The red eye is one of the commonest ophthalmic complaints in patients presenting to non-ophthalmologists. The myriad of aetiology can pose diagnostic difficulties, particularly in settings with non-specialist equipment. A red eye can result from ocular, adnexal or systemic pathologies.

History taking

This should consist of a general history and a more focused ophthalmic history.

General history 

This should aim to elicit history of systemic conditions with known ocular complications, use of oculotoxic drugs, and any history of intercurrent or recent illness.

Ophthalmic history 

History of presenting complaint:

• Onset and duration
• Laterality
• Pain history using a SOCRATES approach, important to distinguish periorbital from ocular pain
• Appearance of the eye
  • Redness, swelling or lumps in the eyelids
  • Redness of the conjunctiva or sclera, visible lesions
  • Cloudiness of the cornea
• Discharge – colour and onset
• Foreign body sensation or itching
• Photophobia
• Visual symptoms such as decreased/blurred vision, diplopia, scotomas and transient visual obscurations
• Possible precipitants such as trauma or chemical injury
• Previous episodes
  • Past ocular history – refractive errors, contact lens wear, previous ocular surgery, congenital problems, chronic eye conditions
  • Drugs applied directly to the eye or peri-ocularly
  • Family history of ophthalmic conditions

References 

• Leibowitz HM. The Red Eye. http://dx.doi.org/101056/NEJM200008033430507 2009; 343: 345–351.
• Diagnosis | Diagnosis | Red eye | CKS | NICE, https://cks.nice.org.uk/topics/red-eye/diagnosis/diagnosis/(accessed 5 May 2022).
• Smith J, Severn P, Clarke L. Assessment of red eye Straight to the point of care. BMJ Best Pract  2022; 1–118.

Clinical examination 

The non-affected eye should also be examined as it gives an idea of the baseline appearance of the patient’s eyes. Clinical examination should include:

• Visual acuity check using a Snellen chart at 6 metres
• Examine the pupils
  • Check for asymmetry in dim and bright light
  • Check for abnormalities of shape or size
  • Check pupillary reactions to light – direct, consensual and presence of a relative afferent pupillary defect
• Examination of the eyelids looking for redness, swelling, lumps, trichiasis, abnormalities of position such as ptosis, entropion and ectropion, and abnormal shapes
• Examination of the conjunctiva to include eversion of the upper lid, checking for foreign bodies, if available, stain with fluorescein and examine under a blue filter on the ophthalmolscope. Check for redness, including location and pattern, such as ciliary (pattern of dilated vessels around the cornea indicating uvea pathology) or conjunctival which is more diffuse
• Examine the cornea for cloudy areas and staining epithelial defects

Based on NICE guidelines, red flag signs and symptoms which may indicate a serious and potentially sight-threatening cause of the person’s red eye include:

• Reduced visual acuity.
• Moderate to severe pain.
• Headache.
• Photophobia — this can be a symptom of acute uveitis, corneal ulcer, contact lens-related red eye, or corneal foreign body. However, systemic causes of photophobia, such as meningitis, should also be considered.
• Significant ciliary injection.
• Fluorescein staining indicating a significant corneal ulcer.
• Unequal or misshapen pupils, or abnormal pupillary reactions.
• Pain on pupillary constriction.
• Loss of red reflex.
• Corneal defect/haze.
• Hyphaema (blood in the anterior chamber) or hypopyon (pus in the anterior chamber).

Other red flag features include:

• A high-velocity injury (for example, injuries occurring while hammering or chiselling), or injuries involving glass.
• Foreign body or penetrating lesion.
• Serious chemical eye injury.
• Contact lens use.
• Conjunctivitis in an infant in the first 28 days of life.

Diagnostic algorithm

The limited exposure to Ophthalmology in the undergraduate medical curriculum means the diversity of possible diagnoses with a red eye can feel staggering4. Algorithms are useful diagnostic aids and can act as a guide towards having an appropriate list of differential diagnoses and recognising salient features. They also reduce bias, errors and increase efficiency.

The Edinburgh Red Eye Diagnostic Algorithm is a validated tool in referral groups that has been shown to have a diagnostic accuracy of 72% overall, 100% in acute angle closure, 82% in iritis and up to 70% in epithelial keratitis. The sensitivity of this algorithm increases with the severity of the condition, which makes it particularly suited to non-ophthalmologists. Once an appropriate list of differential diagnoses is made, further investigations and management is subject to the most probable diagnosis. Below is a traffic light system illustrating the recommended management system from NICE according to the most likely differential diagnosis.

