrounded by normal conjunctiva. This condition is usually asymptomatic. If pain, photophobia, or diminished visual acuity occurs, a more serious pathological condition should be considered (Fig. 1.3).
The differential diagnosis of subconjunctival hemorrhage includes other causes of red eye, such as conjunctivitis, episcleritis, iritis, acute glaucoma, and dendritic ulcer. Kaposi sarcoma, or other conjunctival neoplasms with secondary hemorrhage should be taken into consideration.
Blood pressure should be checked in all patients, and if there is a history of recurrent, unprovoked subconjunctival hemorrhages, a bleeding diathesis should be investigated. The uncomplicated hemorrhage, not associated with any significant trauma or bleeding diathesis, is typically a self-limiting condition that requires only reassurance. Cold compresses for 24 hours and artificial tears can be used for mild irritation. Hemorrhage clears spontaneously in 1 to 2 weeks. Elective use of NSAIDs is typically discouraged.
The conjunctiva is a strong and resilient tissue, but it may be lacerated in cases of ocular trauma with pointed and sharp objects, such as broken glass. It may be isolated or part of more severe intraocular injuries.
Patients usually present with a history of ocular trauma and complain of red eye, mild pain, and foreign body sensation. Slit-lamp examination reveals a conjunctival surface defect. The edges are usually retracted and rolled up, disclosing the underlying white sclera. Subconjunctival hemorrhages and chemosis are often present. Fluorescein staining under the cobalt filter will enhance the visualization of the defect (Fig. 1.4).
An accurate history of ocular trauma and a complete ophthalmic examination are necessary: topical anesthesia may be used to accurately investigate the underlying sclera in search of injuries and subconjunctival foreign bodies. However, patients under topical anesthesia may lose symptoms associated with the presence of a foreign body. A Seidel test should be performed to rule out a ruptured globe.
B-scan ultrasonography and a computed tomographic scan of the orbit may be useful to exclude intraocular or intraorbital foreign bodies.
In the absence of a ruptured globe or perforating injuries, small conjunctival lacerations heal without surgical repair. Large lacerations (e.g., greater than 1.0 to 1.5 cm) may be sutured (e.g., Vicryl 8–0). Pressure patching for 24 hours and prophylactic antibiotic ointment (e.g., gentamicin) three times a day for 4 to 7 days should suffice.
Chemical burns constitute a true ocular emergency and should be treated promptly. Chemical burns may be caused by either acidic or alkaline agents. Acid burns cause coagulative necrosis of the corneal epithelium. The formation of a coagulum limits penetration and corneal damage. Hydrofluoric acid is an exception because it causes liquefactive necrosis. Common acids causing ocular burns include sulfurous acid (present in some bleaches), sulfuric acid (present in car batteries), hydrochloric acid (used in swimming pools), nitric acid, chromic acid, and acetic acid. Alkali burns are typically more severe because alkaline agents are lipophilic and penetrate more rapidly than acids. They combine with cell membrane lipids and cause saponification of cell membranes, cell death, and disruption of the extracellular matrix. The release of collagenases and proteases after the injury leads to corneoscleral melting. Alkali substances that commonly cause ocular burns contain sodium hydroxide (caustic soda), ammonium hydroxide (fertilizer production), potassium hydroxide, and calcium hydroxide. Chemical burns are often bilateral and are frequently due to industrial and occupational exposures.
The diagnosis of ocular chemical burn is typically based on history of contact with alkaline or acid agents. The symptoms usually include pain, photophobia, blepharospasm, reduced vision, and excessive tearing. If the burn is mild or moderate, the conjunctiva is hyperemic. Focal conjunctival chemosis, hyperemia, or hemorrhages can be present. Eyelid edema and first- to second-degree periocular skin burns can be seen. Corneal findings may range from superficial punctate keratitis (SPK) to focal epithelial defects. In severe conditions white areas of conjunctival and limbal ischemia can be seen. Corneal findings usually consist of total epithelial loss, stromal hazing, and, in same cases, complete opacification. Other signs include anterior chamber reaction and second- or third-degree periocular burns. (Fig. 1.5A,B).
