Concussive Trauma

Subconjunctival Hemorrhage

Blood under the conjunctiva creates a dramatic appearance that can alarm the patient. Most frequently, patients present with subconjunctival hemorrhage without a history of antecedent trauma. When trauma has occurred, damage to deeper structures of the eye must be ruled out. Subconjunctival hemorrhage is usually not associated with an underlying systemic disease and rarely has an identifiable cause. Occasionally, a history of vomiting, coughing, or other forms of the Valsalva maneuver can be elicited (Table 13-3).

Table 13-3

Most patients simply require reassurance. However, if a patient suffers from repeated episodes of spontaneous subconjunctival hemorrhage or indicates the presence of a possible bleeding diathesis (easy bruising, frequent bloody noses), a careful medical evaluation may be warranted. Recurrent subconjunctival hemorrhages can be seen in association with systemic illness such as uncontrolled hypertension, diabetes mellitus, or a bleeding diathesis. No therapy is usually necessary for the hemorrhage, as it usually resolves in 7–12 days. If the hemorrhage is elevated, dellen may occur. This condition should be treated with intensive topical lubrication and, occasionally, patching until resolved. Patients should be warned that the hemorrhage might spread around the circumference of the globe before it resolves and that it may change in color from red to yellow during its dissolution.

Corneal Changes

Blunt trauma to the cornea can result in abrasions, edema, tears in Descemet membrane, and corneoscleral lacerations, usually located at the limbus. Traumatic posterior annular keratopathy or traumatic corneal endothelial rings have also been described. The rings, composed of disrupted and swollen endothelial cells, are whitish gray in appearance and occur directly posterior to the traumatic impact. The endothelial rings appear within several hours of a contusive injury and usually disappear within a few days.

Traumatic Mydriasis and Miosis

Blunt injury to the globe may result in traumatic mydriasis or, less commonly, miosis. Traumatic mydriasis is often associated with iris sphincter tears that can permanently alter the shape of the pupil. Miosis tends to be associated with anterior chamber inflammation (traumatic iritis; see the following section). Pupillary reactivity may be sluggish in both situations. Cycloplegia is useful to prevent formation of posterior synechiae.

Traumatic Iritis

Photophobia, tearing, and ocular pain may occur within 24 hours after injury. The inflammation of traumatic iritis is often associated with diminished vision and perilimbal conjunctival injection. The anterior chamber reaction can be surprisingly minimal but is usually present if carefully sought.

Treatment should consist of, at the very least, a topical cycloplegic agent to relieve patient discomfort. Topical corticosteroids may be used if significant inflammation is present. Once the iritis has diminished, cycloplegia may be discontinued, and topical corticosteroids should be tapered slowly to prevent rebound iritis. See BCSC Section 9, Intraocular Inflammation and Uveitis, for a more detailed discussion of uveitis.

Iridodialysis and Cyclodialysis

Iridodialysis

Blunt trauma may cause traumatic separation of the iris root from the ciliary body (Fig 13-6). Frequently, anterior segment hemorrhage ensues, and the iridodialysis may not be recognized until the hyphema has cleared. A small iridodialysis requires no treatment. A large dialysis may cause polycoria and monocular diplopia, requiring surgical repair.

Figure 13-6 Severe iridodialysis resulting from blunt trauma. (Courtesy of David Rootman, MD.)

Cyclodialysis

Traumatic cyclodialysis is characterized by a separation of the ciliary body from its attachment to the scleral spur, resulting in a cleft. Gonioscopically, this cleft appears at the junction of the scleral spur and the ciliary body band. Sclera may be visible through the disrupted tissue. Ultrasound biomicroscopy is useful in identifying the location and extent of the cyclodialysis (Fig 13-7). A

cyclodialysis cleft can cause increased uveoscleral outflow and aqueous hyposecretion, leading to chronic hypotony and macular edema. If treatment with topical cycloplegics does not suffice, closure may be attempted by using argon laser, diathermy, cryotherapy, or direct suturing. If repair is necessary, it should be done after the resolution of the hyphema.

Figure 13-7 Ultrasound biomicroscopy of cyclodialysis. (Courtesy of David Rootman, MD.)

Traumatic Hyphema

Traumatic hyphema occurs most commonly in young males. It results from injury to the vessels of the peripheral iris or anterior ciliary body. Trauma causes posterior displacement of the lens–iris interface and scleral expansion in the equatorial zone, which leads to disruption of the major iris arterial circle, arterial branches of the ciliary body, and/or recurrent choroidal arteries and veins (Fig 13-8). Anterior segment bleeding can often be seen on penlight examination (Fig 13-9). At other times, the bleeding is so subtle that it can be detected only as a few circulating red blood cells on slit-

lamp examination (microscopic hyphema). The prognosis is good in patients who do not develop complications, but it is not dependent on the size of the hyphema itself. Even total, or “eight-ball,” hyphemas can resolve without sequelae, unless secondary complications result (Fig 13-10). Hyphema is frequently associated with corneal abrasion, iritis, and mydriasis, as well as with significant injuries to the angle structures, lens, posterior segment, and orbit.