Image Source: https://cks.nice.org.uk/topics/red-eye/diagnosis/diagnosis/(accessed 5 May 2022).

References 

• Scantling-Birch Y, Naveed H, Tollemache N, et al. Is undergraduate ophthalmology teaching in the United Kingdom still fit for purpose? Eye 2021 362 2021; 36: 343–345.
• Timlin H, Butler L, Wright M. The accuracy of the Edinburgh Red Eye Diagnostic Algorithm. Eye 2015; 29: 619.
• Bhattacharyya A, Patel N. Pocket Tutor Ophthalmology. JP Medical Limited, 2012. Epub ahead of print 2012. DOI: 10.5005/jp/books/11542.

Red eye can be classified into infectious and non-infectious causes of red eye.

Infectious Red Eye

Infectious Conjunctivitis 

Conjunctivitis is inflammation of the conjunctiva as a response to either exogenous or endogenous processes. In infectious conjunctivitis, there is an inflamed conjunctiva in response to infection by a pathogen. It is a common cause of red eye in primary and secondary care. It is usually benign and self-limiting. It can be classified as acute or chronic.

Viral conjunctivitis

This is the commonest cause of infectious conjunctivitis, and adenoviruses account for up to 90% of cases. Viral conjunctivitis may also be caused by viruses of the herpes family or enteroviruses. It is transmitted by direct contact with ocular or respiratory secretions, or via fomites such as towels. Common symptoms include redness, burning sensation, foreign body sensation, mild photophobia, watery discharge and transient blurred vision. It may be bilateral or unilateral. There may be prodromal symptoms such as malaise or recent history of a viral upper respiratory tract infection. This is especially true in children, where pharyngoconjunctival fever presents fever, pharyngitis, periauricular lymphadenopathy, and acute follicular conjunctivitis. This condition is self-limiting and resolves within weeks. The conjunctiva is usually diffusely red, and there may be follicles present, as shown in the image below. There may be haemorrhage, especially in severe infection and pseudo-membranes might be present. Pre-auricular lymphadenopathy is common in viral conjunctivitis.

Image Source: Wikimedia Commons (2015). Conjuntivitis (RPS 03-06-2015), Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Conjuntivitis_(RPS_03-06-2015).png (Accessed on: 5  May 2022).

Diagnosis is clinical, but investigations may be useful in specific cases where there is uncertainty and viruses such as the herpes family are suspected. As it is a self-limiting condition and viral, topical antibiotics are not usually required. Cold compresses and artificial tears will provide symptomatic relief. Adenovirus conjunctivitis is very contagious, and patients should be advised on infection control procedures, such as not sharing towels at home. Herpes simplex keratitis should be treated with antivirals.

Bacterial conjunctivitis

Bacterial conjunctivitis is typically a self-limiting condition that occurs on direct inoculation with bacteria. Common pathogens include Staphyloccoccus Aureus, Streptococcus Pneumoniae, Haemophilus influenza and Moraxella Catarrhis. Other less common but more serious causes include Chlamydia and Gonorrhoea. It is usually more common in children.

Symptoms include mucopurulent discharge, particularly in the morning, redness, burning sensation, foreign body sensation, transient blurred vision and mild photophobia. Eyelid oedema may be present in severe cases. Gonococcal infection presents hyperacutely with copious mucopurulent discharge and rapid progression of symptoms. It is important to take a sexual history in these patients, particularly those with persistent bacterial conjunctivitis not responding to topical treatment such as chloramphenicol.

Examination shows conjunctival hyperaemia, mucopurulent discharge, which may be present only in fornices if the eye has been recently cleaned; papillae and follicles may be present in chlamydia conjunctivitis. Pre-auricular lymphadenopathy can occur in gonococcal conjunctivitis. Less commonly, there may be formation of pseudo-membranes or membranes.

Image Source: Wikimedia Commons (2019). Bacterial conjunctivitis, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Bacterial_conjunctivitis.jpg (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2019). Swollen eye with conjunctivitis, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Swollen_eye_with_conjunctivitis.jpg (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2011). Chlamydial-conjunctivitis, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Chlamydial-conjunctivitis.jpg (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2016). Membranous conjunctivitis, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Membranous_conjunctivitis.jpg (Accessed on: 5  May 2022).

