Eye Trauma

by Serpil Yaylaci and Kamil Kayayurt

Introduction

The most common cause of unilateral blindness in industrialized countries is eye trauma, most of which can be prevented with the use of protective goggles. Every year, more than 55 million people worldwide experience eye traumas, and more than one million suffer total loss of vision. Eye traumas constitute approximately 3% of total emergency department cases; most of these traumas are minor injuries. Major injuries are less frequent; however, the rate of recovery of visual impairments is quite low in these cases. Sixty-five to eighty percent of eye traumas are observed in males, typically 25–44 years of age. About half of eye traumas are the result of occupational accidents, and the use of protective goggles reduces the number of those injuries by 70%.

Anatomy

The eyeball consists primarily of three layers. The outermost layer is a fibrous structure made up of the sclera and the cornea. The middle layer is the vascular layer, called the uvea. The iris, ciliary body, and choroid are located inside the uvea. The innermost layer is the neural layer, called the retina.

The eyeball is located in the bony cavity, called the orbit. The superior wall of the orbit consists of the frontal bone, the lateral wall consists of the zygoma, and the medial and anteromedial walls consist of the maxilla, lacrimal, and ethmoid bones. The video below shows bones of the orbit.

https://www.youtube.com/watch?v=qUjw1IV1u9w

Please visit this link to see detailed Eye Anatomy videos.

Orbital Traumas

Eye traumas can be divided into three groups: globe injuries, periorbital injuries, and chemical injuries. Only selected injuries observed most frequently in emergency departments and that can lead to total loss of vision will be discussed.

Classification of Eye Trauma

Globe Injuries

1. Open-globe injuries ( Rupture of globe)
2. Closed-globe injuries
   • Conjunctival laserations
   • Partial thickness corneal and scleral lacerations
   • Corneal and conjuntival abrasions
   • Hyphema
   • Lens dislocation
   • Traumatic iritis
   • Retinal detachment
   • Vitreous hemorrhage
   • Commotio retina

Periocular trauma

1. Orbita fractures
2. Ekstraocular muscle, vascular, and eyelid injuries
   • Orbital compartment syndrome
   • Eyelid lacerations
   • Retrobulbar hematoma
   • Traumatic optic neuropathy
   • Ophthalmic arter injuries
   • Extraocular muscle entrapment

Globe Injuries

Globe Rupture

It is an ophthalmologic emergency, consisting of a full-thickness injury in the cornea or sclera caused by penetrating or blunt trauma. Anterior rupture is usually observed, as this is the region where the sclera is the thinnest. Posterior rupture is rare and difficult to diagnose. It can be diagnosed through indirect findings such as contraction in the anterior chamber and decrease in intraocular pressure (IOP) in the affected eye. If there is a risk of globe rupture, a slit lamp test with 10% fluorescein must be conducted. Normal tissue is dark orange under a blue cobalt filter; a lighter color is observed in the damaged zone due to a lower dye concentration. Ultrasonography (USG) can be useful in making a diagnosis, especially with posterior ruptures. Computed tomography (CT) sensitivity ranges 56–75%. In cases of anterior globe injuries, USG use, and if there is a risk of a foreign metal body, magnetic resonance imaging, are contraindicated. Prompt ophthalmology consultation is required. While in the emergency department, tetanus prophylaxis, analgesics, bed rest, head elevation, and systemic antibiotic therapy are required. The most commonly preferred antibiotics are cefazolin and vancomycin. Age over 60 years; injury sustained by assault, on the street/highway, during a fall, or by gunshot; and posterior injuries are indications of a poor prognosis.

ectopic pupil after penetrated eye trauma

Foreign Bodies

Orbital foreign bodies are classified as superficial or intraorbital. Superficial foreign bodies constitute the second most common general eye injury, after corneal abrasions, and are the most common work-related injuries. They usually consist of earth, stone, wood and metal pieces. Organic foreign bodies have a higher risk of infection. Intraocular foreign bodies (IOFB) are most commonly observed in young males in the form of hammering injuries. Blast injuries and combat injuries are also frequently observed.

corneal foreign body

corneal foreign body

superglued eye

Diagnosis usually depends on patient history. The patient should be asked the location and intensity of the trauma, as well as time elapsed since the injury. In addition, the patient’s tetanus risk should be determined. There may be multiple foreign bodies. During the diagnosis, a microscopic examination with fluorescein must be conducted, and it must be determined if there is an intraocular foreign object. After applying local anesthesia, superficial foreign bodies can be removed with saline irrigation or a wet cotton swab. If unsuccessful, an attempt can be made to remove the object with a 25G needle under direct vision using a slit lamp. Any buried foreign bodies should be removed by an ophthalmologist. If there is a risk of IOFB, the patient should be referred to an ophthalmologist. If there is an IOFB, the patient should be treated as a case of globe rupture.

