• No se han encontrado resultados

DAÑO A LOS BIENES PERSONALÍSIMOS DE ESPECIAL PROTECCIÓN CONSTITUCIONAL

2. LA CERTEZA DEL DAÑO – ASPECTOS CRÍTICOS

2.2. LA CERTEZA EN LOS PERJUICIOS EXTRAPATRIMONIALES

2.2.3. DAÑO A LOS BIENES PERSONALÍSIMOS DE ESPECIAL PROTECCIÓN CONSTITUCIONAL

1. Observe the patient with periodic examinations and photographs every 3 to 12 months, depending on suspicion of malignancy.

2. Surgical resection is indicated if growth is documented, the tumor interferes with vision, or it produces intractable glaucoma.

3. Diffuse iris melanoma with secondary glaucoma may require enucleation.

Note

Avoid filtering surgery for glaucoma associated with possible melanoma because of the risk of tumor dissemination.

P.127

Chapter 6 Eyelid

6.1 Ptosis Ptosis Symptoms

Drooping upper eyelid, visual loss, especially with reading.

Signs

(See Figure 6.1.1.)

Critical. Drooping upper eyelid.

Other. Concerning associated signs include anisocoria, diplopia, ocular motility changes, headache, or neck pain. See individual entities.

Etiology

Note

Although the vast majority of ptosis is of benign etiology, four entities must be ruled out in every single case by careful examination:

1. Horner syndrome.

2. Third cranial nerve palsy (complete, partial, or aberrant III nerve regeneration).

3. Myasthenia gravis.

4. Superior eyelid or orbital malignancy.

z Myogenic: Decreased levator function (<10mm), weak or absent eyelid crease. Congenital levator dysgenesis may be associated with lagophthalmus in downgaze, poor elevation in upgaze if associated with double elevator palsy; acquired myogenic ptosis from localized or diffuse muscular dystrophy, chronic progressive external ophthalmoplegia (CPEO), Kearns-Sayre syndrome, or oculopharyngeal dystrophy is much less common.

z Aponeurotic: High eyelid crease, moderate degree of ptosis (3 to 4 mm), good levator function (10 to 15 mm), may worsen in downgaze. Levator stretching or dehiscence can be due to normal aging changes, secondary to repetitive trauma in patients who rub eyes, wear rigid contact lenses, or in patients with previous intraocular surgery.

z Neurogenic: Third cranial nerve palsy (often complete ptosis, never an isolated abnormality;

congenital, compressive, vasculopathic, see 10.5, Isolated Third Nerve Palsy); Horner syndrome (subtle upper and lower eyelid ptosis, see 10.2 Horner Syndrome); myasthenia gravis (variable ptosis, worsens with fatigue, see 10.11, Myasthenia Gravis); Marcus Gunn jaw winking syndrome (ptotic eyelid elevates with jaw movement); ophthalmoplegic migraine; multiple sclerosis.

z Mechanical: Retained contact lens in upper fornix; upper eyelid inflammation (chalazion, giant papillary conjunctivitis, posttraumatic edema) or neoplasm.

z Traumatic: History of eyelid laceration with levator transection, contusion injury to the levator, tethering/ischemia within an orbital roof fracture, late dehiscence or cicatricial changes.

z Pseudoptosis: Contralateral eyelid retraction or proptosis, ipsilateral enophthalmos, hypertropia, microphthalmus, phthisis bulbi,

dermatochalasis, brow ptosis, chalazion or other eyelid tumor, eyelid edema, blepharospasm, Duane syndrome.

Work-Up

1. History: Determine onset and duration of ptosis. Present since birth? Acute onset? Old photographs, a driver's license and family member's opinions are useful adjuncts to the history. History of surgery in either eye? Orbital or eyelid trauma (orbital blow-out fractures resulting in enophthalmos can mimic ptosis)? Variability with fatigue? Associated with headache or neck pain? Any history of autoimmune disease (lupus, Sjogren syndrome) or corneal abnormalities (which may predispose the patient to postoperative exposure keratopathy).

2. Mandatory documentation: Must carefully check and document pupillary size and extraocular motility, even if normal. If anisocoria is present, measurements should be documented under light and dark conditions. Additional pharmacologic testing may be indicated (see 10.1, Anisocoria). If extraocular muscle dysfunction is noted, additional testing with prism bars may be indicated.

