Ординатура / Офтальмология / Английские материалы / Practical Ophthalmology A Manual for the Beginning Ophthalmology Residents 4th edition_Wilson_1996

368 Chapter 14: Ophthalmic Kmernencies

Figure 14.6 Orbitai cellulitis.

Diagnostic workup of orbital cellulitis includes blood cultures and, if an evelid wound is present, wound cultures and Gram stains. Computed tomography of the orbit is indicated to exclude a retained foreign bodv, subperiosteal abscess, intracranial involvement, and contiguous sinus disease.

Treatment

Patients with mild preseptal cellulitis can be treated with oral antibiotics on an outpatient basis. Antibiotics are selected to cover the most likely organisms, which include Staphylococcus aureus, S epidermidis, and

Streptococcus pyogenes. In small children, one must also consider Haemophilus in flu en zae.

The treatment of severe preseptal cellulitis or orbital cellulitis should begin urgently, because patients are at risk for cavernous sinus thrombosis, meningitis, and brain abscesses. The patient should be admitted, and broad-spectrum intravenous antibiotics covering Grampositive. Gram-negative, and anaerobic organisms should be administered until the precise infectious agent is identified. Topical antibiotic ointment may be added.

Because sinus drainage may be required in severe cases, otolaryngologic evaluation is obtained in patients with mucoceles or sinusitis. It the patient with orbital cellulitis has diabetes mellitus, particularlv with ketoacidosis, or is otherwise immunocompromised, mucormycosis, a life-threatening fungal infection, must be seriously considered, since immediate surgical debridement and antifungal therapy would be needed to save the patient's life. Affected patients may show a black eschar in the nose or on the root of the mouth.

3 / 0 Chapter 14: Ophthalmic Hmergencies

Central Retinal Artery Occlusion

Patients with central retinal artery occlusion present with unilateral, acute, painless, severe loss of vision. It may result from embolic episodes in patients with carotid or cardiac disease, but it may be associated with giant cell (temporal) arteritis, collagen vascular disease, hypercoagulation disorders, talc emboli with intravenous drug abuse, and trauma.

Affected patients show an afferent pupillary defect. Fundus examination reveals retinal arterial narrowing and blood column segmentation. The retina is white or gray except for a cherry-red spot at the fovea, which is perfused by the choroid, and for areas supplied by a cilioretinal arterv (Figure 14.8). Look for Hollenhorst plaques or other types of emboli. Over time, patients will develop inner retinal atrophy and optic atrophv. The prognosis of central retinal arterv occlusion is generally poor.

Figure 14.8 Central retinal artery occlusion. Note retina! pallor and cherry-red spoi •• •'".-•: ^• — h- ;v\ - * N^^ev,CRA.Courtesy W..K. Kelloqn - - '••--iter, Univ.-

Treatment

Treatment for central retinal artery occlusion is emergent. Irreversible retinal damage is said to occur after 90 minutes, but treatment should be considered in a patient presenting within 24 hours of onset. The goals of treatment are to restore retinal blood flow and to move a potential retinal embolus distally. Emergency treatment is initiated as follows:

1.Lower intraocular pressure to improve retinal perfusion in one or more of the following ways:

a.Massage the globe either digitally or with a fundus contact lens. In addition to lowering the intraocular pressure, this may also dislodge an embolic plaque.

b.Administer acetazolamide (500 mg IV) and/or instill topical timolol 0.5%.

c.Consider performing anterior chamber paracentesis (Clinical Protocol 14.4).

2.Produce arterial dilation by having the patient either inhale a combination of 95% oxygen and 5% carbon dioxide (carbogen) or breathe into a paper bag.

3.All patients with central retinal artery occlusion should undergo

athorough medical evaluation after emergency treatment. In patients older than 55 years, erythrocyte sedimentation rate should be measured at the time of presentation to rule out giant cell arteritis. If the patient's sedimentation rate suggests temporal arteritis, give high-dose corticosteroids.

