Herpes Zoster Ophthalmicus
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Herpes Zoster Ophthalmicus
- 1. Herpes Zoster Ophthalmicus (HZO) Presented by SEA Bunseng, First Year Resident Khmer Soviet Friendship Hospital
- 2. Outline I. What is Herpes Zoster Ophthalmicus (HZO)? II. Anatomy of CN V III. Pathophysiology IV. Risk of Ocular Involvement V. Clinical Manifestation VI. Management
- 3. I. What is Herpes Zoster Opthalmiscus (HZO)? ❖ known as shingles/Zoster, is a viral disease characterized by a painful skin rash in one or more dermatome distributions of the fifth cranial nerve, shared by the eye and orbit.
- 4. II. Anatomy of CN V
- 5. III. Pathophysiology Following Primary infection of VZV Dorsal Root of Sensory neural Ganglion Dormant Activated VZV VZV specific cell mediated immunity faded Central Nervous System Dermatologic involvement Optical system Auditory System
- 6. IV. Risk of Ocular Involvement ✤ Hutchinson Sign ✤ Age ✤ AIDS
- 7. V. Clinical Manifestation A. Acute Shingle ✴ A Prodromal Phase ✴ Skin Lesions ✴ Disseminated Zoster
- 8. V. Clinical Manifestation . Vesicles B. Confluent crusting Haemorrhagic sh with volvement of oth the phthalmic and axillary nerve D. Residual Scarring
- 9. V. Clinical Manifestation B. Acute Eye Diseases ❖ Conjunctivitis (follicular and/or papillary) ❖ Episcleritis, Scleritis ❖ Keratitis (Acute Epithelial, Nummular, Stromal, Disciform) ❖ Anterior Uveitis with Sectoral iris ischeamia and atrophy ❖ IOP elevated ❖ Retinitis, choroiditis ❖ Neurological Complication
- 10. V. Clinical Manifestation A. Dendritic epithelial lesions with tapered ends B. Nummular keratitis C. Stromal Keratitis
- 11. V. Clinical Manifestation C. Chronic Eye Diseases ❖ Neurotrophic keratitis 50% cases ❖ Scleritis patchy slceral atrophy ❖ Mucous plaque keratitis 5%, between 3rd and 6th month ❖ Lipid degeneration in eye with persistent severe nummular or disci form keratitis ❖ Lipid-filled granulomata under tarsal conjunctiva together with subconjunctival scarring ❖ Eyelid scarring result in ptosis, cicatrices entropion and occasionally ectropion
- 12. V. Clinical Manifestation A. Scleral atrophy B. Mucous Plaque Keratitis C. Lipid filled granuloma Cicatricial entropion Cicatricial ectropion
- 13. V. Clinical Manifestation D. Postherpetic Neuralgia ❖ Pain persist > 1 month after rash healed ❖ 75% of patient over 70 Yrs ❖ Pain (Constant or intermittent), worse at night and aggravated by minor stimuli, touch and heat.