3. Complete orbital examination of both eyes: Measure and compare margin-reflex distance, levator function (full upper eyelid excursion while preventing frontalis muscle assistance), upper eyelid crease position of both eyes. Is there lagophthalmus? Associated lower eyelid ‘ptosis' (elevation of ipsilateral lower eyelid) is often seen in Horner syndrome. Proptosis or eyelid lag may masquerade as contralateral ptosis. Exophthal-mometry measurements are useful. Any sign of aberrant eyelid movements like jaw-winking, variability and/or fatigue, orbicularis weakness, eyelid retraction with adduction and/or infraduction? Palpate the superior orbit to rule out a mass or superior orbital rim deformity.

4. Complete ocular examination: Determine if there are associated pupillary or extraocular motility abnormalities. Flip upper eyelid to examine conjunctival surface and superior fornix. Dilated fundus examination to look for pigmentary changes in adolescents and young adults who present with ptosis, poor levator function, and external ophthalmoplegia (i.e., possible Kearns-Sayre syndrome).

5. Corneal protective mechanisms. Document presence or absence of preoperative lagophthalmos, orbicularis function, Bell phenomenon, and tear production. Check the cornea carefully for any abnormalities or dystrophies which may predispose the patient to postoperative keratopathy.

6. Other tests

—Ice test: Apply ice pack to ptotic eye for 2 minutes and reassess degree of ptosis. Improvement with ice suggests myasthenia gravis.

—Neosynephrine test: Instill one drop 2.5% phenylephrine in the ptotic eye(s) and reassess degree of P.129

Figure 6.1.1. Ptosis.

ptosis. Patients with improvement of ptosis after 5 to 7 minutes may be good candidates for ptosis correction by an internal approach.

—Cocaine and hydroxyamphetamine tests. See 10.2, Horner Syndrome.

7. Imaging studies: In very select cases where a systemic or neurologic cause is suspected:

—Computed tomographic (CT) or magnetic resonance imaging (MRI) of orbit if a superior orbital mass is suspected.

—Emergent CT/CTA or MRI/MRA of the head and neck if carotid artery dissection is suspected in a patient with a painful Horner syndrome. Imaging of the head alone is inadequate. See 10.2, Horner Syndrome.

—Emergent CT/CTA, MRI/MRA or conventional angiography if intracranial aneurysm

causing a third cranial nerve palsy with pupillary involvement or a partial third cranial nerve palsy is suspected. See 10.5, Isolated Third Nerve Palsy.

—Chest CT if myasthenia gravis is suspected, to rule out thymoma. See 10.11, Myasthenia Gravis.

8. Ancillary studies:

—Urgent EKG and cardiology consult if Kearns-Sayre syndrome is suspected. Many of these patients can have a high degree heart block which can result in sudden death.

—If myasthenia gravis is suspected, acetylcholine receptor antibody testing, single fiber

electromyography, and/or edrophonium chloride (e.g., Tensilon) testing under monitored conditions may be indicated. See 10.11, Myasthenia Gravis, and Pharmacopoeia.

—If severe dry-eye is found, consider an autoimmune work-up with serologies to rule out lupus and Sjogren syndrome.

Treatment

1. Depends on underlying etiology (see 10.2, Horner Syndrome; 10.5, Isolated Third Nerve Palsy; 10.11, Myasthenia Gravis).

2. Nonsurgical options: Observation. Taping and eyelid crutches attached to glasses in neurogenic and myogenic ptosis. Management of chalazion with warm compresses and/or excision, eyelid and/or orbital neoplasms with excision.

3. Surgical options: Based on initial evaluation and additional testing. Transcutaneous levator advancement, transconjunctival levator advancement, frontalis muscle suspension, Müller muscle resection.

Follow-Up

1. Congenital: Close follow-up is required to monitor for the presence of occlusion amblyopia and exposure keratopathy

2. Traumatic: Observation for 6 months before considering surgical intervention.

3. Neurologic: Reevaluate based on particular entity.

4. Postoperative (after ptosis repair). Acute: monitor for infection and hemorrhage. Subacute: Monitor for exposure keratopathy and for asymmetry that may require postoperative readjustment. Mild

lagophthalmos is common for 2 to 3 weeks after surgical repair and usually resolves. Chronic: Monitor for ptosis recurrence and exposure keratopathy.

6.2 Chalazion/Hordeolum

P.130

Chalazion/Hordeolum

Documento similar