Ординатура / Офтальмология / Английские материалы / Clinical Ophthalmology A Systematic Approach 7th Edition_Kanski, Bowling_2011

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Fig. 6.16 Herpes zoster ophthalmicus. (A) Hutchinson sign; (B) involvement in a child withAIDS

Acute shingles

General features

1A prodromal phase precedes the appearance of the rash. It lasts 3–5 days and is characterized by tiredness, fever, malaise and headache. Symptoms involving the affected dermatome vary from a superficial itching, tingling or burning sensation to a severe deep boring or lancing pain that is either constant or intermittent. Older patients with early severe pain and a larger area of involvement are at particular risk of postherpetic neuralgia.

2Skin lesions

•The rash respects the midline, which may aid in distinguishing shingles from HSV infection.

•Erythematous areas with a maculopapular rash develop, and may also be confused with cellulitis or contact dermatitis.

•Within 24 hours, groups of vesicles appear and these become confluent over 2–4 days (Fig. 6.17A).

•Although the rash itself does not affect the lower lid in HZO, boggy oedema of upper and lower eyelids is common and may sometimes also involve the contralateral side of the face.

•The vesicles often pass through a pustular phase before they crust and dry after 2–3 weeks (6.17B).

•Large, deep haemorrhagic lesions are more common in immunodeficient patients (Fig. 6.17C).

•The lesions heal to leave residual skin destruction and depigmented scars (Fig. 6.17D).

•Rarely, no rash develops (zoster sine herpete)

3Disseminated zoster may rarely develop in immunodeficiency or malignancy. The patient becomes severely ill and the rash progresses to involve multiple dermatomes and multiple organ systems.

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Fig. 6.17 Herpes zoster ophthalmicus. (A) Vesicles; (B) confluent crusting; (C) haemorrhagic rash with involvement of both the ophthalmic and maxillary nerve; (D) residual scarring

(Courtesy of R Fogla – fig. A)

Treatment

1Oral aciclovir 800 mg five times daily for 7–10 days, started within 72 hours of onset, is the treatment of choice. Patients presenting later than 72 hours at the vesicular stage should also be treated as this will still reduce the severity of the acute episode and the risk of postherpetic neuralgia. The incidence of late ophthalmic complications is also reduced by about 50%.

2Intravenous aciclovir 5–10 mg/kg t.i.d. is indicated only for encephalitis.

3Other oral antiviral agents such as valaciclovir 1 g t.i.d., famciclovir 500 mg t.i.d. and brivudine 125 mg once daily are more expensive than but have a more convenient regimen, are better tolerated, and are as effective as aciclovir.

4Systemic steroids (prednisolone 40–60 mg daily) should be used only in conjunction with systemic antivirals. They have a moderate effect to reduce acute pain and accelerate skin healing but have no effect on the incidence or severity of postherpetic neuralgia.

5Symptomatic treatment of skin lesions is by drying, antisepsis and cold compresses. The benefit of topical antibiotic-steroid combinations is uncertain.

6Patients with shingles can transmit chickenpox so that contact with people not known to be immune (particularly pregnant women) and with immunodeficient individuals should be avoided at least until crusting is complete.

Eye disease

Acute eye disease

1Acute epithelial keratitis develops in over 50% of patients within 2 days of the onset of the rash and usually resolves spontaneously within a few days. It is characterized by dendritic lesions which are smaller and finer than herpes simplex dendrites, and have tapered ends without terminal bulbs (Fig. 6.18A). The lesions stain better with rose Bengal than with fluorescein. Treatment, if required, is with a topical antiviral.

2Conjunctivitis (follicular and/or papillary) is common and typically associated with lid margin vesicles. Treatment is not required in the absence of corneal disease.

3Episcleritis occurs at the onset of the rash and usually resolves spontaneously. A mild nonsteroidal anti-inflammatory may be used if necessary.

4Scleritis and sclerokeratitis are uncommon and may develop at the end of the first week. Treatment of indolent lesions is with oral flurbiprofen (Froben) 100 mg t.i.d. Occasionally, oral steroids with antiviral cover may be required for severe involvement.

5Nummular keratitis usually develops at the site of epithelial lesions about 10 days after the onset of the rash. It is characterized by fine granular subepithelial deposits surrounded by a halo of stromal haze (Fig. 6.18B). The lesions fade in response to topical steroids but recur if treatment is discontinued prematurely.

6Stromal (interstitial) keratitis (Fig. 6.18C) develops in about 5% of cases three weeks after the onset of the rash. It responds to topical steroids but can become chronic and require slow tapering.

7Disciform keratitis (immune-mediated endotheliitis) is less common than with herpes simplex infection but may lead to corneal decompensation. Treatment is with topical steroids.

8Anterior uveitis affects at least a third of patients and can be associated with sectoral iris ischaemia and atrophy (see Fig. 11.44B).

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9IOP should be monitored as elevation is common, including steroid-induced. Prostaglandin derivatives should be avoided if treatment is necessary.

10Neurological complications may require intravenous antivirals and systemic steroids.

