Ocular Herpes Simplex: Keratitis & Emergency Care

Ocular herpes simplex is a recurrent viral eye disease that can injure the corneal surface, deeper cornea, iris, eye pressure system and, rarely, retina. A painful red eye with photophobia, blurred vision, reduced corneal sensation or a branching epithelial lesion needs prompt eye assessment. The first emergency decision is to distinguish active epithelial infection from deeper stromal inflammation: the treatment differs, and a steroid used at the wrong stage can worsen infection and threaten sight.

Emergency rule: Suspected HSV keratitis warrants same-day ophthalmology advice when there is reduced vision, a corneal ulcer or opacity, marked photophobia, contact-lens use, immunosuppression/HIV, a one-eyed patient, raised intraocular pressure, anterior-chamber inflammation, rapid progression, a geographic ulcer, stromal thinning, or uncertainty about bacterial/fungal keratitis. Do not prescribe topical corticosteroid for an undiagnosed red eye or active epithelial dendrite. Steroids have an important role in selected stromal disease only under ophthalmology supervision and with antiviral cover.

Learning objectives

Explain HSV types, transmission, trigeminal latency and recurrence without assuming HSV-1 only affects the mouth or HSV-2 only affects the genital tract.
Recognize primary blepharoconjunctivitis, epithelial dendritic/geographic keratitis, stromal keratitis/endotheliitis, herpetic anterior uveitis and retinal warning signs.
Differentiate an HSV dendrite from VZV pseudodendrite, neurotrophic defect, contact-lens infection and bacterial or fungal ulceration.
Perform a structured emergency history and examination, including acuity, pupils, fluorescein, corneal sensation when trained, anterior chamber and referral triggers.
Choose safe initial actions, know when testing is useful, understand antiviral and steroid principles, and arrange follow-up for recurrence or complications.

Coverage of the supplied 38-slide presentation

The supplied SlideShare page exposes a 38-slide teaching deck. The map below accounts for each numbered slide, including clinical-photo, transition and closing slides. Where the older deck describes recurrence triggers or gives treatment schedules as absolutes, this article retains the teaching point and adds current context, dosing cautions and an emergency-medicine perspective.

Slide	Topic addressed
1	Deck title and setting: herpetic eye disease.
2	Outline: virology, pathogenesis, primary and recurrent disease, investigations, treatment, complications and surgery.
3	Herpesvirus structure, types, DNA genome and latency.
4	Frequency of HSV exposure and recurrent infection; epidemiology interpreted without overgeneralizing older estimates.
5	HSV-1/HSV-2 transmission, trigeminal distribution and primary infection.
6	Neural latency, reactivation and proposed triggers; uncertainty around individual triggers.
7	Primary ocular infection: follicular blepharoconjunctivitis, preauricular node, vesicles and possible epithelial keratitis.
8	Clinical image of periocular/skin vesicles and what to inspect.
9	Clinical image of eyelid-margin ulceration.
10	HSV versus adenoviral conjunctivitis: vesicles, epithelial dendrite and membranes; laterality is not enough.
11	Recurrent ocular HSV presentations and the significance, but not diagnostic certainty, of bilateral disease.
12	Recurrent blepharoconjunctivitis.
13	Epithelial keratitis symptoms: foreign-body sensation, photophobia, redness and blurred vision.
14	Epithelial keratitis signs, dendrites/geographic ulcers, mild stromal response and reduced corneal sensation.
15	Differential diagnosis of a branching epithelial lesion.
16	Clinical image of a dendritic epithelial ulcer.
17	Clinical image of a geographic epithelial ulcer.
18	Stromal keratitis and risk of visual morbidity/recurrence.
19	Non-necrotizing versus necrotizing stromal presentations and symptoms.
20	Interstitial stromal keratitis signs without epithelial ulceration.
21	Disciform keratitis/endotheliitis: edema, keratic precipitates and possible iridocyclitis.
22	Differential diagnosis of stromal disease.
23	Clinical image of interstitial keratitis.
24	Clinical image of disciform keratitis.
25	Image/transition in the stromal-to-necrotizing keratitis sequence.
26	Necrotizing herpetic keratitis, ulceration, corneal vascularization and mimics.
27	Herpetic iridocyclitis, raised pressure/trabeculitis and iris transillumination.
28	Laboratory evaluation: when clinical diagnosis is sufficient and when PCR/culture is useful.
29	Clinical image of iridocyclitis.
30	Transition to management principles.
31	Primary ocular HSV management and limits of what treatment can prevent.
32	Recurrent blepharoconjunctivitis and supportive/antiviral care.
33	Epithelial keratitis management, antiviral choices, toxicity and steroid avoidance.
34	Stromal keratitis: specialist-directed antiviral plus carefully monitored corticosteroid; recurrence prevention.
35	HSV iridocyclitis and inflammation control under ophthalmology care.
36	Complications: epitheliopathy, neurotrophic disease, scarring, vascularization and lipid keratopathy.
37	Selected penetrating keratoplasty and antiviral cover around grafting.
38	Closing slide; consolidated emergency take-home messages.