Bacterial conjunctivitis is a clinical diagnosis, but investigations may be appropriate if gonococcal, chlamydial or meningococcal infection is suspected. Investigations are also useful in cases where there is failure of treatment. Although bacterial conjunctivitis is self-limiting, topical treatment can be given to hasten resolution. This includes anti-bacterials such as chloramphenicol and fluoroquinolones. Gonococcal conjunctivitis is treated with one dose of intramuscular Ceftriaxone, and systemic Azithromycin is given for Chlamydial infection.  Advice should be given regarding handwashing and not sharing towels.

Neonatal conjunctivitis

Inflammation of the conjunctiva within the first 28 days of life is termed neonatal conjunctivitis. It can be chemical or infectious in nature. It is the most common infection in neonates. Chlamydia is a leading cause9. Other organisms include staphylococci, streptococci, and chlamydia. Route is typically via vertical transmission during delivery or from caregivers in the post-natal period. History taking should include parental symptoms of sexually transmitted infection, prophylactic eyedrops instilled at birth and systemic illness in the neonate. Symptoms include sticky eyes, mucopurulent or watery discharge, red eyes and eyelid oedema. Examination should include corneal examination to look for ulceration and the tarsal and bulbar conjunctiva.

Image Source: Wikimedia Commons (2016). OSC Microbio 21 02 neonatorum, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:OSC_Microbio_21_02_neonatorum.jpg (Accessed on: 5  May 2022).

Investigation is unnecessary in mild cases, but conjunctival swabs and/or scrapes can be taken and sent for analysis in moderate to severe cases. Untreated, there is a risk of blindness, disability, and significant morbidity. Neonates with suspected infective conjunctivitis should be referred urgently for same-day Ophthalmology assessment9. Mild conjunctivitis can be treated with broad-spectrum topical antibiotics such as Chloramphenicol. Moderate to severe cases Gonococcal conjunctivitis is treated with Ceftriaxone according to weight and chlamydial infections with Azithromycin according to weight.

Keratitis 

Inflammation of the cornea can result from either exogenous insults or endogenous processes. For the purposes of this, keratitis will be discussed in terms of infective processes. Various pathogens such as bacterial, viral, fungi or protozoa can cause corneal infections.

Bacterial keratitis

Bacterial keratitis (bacterial infection of the cornea) is synonymously referred to as corneal ulcer and is the most common infectious keratitis. Although commonly presenting with an epithelial defect (ulcer), there might be a focus of infection (infiltrate) without an ulcer. A healthy cornea with an intact epithelium is a good defensive barrier against pathogens. Predisposing factors such as: contact lens wear (commonest), ocular surface disease, trauma, previous ocular surgery, immunosuppression, and systemic diseases are associated with an increased risk of corneal ulcers. Gram-positive bacteria such as staphylococci and gram-negative species such as pseudomonas are pathogens common in isolates. There are four pathophysiological states: infiltration of the cornea by the pathogen, active ulceration, regression and healing. Disease severity depends on the pathogenicity of the invading organism.

Common presenting complaints include redness, watering, photophobia, foreign body sensation and blurred vision. Patients should be asked about contact lens use/misuse (sleeping, swimming, sleeping, showering, or washing lenses in tap water).

Examination of the cornea should include, if possible, the use of fluorescein. Signs include staining epithelial defect (usually circular), whitish infiltrate or focal haziness of the cornea, mucopurulent discharge, conjunctival hyperaemia, anterior chamber reaction such as cells or hypopyon and eyelid oedema.

Image Source: Wikimedia Commons (2016). Contact Lens Related Small Corneal Ulcer with Sodium Fluorescein Staining 7 copy, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Contact_Lens_Related_Small_Corneal_Ulcer_with_Sodium_Fluorescein_Staining_7_copy.png (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2019). Corneal Ulcer, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Corneal_Ulcer.png (Accessed on: 5  May 2022).

