Slit lamp examination in the cooperative patient may show associated injuries such as iris

transillumination defect (red reflex obscured by vitreous hemorrhage); corneal lacerations;

iris prolapse; hyphema from ciliary body disruption; and lens injuries, including dislocation
or subluxation.
A shallow anterior chamber may be the only sign of occult globe rupture and is associated
with a worse prognosis. A posterior rupture may present with a deeper anterior chamber due
to extrusion of vitreous from the posterior segment.

Physical
In peripheral iris prolapse, the iris appears as a knuckle of colored tissue, resulting in a partial
peripheral synechia. When the prolapse is central, the entire pupillary margin may prolapse,
resulting in a total anterior synechia. In patients with a perforated cornea, the prolapsed iris is
exposed.
Depending on the duration of prolapse, the appearance of the iris may vary. In cases of recent
prolapse, the iris appears viable. With time, the iris appears dry and nonviable. In patients
who have undergone corneal transplant surgery or cataract surgery with a clear corneal
incision, the appearance of the iris is the same as in a perforated cornea. When the iris
prolapses through a scleral wound, it appears as a colored mass beneath the overlying
conjunctiva. In this case, the iris remains viable for a long time.
The pupil appears peaked in the region of the iris prolapse. The anterior chamber is
formed as the prolapsed iris seals the wound. Minimal or no wound leakage occurs.
Wound leak is verified using the Seidel test. A drop of 2% fluorescein sodium is
instilled in the conjunctival sac. The wound is examined under the slit lamp with
cobalt blue light. The fluorescein appears greenish. Wound leak can be easily
identified when the fluorescein is diluted by the aqueous humor. Gentle pressure on
the eye may be needed to induce leakage.
Intraocular pressure is lower than normal, but hypotony is uncommon after iris
prolapse.
In long-standing iris prolapse, chronic iridocyclitis, cystoid macular edema, or
glaucoma may be seen. The prolapsed iris may act as a scaffold for infection,
epithelial downgrowth, or fibrous ingrowth. Rarely, sympathetic ophthalmia may
occur. Carefully examining the fellow eye for cells and flare is important
3.5 Traumatic Iritis
Traumatic Iritis
Symptoms
Dull, aching/throbbing pain, photophobia, tearing, onset of symptoms within 3 days of
trauma.
Signs
Critical. White blood cells and flare in the AC (seen under high-power magnification by
focusing into the AC with a small, bright beam from the slit lamp).
Other. Pain in the traumatized eye when light enters either eye; lower (although sometimes
higher) IOP; smaller pupil (which dilates poorly) or larger pupil (caused by iris sphincter
tears) in the traumatized eye; perilimbal conjunctival injection; occasionally, decreased
vision.
Differential Diagnosis
Nongranulomatous anterior uveitis (NGAU): No history of trauma, or the degree of
trauma is not consistent with the level of inflammation. See 12.1, Anterior Uveitis.
Traumatic microhyphema: RBCs suspended in the AC. See 3.6, Hyphema and
Microhyphema.
Traumatic corneal abrasion: May have an accompanying AC reaction. See 3.2,
Corneal Abrasion.
Traumatic retinal detachment: May produce an AC reaction or may see pigment in the
anterior vitreous. See 11.3, Retinal Detachment.
Work-Up
Complete ophthalmic examination, including IOP measurement and dilated fundus
examination.
Treatment
Cycloplegic agent (e.g., cyclopentolate 2% t.i.d. or scopolamine 0.25% t.i.d.). If the patient is
very symptomatic, may use a steroid drop (e.g., prednisolone acetate 0.125% to 1% q.i.d.).
Avoid topical steroids if an epithelial defect is present.
Follow-Up
Recheck in 5 to 7 days.
If resolved, the cycloplegic agent is discontinued and the steroid is tapered.
One month after trauma, perform gonioscopy to look for angle recession and indirect
ophthalmoscopy with scleral depression to detect retinal breaks or detachment.
3.6 Hyphema and Microhyphema
Traumatic Hyphema
Symptoms
Pain, blurred vision, history of blunt trauma.
Signs
(See Figure 3.6.1.)
Blood or clot or both in the AC, usually visible without a slit lamp. A total (100%)
P.20

hyphema may be black or red. When black, it is called an 8-ball or black ball hyphema;
when red, the circulating blood cells may settle with time to become less than a 100%
hyphema.

