OCULAR MOTOR SYSTEM

Ocular and orbital trauma frequently involves neurologic damage. In addition to containing the eye, the orbit is tightly packed with ocular support

structures, including nerves, blood vessels, muscles, and fat. Concurrent trauma to the globe and orbit may easily become an “orbital multisystem trauma.” The treatment of orbital and globe injuries requires a thorough knowledge of the ocular motor systems.

EPIDEMIOLOGY (USEIR DATA)

Rate of extraocular muscle involvement among all serious injuries: 3%.

Age (years):

•range: 2–81;

•average: 26;

•rate of 0- to 9-year-olds among the total: 10%;

•rate of 10to 19-year-olds among the total: 20%;

•rate of 60-year-olds among the total: 6%.

Sex: 80% male.

Place of injury:

•home: 32%;

•street and highway: 22%;

•recreation and sport: 14%;

•industrial premises: 13%;

•public building: 5%.

Source of injury:

•various blunt objects: 32%;

•various sharp objects: 15%;

•MVC: 15%;

•gunshot: 14%;

•BB/pellet gun: 6%;

•fall: 5%.

Globe involvement among the total: 50%.

PATHOPHYSIOLOGY

The globe and orbit are innervated by 6 of the 12 cranial nerves. The anatomy of the nerve pathways and origins has been well described and may be significant for the evaluation of patients and their management. The involved nerves are:

•II (optic);

•III (oculomotor);

•IV (trochlear);

•V (trigemineal);

•VI (abducens); and

•VII (facial)

EVALUATION

Examination of patients in an ER setting always involves an assessment of the neurologic system.

•A detailed history will often guide subsequent steps of the examination. In patients with orbital injuries, extra care must be taken to evaluate for nerve damage.

•The visual acuity is crucial to take in the orbital trauma victim. Vision testing and the swingingflashlight test (see Chapters 9 and 37) will establish whether the optic nerve is functioning, and whether symmetrically.

406 • SECTION V NONGLOBE INJURIES

•An equally important neurologic test is the pupillary examination (see Chapter 3, 9, and 37). An APD indicates that the optic nerve is disrupted somewhere anterior to the chiasm; this should instigate further investigation, including an orbital CT scan.

•Evaluation of the extraocular muscles’ movement can reveal information about cranial nerves III, IV, and VI.

PEARL... A complete extraocular muscle examination, which takes seconds to perform, will establish the function of both

the muscles and the nerves.

•If extraocular muscle movement abnormalities are seen in a traumatic setting, further radiologic investigation should be initiated. One exception to this is the simple blowout fracture, which may be diagnosed clinically (see Chapter 36). Radiologic examination of patients with obvious blowout fractures may be delayed for 1 week, pending the spontaneous resolution of symptoms. If the diplopia and restrictive strabismus seen in simple blowout fractures resolve, then an orbital CT scan is not necessary (see Chapter 36).

•In cases of orbital injury involving neurologic damage, a CT scan is the radiologic test of choice. The relationship between the bones and soft tissues of the orbits is best delineated with a CT scan. The CT scan is also the most useful radiologic test for preoperative surgical planning.

PEARL... An MRI scan is the test of choice when orbital injury is accompanied

by CNS trauma.

•Neurological injury to the orbit is almost always associated with trauma to the surrounding tissue(s). The neurological assessment of the globe and orbital injuries must be part of a comprehensive evaluation of the patient.

P I T F A L L

The risk of CNS injuries must be meticulously evaluated.

CLINICAL CONDITIONS

TON

See Chapter 37.

Bell’s Palsy

Pathophysiology

Because it has an extensive superficial plexus, the facial nerve is rather susceptible to trauma. The nerve exits the skull at the stylomastoid foramen and innervates the muscles of facial expression. The facial nerve innervates the orbicularis oculi muscle, and its dysfunction leads to Bell’s palsy.

Diagnosis

The clinical appearance is one of facial paralysis. In traumatic cases, lacerations or evidence of contusion trauma are usually found. Ocular manifestations of Bell’s palsy include:

•ectropion;

•lagophthalmos;

•brow ptosis; and

•ocular exposure symptoms.

Management

In the early phases, a search for the underlying cause is indicated. The initial treatment of the ocular manifestations of Bell’s palsy is supportive (Fig. 38–1). The use of ocular lubricants and patching may significantly improve the patient’s comfort. Spontaneous improvement and resolution of Bell’s palsy are common. Supportive measures should be maintained for 6 months prior to contemplating surgical intervention. Surgical repair of a lacerated facial nerve may be attempted.1 The use of steroids to modulate swelling and protect the nerve is controversial.