Corneal Abrasions

These are epithelium defects following a non-penetrating eye trauma; they constitute the most common eye pathology caused by trauma. The most common cause is chronic contact lens use. Other causes include blunt trauma, foreign bodies, burns, and radiation. Symptoms include stinging, burns, pain, and a feeling that there is a foreign object present. During diagnosis, a slit lamp examination must be conducted with fluorescein, and the dimensions and shape of the defect must be ascertained. Linear defects indicate the possibility of a foreign body located in the inner part of the eyelid. Therefore, the inner parts of the eyelid must be examined for foreign bodies as well. In the treatment, preventing bacterial superinfections that might be caused as a result of the defect, relieving pain, and speeding up recovery must be targeted. Fluoroquinolones are preferred as antibiotics, and oral analgesics are preferred for relieving pain. Topical non-steroids and anesthetics should not be used.

Fluorescein staining confirms the presence of a corneal abrasion Courtesy of Simon Arunga. Retrieved from Flickr.

Hyphema

It is defined as bleeding in the anterior chamber; the source of the bleeding is the iris root or ciliary body. Although hyphema can be caused by many medical conditions, the most common one is trauma. Among the causes of trauma, athletic injuries rank the highest. In children without underlying diseases, non-accidental injuries should come to mind. Bleeding itself does not usually lead to loss of vision; however, the source of the bleeding is important. There is no correlation between the amount of bleeding and tissue damage; small amounts of bleeding can be observed in major injuries. When evaluating a patient with hyphema, the manner in which the trauma occurred, its intensity, and time should be determined. There is usually more than one eye pathology in patients with hyphema, and missing them could have serious consequences. For this reason, these patients must be evaluated by an ophthalmologist. During emergency department treatment, bed rest, head elevation, eye patching, mydriatic/cycloplegic agents, antifibrinolytics (tranexamic acids), and anti-glaucoma drugs (beta blockers, carbonic anhydrase inhibitors) can be used. Complications such as glaucoma, corneal blood staining, rebleeding, and optic atrophy can develop.

Hyphaema. Courtesy of Allen Foster. Retreived from Flickr.

Hyphaema from blunt trauma. Some iris detail is visible. A level cannot be seen. Secondary glaucoma is likely until the blood has absorbed. Courtesy of International Centre for Eye Health. Retrieved from Flickr.

Lens dislocation

Rupture of the fibrils attaching the lens to the ciliary body, following trauma can result in subluxation or dislocation of the lens. The most frequently posterior dislocations; due to the restrictive effect of the iris, anterior dislocations are less frequent. Sudden onset of loss of vision, monocular diplopia, photosensitivity, red eye, subconjunctival hemorrhage, and periorbital ecchymosis can be observed in these patients. Anterior dislocations can cause acute angle closure glaucoma by disrupting the flow of aqueous humor. USG and CT can be used for diagnosis. Treatment can vary from observation to surgical treatment, based on whether there are additional injuries and on the region of dislocation.

Dislocated lens after trauma. Courtesy of Bruce Noble. Retrieved from Flickr.

Retinal Detachment

Traumatic retinal detachment (TRD) is the separation of the neurosensorial retina from the retinal pigment epithelia underneath it, leading to a disruption of its nourishment, and thus, a loss of vision. TRD typically develops months or years after trauma. Although it can also be observed immediately after trauma due to distracting injuries and poor patient cooperation and poor visualization as a result of periocular edema, it is difficult to diagnose at the acute stage. While the most common cause is closed blunt trauma, it has a higher incidence of open globe injuries. Symptoms include unilateral floaters, photopsia, and visual impairment. During the physical examination, visual acuity, visual field, and light reflex must be evaluated, and IOP should be measured. Retinal detachment and vitreous bleeding can be seen via ophthalmoscopy. Retinal detachment can be detected with USG, and a characteristic detachment pattern in the form of a “V” can be observed with CT. Early diagnosis is to ensure surgical intervention by an ophthalmologist. The prognosis depends on the size of the TRD, whether it involves the macula and length of time.