Figure 3.6.1. Hyphema.
Work-Up
History: Mechanism (including force, velocity, type, and direction) of injury?
Protective eyewear? Time of injury? Time of visual loss? Usually the visual
compromise occurs at the time of injury; decreasing vision over time suggests a
rebleed or continued bleed. Use of medications with anticoagulant properties [aspirin,
NSAIDs, warfarin (e.g., Coumadin), or clopidogrel (e.g., Plavix)]? Personal or family
history of sickle cell disease/trait? Symptoms of coagulopathy (e.g., bloody nose-
blowing, bleeding gums with tooth brushing, easy bruising)?
Ocular examination, first ruling out a ruptured globe (see 3.14, Ruptured Globe and
Penetrating Ocular Injury). Evaluate for other traumatic injuries. Document the extent
(e.g., measure the hyphema height) and location of any clot and blood. Measure the
IOP. Perform a dilated retinal evaluation without scleral depression. Consider a gentle
UBM if the view of the fundus is poor. Avoid gonioscopy unless intractable increased
IOP develops. If gonioscopy is necessary, gently use a Zeiss 4 mirror lens. Consider
UBM to evaluate the anterior segment if the view is poor and lens capsule rupture,
IOFB, or other anterior segment abnormalities are suspected.
Consider a CT scan of the orbits and brain (axial and coronal views, with 1- to 3-mm
sections through the orbits) when indicated (e.g., suspected orbital fracture or IOFB,
loss of consciousness).
Black and Mediterranean patients should be screened for sickle cell trait or disease
(order Sickledex screen; if necessary, may check hemoglobin electrophoresis).
Treatment
Many aspects remain controversial, including whether hospitalization and absolute bed rest
are necessary, but an atraumatic upright environment is essential. Consider hospitalization for
noncompliant patients, patients with bleeding diathesis or blood dyscrasia, patients with other
severe ocular or orbital injuries, and patients with concomitant significant IOP elevation and
sickle cell. In addition, consider hospitalization and aggressive treatment for children,
especially those at risk for amblyopia (e.g., those under age 7 to 8) or when child abuse is
suspected.
Confine either to bed rest with bathroom privileges or to limited activity. Elevate head
of bed to allow blood to settle.
Place a shield (metal or clear plastic) over the involved eye at all times. Do not patch
because this prevents recognition of sudden visual loss in the event of a rebleed.
Atropine 1% solution b.i.d. to t.i.d. or scopolamine 0.25% b.i.d. to t.i.d.
No aspirin-containing products or NSAIDs.
Mild analgesics only (e.g., acetaminophen). Avoid sedatives.
Use topical steroids (e.g., prednisolone acetate 1% four to eight times per day) if any
suggestion of iritis (e.g., photophobia, deep ache, ciliary flush), evidence of lens
capsule rupture, any protein (e.g., fibrin), or definitive white blood cells in anterior
P.21

chamber. Reduce the frequency of steroids as soon as signs and symptoms resolve to
reduce the likelihood of steroid-induced glaucoma.
For increased IOP:
o Nonsickle cell disease/trait (>30 mm Hg):
Start with a beta-blocker (e.g., timolol or levobunolol 0.5% b.i.d.).
If IOP still high, add topical alphaagonist (e.g., apraclonidine 0.5%, or
brimonidine 0.2% t.i.d.) or topical carbonic anhydrase inhibitor (e.g.,
dorzolamide 2%, or brinzolamide 1% t.i.d.). Avoid prostaglandin
analogs and miotics (may increase inflammation). In children under 5,
topical alphaagonists are contraindicated.
If topical therapy fails, add acetazolamide (500 mg p.o., q12h for
adults, 20 mg/kg/day divided three times per day for children) or
mannitol [1 to 2 g/kg intravenously (i.v.) over 45 minutes q24h]. If
mannitol is necessary to control the IOP, surgical evacuation may be
imminent.
o Sickle cell disease/trait (24 mm Hg):
Start with a beta-blocker (e.g., timolol or levobunolol 0.5% b.i.d.).
All other agents must be used with extreme caution: Topical
dorzolamide and brinzolamide may reduce aqueous pH and induce
increased sickling; topical alphaagonists (e.g., brimonidine or
apraclonidine) may affect iris vasculature; miotics and prostaglandins
may promote inflammation.
If possible, avoid systemic diuretics because they promote sickling by
inducing systemic acidosis and volume contraction. If a carbonic
anhydrase inhibitor is necessary, use methazolamide 50 mg p.o., q8h
instead of acetazolamide (controversial). If mannitol is necessary to
control the IOP, surgical evacuation may be imminent.
AC paracentesis is safe and effective if IOP cannot be safely lowered
medically (see Appendix 13, Anterior Chamber Paracentesis). This
procedure is often only a temporizing measure when the need for
surgical evacuation is anticipated.
If hospitalized, use antiemetics p.r.n. for severe nausea or vomiting [e.g.,
prochlorperazine 10 mg intramuscularly (i.m.) q8h or 25 mg q12h p.r.n.; <12 years of
age, trimethobenzamide suppositories, 100 mg PR q6h p.r.n.].
Indications for surgical evacuation of hyphema:
o Corneal stromal blood staining.
o Significant visual deterioration.
o Hyphema that does not decrease to <50% by 8 days [to prevent peripheral
anterior synechiae (PAS)].
o IOP >60 mm Hg for >48 hours, despite maximal medical therapy (to
prevent optic atrophy).
o IOP >25 mm Hg with total hyphema for >5 days (to prevent corneal stromal
blood staining).
o IOP 24 mm Hg for >24 hours (or any transient increase in IOP >30 mm Hg)
in sickle trait/disease patients.
Note
In children, particular caution must be used regarding topical steroids. Children often get
rapid rises in IOP and with prolonged use there is a significant risk for cataract. As outlined
above, in certain cases steroids may be beneficial, but steroids should be prescribed in an
individualized manner. Children must be monitored closely for increased IOP and should be
tapered off the steroids as soon as possible.
Note
Increased IOP, especially soon after trauma, may be transient, secondary to acute mechanical
plugging of the trabecular meshwork. Elevating the patient's head may decrease the IOP by
causing RBCs to settle inferiorly.
Note
Previously, systemic aminocaproic acid was used in hospitalized patients to stabilize the clot
and to prevent rebleeding. This therapy is rarely used now. Topical aminocaproic acid (e.g.,
Caprogel) is currently under research and development. Preliminary studies suggest it may be
useful in reducing risk of rebleeding. Further research is needed before the role for topical
aminocaproic acid in the management of hyphemas can be determined.
P.22