1. What ocular HSV is

Herpes simplex virus (HSV) is an enveloped, double-stranded DNA virus in the Herpesviridae family. HSV-1 and HSV-2 can both infect the eye. HSV-1 is the more frequent cause of ocular disease in many settings, but the familiar shorthand “HSV-1 above the waist, HSV-2 below the waist” is not a rule: either type can infect the mouth, skin, genital tract or eye. Transmission occurs through direct contact with infectious secretions or lesions, including when the source is not obvious.

After initial infection in skin or mucosa, HSV travels in sensory nerves to a sensory ganglion, most often the trigeminal ganglion for ocular/facial disease. The virus persists in a latent state. Reactivation can send virus back along a nerve branch to the eyelid, conjunctiva or cornea; later episodes may also involve a damaging host inflammatory response. This is why “herpetic eye disease” is not one single lesion and why a person may have recurrences despite treatment of the first episode. Antivirals suppress viral replication; they do not remove latent virus or cure infection.

Many primary infections are asymptomatic or mild. Primary ocular disease classically affects children or young adults and may look like follicular conjunctivitis with eyelid vesicles, small ulcers or blepharitis. Recurrent disease is more often unilateral and corneal, but either primary or recurrent disease can be atypical, bilateral or extensive, particularly with immune dysfunction, atopy or topical steroid exposure. Bilateral disease should prompt a careful review for immune suppression or an alternative diagnosis; it does not establish either.

2. Primary infection, recurrence and the HIV context

Primary ocular infection

Primary infection may produce watery red eye, follicular conjunctival reaction, lid-margin vesicles or ulcers, mild discomfort, a tender preauricular node and sometimes punctate epithelial keratitis. A first episode may be mistaken for adenovirus. Stromal keratitis and uveitis are less common in primary presentation than in reactivation, but they are possible. Fever, malaise or oral lesions may accompany a first infection. Do not infer a person’s exposure history, sexual behaviour or route of infection from ocular disease.

Recurrent infection

Reactivation may present as blepharoconjunctivitis, epithelial keratitis, immune stromal keratitis, endothelial inflammation, anterior uveitis or combinations. Prior episodes, old corneal scars, reduced sensation and a characteristic dendrite increase suspicion. A history of cold sores can help but is often absent. The source deck lists psychological stress, febrile/systemic illness, sunlight, menstruation and contact-lens wear as possible triggers, while also noting that triggers have not been reliably established by the Herpetic Eye Disease Study. Explain that individual episodes often have no identifiable trigger; avoid making the patient feel responsible for recurrence.

HIV and immunosuppression

HSV ocular disease can occur in people with and without HIV. HIV and other immunosuppressive conditions increase concern for prolonged, atypical, bilateral, extensive or treatment-resistant disease, but a dendrite alone is not an HIV test. In a person living with HIV, ask about ART and general clinical status, review renal function before systemic acyclovir when feasible, and coordinate eye care with the HIV team. Do not delay treatment or urgent ophthalmology referral while waiting for a CD4 count or viral load. Acute retinal necrosis and disseminated HSV are uncommon but sight- or life-threatening possibilities when symptoms, examination or immune status point to posterior or systemic disease.

In Uganda, use local consent and confidentiality standards if offering HIV testing. Testing should be voluntary and connected to counselling and follow-up. Avoid stigmatizing language: ocular HSV is not proof of HIV, a particular sexual history, or recent transmission.

3. Clinical syndromes and what they mean

A. Blepharitis and blepharoconjunctivitis

Small clustered vesicles may appear on the eyelid skin or margin, then erode into shallow ulcers or crusts. The conjunctiva is often watery and follicular; a preauricular node may be palpable. Fluorescein may reveal punctate epithelial lesions if the cornea is involved. Inspect lid margins, medial and lateral canthi, brow and periocular skin. Vesicles may already have crusted by the time the patient is seen. A periocular eruption in the ophthalmic division with pain or forehead/nasal involvement may instead represent herpes zoster ophthalmicus (HZO); distinguish HSV from VZV because the skin distribution and systemic treatment pathways differ.