Vitreous hemorrhage: is bleeding in the posterior segment as a result of damage to the retinal veins following blunt trauma. It is usually accompanied by retinal detachment, and the patient complains of a sudden loss of vision. Fundoscopy, USG, and CT can be used for diagnosis. Treatment is surgical; although there are differing views on its timing, due to high TRD frequency, it is suggested that the surgery is performed at an early stage.

Periorbital Injuries

Orbital Fractures

It can occur as isolated incidents, as well as together with other facial bone fractures. The most commonly observed isolated orbital fracture is a blow-out fracture. There are three theories regarding its formation: indirect impact related to increasing intraorbital pressure caused by trauma (hydraulic mechanism); direct conveying of energy during orbital wall trauma (the buckling mechanism); and a combination of the two mechanisms. The most common fractures are in the inferior and medial walls.

Examination findings can vary from a simple ecchymosis and edema to loss of vision. Sensitivity in the orbital wall, subcutaneous emphysema, and irregularity in orbital rhythms can be observed. Pupil diameters and light reflexivity must be evaluated. Upper and lower eyesight restriction and diplopia can develop if the inferior rectus and inferior oblique muscles are caught in the fracture line. In cases of medial wall fractures, patients can suffer epistaxis. When orbital pressure increases to very high levels, optic nerve damage and loss of vision can occur.

The gold standard in diagnosis is CT, and it should be used to evaluate the axial and coronal planes. Fractures can manifest in two ways in CT: the first one is direct visualization of irregularity and dislocations in bone cortexes, and the second one is visualization of air-liquid level in the sinuses around the orbit and air in the orbital cavity. Immediate surgery is rarely necessary for treatment. Surgical treatment indications include enophthalmos greater than 2 mm, significant hypoglobus or diplopia, and an increase inorbital volume greater than 1 cm3.

Orbital Compartment Syndrome

This condition is an ophthalmologic surgical emergency that develops following an acute increase in intraorbital volume and pressure. A sudden increase in pressure can cause blindness via compression of the optic nerves and/or vascular structures when not diagnosed at an early stage and treated. The most common causes are trauma, intraocular injections, and surgery. Orbital cellulite or abscess, orbital emphysema, foreign bodies, and tumors can also lead to this condition. Orbital volume is about 30 ml, and it is surrounded by the bony orbit, which prevents expansion. The only possibility is to expand toward the anterior, but that movement is limited by the canthal ligaments attached to the eyelids. Diagnosis is clinical. In patients with the predisposing causes mentioned above, it should be considered as a possibility if there are findings such as reduced eyesight, diplopia, pain, and proptosis. Reduced eyesight, afferent pupil defect, elevated IOP, painful eye movement, and proptosis can be detected during a physical examination. Widened blind spot, reduced color sight (especially red), and afferent pupil defect detected during a visual field test are the most reliable findings that suggest optic nerve damage. The possibility of optic disc edema and retinal vein occlusion or congestion should be investigated with fundoscopy. If the patient history and physical examination support the findings, no time should be lost with visualization methods. Normal IOP level is 3–6 mmHg. Although there is not a specific pressure limit defined for orbital compartment syndrome, values ≥30 mmHg are considered to be high. The most important factor in making a treatment decision is the presence of clinical findings. Treatment is surgical, and lateral canthotomy and cantholysis are the surgeries preferred most often.

Eyelid Lacerations

Eyelids anatomically consist of five layers. The outermost layer is the thin skin layer; beneath it is the subcutaneous tissue, and beneath that are the orbicularis oculi muscle, which allows the eyelids to be shut, the meibomian glands and the tarsal plate containing the eyelashes, and the innermost layer is the conjunctiva. Eyelid lacerations (ELLs) are injuries caused by blunt or penetrating mechanisms. Because the eyelid is anatomically thin, it provides little protection against penetrating injuries, and the risk of globe injury is high in penetrating traumas. ELLs are injuries that require special attention, and certain points must be considered. Before repairing the laceration, a complete physical examination must be undertaken. During the examination, lid and globe movements, visual field, corneal injuries, foreign bodies, and globe perforation should be evaluated. All patients must be asked about tetanus immunization. If there has been no immunization, immunoglobulin (250 U) and toxoid should be administered together. Superficial lacerations can be sutured with 6.0 nylon or polypropylene. Eyelids have a risk of edema, and a cold compress after repair can decrease swelling and wound tension. Sutures can be removed on the fifth day. Ptosis in the eye, lacerations closer than 1 cm to the medial canthus, and cuts reaching the tarsal plate should be evaluated by an ophthalmologist or plastic surgeon.