Follow-Up
The patient should be seen daily for 3 days after initial trauma to check visual acuity,
IOP, and for a slit-lamp examination. Look for new bleeding, increased IOP, corneal
blood staining, and other intraocular injuries as the blood clears (e.g., iridodialysis;
subluxated, disclocated, or cataractous lens). Hemolysis, which may appear as bright
red fluid, should be distinguished from a rebleed, which forms a new, bright red clot.
If the IOP is increased, treat as described earlier.
The patient should be instructed to return immediately if a sudden increase in pain or
decrease in vision is noted (which may be symptoms of a rebleed or secondary
glaucoma).
If a significant rebleed or an intractable IOP increase occurs, the patient should be
hospitalized.
After the initial close follow-up period, the patient may be maintained on a long-
acting cycloplegic (e.g., atropine 1% solution q.d. to b.i.d., scopolamine 0.25% q.d. to
b.i.d.), depending on the severity of the condition. Topical steroids may be tapered as
the blood, fibrin, and white blood cells resolve.
Glasses or eye shield during the day and eye shield at night. As with any patient,
protective eyewear (polycarbonate or Trivex lenses) should be worn any time
significant potential for an eye injury exists.
The patient must refrain from strenuous physical activities (including bearing down or
Valsalva maneuvers) for 1 week after the initial injury or rebleed. Normal activities
may be resumed 1 week from the date of injury or rebleed. This period should be
extended if blood remains in the anterior chamber.
Future outpatient follow-up:
o If patient was hospitalized, see 2 to 3 days after discharge. If not
hospitalized, see several days to 1 week after initial daily follow-up period,
depending on severity of condition (amount of blood, potential for IOP
increase, other ocular or orbital pathologic processes).
o Four weeks after trauma for gonioscopy and dilated fundus examination
with scleral depression for all patients.
o Some experts suggest annual follow-up because of the potential for
development of angle-recession glaucoma.
o If any complications arise, more frequent follow-up is required.
o If filtering surgery was performed, follow-up and activity restrictions are
based on the surgeon's specific recommendations.
3.13 Corneal Laceration
Parital-Thickness Laceration
Signs
(See Figure 3.13.1.)
The anterior chamber is not entered and, therefore, the cornea is not perforated.
Work-Up
Careful slit-lamp examination should be performed to exclude ocular penetration.
Carefully evaluate the conjunctiva, sclera, and cornea, checking for extension beyond
the limbus in cases involving the corneal periphery. Evaluate the depth of the AC and
compare with the fellow eye. A shallow AC indicates an actively leaking wound or a
self-sealed leak (see Full-Thickness Laceration below). Deeper AC in the involved
eye can be an indication of a posterior rupture. Check iris for transillumination defects
(TIDs) and evaluate lens for a cataract or a foreign body tract (must have a high level
of suspicion with
P.39

projectile objects). Presence of TIDs and lens abnormalities are an indication of a
ruptured globe. IOP should be measured only after a ruptured globe is ruled out. Use
applanation only if the laceration site can be avoided. Otherwise, use a Tono-Pen to
check the IOP.

Figure 3.13.1. Corneal laceration.
Seidel test (see Appendix 5, Seidel Test to Detect a Wound Leak). If the Seidel test is
positive, a full-thickness laceration is present (see Full-Thickness Laceration below).
Treatment
A cycloplegic (e.g., scopolamine 0.25%) and an antibiotic [e.g., frequent polymyxin
B/ bacitracin ointment (e.g., Polysporin) or fluoroquinolone drops, depending on the
nature of the wound].
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.