B. Epithelial keratitis: active viral replication

Active epithelial keratitis commonly begins with coarse punctate epithelial disease or small raised vesicles that join into a branching “dendrite.” Classic HSV dendrites have terminal bulbs at the branch ends and stain brightly at the epithelial ulcer bed with fluorescein. Rose bengal or lissamine green can highlight devitalized epithelium at the margins when available. Symptoms include pain, foreign-body sensation, tearing, photophobia, redness and blurred vision. Ciliary flush may be present. Corneal sensation often falls because HSV injures trigeminal corneal nerves; however, sensation may be preserved early, and severe pain does not rule HSV out.

A larger irregular geographic epithelial ulcer can form when branches enlarge or coalesce, especially with topical steroid exposure, atopy or immune compromise. A geographic ulcer is a reason for urgent specialist review because it can heal slowly and scar, and because the differential includes microbial keratitis. A defect can be deceptively painless in an anaesthetic/neurotrophic cornea; examine the cornea carefully even when symptoms seem mild.

Fluorescein findings should be interpreted in context. Fluorescein stains exposed epithelium; it is not an HSV-specific test. A dendritic shape supports HSV but can be mimicked by VZV, healing epithelium, toxic drops, contact-lens injury, neurotrophic disease and Acanthamoeba. A central or large ulcer, stromal infiltrate, hypopyon, purulent discharge, trauma with vegetative material, contact lenses or rapid tissue loss requires bacterial/fungal evaluation rather than assuming HSV and giving antiviral drops alone.

C. Stromal keratitis: immune inflammation and tissue injury

Stromal disease is a major cause of visual loss from ocular HSV. It may be non-necrotizing/interstitial or necrotizing. In non-necrotizing stromal keratitis, the epithelium is often intact and the haze or opacity reflects inflammation within the stroma. There may be one or several areas of stromal infiltrate, edema, thinning or new vessels. Symptoms can be more gradual than epithelial disease: blurred vision, haloes, mild redness or discomfort. Repeat episodes raise the risk of scarring, irregular astigmatism and permanent loss of corneal clarity.

Necrotizing stromal keratitis is less common but more dangerous. There can be epithelial breakdown over an inflamed infiltrate, dense opacity, vascularization, stromal melt and risk of perforation. It may look indistinguishable from bacterial, fungal or Acanthamoeba keratitis at first glance. Treat it as a corneal emergency; urgent ophthalmology must determine sampling and combined therapy. A history of HSV does not exclude a second infection.

D. Endotheliitis/disciform keratitis

HSV endotheliitis can produce a localized round or oval area of corneal edema, sometimes with epithelial edema, keratic precipitates on the posterior corneal surface under the edematous region, Descemet membrane folds and anterior-chamber inflammation. “Disciform keratitis” is a commonly used clinical label for this pattern. The endothelium pumps fluid out of the cornea; dysfunction produces edema and blurred vision. Intraocular pressure may rise if inflammation affects the trabecular meshwork. The appearance overlaps with other viral endotheliitides, so classification and treatment belong with an ophthalmologist.

E. Anterior uveitis / iridocyclitis

HSV may cause unilateral anterior uveitis, with or without obvious epithelial keratitis. Look for pain, photophobia, ciliary flush, a small or irregular pupil, cells and flare, keratic precipitates, localized corneal edema, patchy iris atrophy or transillumination, and elevated intraocular pressure. Trabeculitis and inflammatory cells can obstruct aqueous outflow; pressure can be substantially raised. A unilateral hypertensive uveitis with corneal scars or reduced sensation raises suspicion for HSV, but VZV, CMV, syphilis and non-infectious causes remain in the differential. Do not treat presumed uveitis with steroid drops before excluding epithelial HSV and arranging eye review.

F. Neurotrophic keratopathy / metaherpetic ulcer

Damage to corneal sensory nerves can reduce blinking, tear reflex and epithelial healing. A persistent defect may remain after active virus is controlled and can progress to stromal thinning, infection or perforation. The resulting ulcer may cause surprisingly little pain. This is not necessarily ongoing viral replication, so simply extending antiviral drops can worsen ocular-surface toxicity without healing the defect. Ophthalmology assesses epithelial status, sensation, exposure, tear film and microbial superinfection; lubrication, protection, serum tears, amniotic membrane, tarsorrhaphy or other measures may be needed.