Retrobulbar hematoma

Retrobulbar hematomas are hemorrhages formed behind the globe due to trauma, surgery, and posterior injections. They are usually arterial in origin; the inferior orbital arteries and anterior ethmoidal arteries are most commonly injured. The clinical importance is that this condition leads to compartment syndrome by causing increased pressure inside the orbital cavity. Patients can suffer decreased visual acuity, sluggish light reflex, restricted eye movement, painful proptosis, and afferent pupil defect. CT is the most commonly preferred visualization method for diagnosis. Although there is not a globally accepted algorithm for treatment, there are medical and surgical treatment options. Corticosteroids are used in medical treatments, and lateral canthotomy and cantholysis are the surgical treatments.

Chemical Injuries

Eye traumas caused by chemical substances constitute a wide spectrum ranging from corneal abrasions, which are simple burn symptoms, to serious burns that can result in permanent blindness. The most commonly encountered chemicals are cleaning materials, personal care items, and automobile chemicals. Alkaline chemical injuries are more common than acidic ones. Because acidic materials lead to coagulation necrosis and scar formation, deep penetration is restricted. Alkaline materials cause deeper wounds due to liquefaction necrosis. Burns are grouped into four grades, based upon intensity.

• Grade 1: Only epithelial damage; no limbal ischemia.
• Grade 2: Obscurity on the cornea; however, iris details can be spotted and there is ischemia in less than 1/3 of the limbus.
• Grade 3: Total loss of corneal epithelia. Stromal obscurity prevents spotting iris details. 1/3–1/2 limbal ischemia.
• Grade 4: The cornea is completely opaque and there is >50% limbal ischemia.

While the prognosis is good for grades 1 and 2, it is poor for grades 3 and 4. The first thing to do when a chemical substance contacts the eye is to irrigate it with normal saline or Ringer’s lactate solution in order to neutralize the eye’s pH. Applying a local anesthetic will relieve the patient’s pain. If care is being administered at the scene, tap water can be used for irrigation. Grade 1 and 2 injuries can be treated with antibiotics, steroids, and cycloplegic drugs. As antibiotics, preparations containing tobramycin or quinolone (ciprofloxacin, ofloxacin) can be used 4–5 times per day. Steroids decrease inflammation and prevent neutrophil activation. Grade 3 and 4 injuries may require surgical treatment.

