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

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• Familial

2Congenital

•Oliver–McFarlane syndrome – pigmentary retinopathy, dwarfism and mental handicap

•Cornelia de Lange syndrome – mental and physical developmental abnormalities.

•Goldstein–Hutt syndrome – cataract and hereditary spherocytosis.

•Hermansky–Pudlak syndrome – albinism and bleeding diathesis.

Madarosis

Madarosis is a decrease in the number of lashes (Fig. 1.37C); the main causes are shown in Table 1.2

Table 1.2 -- Cause of madarosis

1Local

•Chronic anterior lid margin disease

•Infiltrating lid tumours

•Burns

•Radiotherapy or cryotherapy of lid tumours

2Skin disorders

•Generalized alopecia

•Psoriasis

3Systemic diseases

•Myxoedema

•Systemic lupus erythematosus

•Acquired syphilis

•Lepromatous leprosy

4Following removal

•Iatrogenic for trichiasis

•Trichotillomania – psychiatric disorder of hair removal

Poliosis

Poliosis is a premature localized whitening of hair, which may involve the lashes and eyebrows (Fig. 1.37D); the main causes are shown in Table 1.3.

Table 1.3 -- Causes of poliosis

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Allergic disorders

Acute allergic oedema

Acute allergic oedema is usually caused by pollen or by insect bites.

1 Signs. Sudden onset of bilateral pitting periorbital oedema (Fig. 1.38A), often accompanied by conjunctival swelling (chemosis).

2Treatment with systemic antihistamines may be helpful.

Fig. 1.38 Allergic disorders. (A) Acute allergic oedema; (B) contact dermatitis; (C) atopic dermatitis

Contact dermatitis

Contact dermatitis is an inflammatory response that usually follows exposure to a medication or preservative, cosmetics or metals. An irritant can also cause a non-allergic toxic dermatitis. The individual is sensitized on first exposure and develops an immune reaction on further exposure. Reaction is mediated by a delayed type IV hypersensitivity response.

1 History of exposure and re-exposure to a potential allergen. 2 Symptoms include itching and tearing following exposure.

3Signs

•Lid oedema, scaling, angular fissuring and tightness (Fig. 1.38B).

•Chemosis, redness and papillary conjunctivitis.

•Punctate corneal epithelial erosions.

4Treatment

•Stopping exposure to the allergen, if it can be identified.

•Use of non-preserved drops, if sensitivity to preservatives suspected.

•Cold compresses for symptomatic relief.

•Topical steroids may be helpful but are rarely required.

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•Oral antihistamine for severe cases.

•Care to avoid re-exposure (record in notes).

Atopic dermatitis

Atopic dermatitis (eczema) is a very common idiopathic condition, typically associated with asthma and hay fever. Eyelid involvement is relatively infrequent but when present is invariably associated with generalized dermatitis.

1Signs. Thickening, crusting and vertical fissuring of the lids associated with staphylococcal blepharitis and madarosis (Fig. 1.38C).

2Treatment is with emollients to hydrate the skin and the judicious use of mild topical steroids such as hydrocortisone 1%. It is also important to treat associated infection.

3Ocular associations:

a Common include vernal disease in children and chronic keratoconjunctivitis in adults. b Uncommon include keratoconus, presenile cataract and retinal detachment.

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Necrotizing fasciitis is an extremely rare rapidly progressive necrosis initially involving subcutaneous soft tissues and later the skin. It is usually caused by S. pyogenes and occasionally S. aureus. The most frequent sites of involvement are the extremities, trunk and perineum, as well as postoperative wound sites. Unless treatment is early and appropriate death may result. Periocular infection is rare and may be secondary to trauma or surgery.

1Signs. Periorbital redness and oedema leading to formation of large bullae and black discoloration of skin due to gangrene secondary to underlying thrombosis (Fig. 1.39D).

2Complications include ophthalmic artery occlusion, lagophthalmos and disfigurement.

3Treatment involves intravenous benzylpenicillin, debridement of necrotic tissue and reconstructive surgery.