G. Posterior disease and acute retinal necrosis

HSV or VZV can cause acute retinal necrosis, an uncommon but rapidly progressive posterior-segment emergency that can cause retinal detachment and profound visual loss. New floaters, flashes, a curtain/field defect, sudden reduction in vision, vitreous haze or retinal whitening in a person with a herpes history or immunosuppression needs same-day retinal specialist assessment. This presentation is not managed as simple surface keratitis. Initiation of systemic antiviral treatment and possible intravitreal treatment are specialist decisions; do not wait for outpatient routine review if this is suspected.

4. Distinguishing HSV from other red-eye and corneal emergencies

Condition	Helpful clues	Emergency implication
HSV epithelial keratitis	Branching ulcer with terminal bulbs; fluorescein-staining base; reduced corneal sensation; often recurrent and unilateral.	Antiviral treatment and prompt eye review; no steroid monotherapy.
VZV pseudodendrite / HZO	Often elevated, less intensely staining branching lesion without classic terminal bulbs; forehead, lid or nasal rash in V1 distribution may be present. HZO can occur without rash.	Systemic antiviral and urgent ocular assessment when eye involvement is possible.
Adenoviral conjunctivitis	Follicles, watery discharge, possible membranes or pseudomembranes, often sequential bilateral involvement; corneal infiltrates may follow.	Infection-control advice; reconsider HSV if vesicles or dendritic keratitis are present.
Bacterial keratitis	Focal stromal infiltrate with epithelial defect, pain, discharge, contact lens, trauma or rapid progression; may have hypopyon.	Urgent corneal sampling and antimicrobial management by trained eye service.
Fungal keratitis	Trauma with plant/soil matter, feathery infiltrate, satellite lesions or indolent ulcer; common in warm climates.	Urgent corneal assessment and scraping; antiviral-only treatment delays care.
Acanthamoeba keratitis	Contact-lens exposure or contaminated water, pain often out of proportion, perineural infiltrates or ring infiltrate later.	Urgent specialist work-up; early disease may resemble HSV.
Neurotrophic defect/toxic epitheliopathy	Poorly healing smooth-edged defect, reduced sensation, chronic topical medication use; branching healing lines can mimic a dendrite.	Check sensation and medication exposure; avoid repeated toxic drops and arrange eye review.
Acute angle closure	Severe pain/headache, halos, nausea, shallow chamber, fixed mid-dilated pupil and markedly raised pressure; corneal edema can blur fluorescein findings.	Immediate emergency treatment and ophthalmology; do not assume HSV.

More than one process can coexist. A patient with a dendrite may also have bacterial superinfection, and a patient with HZO may have corneal pseudodendrites. If the lesion does not fit, worsens or fails to improve as expected, revisit the diagnosis rather than repeating the same prescription.

5. Emergency history

Onset, duration and progression of redness, pain, tearing, photophobia and blurred vision; sudden versus gradual change.
Previous HSV eye disease, cold sores, recurrent unilateral “pink eye,” corneal scars, grafts, glaucoma or prior ocular surgery.
Periocular rash, grouped vesicles, lid-margin ulcers, facial pain, nose lesions, fever, oral ulcers or other mucocutaneous symptoms.
Contact-lens type and wear, overnight use, water exposure, hygiene, trauma, foreign body, chemical exposure, plant matter and recent procedures.
All eye medicines used, including topical steroids, leftover antibiotics, traditional remedies, topical anesthetic and frequency/duration of antiviral drops.
HIV status when known, ART, transplant, chemotherapy, systemic corticosteroids, atopic dermatitis and other immune-suppressing conditions.
Renal disease, dehydration, pregnancy, drug allergy and medicines that may affect renal function if systemic antiviral treatment is being considered.
Symptoms suggesting posterior disease: floaters, flashes, curtain/field defect, new severe visual loss, headache, diplopia or neurologic symptoms.