Chemical burns are considered a true ophthalmologic emergency and require immediate care. The first priority is immediate and copious irrigation with sterile irrigating solution or saline solution. If these solutions are not available, tap water can be used. Irrigation should be continued until neutral pH is reached. Insertion of a lid speculum and topical anesthetic prior to irrigation facilitates the procedure. After irrigation a good history with an exact identification of the chemical agent should be obtained. Slit-lamp examination with fluorescein staining should be performed. Eyelids should be everted to search for residual chemicals and foreign bodies. The goal of therapy is to reduce pain, inflammation, and risk of infection. Thus cycloplegic agents (avoid phenylephrine because it is a vasoconstrictor), oral analgesics (avoid repeated applications of topical anesthetics because they can delay epithelial healing), and ophthalmic antibiotics (avoid aminoglycoside antibiotics because they impair epithelial healing) should be administered. The use of topical steroids remains controversial. They can limit inflammation-mediated ocular damage, but they retard wound healing and predispose to infection. Severe burns can be managed with adjunctive therapy: ocular hypotensive medications if the intraocular pressure is elevated, collagenase inhibitors if any melting of the cornea occurs, lysis of conjunctival adhesions if present, and active surgical removal of necrotic tissue. Long-term complications of chemical burns include perforation, scarring, corneal neovascularization, symblepharon, glaucoma, cataracts, and retinal damage. Ultimate prognosis is related to the degree of limbus ischemia, the depth of the corneal injury, and the presence of symblepharon.
Corneal abrasions represent one of the most common ophthalmic problems seen in emergency departments. A corneal abrasion is the disruption of the protective epithelium covering the cornea; it may be caused by direct or tangential impact. Common causes are scratches from fingernails, animal paws, tree branches, or a paper cut. Another common cause is contact lens overwear. A large number of corneal abrasions are preventable. High-risk workers (e.g., woodworkers, metal workers) and players of certain sports (e.g., hockey, racquetball, cross-country skiing, mountain biking) should wear appropriate eye protection.
The patient’s history typically includes eye trauma and subsequent acute pain. Presenting symptoms usually include severe pain, excessive tearing, photophobia, foreign body sensation, blepharospasm, and blurred vision. At slit-lamp examination diffuse corneal edema, epithelial disruption, and circumcorneal injection can be seen (Fig. 1.6).
Acute angle glaucoma, herpes ulcers and other corneal ulcers, corneal foreign body, and corneal perforation
Visual acuity should be assessed because it may be significantly reduced if the abrasion is on the optic axis. Upper and lower tarsal conjunctiva should be inspected carefully for foreign bodies. If examination is limited by excessive pain, one drop of topical anesthetic could be administered for diagnostic purposes. At slit-lamp examination the visualization of the corneal abrasion can be improved using fluorescein staining under blue-cobalt filtered light. The abrasion should be documented in size, shape, depth, and localization. A Seidel test should be performed to rule out possible full-thickness injury. Intraocular pressure should be measured in both eyes, and the anterior chamber should be carefully investigated for evidence of iritis. Prevention of infection is a key point in corneal abrasion treatment. An antibiotic ointment should be used; consider antipseudomonas coverage for abrasions due to contact lens overwear. Patients with contact lens–associated corneal abrasion or a wound that is caused by vegetable matter should have antipseudomonas coverage (e.g., tobramycin, ciprofloxacin, gentamicin, ofloxacin). Oral analgesics are often necessary owing to the severity of pain. Topical NSAIDs (e.g., diclofenac, ketorolac) may be useful in reducing pain. Patients using topical NSAIDs may take fewer oral analgesics. Never provide topical anesthetics to take home because they can delay wound healing. One drop of topical cycloplegic can be used if the patient is really photophobic. This relieves ciliary spasm, reduces pain, and improves comfort. Pressure patching is no longer recommended. It should be used for 6 hours only if pain is severe. Given the risk of infection, do not patch if the lesion is caused by vegetable matter or contact lenses. Healing of small abrasions is expected within 24 to 48 hours. Deep and large abrasions may require 5 to 7 days to heal. Most corneal abrasions (small and peripheral) do not need any follow-up. However, contact lens wearers or patients with a central or large abrasion should be reevaluated in 24 hours and every 2 to 3 days until abrasion clears. Patients should return sooner if symptoms worsen.
Corneal Foreign Body
A corneal foreign body is a common cause of visits for ophthalmic emergencies. It frequently occurs when one is grinding and drilling steel without wearing protective goggles.
