It constitutes approximately 10 percent of all cases of herpes zoster.
Etiology
Varicella zoster virus. It is a DNA virus and produces acidophilic intranuclear inclusion bodies. It is neurotropic in nature.Comprehensive OPHTHALMOLOGY
Mode of infection. The infection is contracted in childhood, which manifests as chickenpox and the child develops immunity. The virus then remains dormant in the sensory ganglion of trigeminal nerve.It is thought that, usually in elderly people (can occur at any age) with depressed cellular immunity, the virus reactivates, replicates and travels down along one or more of the branches of the ophthalmic division of the fifth nerve.
Clinical features
In herpes zoster ophthalmicus, frontal nerve is more frequently affected than the lacrimal and nasociliary nerves.About 50 percent cases of herpes zoster ophthalmicus get ocular complications.
The Hutchinson's rule, which implies that ocular involvement is frequent if the side or tip of nose presents vesicles (cutaneous involvement of nasociliary nerve), is useful but not infallible.
Lesions of herpes zoster are strictly limited to one side of the midline of head.
Clinical phases of H. zoster ophthalmicus are :
1. Acute, which may totally resolve.
2. Chronic, which may persist for years.
3. Relapsing, where the acute or chronic lesions reappear sometimes years later.
Clinical features of herpes zoster ophthalmicus include general features, cutaneous lesions and ocular lesions. In addition, there may be associated other neurological complications as described below:
A. General features. The onset of illness is sudden with fever, malaise and severe neuralgic pain along the course of the affected nerve. The distribution of pain is so characteristic of zoster that it usually arouses suspicion of the nature of the disease before appearance of vesicles.
B. Cutaneous lesions. Cutaneous lesions in the area of distribution of the involved nerve appear usually after 3-4 days of onset of the disease. To begin with, the skin of lids and other affected areas become red and oedematous (mimicking erysipelas), followed by vesicle formation. In due course of time vesicles are converted into pustules, which subsequently burst to become crusting ulcers. When crusts are shed, permanent pitted scars are left. The active eruptive phase lasts for about 3 weeks.
Main symptom is severe neuralgic pain which usually diminishes with the subsidence of eruptive phase, but sometimes it may persist for years with little diminution of intensity. There occurs some anaesthesia of the affected skin which when associated with continued post-herpetic neuralgia is called anaesthesia dolorosa.
C. Ocular lesions. Ocular complications usually appear at the subsidence of skin eruptions and may present as a combination of two or more of the following lesions:
1. Conjunctivitis is one of the most common complication of herpes zoster. It may occur as mucopurulent conjunctivitis with petechial haemorrhages or acute follicular conjunctivitis with regional lymphadenopathy. Sometimes, severe necrotizing membranous inflammation may be seen.
2. Zoster keratitis occurs in 40 percent of all patients and sometimes may precede the neuralgia or skin lesions. It may occur in several forms, which in order of chronological clinical occurrence are :
- Fine or coarse punctate epithelial keratitis.
- Microdendritic epithelial ulcers. These unlike dendritic ulcers of herpes simplex are usually peripheral and stellate rather than exactly dendritic in shape. It contrast to Herpes simplex dendrites, they have tapered ends which lack bulbs.
- Nummular keratitis is seen in about one-third number of total cases. It typically occurs as multiple tiny granular deposits surrounded by a halo of stromal haze.
- Disciform keratitis occurs in about 50 percent of cases and is always preceded by nummular keratitis.
D. Associated neurological complications. Herpes zoster ophthalmicus may also be associated with other neurological complications such as :
1. Motor nerve palsies especially third, fourth, sixth and seventh.
2. Optic neuritis occurs in about 1 percent of cases.
3. Encephalitis occurs rarely with severe infection.
Herpes zoster ophthalmicus treatment
Therapeutic approach to herpes zoster ophthalmicus should be vigorous and aimed at preventing severe devastating ocular complications and promoting rapid healing of the skin lesions without the formation of massive crusts which result in scarring of the nerves and postherpetic neuralgia. The following regime may be followed:I. Systemic therapy for herpes zoster :
1. Oral antiviral drugs. These significantly decrease pain, curtail vesiculation, stop viral progression and reduce the incidence as well as severity of keratitis and iritis. In order to be effective, the treatment should be started immediately after the onset of rash. It has no effect on post herpetic neuralgia.
- Acyclovir in a dose of 800 mg 5 times a day for 10 days, or
- Valaciclovir in a dose of 500mg TDS.
2. Analgesics. Pain during the first 2 weeks of an attack is very severe and should be treated by analgesics such as combination of mephenamic acid and paracetamol or pentazocin or even pethidine (when very severe).
3. Systemic steroids. They appear to inhibit development of post-herpetic neuralgia when given in high doses. However, the risk of high doses of steroids in elderly should always be taken into consideration. Steroids are commonly recommended in cases developing neurological complications such as third nerve palsy and optic neuritis.
4. Cimetidine in a dose of 300 mg QID for 2-3 weeks starting within 48-72 hours of onset has also been shown to reduce pain and pruritis in acute zoster - presumably by histamine blockade.
5. Amitriptyline should be used to relieve the accompanying depression in acute phase.
Types of zoster keratitis
A. Punctate epithelial keratitis.B. Microdendritic epithelial ulcer.
C. Nummular keratitis.
D. Disciform keratitis.
3. Episcleritis and scleritis occur in about one-half of the cases. These usually appear at the onset of the rash but are frequently concealed by the overlying conjunctivitis.
4. Iridocyclitis is of a frequent occurrence and may or may not be associated with keratitis. There may be associated hypopyon and hyphaema (acute haemorrhagic uveitis).
5. Acute retinal necrosis may occurs in some cases.
6. Anterior segment necrosis and phthisis bulbi. It may also result from zoster vasculitis and ischemia.
7. Secondary glaucoma. It may occur due to trabeculitis in early stages and synechial angle closure in late stages.
II. Local therapy for skin lesions.
1. Antibiotic-corticosteroid skin ointment or lotions. These should be used three times a day till skin lesions heal.
2. No calamine lotion. Cool zinc calamine application, as advocated earlier, is better avoided, as it promotes crust formation.
III. Local therapy for ocular lesions.
1. For zoster keratitis, iridocyctitis and scleritis :
a. Topical steroid eye drops 4 times a day.
b. Cycloplegics such as cyclopentolate eyedrops BD or atropine eye ointment OD.
c. Topical acyclovir 3 percent eye ointment should be instilled 5 times a day for about 2 weeks.
2. To prevent secondary infections topical antibiotics are used.
3. For secondary glaucoma
a. 0.5 percent timolol or 0.5% betaxolol drops BD.
b. Acetazolamide 250 mg QID.
4. For neuroparalytic corneal ulcer caused by herpes zoster, lateral tarsorrhaphy should be performed.
5. For persistent epithelial defects use : Lubricating artificial tear drops, and Bandage soft contact lens.
6. Keratoplasty. It may be required for visual rehabilitation of zoster-patients with dense scarring. However, these are poor risk patients.
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