6. Emergency examination: a repeatable sequence

Visual acuity first: measure each eye separately with habitual correction and pinhole if appropriate. Record any new asymmetry. Reduced acuity raises urgency even when the external eye looks mildly red.
General and external exam: assess temperature and systemic illness when relevant; inspect brow, forehead, nose, eyelid skin, lid margin and periocular area for vesicles, ulcers, crusts, swelling or rash. Check for proptosis and orbital signs.
Pupils and function: compare pupils, reactivity and relative afferent pupillary defect; assess extraocular movements, diplopia, visual fields when possible, and pain with movement. A new RAPD, field loss or motility deficit suggests disease beyond uncomplicated epithelial keratitis.
Conjunctiva and cornea: inspect discharge, follicles, chemosis and ciliary flush. With fluorescein and cobalt-blue illumination, map epithelial defects, branching edges, terminal bulbs, infiltrates, thinning and leakage. Document location, dimensions and whether the visual axis is involved.
Corneal sensation: compare both eyes before instilling anesthetic, using a clean cotton wisp only if trained and safe. Reduced sensation supports herpetic nerve injury but is not diagnostic. Never use a pin, touch a damaged cornea forcefully, or perform this test if it risks injury.
Anterior chamber and pressure: slit-lamp examination for cells/flare, hypopyon, keratic precipitates, corneal edema and iris changes. Measure IOP only when appropriate, equipment/training are available and open globe is not suspected. Do not press on an injured or potentially perforated eye.
Fundus/retina: assess red reflex and posterior segment when trained and view is possible. Floaters, flashes, field loss or retinal whitening require urgent dilated specialist examination even when the cornea is also affected.
Document and communicate: note laterality, acuity, pupil findings, fluorescein pattern, corneal clarity, IOP if measured, anterior chamber, contact lens status and immune context. A secure clinical photograph can help follow progression if consent and local policy permit.

Do not send a patient away with “viral conjunctivitis” when there is photophobia, reduced acuity, a corneal epithelial defect, opacity, severe pain, abnormal pupil, high pressure or an uncertain diagnosis. Avoid eye patching; it can hinder observation and may encourage microbial growth in an ulcer. Stop contact-lens wear and do not share eye drops. A topical anesthetic may be used by a clinician for examination, but should not be prescribed for home use because repeated use damages the cornea and masks progression.

7. Investigations

Typical recurrent epithelial HSV can often be diagnosed clinically by an experienced eye clinician; testing every classic episode is not necessary. Fluorescein helps identify the defect but does not identify the virus. Serum HSV antibody is generally not useful for diagnosing recurrent ocular disease because past exposure is common and does not prove that a current corneal lesion is HSV.

Consider corneal/lesion PCR, viral culture, antigen testing or other laboratory assessment when the presentation is atypical, severe, bilateral, neonatal, immunocompromised, treatment-resistant or not responding as expected; when distinguishing HSV from VZV or another infection changes management; or when the diagnosis is uncertain. Corneal scraping for microscopy and bacterial/fungal culture may be needed for an ulcer with stromal infiltrate, contact-lens exposure, trauma or possible coinfection. Sampling should be organized by an ophthalmologist/qualified corneal clinician; do not delay urgent treatment of sight-threatening disease to obtain a test that is not immediately available.

With suspected uveitis, glaucoma, retinal necrosis or orbital involvement, investigations are directed by the specialist: IOP and gonioscopy, dilated fundus exam, ocular imaging, aqueous/vitreous PCR in selected cases, and systemic tests based on the differential. HIV testing, if appropriate, follows local confidential consent pathways and is not a substitute for eye examination.

8. Treatment principles by disease layer

Treatment depends on whether disease is on the epithelium, in the stroma/endothelium, inside the anterior chamber, or at the retina. The following adult examples are common reference regimens for teaching; actual drug choice, formulation and duration must follow current Uganda protocols, availability, pregnancy status, renal function, age and ophthalmology advice. Children and neonates require weight-based/specialist dosing. Acyclovir is renally cleared: adjust for renal impairment, maintain appropriate hydration and review nephrotoxic co-medications.

Clinical pattern	Core principle	Important safety point
Primary blepharoconjunctivitis without corneal involvement	Supportive care; an oral antiviral may shorten more significant disease, depending on extent, immune status and eye-service advice.	Re-examine the cornea if pain, photophobia or vision change develops.
Active epithelial dendrite/geographic ulcer	Topical antiviral such as acyclovir 3% ophthalmic ointment five times daily, or an appropriate oral antiviral regimen; local availability and clinician/ophthalmologist guidance determine the choice. Ganciclovir gel is another option where available.	No topical corticosteroid monotherapy. Avoid prolonged topical antiviral courses because surface toxicity can delay healing.
Non-necrotizing stromal keratitis/endotheliitis	Antiviral cover plus carefully titrated topical corticosteroid under ophthalmologist direction; slow taper and monitoring are often required.	Do not start, stop or rapidly taper steroid without eye-service direction; monitor epithelial disease and IOP.
Necrotizing keratitis, melt or perforation risk	Urgent corneal specialist; systemic antiviral and tailored anti-inflammatory/infection management, sampling and possible admission.	Must consider bacterial/fungal coinfection. A perforation is an emergency requiring protection and immediate surgery-capable referral.
Anterior uveitis/trabeculitis	Ophthalmologist-directed systemic antiviral, inflammation control and pressure-lowering therapy where needed.	Topical steroid and cycloplegic use depends on corneal epithelium and specialist assessment; IOP may be very high.
Acute retinal necrosis / disseminated disease	Emergency retina/infectious disease assessment; systemic antiviral treatment, sometimes IV or intravitreal therapy.	Do not manage as uncomplicated outpatient keratitis or wait for routine review.