FIGURE 38–1 Right Bell’s palsy manifest by brow ptosis, ectropion, and lagophthalmos.

For the first 6 months following the onset of Bell’s palsy, the goal of treatment is the patient’s comfort and safety.

•The use of artificial tears and ocular lubricants is often sufficient to provide improvement regarding the symptoms.

•Occasional patching of the eye at night may be necessary.

If simple remedies such as artificial tears and ocular lubricants are sufficient, then further treatment can be avoided or evaluated from an aesthetic perspective.

In chronic cases (patients who have had Bell’s palsy for over 6 months), surgery is recommended. In reconstructive surgery2, both functional and cosmetic considerations need to be addressed; the primary goal is to provide improved ocular function and comfort; the second goal is to improve the appearance.

P I T F A L L

A stepwise approach to the surgical management of chronic Bell’s palsy is usually followed to avoid overtreatment.

The surgical steps/goals are the following:

•optimize ocular lubrication;

•correct lower eyelid ectropion;

•repair brow ptosis;

•gold weight implant if symptomatic lagophthalmos is present; and

•tarsorrhaphy.

CHAPTER 38 OCULAR MOTOR SYSTEM • 407

Additional noteworthy details are listed below.

•Lacking seventh-nerve innervation, the eyebrow and lower eyelid become ptotic.

•Any laxity already present will be exaggerated, and brow ptosis and ectropion will become manifest.

•The lower eyelid ectropion may lead to a worsening of exposure symptoms, ocular irritation, and tearing. If symptomatic ectropion is present, a horizontal eyelid-tightening procedure often improves patient comfort.

PEARL... Brow ptosis may not only produce dramatic facial asymmetry, which is aesthetically unappealing, but also affect the superior visual field, whose loss can easily be

documented by visual field testing.

•The repair of brow ptosis is usually performed by removing an adjacent strip of skin superior to the eyebrow. An adjacent brow lift will restore the superior visual field and enhance facial symmetry (Fig. 38–2).

•A gold weight implant remained the “gold standard”a for the treatment of paralytic lagophthalmos.3 A 6- to 16-g gold weight implant sewn to the superior tarsal border provides enough weight to augment gravity in the closure of the eyelid (Fig. 38–3).

a A variety of other devices have been described over the years, including springs, magnets, and slings.4–9

FIGURE 38–4 A 10-gram gold weight implant for treatment of paralytic lagophthalmos.

•If the patient is symptomatic in spite of the maximal use of the measures outlined previously (i.e., ocular lubricants, correction of lower eyelid laxity and brow ptosis, gold weight implants), tarsorrhaphy is effective at relieving pain associated with ocular exposure (Figs. 38–4 and 38–5).

P I T F A L L

The major disadvantage of tarsorrhaphy is that it causes a noticeable facial asymmetry, which can be rather distracting. If control of the pain is needed and/or the health of the cornea is compromised, a tarsorrhaphy should be performed as a last resort in the treatment of Bell’s palsy.

Neurogenic Ptosis

The development of ptosis after eyelid or orbital trauma is quite common. In some cases the superior division of the third nerve is damaged, leading to neurogenic ptosis. This type of ptosis may be indistinguishable from other forms of ptosis (see Chapter 35) during the initial phase of recovery.

Traumatic ptosis often improves spontaneously weeks to months following the initial injury.10 Associated swelling of the eyelid and orbit may lead to a dehiscence of the levator aponeurosis. The diagnosis of a neurogenic ptosis must encompass the following physical findings:

•poor levator function;

•history of eyelid or orbital trauma; and

•no lid function recovery after 6 months.

FIGURE 38–5 Improved eyelid closure following implantation of a gold weight implant in a Bell’s palsy patient.

If the lid function does not recover by 6 months after injury, reconstructive surgery may be contemplated.

A sling procedure is usually necessary to elevate the eyelid margin. The Supramid sling ptosis repair is often the procedure of choice.11 This sling is easy to place and also easy to remove.

The most frequent complication of sling procedures in older patients is the development of dry eyes, caused by iatrogenic lagophthalmos. In severe and refractory cases, the Supramid sling can be easily removed to allow the eyelid to return to its ptotic position and protect the cornea.

PEARL... If the Supramid sling is well tolerated over the years, it can be replaced

with an autogenous fascia lata implant.