Diagnosis is primarily clinical. Corneal scrapes for microscopy, culture and sensitivities are usually sent for ulcer >2mm, deeper or not responding to treatment. Contact lenses should be discontinued. Treatment typically involves topical broad-spectrum antibiotics, which can be changed according to sensitivities. In patient with anterior chamber reaction will benefit from cycloplegia and/or initiation of steroids once antibiotic therapy has been established. Patients with suspected corneal ulcers need urgent ophthalmology assessment. Sequelae of bacteria keratitis include corneal abscess, perforation and corneal scarring.

Herpes Simplex Keratitis (HSK)

Most people would have been exposed to herpes simplex, and the prevalence of herpes simplex is high in developing countries. Herpes simplex can cause a primary or secondary infection. Primary infection occurs on direct contact of the eye with the virus and is usually subclinical. The virus then stays dormant in the trigeminal nerve with reactivation, causing a secondary infection. Risk factors for reactivation are shown below. Recurrent activation has sight-threatening complications. Herpes can cause inflammation in every ocular tissue, but for the purpose of this, we shall only discuss herpes simplex keratitis. HSK is mainly caused by HSV-1.

Based on the Herpetic Eye Disease Study Group’s ‘Predictors of Recurrent Herpes Simplex Virus Keratitis’,  reactivation can be triggered by a variety of stimuli:

• Psychological stress
• UV light
• Fever
• Immunosuppression
• Trauma such as injury or surgery
• Intercurrent illness
• Previous episodes of disease recurrence

Herpes Simplex Keratitis can present clinically as two entities: Herpes Simplex Epithelitis and stromal keratitis.

Herpes Simplex Epithelitis occurs due to reactivation and anterograde migration of the virus through the trigeminal nerves to the corneal nerves. Active replication of the virus leads to loss of epithelial cells in a geographic, dendritic/branching pattern. Risk factors for activation include sunlight, stress, trauma and immunosuppression. Patient presents with unilateral (rarely bilateral) redness, pain, photophobia, eye-watering and blurry vision. Examination of the Fluorescein- stained cornea will reveal a characteristic branching defect with terminal bulbs. Diagnosis is usually clinical. In cases of diagnostic uncertainty, a corneal swab or scrap can be sent for PCR; PCR is highly sensitive in epithelial disease. Treatment consists of topical antiviral agents such as Ganciclovir. Antiviral agents are only beneficial in cases of active viral replication such as this.

Image Source: Wikimedia Commons (2012). Herpes simplex geographic corneal ulcer, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Herpes_simplex_geographic_corneal_ulcer.jpeg (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2017). Dendritic corneal ulcer, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Dendritic_corneal_ulcer.jpg (Accessed on: 5  May 2022).

Stromal keratitis occurs as a result of both the viral-mediated destruction and the host’s immunological response to the virus. Inflammation in the stroma leads to a stromal opacity, which is often accompanied by neovascularisation. Stromal keratitis can be further classified based on the integrity of the epithelium. In the necrotising form, there is an overlying epithelial defect and a high risk of cornea perforation. In the non-necrotising form, the epithelium is intact. Presenting symptoms can include redness, pain, photophobia, decrease in visual acuity and noticeable opacification of the cornea. Clinical signs include evidence of active inflammation such as redness, vascularisation, evidence of anterior chamber activity and raised intraocular pressure. There is often corneal stromal opacity, which can present in a classic disciform shape. Diagnosis is clinical. PCR and viral culture may have a positive yield, but this is greatly reduced in the absence of epithelial defects. The principles of treatment are to inhibit viral replication and reduce damage caused by inflammation. First line treatment often includes topical steroids and antivirals. In cases of epithelial defects and raised intraocular pressure, antibacterial and intraocular pressure-lowering drugs are indicated respectively. The Herpetic Eye Disease study showed that in patients with recurrent disease, systemic antiviral can reduce recurrence by up to 50%. Complications from recurrent or severe infections include corneal scarring, corneal vascularisation, lipid keratopathy and increased risk of transplant rejection. There are also associated complications from prolonged steroid therapy.