Figure 3.13.2. Full-thickness corneal laceration with positive Seidel test.
Tetanus toxoid for dirty wounds (see Appendix 2, Tetanus Prophylaxis).
Follow-Up
Reevaluate daily until the epithelium heals.
Full-Thickness Laceration
(See Figure 3.13.2.)
See 3.14, Ruptured Globe and Penetrating Ocular Injury. Note that small, self-sealing, or
slow-leaking lacerations may be treated with aqueous suppressants, bandage soft contact
lenses, fluoroquinolone drops q.i.d., and precautions as listed in 3.14. Alternatively, a
pressure patch and twice-daily antibiotics may be used. Avoid topical steroids. If an IOFB is
pres-ent, see 3.15, Intraocular Foreign Body.
3.14 Ruptured Globe and Penetrating Ocular Injury
Ruptured Globe and Penetrating Ocular Injury
Symptoms
Pain, decreased vision, loss of fluid from eye. History of trauma, fall, or sharp object entering
globe.
Signs
(See Figure 3.14.1.)
Critical. Full-thickness scleral or corneal laceration, severe subconjunctival hemorrhage
P.40

(especially involving 360 degrees of bulbar conjunctiva, often bullous), a deep or shallow AC
compared to the fellow eye, peaked or irregular pupil, iris TIDs, lens material in the AC,
foreign body tract in the lens, or limitation of extraocular motility (greatest in direction of
rupture). Intraocular contents may be outside of the globe.

Figure 3.14.1. Ruptured globe showing flat anterior chamber, iris prolapse, and peaked pupil.
Other. Low IOP (although it may be normal or increased), iridodialysis, cyclodialysis,
hyphema (i.e., clotted blood in AC), periorbital ecchymosis, vitreous hemorrhage, dislocated
or subluxed lens, and traumatic optic neuropathy. Commotio retinae, choroidal rupture, and
retinal breaks may be seen but are often obscured by vitreous hemorrhage.
Work-Up/Treatment
Once the diagnosis of a ruptured globe is made, further examination should be deferred until
the time of surgical repair in the operating room. This is to avoid placing any pressure on the
globe and risking extrusion of the intraocular contents. Diagnosis should be made by
penlight, or if possible, by slit-lamp examination (with very gentle manipulation). Once the
diagnosis is made, then the following measures should be taken:
Protect the eye with a shield at all times.
Obtain CT scan of the brain and orbits (axial and coronal views, 1-mm sections) to
rule out IOFB in most cases.
Gentle UBM may be needed to localize posterior rupture site(s) or to rule out
intraocular foreign bodies not visible on CT scan (nonmetallic, wood, etc.). However,
UBM should not be done in patients with an obvious anterior rupture for the risk of
extrusion of intraocular contents. A trained ophthalmologist should evaluate the
patient before UBM or other manipulation is performed on a ruptured globe suspect.
Admit patient to the hospital with no food or drink (NPO).
Place patient on bed rest with bathroom privileges. Avoid bending over and Valsalva
maneuvers.
Systemic antibiotics should be administered within 6 hours of injury. For adults, give
cefazolin 1 g i.v. q8h or vancomycin 1 g i.v. q12h. Also give ciprofloxacin 400 mg
p.o./i.v. b.i.d. (fourth-generation fluoroquinolones, such as gatifloxacin 400 mg q.d. or
moxifloxacin 400 mg q.d. may have better vitreous penetration). For children <12
years, give cefazolin 25 to 50 mg/kg/ day i.v. in three divided doses, and gentamicin 2
mg/kg i.v. q8h.
Administer tetanus toxoid p.r.n. (see Appendix 2, Tetanus Prophylaxis).
Administer antiemetic (e.g., prochlorperazine (Compazine) 10 mg i.m. q8h) p.r.n. for
nausea and vomiting to prevent Valsalva.
Consider pain medicine before and after surgery p.r.n.
Determine the time of the patient's most recent meal. The timing of surgical repair is
often influenced by this information.
Arrange for surgical repair to be done as soon as possible.
Note
Antibiotic doses may need to be reduced if renal function is impaired. Gentamicin peak and
trough levels are obtained one-half hour before and after the fifth dose, and blood urea
nitrogen and creatinine levels are evaluated every other day. See Pharmacopoeia.
Note
In any severely traumatized eye in which there is no chance of restoring vision, enucleation
should be considered initially or within 7 to 14 days after the trauma to prevent the rare
occurrence of sympathetic ophthalmia.
Infection is more likely to occur in eyes with dirty injuries, retained intraocular foreign
bodies, rupture of lens capsule, and in patients with a long delay until primary surgical repair.
In patients at high risk of infection, some groups recommend intravitreal antibiotics (see
12.15, Traumatic Endophthalmitis).