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Viral infections

Molluscum contagiosum

Molluscum contagiosum is a skin infection caused by a human specific double-stranded DNA poxvirus which typically affects otherwise healthy children, with a peak incidence between 2 and 4 years. Transmission is by contact and subsequently by autoinoculation. Multiple, and occasionally confluent, lesions may develop in immunocompromised patients. A distribution in the chin-strap region is common in HIVpositive individuals.

1Histology shows a central pit and lobules of hyperplastic epidermis with intracytoplasmic (Henderson-Patterson) inclusion bodies that displace the nuclear remnant to the edge of the cell. The bodies are small and eosinophilic near the surface and large and basophilic deeper down (Fig. 1.40A).

2Signs

•Single or multiple pale, waxy, umbilicated nodules (Fig. 1.40B).

•Lesions on the lid margin (Fig. 1.40C) may shed virus into the tear film and give rise to a secondary ipsilateral chronic follicular conjunctivitis. Unless the lid margin is examined carefully the causative molluscum lesion may be overlooked.

•White cheesy material consisting of infected degenerate cells can be expressed from the lesion.

3Treatment may not be necessary unless the lesion is very close to the lid margin. Options include shave excision, cauterization, cryotherapy or laser.

Fig. 1.40 Molluscumcontagiosum. (A) Histology shows lobules of hyperplastic epidermis and a pit containing intracytoplasmic inclusion bodies which are small and eosinophilic near the surface and larger and basophilic more deeply; (B) multiple molluscumnodules; (C) lid margin nodule

(Courtesy of A Garner – fig. A; N Rogers – fig. B)

Herpes zoster ophthalmicus

Herpes zoster ophthalmicus (HZO) is a common, unilateral infection caused by varicella-zoster virus. It typically affects the elderly but may occur at an earlier age. It tends to be more severe in immunocompromised individuals.

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1Presentation is with pain in the distribution of the first division of the trigeminal nerve.

2Signs

•A maculopapular rash on the forehead (Fig. 1.41A).

•Progression through vesicles and pustules to crusting.

•Periorbital oedema may spread to the other side (Fig. 1.41B), giving the erroneous impression that the condition is bilateral.

3Ocular complications (see Ch. 6).

4Treatment

•Oral aciclovir 800 mg five times daily for 7–10 days; alternatives include valaciclovir 1 g t.i.d., famciclovir 500 mg t.i.d. and brivudine 125 mg once daily.

•Topical aciclovir or penciclovir cream, and a steroid-antibiotic combination such as Fucidin-H (hydrocortisone 1%, fusidic acid 2%) can be used t.i.d. until the crusts have separated.

Fig. 1.41 Herpes zoster ophthalmicus (A) Maculopapular rash; (B) vesicles and crusts, and periorbital oedema

Herpes simplex

1Pathogenesis. Primary infection or rarely reactivation of herpes simplex virus previously dormant in the trigeminal ganglion.

2Diagnosis

•Prodromal facial and lid tingling, lasting about 24 hours.

•Eyelid and periorbital vesicles on the lid margin (Fig. 1.42A) that break down over 48 hours.

•Associated papillary conjunctivitis, discharge and lid swelling.

•Dendritic corneal ulcers can develop, especially in atopic patients.

•Gradually settles over 6–8 days.

•Involvement can be very severe in atopic patients (eczema herpeticum – Fig. 1.42B).

3Treatment

•Topical antiviral (aciclovir cream) 5 times daily for 5 days.

•Oral aciclovir 400–800 mg 5 times daily for 3–5 days; famciclovir and valaciclovir are alternatives.

•Add co-amoxiclav or erythromycin for secondary staphylococcal infection in patients with eczema

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herpeticum.

Fig. 1.42 Herpes simplex. (A) Vesicular rash; (B) eczema herpeticum

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Blepharitis

Chronic anterior blepharitis

Chronic marginal blepharitis is a very common cause of ocular discomfort and irritation. Involvement is usually bilateral and symmetrical. Blepharitis may be subdivided into anterior and posterior although there is considerable overlap and both are often present. The poor correlation between symptoms and signs, the uncertain aetiology and mechanisms of the disease process all conspire to make management difficult.