The patient’s history usually includes an ocular trauma. The more frequent symptoms are mild or moderate pain, foreign body sensation, excessive tearing, photophobia, and blurred vision. At slit-lamp examination one or more objects can be seen lodged superficially or embedded within the cornea. Metallic foreign bodies may leave rust rings in the surrounding cornea. Other signs include a circumlimbal conjunctival injection, eyelid edema, and a sterile infiltrate surrounding the foreign body (Fig. 1.7).
After having assessed visual acuity, it is important to rule out a possible perforating injury. This can be done using a Seidel test (instill fluorescein to inspect for aqueous leakage), measuring intraocular pressure, and paying attention to anterior chamber reaction. Consider a b-scan ultrasound and an orbital computed tomographic scan to exclude intraocular and intraorbital foreign bodies. If there is no perforation, the object can be removed under topical anesthesia (e.g., proparacaine 0.5%) using a foreign body spud or a 25-gauge needle. This operation can be facilitated by sterile irrigation. The rust ring can be removed using an ophthalmic drill. These procedures should be performed at slit lamp by well-trained and experienced physicians. Before and after the removal, antibiotic drops should be applied until healing. A topical cycloplegic can be used to reduce photophobia and pain. Patients should be reevaluated every 2 to 3 days until the wound is healed and the infiltrate resolved.
The laceration can be partial thickness or full thickness.
In partial-thickness laceration, the anterior chamber is not entered, and, therefore, the cornea is not perforated. If the Seidel test is positive, a full-thickness laceration is present. In full-thickness laceration the patient presents with tearing, pain, and loss of vision. Associated findings include: shallow anterior chamber, anterior synechiae, corneal opacity with endothelial dysfunction, or cataract. Intraocular pressure may be very low (Fig. 1.8).
A history and complete ophthalmic examination are required to ascertain the diagnosis. While managing a partial-thickness laceration, a cycloplegic (e.g., scopolamine 0.25%) and an antibiotic (e.g., frequent polymyxin B/bacitracin ointment such as polysporin) or fluoroquinolone drops, depending on the nature of the wound, are started immediately.
When a moderate to deep corneal laceration is accompanied by wound gape, it is often best to suture the wound closed in the operating room to avoid excessive scarring and corneal irregularity, especially in the visual axis. Tetanus toxoid for dirty wounds is a must.
Note that small, self-sealing, or slow-leaking lacerations may be treated with aqueous suppressants, bandage soft contact lenses, fluoroquinolone drops four times a day. Alternatively, a pressure patch and twice-daily antibiotics may be used. Avoid topical steroids.
A blunt trauma to the eye can cause traumatic inflammation of the iris or, more accurately, of the anterior uveal tract. This leads to the presence of inflammatory cells in the anterior chamber of the eye. Traumatic iritis generally develops quickly after the trauma and usually affects only the injured eye.
Patients usually present with a history of ocular trauma. Symptoms include pain, photophobia, and possibly headache. Pain typically worsens when either the injured eye or the uninvolved eye is exposed to bright light (due to consensual pupillary constriction). Signs include cells and flare in the anterior chamber and perilimbar injection (Fig. 1.9). The iris pupillary margin of the involved eye may be different in shape compared with the contralateral.
Traumatic corneal abrasion, traumatic microhyphema, other causes of anterior uveitis
Posttraumatic pain without corneal abrasion or ulcer should suggest the diagnosis of traumatic iritis. This diagnosis can be confirmed by the presence of cells and flare in the anterior chamber at slit-lamp examination. A complete ophthalmic evaluation should be performed, including tonometry and fundus examination. Treatment typically consists of cycloplegic agents. In refractory cases and if no corneal epithelial defect is detected, a steroid drop could be given. Patients should be re-evaluated within a week; if iritis is resolved, medication can be discontinued.
Iris Sphincter Tear
Blunt injury often causes tears in the sphincter pupillae of the iris.
The patient may be asymptomatic or may have glare and photophobia. The tears in the pupillary margin can be visualized on slit lamp examination (Fig. 1.10)
A thorough ocular examination is done to rule out any other coexisting damage. It may be left alone untreated. If causing symptoms, and if cataract extraction is also being planned, one may perform a pupilloplasty or use aniridia segments.