Practical epithelial keratitis details

Uganda’s Clinical Guidelines for eye conditions list acyclovir ophthalmic ointment five times daily for herpes simplex/viral keratitis and warn against topical corticosteroids in infective keratitis. A topical antiviral course is usually limited to the period needed for epithelial healing according to the product and eye clinician; extended frequent dosing can produce epitheliopathy. Where oral therapy is selected, common adult regimens for epithelial HSV use oral acyclovir 400 mg five times daily for about 7–10 days; dosing varies across guidelines and patient groups. The ophthalmologist may choose topical acyclovir, ganciclovir, trifluridine or oral acyclovir/valacyclovir based on access, disease extent, tolerance and clinical history. Check renal function and dose adjustment when systemic treatment is given.

Routine mechanical debridement is not a general emergency-department treatment. An eye specialist may consider debridement in selected cases, but it can injure healthy epithelium and should not be done without a clear indication, adequate magnification and follow-up. Do not prescribe prophylactic topical antibiotic automatically for every classic dendrite; use it only if indicated by epithelial defect, contamination, superinfection concern or local ophthalmology protocol.

Steroids: a distinction students must retain

For active HSV epithelial keratitis, topical steroid can enlarge the dendrite into a geographic ulcer, increase viral replication and delay healing; avoid it unless an ophthalmologist has a specific, covered plan. In non-necrotizing stromal keratitis, inflammation itself can scar the cornea. Controlled trials support specialist-supervised topical corticosteroid with antiviral cover to reduce persistence/progression and shorten inflammation. The dose is tapered gradually according to response; abrupt withdrawal can cause rebound inflammation. Steroids can raise IOP and increase infection risk, so follow-up must assess pressure, epithelium and stromal response.

The treatment depends on the affected corneal layer: avoid steroid monotherapy while virus is actively replicating in the epithelium; consider topical steroid only for selected stromal inflammation under specialist supervision and with antiviral cover. When the corneal layer cannot be determined, withhold unsupervised steroid and arrange urgent ophthalmology advice.

Uveitis and pressure control

Herpetic uveitis often requires antiviral therapy plus anti-inflammatory treatment and a cycloplegic for pain/synechiae prevention, all selected by ophthalmology. Raised pressure may require topical aqueous-suppressant therapy; drug choice depends on contraindications, pregnancy, respiratory/cardiac history and the clinical context. Avoid starting a miotic or steroid without appropriate assessment. Urgent referral is particularly important with very high IOP, corneal edema, reduced acuity, severe pain, abnormal pupil or a one-eyed patient.

HIV, severe disease and resistance

For people with HIV or other immunosuppression, use a lower threshold for urgent specialist review and more reliable follow-up. Extensive, bilateral, progressive, disseminated or posterior disease may need higher-dose systemic or intravenous antiviral therapy and inpatient care. If a lesion persists or progresses despite an appropriate course, review adherence, diagnosis, drug formulation, renal-adjusted dose, possible coinfection and resistance. Acyclovir resistance is uncommon in immunocompetent patients but matters in immunocompromised patients with nonhealing disease; discuss resistant HSV with infectious disease/ophthalmology rather than simply extending ineffective drops.

9. Admission, referral and disposition

Immediate/same-day eye service or hospital discussion

Any new reduction in visual acuity, central/large dendrite, geographic ulcer, stromal infiltrate or opacity, corneal thinning, melt or suspected perforation.
Marked pain or photophobia, abnormal pupil, anterior-chamber cells/hypopyon, high IOP, corneal edema, suspected uveitis/endotheliitis or inability to examine safely.
Contact-lens wearer, recent trauma, organic material exposure, possible bacterial/fungal/Acanthamoeba keratitis or uncertain diagnosis.
Known HIV/immunosuppression with bilateral, atypical, severe, recurrent or nonhealing disease; inability to take/absorb medication or unreliable follow-up.
Floaters, flashes, curtain/field defect, new severe visual loss, retinal whitening or suspected acute retinal necrosis.
Neonate/young infant with vesicles, red eye or suspected HSV exposure; possible neonatal herpes needs urgent paediatric and ophthalmology assessment.