Acute Angle-Closure Glaucoma

Aqueous normally flows from the posterior chamber to the anterior chamber through the pupil, and then drains through the trabecular meshwork. Acute angle-closure glaucoma occurs when the iris becomes apposed to the trabecular meshwork, blocking aqueous humor drainage (Figure 14.9). Some patients are anatomically predisposed to developing pupillary block, the most common cause of angle-closure glaucoma, wherein aqueous cannot readily access the anterior chamber through the pupil. Predisposing factors include a small, hyperopic eye and a narrow chamber angle. Pupillary block leads to buildup of aqueous behind the iris, forward bowing of die iris, closure of tire anterior chamber angle, and acute rise in the intraocular pressure (IOP). Pupillary block is more likely to occur when the pupil is mid-dilated. Therefore, attacks can be precipitated by topical mydriatics, svstemic anticholinergics, stress, excitement (sympathetic release), or dim illumination.

Treatment

Medical treatment is used initially to break the acute attack, paving the way for definitive surgical treatment. Stepwise medical treatment consists of the following:

1.Attempt to terminate the attack by compressing the central cornea with a muscle hook or Zeis gonioprism. This may he helpful in cases of recent onset.

2. Instill a topical beta blocker (eg, 1 drop of timolol 0.5%).

3.Only in phakic patients, instill pilocarpine 1 % - 2 % ql5 minutes x 3.

4.Instill topical corticosteroid drops (prednisolone acetate 1%).

5.Instill topical mydriatic or cycloplegic drops (eg, phenylephrine

2.5% or tropicamide 1%) q 15 minutes x 3 (used in pseudophakic or aphakic pupillary block).

6.Administer systemic carbonic anhydrase inhibitors (eg, aceta/.olamide 250 mg po or IV).

7.Administer systemic osmotic agents (eg, isosorbide 50-100 mg po over crushed ice, to be drunk slowlv; intravenous mannitol). Avoid these medications in patients with congestive heart failure.

8.Administer svstemic analgesics (eg, acetaminophen).

9.Apply topical glycerin, which may temporarily reduce corneal edema and swelling, allowing adequate view for examination and laser iridotomy.

Definitive treatment, performed when the acute attack is broken, consists of laser iridotomy or, if not possible or not available, surgical iridectomy. The fellow eye should be treated prophylacticallv in the immediate future since it is at high risk for developing acute angle closure as well.

Pitfalls and Pointers

•Make appropriate follow-up arrangements after evaluating the patient in the emergency room.

•Make the medical records sufficiently detailed for later medico-

374Chapter 14: Ophthalmic Emergencies

•Do not use depolarizing muscular relaxants (eg, succinylcholine) in a patient with a ruptured globe.

•Embedded, hidden foreign bodies are sometimes overlooked.

In cases of perforating trauma, neuroimaging studies may be indicated to rule out a hidden foreign body.

•If significant head trauma exists, avoid dilating the patient's pupils for ophthalmoscopy until neurologic evaluation is completed. When you do dilate, be sure to notify other health care personnel and note the dilation on the chart.

•Traumatic hyphema in children is often associated with lethargy or somnolence; avoid confusing these symptoms with those associated with neurologic injury, and vice versa.

•Do not apply pressure (eg, ocular palpation, scleral depression) to

•Do not use a papoose board for restraining a child with an open or potentially ruptured globe.

•Give priority to the treatment of life-threatening conditions over

the treatment of ocular trauma.

•Do not prescribe or give a patient a bottle of anesthetic eyedrops.

Keep all ophthalmic medications out of reach.

•Accidental swallowing of the contents of a bottle of atropine or pilocarpine is fatal.

•Do not administer carbonic anhydrase inhibitors to individuals with possible or proven sickle-cell disease or trait, or patients with severe chronic obstructive pulmonary disease.

Suggested Resources

Bacterial Keratitis [Preferred Practice Pattern]. San Francisco:

American Academy of Ophthalmology; 1995.

Catalano RA, Belin M, eds. Ocular Emergencies. Philadelphia: WB Saunders; 1992.