•Cranial nerve palsies affecting the third (most common), 4th and 6th nerves usually recover within 6 months.

•Optic neuritis is rare.

•CNS manifestations are rare but include encephalitis, cranial arteritis, and Guillain-Barré syndrome.

Fig. 6.18 Acute lesions in herpes zoster ophthalmicus. (A) Dendritic epithelial lesions with tapered ends; (B) nummular keratitis; (C) stromal keratitis

(Courtesy of J Krachmer, M Mannis and E Holland, from Cornea, Elsevier 2005 – fig. A; C Barry – fig. C)

Chronic eye disease

1 Neurotrophic keratitis develops in about 50% of cases, although it is usually relatively mild and settles over several months.

2Scleritis may become chronic and lead to patchy scleral atrophy (Fig. 6.19A).

3Mucous plaque keratitis develops in about 5% of patients, most commonly between the 3rd and 6th months. It is characterized by the sudden appearance of elevated mucous plaques that stain with rose bengal (Fig. 6.19B). Treatment involves a combination of topical steroid and acetylcysteine. Untreated, plaques resolve after a few months, leaving a faint diffuse corneal haze.

4 Lipid degeneration may develop in eyes with persistent severe nummular or disciform keratitis.

5Lipid-filled granulomata may develop under the tarsal conjunctiva, together with subconjunctival scarring (Fig. 6.19C).

6Eyelid scarring may result in ptosis, cicatricial entropion (Fig. 6.20A) and occasionally ectropion (Fig. 6.20B), trichiasis, lid notching and madarosis.

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Fig. 6.19 Chronic lesions in herpes zoster ophthalmicus. (A) Scleral atrophy; (B) mucous plaque keratitis; (C) lipid-filled granulomas

(Courtesy of R Marsh – fig. B)

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Fig. 6.20 Eyelid scarring in herpes zoster ophthalmicus. (A) Cicatricial entropion; (B) cicatricial ectropion

(Courtesy of D Meyer – fig. B)

Relapsing eye disease

In the relapsing phase lesions may reappear years after an acute episode, which may have been forgotten; eyelid scarring may be the only diagnostic clue. Reactivation of keratitis, episcleritis, scleritis or iritis can occur.

Post-herpetic neuralgia

Post-herpetic neuralgia is defined as pain that persists for more than one month after the rash has healed. It develops in up to 75% of patients over 70 years of age. Pain may be constant or intermittent, worse at night and aggravated by minor stimuli (allodynia), touch and heat. It generally improves slowly with time with only 2% of patients affected after 5 years. Neuralgia can impair the quality of life, and may lead to depression of sufficient severity to present the danger of suicide. Patients severely affected should be referred to a specialist pain clinic. Treatment involves the following:

1Topical treatment with cold compresses, topical capsaicin 0.025% or 0.075% cream or local anaesthetic (lidocaine 5%) creams may be effective. Capsaicin takes up to 3 weeks to provide relief and may need to be continued long-term.

2Systemic treatment should be increased in steps as follows:

•Simple analgesics such as paracetamol up to 4 g daily.

•Stronger analgesics such as codeine up to about 240 mg daily.

•Amitriptyline 10–25 mg at night increasing gradually to 75 mg daily if appropriate.

•Carbamazepine 400 mg daily for lancinating pain.

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Interstitial keratitis

Pathogenesis

Interstitial keratitis (IK) is an inflammation of the corneal stroma without primary involvement of the epithelium or endothelium. In most cases, the inflammation is an immune-mediated process triggered by an appropriate antigen. Syphilis-related (usually congenital and sometimes acquired) IK is the archetype, but no longer the most common in developed countries. Others include herpetic keratitis (including chickenpox), other viral infections, tuberculosis, sarcoidosis, Cogan syndrome (see below), and a range of other infections.

Syphilitic IK

Syphilis is caused by the spirochaete Treponema pallidum. The organism is very fragile, easily eliminated by drying or heating, and does not survive in culture.

Acquired infection

1The systemic features and investigations are described in Chapter 11.

2Ocular manifestations include uveitis, IK, madarosis, optic neuritis, ocular motor nerve palsies and Argyll Robertson pupils.

3Treatment is with procaine penicillin, (10 days in primary and secondary syphilis, 4 weeks in tertiary syphilis); alternatives in penicillin-allergic patients include doxycycline, tetracycline and erythromycin.

Congenital infection

Infection of the fetus can occur transplacentally. It may lead to stillbirth, be subclinical, or can result in a range of clinical features. It is important to diagnose and treat infants as early as possible.

1Early systemic features include rhinitis and failure to thrive, maculopapular rash (especially on the buttocks and thighs), mucosal ulcers, fissures around the lips, nares and anus (rhagades), pneumonia, hepatosplenomegaly, lymphadenopathy and jaundice. Neurological and cardiovascular problems can also occur.

2Late systemic features include sensorineural deafness, saddle-shaped nasal deformity (Fig. 6.21A), ‘sabre’ tibiae (Fig. 6.21B), bulldog jaw (mandibular prominence due to maxillary underdevelopment), malformed incisors, Hutchinson's teeth (notched, small, widely spaced teeth – Fig. 6.21C), mulberry molars and Clutton joints (painless effusions in large joints, especially the knees).