Figure 13-8 Mechanism of hyphema and blunt force injury to the eye. Blunt force applied to the eye displaces the aqueous volume peripherally, causing an increase in hydraulic pressure at the lens, iris root, and trabecular meshwork. If this “wedge of pressure” exceeds the tensile strength of ocular structures, the vessels in the peripheral iris and face of the ciliary body may rupture, leading to hyphema. The force may cause scleral ruptures, typically at the limbus and posterior to the muscle insertions, where the sclera is thinner and unsupported by the orbital bones. Severe trauma leads to subluxation of the lens, retinal dialysis, optic nerve avulsion, and/or vitreous hemorrhage. (Illustration by C.H. Wooley.)

Figure 13-9 Layered hyphema from blunt trauma.

Figure 13-10 Total, or “eight-ball,” hyphema.

Spontaneous hyphema is much less common and should alert the examiner to the possibility of rubeosis iridis, clotting abnormalities, herpetic disease, or intraocular lens (IOL) problems. Juvenile xanthogranuloma, retinoblastoma, and leukemia are associated with spontaneous hyphema in children.

Rebleeding

The major concern after a traumatic hyphema is rebleeding, for which most studies report an incidence of less than 5%. Complications associated with secondary hemorrhage include glaucoma, optic atrophy, and corneal blood staining (Fig 13-11).

Figure 13-11 Dense corneal blood staining after a traumatic hyphema. (Courtesy of Vincent P. deLuise, MD.)

Rebleeding may complicate any hyphema, regardless of size, and occurs most frequently between 3 and 7 days after injury. The timing of the rebleeding may be related to the lysis and clot retraction that occur during this period. Rebleeding is an important indicator of poor visual outcome.

Approximately 50% of patients with rebleeding develop elevated IOP. The combination of elevated IOP, endothelial dysfunction, and anterior chamber blood predisposes the eye to corneal blood staining, which is difficult to detect when blood is in apposition to the endothelium. Red blood cells within the anterior chamber release hemoglobin that penetrates the posterior corneal stroma, where it is absorbed by keratocytes. Hemoglobin is converted to hemosiderin within the keratocytes, which in turn causes keratocyte death. On slit-lamp examination, early blood staining is detected by yellow granular changes and reduced fibrillar definition in the posterior corneal stroma. Blood staining leads to a reduction in corneal transparency that may be permanent. Histologically, red blood cells and their breakdown products can be seen within the corneal stroma. Corneal blood staining often slowly clears in a centripetal pattern starting in the periphery.

Medical management

The overall treatment plan for traumatic hyphema should be directed at minimizing the possibility of secondary hemorrhage. Elevated IOP may require treatment in order to reduce the risk of corneal

blood staining and optic atrophy. Specifics of medical management remain controversial; however, most patients are treated with the following: protective shield over the injured eye, restriction of physical activity, elevation of the head of the bed, and daily observation.

To reduce the risk of rebleeding, nonaspirin analgesics should be used for pain relief; however, even nonsteroidal anti-inflammatory medications can increase the risk of rebleeding. Most patients can be managed on an outpatient basis. But if satisfactory home care and outpatient observation cannot be ensured, hospitalization may be required.

Most ophthalmologists administer long-acting topical cycloplegic agents initially for comfort, to facilitate posterior segment evaluation, and to eliminate iris movement. Topical corticosteroids are beneficial in controlling anterior chamber inflammation and preventing synechiae formation, and they may play a role in preventing rebleeding. Oral corticosteroids may be used to facilitate the resolution of severe inflammation and/or to prevent rebleeding. Topical antihypertensives (β- blockers and α-agonists) are the mainstay of therapy, although occasionally intravenous or oral hyperosmotic agents may be required.

Several prospective studies supported the efficacy of antifibrinolytic agents (aminocaproic acid [Amicar], tranexamic acid, prednisone) in reducing the incidence of rebleeding; however, these studies failed to show a statistical improvement in visual outcome. In addition, these agents may produce significant adverse effects, such as nausea, vomiting, postural hypotension, muscle cramps, conjunctival suffusion, nasal stuffiness, headache, rash, pruritus, dyspnea, toxic confusional states, and arrhythmias, as well as the risk of increased IOP on discontinuation. As a result, these medications are rarely used today.

Surgery

Surgery (to evacuate blood) may be required to prevent irreversible corneal blood staining and optic atrophy from persistently elevated IOP. Surgery is generally recommended at the earliest definitive detection of blood staining. Some authors suggest that surgery may be indicated if the IOP averages greater than 25 mm Hg for 5 days with a total hyphema. Surgical intervention should be considered when the IOP is greater than 60 mm Hg despite maximal medical management for 2 days to prevent optic atrophy. Patients with preexisting optic nerve damage or sickle hemoglobinopathies may require earlier intervention. Table 13-4 has guidelines on surgical intervention.

Table 13-4

The simplest surgical technique is anterior chamber irrigation with balanced salt solution through a paracentesis. The goal is to remove circulating red blood cells that may obstruct the trabecular meshwork; removal of the entire clot is neither necessary nor wise. This procedure can be repeated. If irrigation is not successful, the I/A handpiece, which integrates irrigation and aspiration in cataract surgery, may be effective in many cases. The use of a cutting instrument or intraocular diathermy may be necessary in severe cases. Iris damage, lens injury, endothelial cell trauma, and additional bleeding are the major complications of surgical intervention.