- 14. VI. Management A. Acute Shingles ✦ Oral Aciclovir 800mg 5t/day for 7-10 days, start within 72 hours of onset ✦ Intravenous aciclovir 5-10mg/kg t.i.d is indicated for encephalits ✦ Other Oral antiviral agents Valaciclovir 1g tid, famiciclovir 500mg tid and brivudine 125mg qd ✦ Systemic steroids (prednisone 40-60 mg daily) ✦ Symptomatic Remember it’s contagious to get ChickenPox
- 15. VI. Management B. Ocular Involvement 1. Conjunctival involvement: Cool compress and erythromycin ointment b.i.d 2. SPK: lubrication with preservative-free artificial tears q1-2h and ointment q.h.s 3. Corneal or conjunctival pseudodentrites: lubrication with preservative-free artificial tears q1-2h, topical antivirals (e.g ganciclovir 0.15% or vidarabine 3% ointment) tid or aid 4. Immune stromal keratitis: topical steroid (prednisonelone acetate 1%) tapering over months to years using weaker steroids and less than daily dosing 5. Uveitis (with or without immune stromal keratitis): Topical Steroid (prednisolone acetate 1%) and cycloplegic (scopolamine o.25% bid) Treat increased IOP with aggressive aqueous suppression; avoid prostaglandin analogues
- 16. VI. Management B. Ocular Involvement 6. Neurotrophic Keratitis: treat mild epithelial defects with erythromycin ointment 4-8 times/days. if corneal ulceration occurs, smears and cultures to rule out infection. If sterile, no response to ointment, consider a bandage contact lens, tarsorrhaphy, amniotic membrane graft or conjunctival flap. 7. Retinitis, choroiditis, optic neuritis or cranial nerve palsy: Acyclovr 5-10 mg/kg i.v q8h for 1 week and prenisolone 60mg p.o for 3 days, then taper over 1 week. Management of Acute retinal necrosis may require intraocular antivirales. 8. Increased IOP: maybe steroid response or secondary to inflammation. if uveitis, increase frequency of steroid for a few days and use topical aqueous suppressants eg. timolol 0.5% bid, brimonidine 0.2% tid or dorzolamide 2% tie. Oral carbonic anhydrase inhibitors if IOP > 30mmhg. If IOP still increased but inflammation controlled, substitue fluorometholone 0.25%, rimexolone 1% or loteprednol 0.5% drops for prednisolone acetate and taper dose
- 17. References ✴Section 8, External Disease and Cornea. (2012-2013). The American Association of Ophthalmology. page: 119-122 ✴Kenski, J. Jack. MD, (2011). Clinical Ophthalmology: A Systemic Approach, 7th Edition. Elsevier Saunders, UK. page: 248-253 ✴Ehlers, Justis, P.; Shah, Chirag, P. (2008). Will’s Eye Manual, The Office and Emergency Room Diagnosis and Treatment of Eye Diseases, 5th Edition. Lippincott Williams & Wilkins ✴http://emedicine.medscape.com/article/1132465-overview ✴http://eyewiki.aao.org/Herpes_Zoster_Ophthalmicus
Notas del editor
- VZV is one of Human Herpes Virus (HHV). There are 8 recognised of Human Herpes virus Type 1: HSV1 (herpes Simplex virus 1): Infection above the waist (orofacial and ocular infection etc) Type 2: HSV 2 (Herpes Simplelx virus 2): below the waist (genital infection) Type 3: VZV (Varicella-Zoster Virus): Varicelle (Chicken pox) and herpes zoster (Shingle) Type 4: EBV (Epstein-Barr Virus) Type 5: CMV (Cytomegalovirus) Type 6, 7: Rose-olovirus: Roseola infantum and encephalitis Type 8: Associated with Kaposi sarcoma and HIV lymphomas.
- CN V- largest and most complex of 12 CN, Mix nerve (Sensory and motor), supplies sensations to face, mucous membranes and other structure of head. motor for the muscles of mastication and contains proprioceptive fibbers. Exit the brain by a large sensory root and smaller motor root coming out of the pons at its junction with middle cerebral peduncle. join gasserian gg in the meckel cave. 3 branches: Ophthalmic, maxillary and mandicular leave skull through 3 separate foramina: superior orbital fissure, foramen rotundum and foramen oval. Ophthalmic V1 (Sensory) have 3 branches: Frontal Nerve: Supraorbital nerve: upper lid, frontalis muscle, scalp Supratrochlear nerve: conjunctiva, upper lid, forehead Lacrimal nerve: receive branches of zygomatic nerve of maxillary: lacrimal glance Conjuntiva and apparelled Nasocilliary: Anterior ethmoid : Frontal, anterior ethmoid sinuses Branches to cilliary gg: anterior septum, nasal wall Posterior ethmoid: Cornea, iris, cilliary body 2-3 long ciliary nerve: Posterior ethmoid sphenoid sinus Maxillary V2 (Sensory) lower eyelid and cheek, the nares and upper lip, the upper teeth and gums, the nasal mucosa, the palate and roof of the pharynx, the maxillary, ethmoid and sphenoid sinuses and parts of the meninges. 3 branches: zygomatic, pterygopalatine and posterior superior alveolar nerves. Maxillary V3 (Sensory & motor): Sensory: lowerlip, lower teeth, gums, chin and jaw, touch/position and pain/temperature sensations from the mouth. 9 branches: Recurrent meningeal nerve Medial pterygoid nerve Masseteric nerve Deep temporal nerves Lateral ptergoid nerve Buccal nerve Auriculotemporal nerve Lingual nerve Inferior alveolar nerve