Pathogenesis

Anterior blepharitis affects the area surrounding the bases of the eyelashes and may be staphylococcal or seborrhoeic. The former is thought to be the result of an abnormal cell mediated response to components of the cell wall of S. aureus which may also be responsible for the red eyes and the peripheral corneal infiltrates seen in some patients. Seborrhoeic blepharitis is often associated with generalized seborrhoeic dermatitis that may involve the scalp, nasolabial folds, behind the ears, and the sternum. Because of the intimate relationship between the lids and ocular surface, chronic blepharitis may cause secondary inflammatory and mechanical changes in the conjunctiva and cornea.

Diagnosis

1Symptoms do not provide a reliable clue to the type of blepharitis and are caused by disruption of normal ocular surface function and reduction in tear stability. Because of poor correlation between the severity of symptoms and clinical signs it can be difficult to objectively assess the benefit of treatment.

•Burning, grittiness, mild photophobia, and crusting and redness of the lid margins with remissions and exacerbations are characteristic.

•Symptoms are usually worse in the mornings although in patients with associated dry eye they may increase during the day.

2Signs

aStaphylococcal blepharitis

•Hard scales and crusting mainly located around the bases of the lashes (collarettes; Fig. 1.43A).

•Mild papillary conjunctivitis and chronic conjunctival hyperaemia are common.

•Long-standing cases may develop scarring and notching (tylosis) of the lid margin (Fig. 1.43B), madarosis, trichiasis and poliosis.

•Secondary changes include stye formation, marginal keratitis and occasionally phlyctenulosis.

•Associated tear film instability and dry eye syndrome are common.

bSeborrhoeic blepharitis

•Hyperaemic and greasy anterior lid margins with sticking together of lashes (Fig. 1.43C).

•The scales are soft and located anywhere on the lid margin and lashes.

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Fig. 1.43 Chronic anterior blepharitis. (A) Collarettes; (B) scarring of the lid margin; (C) greasy lid margin with sticky lashes

Treatment

There is little evidence to support any particular treatment protocol for anterior blepharitis. Patients should be advised that a permanent cure is unlikely, but control of symptoms is usually possible.

1Lid hygiene

•A warm compress applied for several minutes to soften crusts at the bases of the lashes.

•Lid cleaning to mechanically remove crusts involves scrubbing the lid margins once or twice daily with a cotton bud dipped in a dilute solution of baby shampoo or sodium bicarbonate.

•Commercially produced soap/alcohol impregnated pads for lid scrubs are available but care should be taken not to induce mechanical irritation.

•The eyelids can also be cleaned with diluted shampoo when washing the hair.

•Gradually, lid hygiene can be performed less frequently as the condition is brought under control but blepharitis often recurs if it is stopped completely.

2Antibiotic

aTopical sodium fusidic acid, bacitracin or chloramphenicol is used to treat acute folliculitis but is of limited value in longstanding cases. Following lid hygiene the ointment should be rubbed onto the anterior lid margin with a cotton bud or clean finger.

bOral azithromycin (500 mg daily for three days) may be helpful to control ulcerative lid margin disease.

3Weak topical steroid such as fluorometholone 0.1% q.i.d. for one week is useful in patients with severe papillary conjunctivitis, marginal keratitis and phlyctenulosis although repeated courses may be required.

4Tear substitutes are required for associated tear film instability and dry eye.

Chronic posterior blepharitis

Pathogenesis

Posterior blepharitis is caused by meibomian gland dysfunction and alterations in meibomian gland secretions. Bacterial lipases may result in the formation of free fatty acids. This increases the melting point of the meibum preventing its expression from the glands, contributing to ocular surface irritation and possibly enabling growth of S. aureus. Loss of the tear film phospholipids that act as surfactants results in increased tear evaporation and osmolarity, and an unstable tear film.

Diagnosis

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