What emergency medicine can do while arranging review

Protect the eye from rubbing/contamination; remove contact lenses and keep them for possible microbiology if requested.
Record acuity and key ocular findings before treatment when safe; avoid pressure on a potentially open globe.
Do not patch, dispense topical steroid, use topical anesthetic at home or attempt corneal debridement.
Start an antiviral only when indicated by local protocol and available eye-service advice; do not let an empiric prescription replace urgent referral or exclude a bacterial/fungal ulcer.
Provide simple analgesia and lubrication as appropriate; consider cycloplegic only under trained clinician/ophthalmology protocol.
Arrange a definite review time and transport/pathway. If specialist review is unavailable locally, contact the nearest referral centre directly and document the handover.

A stable patient with a small peripheral epithelial dendrite and good acuity may be managed as an outpatient only when an ophthalmologist/qualified eye clinician agrees, antiviral therapy is available, adherence is realistic and review is arranged within about 24–48 hours or the interval specified by the eye team. Worsening pain, new blur, enlarging lesion, discharge, increased redness or inability to return requires earlier reassessment. Stromal, uveitic and retinal disease should not be placed on a routine outpatient pathway without specialist oversight.

10. Complications and longer-term care

Corneal scar and irregular astigmatism: repeated stromal episodes, ulceration or delayed healing can permanently reduce vision.
Corneal neovascularization and lipid keratopathy: chronic inflammation can bring vessels into the normally clear cornea; lipid may deposit around vessels.
Neurotrophic keratopathy: sensory loss causes recurrent/persistent epithelial breakdown and may lead to infection, thinning or perforation.
Medication toxicity: frequent topical antivirals can damage epithelium; preservatives and multiple drops also contribute.
Secondary glaucoma and cataract: uveitis/trabeculitis and repeated or prolonged steroid exposure may raise pressure or cloud the lens.
Corneal melt or perforation: a thinned or leaking cornea needs emergency protection and surgical-capable ophthalmology.
Retinal detachment after acute retinal necrosis: a posterior complication requiring retina-specialist monitoring and treatment.
Amblyopia in children: visual-axis scarring or prolonged blur during visual development can impair vision; prompt paediatric eye review is essential.

Follow-up should verify epithelial closure, reduction of stromal inflammation, stable IOP and visual recovery. The appropriate interval depends on layer, severity, treatment and response. Recheck sooner for epithelial defects, steroids, pressure elevation, immunosuppression or suspected microbial coinfection. A patient with repeated stromal disease may be offered oral suppressive acyclovir, commonly 400 mg twice daily for 12 months in the HEDS prevention trial population, after the acute episode resolves. This is a specialist prevention decision; renal insufficiency and prior keratoplasty were among the factors excluded from the trial, and the evidence does not mean every first episode needs long-term therapy.

Surgery and corneal grafting

Penetrating keratoplasty may be considered for visually significant scarring, severe thinning/perforation or a cornea too damaged to restore function by nonsurgical means. Grafting during active HSV carries substantial recurrence and graft-failure risk. Corneal surgeons plan timing, antiviral prophylaxis and careful topical-steroid use. Emergency clinicians should know that grafting is a selected reconstructive/sight-restoring intervention, not an acute treatment for a simple dendrite.

11. Patient counselling and prevention

Explain that HSV can remain latent and recur; treatment controls active disease but does not eradicate the virus.
Encourage handwashing before and after touching the face/eye, avoid rubbing, and do not touch a cold sore then the eye. Avoid sharing towels, eye cosmetics or eye drops during active lesions.
Stop contact-lens use during active eye disease; resume only when the eye clinician says the surface has healed and lenses/case have been appropriately replaced or cleaned.
Take antiviral medicine for the full prescribed course; do not use another person’s medication, leftover steroid drops or topical anesthetic at home.
Keep the follow-up appointment even if redness improves; stromal inflammation or pressure problems can evolve after surface symptoms change.
Seek urgent care for worse blur, pain, photophobia, new floaters/flashes, a curtain in the visual field, swelling or a new rash around the eye.
Discuss recurrent disease without blame. Triggers are uncertain, and recurrence can happen without a preventable cause.

12. Case-based application

Case 1: painful unilateral red eye

A 27-year-old has 2 days of unilateral pain, photophobia and tearing. Vision is slightly reduced. Fluorescein shows a branching epithelial defect with terminal bulbs; corneal sensation is lower than in the other eye. No contact lenses, trauma or stromal infiltrate.

Interpretation: Classic epithelial HSV keratitis is likely. Document visual acuity and ulcer location, avoid steroid, arrange same-day or prompt ophthalmology review and antiviral treatment through the local pathway. Recheck to confirm healing. Reduced sensation supports but does not prove HSV.