- VZV immunity faded due to aging, immunosuppressive therapy, psychological stress, or other factors. CNS- Anterior horn lead to muscular weakness, Cranial nerve palsies, diaphragmatic paralysis, neurogenic bladder, and colonic pseudo obstruction, (Winder involvement) Guillain barre syndrome, transverse myelitis and myositis. Severely, Meningoencephalitis or encephalitis. Dermatologic involvement- cutaneous rash Optical System- (Ramsay Hunt syndrome, geniculate neuralgia, or herpes zoster auricularis) Vesicular eruptions may manifest on the pinna, tragus, or tympanic membrane or in the auditory canal, as well as anywhere in the facial nerve distribution. The patient may experience hearing impairment, nystagmus, vertigo, or a facial nerve palsy mimicking Bell palsy.
- Hutchinson Sign: Involvement of Skin supplied by the external nasal nerve, a branch of the nasociliary nerve supplying the tip, side and root of the nose. The sign correlates strongly with ocular involvement although there is no correlation between the severity of the rash and the severity of ocular complications. Age: frequently in the 6th and 7th decades. Elderly, sign & symptoms tend to be more severe and to be of longer duration. AIDS: Shingles can be early indicator of HIV infection. The development of Shingles in children or young adults should be prompt a search for immunodeficiency or malignancy, though found in only a minority.
- A Prodromal Phase: Precedes appearance of the rash. last 3-5 days and is characterised by tiredness, fever, malaise and headache. Symptoms on dermatome: 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. Skin Lesions: Rash respect midline- distinguishing Shingle from HSV Erythematous areas with a maculopapular rash, may confused with cellulitis or contact dermatitis. 24H, groups of vesicles appear and these become confluent over 2-4 days Rash does not affect the lower lid in HZO, but boggy odema of upper and lower eyelids is common. Vesicles often pass through a pustular before they crust and dry after 2-3 weeks Large, deep haemorrhage lesions are more common in immunodeifcient patients. Lesion heal to leave residual skin destruction and depigmented scars. Disseminated 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.
- Conjunctivitis: associated with lid margin vesicles. Episcleritis: occurs at onset of the rash and usually resolves spontaneously. Scleritis & sclerokeratitis: uncommon, end of first week. Acute Epithelial: 50% in 2 days of onset of rash, resolve spontaneously within a few days, characterised by dentritic lesions which are smaller and finer than herpes simplex and have a taper ends with terminal bulbs. Stained better with Rose Bengal than fluorescein. Nummular: at site of epithelial lesions about 10 days after onset of the rash. Charaterised by fine granular sub epithelial deposits surrounded by a halo of stromal haze. Lesions fade in respond to steroids. Stromal Keratitis: 5% of cases 3 weeks after onset of rash, respond to topical steroids, chronic need slow tapering. Disciform keratitis: (immune-mediated endothelilits), less common than herpes simplex infection, may lead to cornea decompensation. Anterior uveitis: 1/3 of patients with sectoral iris ischaemia and atrophy Neurological complication: CN palsies ( CN3, 4 and 6), Optic neuritis (rare), CNS manifestation: encephalitis, cranial arteritis, guillain-barre syn.
- Mucous Plaque keratits: sudden appearance of elevated mucous plaques that stain with rose bengal.
- Systemic steroids used with antiviral. have moderate effect to reduce acute pain and accelerate skin healing but no effect on the incident or severity of postherpetic neuralgia. Symptomatic: treatment of skin lesions is by drying, antisepsis and cold compresses.