Ординатура / Офтальмология / Английские материалы / Oxford American Handbook of Ophthalmology_Tsai, Denniston, Murray_2011

466 CHAPTER 13 Medical retina

Laser procedures in diabetic eye disease

Panretinal photocoagulation

Indication

•Active proliferative retinopathy, some cases of high-risk preproliferative retinopathy in patients with poor control of glucose or poor follow-up.

Method

•Consent: explain what the procedure does (the aim is to stop disease progression; that further laser treatment may well be required), what it does not do (it does not improve vision; is not an alternative to glycemic control), what to expect, and possible complications, e.g., pain, loss of peripheral field (with driving implications), scotoma, worsened acuity (e.g., macular decompensation), choroidal or retinal detachment.

•Instill topical anesthetic and position fundus contact lens (e.g., transequator) with coupling agent.

•Set argon laser for 200–500 μm spot size, 0.1 sec, and adjust power to produce a gently blanching burn.

Consider placing a temporal barrier at least 2–3 disc diameters from the fovea to help demarcate a “no-go” zone. Then place 1000 burns outside the vascular arcades, leaving burn-width intervals between them. A second session of 1000 is usually performed a few weeks later.

The power may need to be adjusted according to variable retinal take-up. Follow up monthly until there is evidence of neovascular regression, ± fill-in PRP until there is a response.

Macular laser (focal or grid)

Indication

• Clinically significant macular edema (Table 13.3).

Method

•Consent: explain what the procedure does (reduce sight loss; further laser treatment may be required), what to expect, and possible complications, e.g., pain, scotomata, worsened acuity, retinal detachment.

•Instill topical anesthetic and position fundus contact lens (e.g., area centralis) with coupling agent.

•Set argon laser for 50–200 μm spot size, 0.08–0.1 sec, and adjust power to produce a very gently blanching burn. Generally, smaller spot sizes and shorter durations are used for more central burns.

468 CHAPTER 13 Medical retina

Intravitreal injection in retinal diseases

Indications

These include cystoid macular edema, diabetic macular edema, posterior uveitis, neovascular glaucoma, proliferative diabetic retinopathy, choroidal neovascular membrane, and neovascular age-related macular degeneration.

Method

•Explain to the patient the rationale for the injection and the possible need for future injections.

•Provide local or topical anesthetic. Prepare the injection site with 50% Betadine solution.

•Measure and mark the proper location of the injection with a sterile caliper.

•The injection is placed in the inferior sclera, especially for triamcinolone injections, to prevent short-term loss of vision due to clouding of the vitreous.

•The intraocular pressure is checked to ensure central retinal artery perfusion.

Orbit

Anatomy and physiology 470

Orbital and preseptal cellulitis 472

Mucormycosis (phycomycosis) 474

Thyroid eye disease: general 475

Thyroid eye disease: assessment 478

Thyroid eye disease: management 481

Other orbital inflammations 483

Cystic lesions 485

Orbital tumors: lacrimal and neural 487

Orbital tumors: vascular 489

Orbital tumors: lymphoproliferative 490

Orbital tumors: other 491

Vascular lesions 492

Related pages:

Orbital and preseptal cellulitis in children bp. 623

470 CHAPTER 14 Orbit

Anatomy and physiology

The bony orbit forms a pyramid comprising a medial wall lying anteroposteriorly, a lateral wall at 45*, a roof, and a floor (Table 14.1). It has a volume of around 30 mL and contains most of the globe and associated structures: extraocular muscles (p. 572), optic nerve (p. 514), cranial nerves (p. 516), vascular supply, and lacrimal system (p. 128) (see also Table 14.2).

Being effectively a rigid box, the only room for expansion is forward. Most orbital pathology, therefore, presents initially with proptosis, followed by disruption of eye movements.

Table 14.1 Orbital bones

Table 14.2 Orbital apertures

472 CHAPTER 14 Orbit

Orbital and preseptal cellulitis

Orbital cellulitis is an ophthalmic emergency that may cause loss of vision and even death. Assessment, imaging, and treatment should be under the combined care of an ophthalmologist and ENT specialist (and pediatrician in children). Part of the ophthalmologist’s role is to assist in differentiating orbital cellulitis from the much more limited preseptal cellulitis.

In younger children in whom the orbital septum is not fully developed, there is a high risk of progression, thus it should be treated similarly to orbital cellulitis. For orbital and preseptal cellulitis in children, see p. 623.

Orbital cellulitis

Infective organisms include Streptococcus pneumoniae, Staphylococcus aureus, Streptococcus pyogenes, and Hemophilus influenza.

Risk factors

•Sinus disease: ethmoidal sinusitis (common), maxillary sinusitis.

•Infection of other adjacent structures: preseptal or facial infection, dacryocystitis, dental abscess.

•Trauma: septal perforation.

•Surgical: orbital, lacrimal, and vitreoretinal surgery.

Clinical features

•Fever, malaise, painful, swollen orbit.

•Inflamed lids (swollen, red, tender, warm) ± chemosis, proptosis, painful restricted eye movements ± optic nerve dysfunction (dVA, dcolor vision, RAPD).