Case 2: red eye after steroid drops

A patient with a prior “viral red eye” has used leftover prednisolone for a week. The corneal lesion is now a broad geographic ulcer and vision is worse.

Interpretation: Steroid-exacerbated active epithelial HSV is possible, but bacterial/fungal coinfection and other ulcerative keratitis must be excluded. This is an urgent corneal referral. Do not continue unsupervised steroid or assume the original diagnosis was correct.

Case 3: quiet pain, nonhealing defect

A 63-year-old with previous HSV keratitis has a persistent epithelial defect but reports little pain. There is reduced corneal sensation and mild stromal thinning.

Interpretation: Neurotrophic keratopathy is likely; an active viral ulcer is not the only explanation. Urgent ophthalmology should assess for infection, thinning and exposure. Repeated antiviral drops alone may increase toxicity and delay healing.

Case 4: red eye with high pressure and irregular pupil

A 44-year-old has unilateral blurred vision, photophobia, keratic precipitates and a markedly raised IOP. There is patchy iris atrophy and a faint old corneal scar.

Interpretation: Herpetic hypertensive anterior uveitis/trabeculitis is possible. Same-day ophthalmology is needed for antiviral, anti-inflammatory and pressure-lowering treatment. Steroid initiation and taper must be supervised; check the corneal epithelium.

Case 5: flashes and floaters in an immunosuppressed patient

A patient receiving immunosuppressive therapy develops sudden floaters, flashes and a field defect. There is little external redness.

Interpretation: Retinal tear/detachment and acute retinal necrosis are urgent possibilities. Arrange immediate retina-capable assessment; a quiet anterior eye does not make this low risk.

13. Knowledge check

What is the key clinical distinction between a typical HSV dendrite and a VZV pseudodendrite?
Why can reduced corneal sensation coexist with a persistent ulcer but little pain?
Which disease compartment generally should not receive topical steroid monotherapy?
When can topical corticosteroid be useful in ocular HSV, and what must accompany it?
Why is fluorescein staining not a confirmatory HSV test?
Name three reasons to arrange same-day ophthalmology review.
Which symptoms suggest posterior-segment disease rather than uncomplicated keratitis?
What is the role of oral acyclovir prophylaxis in recurrent stromal disease?

Answers

HSV dendrites classically branch with terminal bulbs and a fluorescein-staining ulcer bed; VZV pseudodendrites are often elevated and lack classic terminal bulbs, but overlap exists.
HSV injures corneal sensory nerves, leading to anaesthesia, impaired blinking/tearing and poor epithelial repair; the ulcer may be neurotrophic and surprisingly painless.
Active epithelial keratitis with viral replication should not receive steroid alone.
Selected stromal/endothelial inflammation may need a carefully monitored steroid taper under ophthalmology, with antiviral cover and IOP/epithelium follow-up.
It shows exposed epithelium, not the pathogen; HSV, VZV, trauma, toxic injury and other ulcers can stain.
Examples include reduced acuity, central/geographic ulcer, stromal infiltrate or thinning, high pressure/uveitis, immunosuppression, contact-lens ulcer, uncertain bacterial/fungal disease, or inability to follow up.
Floaters, flashes, curtain/field defect, sudden major visual loss or suspected retinal whitening/necrosis.
For selected recurrent disease—especially a history of stromal keratitis—specialists may prescribe suppressive oral acyclovir after active disease resolves. In HEDS, 400 mg twice daily for 12 months reduced recurrence; this is not automatic treatment for every first episode.

Key takeaways

HSV can affect the eyelid, conjunctiva, corneal epithelium, stroma/endothelium, anterior chamber and retina.
Record visual acuity and inspect the cornea with fluorescein in a painful or photophobic red eye.
Terminal-bulb dendrites support HSV, but atypical ulcers still need assessment for VZV, bacterial, fungal, Acanthamoeba and neurotrophic disease.
Never treat an active epithelial dendrite with unsupervised topical steroid. Steroids may be needed for selected stromal disease only with antiviral cover and ophthalmology monitoring.
Vision loss, corneal opacity/thinning, raised IOP, uveitis, HIV/immunosuppression, contact-lens use or retinal symptoms lower the threshold for urgent referral.
Long-term antiviral suppression is considered for selected recurrent disease, especially stromal recurrences; it does not cure latent HSV.

References and further reading

For emergency medicine education. Follow current Uganda Ministry of Health protocols, local drug availability, referral pathways and ophthalmology advice. This material does not replace in-person eye assessment.