corneal chemical burn

References and Further Reading

• Négrel AD, Thylefors B. The global impact of eye injuries. Ophthalmic Epidemiol 1998; 5:143.
• Romaniuk WM. Ocular trauma and other catastrophes. Emerg Med Clin North Am. 2013;31(2):399-411
• Oum BS, Lee JS, Han YS. Clinical features of ocular trauma in emergency department. Korean J Ophthalmol. 2004;18(1):70-78
• Northey LC, Bhardwaj G, Curran S, Mc Girr J. Eye trauma epidemiology in regional Australia. Ophthalmic Epidemiol. 2014;21(4):237-246
• Kels BD, Grzybowski A, Grant-Kels JM. Human ocular anatomy. Clin Dermatol. 2015;33(2): 140-146
• Sharma R, Brunette DD. Ophthalmology. In: Marx J, Hockberger R, and Walls R, editors. Rosen’s Emergency Medicine—Concepts and Clinical Practice, vol 2, 8th ed. Philadelphia: Saunders; 2013:909-930
• Bowling B. Kanski’s clinical ophthalmology-A systematic approach. 8th ed. Australia: Elsevier; 2016: 862-885
• Cain W, Sinskey RM. Detection of anterior chamber leakage with Seidel’s test. Arch Ophthalmology. 1981; 99(11):2013.
• Sung EK, Nadgir RN, Fujita A, Siegel C, Ghafouri RH, Traband A, Sakai O. Injuries of the globe: what can the radiologist offer? Radiographics. 2014;34(34):764-776
• Kuhn F, Morris R, Witherspoon CD, Mann L. Epidemiology of blinding trauma in the United States Eye Injury Registry. Ophthalmic Epidemiol. 2006;13(3):209-216
• Mc Gwin G Jr, Owsley C. Incidence of emergency department-treated eye injury in the United States. Arch Ophthalmol 2005;123(5):662-666
• Ahmed F, House RJ, Feldman BH. Corneal abrasions and corneal foreign bodies. Prim Care. 2015;42(3):363-375
• Pargament JM, Armenia J, Nerad JA. Physical and chemical injuries to eyes and eyelids. Clin Dermatol. 2015;33(2):234-237
• Bansal S, Gunasekeran DV, Ang B, Lee J, Khandelwal R, Sullivan P, Agrawal R. Controversies in the pathophysiology and management of hyphema. Surv Ophthalmol. 2015 Nov 26. doi:10.1016/j.survophthal.2015.11.005. [Epub ahead of print]
• Eken C, Yuruktumen A, Yildiz G. Ultrasound diagnosis of traumatic lens dislocation. J Emerg Med. 2013;44(1):e109-110
• Hoogewoud F, Chronopoulos A, Varga Z, Souteyrand G, Thurman G, Schutz JS. Traumatic retinal detachment-the diffuculty and importance of correct diagnosis. Surv Ophthalmol. 2015 Jul 24. doi: 10.1016/j.survophthal.2015.07.003. [Epub ahead of print]
• Yeung L, Chen TL, Kuo YH, Chao AN, Wu WC, Chen KJ, Hwang YS, Chen y, Lai CC. Severe vitreous hemorrhage associated with closed-globe ınjury. Graefes Arch Clin Exp Ophthalmol. 2006;244(1):52-57.
• Pfeiffer RL. Traumatic enophthalmus. Trans Am Opthalmol Soc. 1943;41:293-306
• Le Fort R. Experimental study of fractures of the upper jaw: In Tessier P (trans). The classic reprints I and II. Plast Reconstr Surg 1972;50:497-506
• Nagasao T, Miyamoto J, Jiang H, Tamaki T, Kaneko T. Interaction of hydraulic and buckling mechanism in bolwout fractures. Ann Plast Surg. 2010;64(4):471-476
• Broder JS. Imaging the face. In: Broder JS, author. Diagnostic imaging for the emergency physician.1st ed. Philadelphia: Saunders; 2011:46-72
• Kontio R, Lindqvist C. Management of orbital fractures. Oral Maxillofac Surg Clin North Am. 2009;21(2):209-220
• Lima V, Burt B, Leibovitch I, Prabhakaran V, Goldberg RA, Selva D. Orbital compartment syndrome: the ophthalmic surgical emergency. Surv Ophthalmol. 2009;54(4):441-449.
• McInnes G, Howes DW. Lateral canthotomy and cantholysis: a simple,vision-savin procedure. CJEM. 2002;4(1):49-52
• Mohammadi F, Rashan A, Psaltis A, Janisewicz A, Li P, El-Sawy T, Nayak JV. Intraocular pressure changes in emergennt surgical decompression of orbital compartment syndrome. JAMA Otolaryngol Head Neck Surg. 2015;141(6):562-565
• Sabatino F, Moskovitz JB. Facial wound management. Emerg Med Clin N Am 2013;31(2):529-538
• Lammers RL, Smith ZE. Methods of wound closure. In: Roberts JR, Hedges JR, Custalow CB, Thomsen TW, editors. Roberts and Hedges’ Clinical Procedures in Emergency Medicine. 6th ed. Philadelphia: Elsevier/Saunders; 2014:644-689
• Ing E. Eyelid lacerations.http://emedicine.medscape.com/article/1212531 Accessed December 26,2015.
• Allen M, Perry M, Burns F.When is a retrobulbar haemorrage not a retrobulbar haemorrage? Int J Oral Maxillofac Surg 2010;39(11):1045-49
• Chen YA, Singhal D, Chen YR, Chen CT. Management of acute traumatic retrobulbar haematomas: a 10-year retrospective review. J Plast Reconstr Aesthet Surg. 2012;65(10):1325-30.
• Han JK, Caughey RJ, Gross CW, Newman S. Management of retrobulbar hematoma. Am J Rhinol. 2008;22(5):522-524
• Blackburn J, Levitan EB, MacLennan PA, Owsley C, McGwin G Jr. The epidemiology of chemical eye injuries. Curr Eye Res. 2012;37(9):787-793
• Roper-Hall MJ. Thermal and chemical burns. Trans Ophthalmol Soc UK 1965;85:631-653
• Fish R, Davidson RS. Management of ocular thermal and chemical injuries, including amniotic membrane therapy. Curr Opin Ophthalmol. 2010;21(4):317-321
• Davis AR, Ali QK, Aclimandos WA, Hunter PA. Topical steroid use in the treatment of ocular alkali burns. Br J Ophthalmol. 1997;81(9):732-734