3Ocular features include anterior uveitis, IK, dislocated/subluxated lens, optic atrophy, ‘salt and pepper’ pigmentary retinopathy and Argyll Robertson pupils.

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Fig. 6.21 Stigmata of congenital syphilis. (A) Saddle-shaped nasal deformity; (B) ‘sabre’ tibia; (C) Hutchinson teeth

(Courtesy of R Marsh and S Ford – fig. C)

Syphilitic IK

1Presentation in congenital syphilis is between the ages of 5 and 25 years. The initial symptoms consist of those of acute anterior uveitis with severe blurring. Involvement is usually bilateral, although usually not simultaneous. In acquired disease IK is less common and usually unilateral, typically occurring years after the age at which the disease is contracted, although it can occur as part of primary infection.

2Signs in chronological order:

•Limbitis associated with deep stromal vascularization, with cellular infiltration and clouding that may obscure the stillperfused vessels to give the characteristic ‘salmon-patch’ appearance (Fig. 6.22A).

•Granulomatous anterior uveitis which may be obscured by corneal clouding.

•After several months the cornea begins to clear and the vessels become non-perfused (ghost vessels – Fig. 6.22B).

•If the cornea later becomes inflamed, the vessels may re-fill with blood and, rarely, bleed into the stroma (Fig. 6.22C).

•The healed stage is characterized by ‘ghost vessels’, feathery deep stromal scarring (Fig. 6.22D), and sometimes thinning, astigmatism and band keratopathy.

3Treatment of active IK is with systemic antibiotics, and topical steroids and cycloplegics. All patients with positive treponemal serology should be referred to a genitourinary medicine specialist for evaluation, treatment and screening of siblings, parents and partners.

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Fig. 6.22 Syphilitic interstitial keratitis. (A) ‘Salmon patch’; (B) ‘ghost vessels’ in inactive disease; (C) intrastromal corneal haemorrhage fromre-perfused vessels; (D) patchy residual scarring

(Courtesy of Krachmer, Mannis and Holland from Cornea, Mosby 2005 – fig. A)

Cogan syndrome

Cogan syndrome is a rare systemic autoimmune vasculitis characterized by intraocular inflammation and vestibuloauditory dysfunction (particularly neurosensory deafness but also tinnitus and vertigo) developing within months of each other. The disease primarily occurs in young adults, with both sexes affected equally.

1Systemic features include necrotizing vasculitis of the renal, gastrointestinal and cardiovascular systems that may be associated with polyarteritis nodosa in some patients.

2Ocular signs

•Redness, pain, photophobia and blurred vision.

•Early faint bilateral peripheral anterior stromal opacities.

•Deeper opacities and corneal neovascularization then ensue that may remain peripheral (Fig. 6.23) or progress centrally.

•Uveitis, scleritis and retinal vasculitis may develop.

3Treatment is with topical steroids for keratitis. Systemic steroids are usually required for scleritis or retinal vasculitis. Vestibuloauditory symptoms mandate immediate treatment with systemic steroids to prevent hearing loss; immunosuppressive therapy may also be required.

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Fig. 6.23 Old peripheral interstitial keratitis in Cogan syndrome

(Courtesy of R Curtis)

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Protozoan keratitis

Acanthamoeba

Pathogenesis

Acanthamoeba spp. are ubiquitous free-living protozoa commonly found in soil, fresh or brackish water and the upper respiratory tract. The cystic form (Fig. 6.24A) is highly resilient. Under appropriate environmental conditions, the cysts turn into trophozoites, which produce a variety of enzymes, leading to tissue penetration and destruction. In developed countries keratitis is most frequently associated with contact lens wear, especially if tap water is used for rinsing.

Fig. 6.24 Acanthamoeba keratitis. (A) Cysts in a corneal biopsy; (B) epithelial pseudodendrites; (C) focal anterior stromal infiltrates; (D) radial perineuritis; (E) ring abscess; (F) melting

(Courtesy of J Harry – fig. A; S Tuft – figs E and F)

Diagnosis

Early misdiagnosis as herpes simplex keratitis is relatively common. In advanced disease the possibility of fungal keratitis should be remembered.

1Presentation is with blurred vision and pain, which may be severe and disproportionate to the clinical signs.

2Signs

•In early disease the epithelial surface is irregular and greyish.

•Epithelial pseudodendrites (Fig. 6.24B) that may be mistaken for herpes simplex keratitis.

•Limbitis with diffuse or focal anterior stromal infiltrates (Fig. 6.24C).

•Perineural infiltrates (radial keratoneuritis – Fig. 6.24D) are seen during the first 1–4 weeks and are pathognomonic.

•Gradual enlargement and coalescence of the infiltrates to form a ring abscess (Fig. 6.24E).

•Scleritis may develop and is generally reactive rather than extension of infection.

•Slowly progressive stromal opacification and vascularization.

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