Traumatic Carotid Cavernous Fistula

A communication between the cavernous sinus and the carotid artery can develop following trauma. The fistula leads to the arterialization of the orbital vein.

Clinical signs of a traumatic carotid cavernous fistula are:

•pulsating proptosis;

•diplopia;

•elevated IOP; and

•dilated conjunctival vessels.

The natural history of a traumatic carotid cavernous fistula is often spontaneous embolization and resolution.

P I T F A L L

A persistent carotid cavernous fistula can lead to vision loss, primarily due to IOP.

Treatment of the traumatic carotid cavernous sinus fistula is indicated if prolonged elevation of the IOP is detected and visual field loss is developing. Two embolization options are available.

1.In most cases, embolization of the carotid cavernous sinus fistula is performed via a femoral approach.

PEARL... Prior to treatment, an arteriogram is required to pinpoint the

location of the fistula.

REFERENCES

CHAPTER 38 OCULAR MOTOR SYSTEM • 409

2.In difficult cases in which the fistula is not accessible by the femoral approach, the best access can be achieved by cannulating the superior ophthalmic vein.12–15 With the arterialization of the orbital veins caused by the carotid cavernous fistula, the superior ophthalmic vein is often quite large. The vein can be accessed by a superior medial anterior orbitotomy. A cannula for embolization is placed into the superior ophthalmic vein to provide access for the interventional radiologist. The cannula is removed following effective embolization.

SUMMARY

Orbital and ocular damage involving neurologic injury is relatively common. Unlike the approach to most problems in ophthalmology, one of the main “treatments” for neurologic injury is stabilization and observation because repair of trauma-related neurologic damage is often unavailable. We support the human body and allow nature to take its course. This ancient and traditional treatment may yield to more aggressive and invasive treatments in the years ahead.

1.Hoffman WY. Reanimation of the paralyzed face. Otolaryngol Clin North Am. 1992;25:649–667.

2.Kinney SE, Seeley BM, Seeley MZ, Foster JA. Oculoplastic surgical techniques for protection of the eye in facial nerve paralysis. Am J Otol. 2000;21:275–283.

3.Kaplan C, Sela M, Peled I, Rousso M, Wexler MR. Gold implant to upper eyelid for correction of lagophthalmos. Ann Ophthalmol. 1980;12:1214–1215.

4.D’Hooge PJ, Hendrickx EM. Upper lid loading with dermis graft and levator weakening. Management of lagophthalmos due to facial palsy. Ophthalmologica. 1975;171:419–424.

5.Duetinger M, Freilinger G. Temporalis transfer for correction of lagophthalmos. Eur Arch Otorhinolaryngol Suppl. 1994:S142–S144.

6.Goumain AJ, Fevrier JC. Treatment of lagophthalmos in facial paralysis by Morel-Fatio’s Aspring insertion operation. J Med Bord. 1965;142:797–801.

7.Lessa S, Carreirae S. Use of an encircling silicone rubber string for the correction of lagophthalmos. Plast Reconstr Surg. 1978;61:719–723.

8.McNeill JI, Oh YH. An improved palpebral spring for the management of paralytic lagophthalmos. Ophthalmology. 1991;98:715–719.

9.Sen DK. Temporalis transplantation for paralytic lagophthalmos. Br J Ophthalmol. 1970;54:680–682.

10.Silkiss RZ, Baylis HI. Management of traumatic ptosis.

Adv Ophthalmic Plast Reconstr Surg. 1988;7:149–155.

11.Katowitz JA. Frontalis suspension in congenital ptosis using a polyfilament, cable-type suture. Arch Ophthalmol. 1979;97:1659–1663.

12.Derang J, Ying H, Long Y, et al. Treatment of carotidcavernous sinus fistulas retrograde via the superior ophthalmic vein (SOV). Surg Neurol. 1999;52:286–292.

13.Gioulekas J, Mitchell P, Tress B, McNab AA. Embolization of carotid cavernous fistulas via the superior ophthalmic vein. Aust N Z J Ophthalmol. 1997;25:47–53.

14.Liang CC, Michon JJ, Cheng KM, Chan CM, Cheung YL. Ophthalmologic outcome of transvenous embolization of spontaneous carotid-cavernous fistulas: a preliminary report. Int Ophthalmol. 1999;23:43–47.

15.Monsein LH, Debrun GM, Miller NR, Nauta HJ, Chazaly JR. Treatment of dural carotid-cavernous fistulas via the superior ophthalmic vein. AJNR. 1991;12: 435–439.