•Complications: exposure keratopathy, iIOP, CRAO, CRVO, inflammation of optic nerve.

•Systemic: orbital or periorbital abscess, cavernous sinus thrombosis, meningitis, cerebral abscess.

Investigation

•Temperature.

•CBC, blood culture.

•CT (orbit, sinuses, brain): diffuse orbital infiltrate, proptosis ± sinus opacity.

Treatment

•Admit for intravenous antibiotics (e.g., either floxacillin 500–1000 mg 4x/day or cefuroxime 750–1500 mg 3x/day with metronidazole 500 mg 3x/day).

•ENT to assess for sinus drainage (required in up to 90% of adults).

Preseptal cellulitis

Preseptal cellulitis is not truly an orbital disease. It is much more common than orbital cellulitis, from which it must be differentiated (Table 14.3). The main causative organisms are Staphylococci and Streptococci spp. It is generally a much less severe disease, at least in adults and older children.

ORBITAL AND PRESEPTAL CELLULITIS 473

Risk factors

•Infection of adjacent structures (dacryocystitis, hordeolum) or systemic (e.g., upper respiratory tract infection).

•Trauma: laceration.

Clinical features

•Fever, malaise, painful, swollen lid/periorbita.

•Inflamed lids but no proptosis, normal eye movements, normal optic nerve function.

Investigation

Investigation is not usually necessary unless there is concern over possible orbital or sinus involvement.

Treatment

•Daily review until resolution (admit young or unwell children).

•Treat with oral antibiotics (e.g., floxacillin 500 mg 4x/day for 1 week and metronidazole 400 mg 3x/day for 1 week).

Table 14.3 Orbital vs. preseptal cellulitis

474 CHAPTER 14 Orbit

Mucormycosis (phycomycosis)

This is a rare, very aggressive life-threatening fungal infection caused by Mucor species or Rhizopus. Mucormycosis is a disease of the immunosuppressed, most commonly seen in patients who are also acidotic, such as in diabetic ketoacidosis or renal failure. However, the disease also occurs in malignancy and therapeutic immunosuppression. It represents fungal septic necrosis and infarction of tissues of nasopharynx and orbit.

Clinical features

•Black crusty material in nasopharynx, acute evolving cranial nerve palsies (II, III, IV, V, VI) ± obvious orbital inflammation.

Investigation

•Biopsy: fungal stains show nonseptate branching hyphae.

•CBC, UA, Glu.

Treatment

•Admit and coordinate care with microbiologist and infectious disease specialist, ENT specialist, ± PCP.

•Correct underlying disease (e.g., diabetic ketoacidosis) where possible.

•Intravenous antifungals (as guided by microbiology; e.g., amphotericin B).

•Early surgical debridement by ENT specialist ± orbital exenteration (for severe or unresponsive disease).

THYROID EYE DISEASE: GENERAL 475

Thyroid eye disease: general

Thyroid eye disease (TED; also called thyroid ophthalmopathy, dysthyroid eye disease, Graves eye disease) is an organ-specific autoimmune disease that may be both sight threatening and disfiguring. Acute progressive disease is an ophthalmic emergency as it may threaten the optic nerve and cornea (see Box 14.1).

While most patients with TED have clinical and/or biochemical evidence of hyperthyroidism or hypothyroidism, some are euthyroid—at least at the time of presentation. Thyroid dysfunction may precede, be coincident with, or follow thyroid eye disease.

Incidence is around 10/100,000/year.

Risk factors

•Female sex (F:M 4:1).

•Middle age.

•HLA-DR3, HLA-B8, and the genes for CTLA4 and the thyroidstimulating hormone (TSH) receptor.

•Smoking.

•Autoimmune thyroid disease.

Autoimmune thyroid disease

TED is most commonly associated with Graves’ disease but may occur in 3% of Hashimoto’s thyroiditis.

Graves’ disease

This is the most common cause of hyperthyroidism. Anti-TSH receptor antibodies cause overproduction of thyroxine (T4) and/or T3. Classic features include hyperthyroidism, goiter, thyroid eye disease, thyroid acropachy (clubbing), and pretibial myxedema.

Autoimmune thyroiditis (e.g., Hashimoto’s thyroiditis)

This is the most common cause of hypothyroidism. It may have a transient hyperthyroid stage, before leaving the patient hypothyroid. The associated goiter is usually firm.

Pathogenesis of TED

The cause is unclear. The target antigen is likely shared between the extraocular muscles and thyroid gland. Activated T cells probably act on cells of the fibroblast-adipocyte lineage within the orbit, thus stimulating adipogenesis, fibroblast proliferation, and glycosaminoglycan synthesis.

Clinical features

Ophthalmic

•Ocular irritation, ache (worse in mornings), red eyes, cosmetic changes, diplopia.

•Proptosis (exophthalmos), lid retraction (upper > lower) (Fig. 14.2), lid lag (on downgaze), conjunctival injection/chemosis, orbital fat prolapse, keratopathy (exposure/superior limbic keratoconjunctivitis or keratoconjunctivitis sicca), restrictive myopathy, optic neuropathy.