Herpes Zoster Ophthalmicus (Shingles)

Primary infection with Varizella Zoster typically occurs in childhood, with the virus then lying dormant with a sensory nerve ganglion. 10-20% of Herpes Zoster infections present with Herpes Zoster Ophthalmicus. Herpes Zoster Ophthalmicus (HZO)occurs when a reactivation of latent Varicella Zoster Virus (VZV) hidden in the sensory ganglia affects the ophthalmic division (V1) of the trigeminal nerve. V1 is a sensory nerve supplying:

• Related areas of the meninges and tentorium cerebelli
• The forehead and scalp
• Sinuses – Frontal, ethmoidal and sphenoidal
• Lacrimal gland
• Upper eyelid and conjunctiva
• Cornea
• Dorsum of the nose

Herpes Zoster Ophthalmicus does not in itself imply ocular involvement, but there is ocular infection in about 50% of cases. The reactivated virus travels to the sensory axons in the skin, forming a vesicular rash which blisters. The local immune response results in blisters and perinueritis, leading to significant neuropathic pain in the nerve distribution. Ocular involvement results in inflammatory conditions such as conjunctivitis, keratitis and uveitis.

Risk factors for reactivation are:

• Increasing Age
• Immunosuppression
• Stress
• Chronic illness such as diabetes
• Organ or bone marrow transplantation
• Malignancy
• Chemotherapy

An episode presents as a blistering rash in V1 (usually unilateral) associated with subcutaneous oedema. The rash starts off as a maculopapular rash, which then becomes vesicular and pustular before blistering and scabbing over. There is usually a prodromal phase of malaise, fever, paraesthesia or neuropathic pain (typically burning or shooting) in the affected dermatome and headache. In cases of ocular involvement, patients can present with redness, watering, pain, photophobia and blurry vision. General examination should assess for the presence of Hutchinson’s sign. A positive Hutchinson’s sign is when the rash involves the nasociliary branch of the trigeminal nerve (any area from the root to the tip of the nose) and is a strong predictor of ocular involvement. The eye should be examined for conjunctival redness and cornea stained with fluorescein to look for punctate keratitis or pseudo-dendrites. Decrease in corneal sensation may be present. Eyelid swelling and ptosis might occur due to gravitational oedema from the forehead.

Image Source: Wikimedia Commons (2018). Herps zoster ophthalmicus, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Herps_zoster_ophthalmicus.jpg (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2015). Day07 shingles or Herpes Zoster Virus attacking forehead and eye, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Day07_shingles_or_Herpes_Zoster_Virus_attacking_forehead_and_eye.jpg (Accessed on: 5  May 2022).

Diagnosis is clinical, but on occasion of diagnostic uncertainty, a viral swab can be sent for PCR. Antiviral treatment should be started – ideally within 72 hours of onset. PO Aciclovir 800mg 5x/day for 7-10 days is the mainstay of oral treatment. Immunocompromised patients might require intravenous antiviral agents. In patients with suspected ocular involvement, ophthalmology input should be sought within 24 hours. Surface ocular disease can be treated with topical Ganciclovir, but substantial inflammation will require steroids. Bacterial superinfection should also be treated. Vesicles blister and typically heal by 6 weeks. Patients commonly develop post-herpetic neuralgia, which can be debilitating and will require treatment with neuropathic pain medication. Inflammation around the eyelids can cause scarring, which expose the cornea, leading to exposure keratopathy and its sequelae – this is a sight-threatening condition. Direct corneal inflammation, if prolonged, also risks sight loss. Shingles vaccination has been demonstrated to decrease disease recurrence and is currently available on the NHS to people in their 70s.

Acanthamoeba keratitis

Acanthamoeba is a free-living protozoan which can rarely cause a severe opportunistic corneal infection. It exists in two forms: trophozoites (active organism) and cysts (encased and resistant to a variable of external factors). Risk factors include contact lens wear inoculation through contaminated water or via trauma. Patients typically present with pain disproportionate to clinical findings. They also complain of non-specific symptoms of keratitis. Early clinical findings include an irregular epithelium, infiltrates and pseudodendrites. Late signs can include characteristic ring-shaped or disciform stromal infiltrates, as shown in the image below, corneal perforation, anterior uveitis and scleritis. Diagnosis is often through corneal scrapes grown on specific agar or confocal microscopy.

Image Source: Wikimedia Commons (2015). Parasite140120-fig1 Acanthamoeba keratitis, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Parasite140120-fig1_Acanthamoeba_keratitis.png (Accessed on: 5  May 2022).

Urgent ophthalmology assessment is needed with even a marginal suspicion of acanthamoeba keratitis. Current treatment options include combinations of antibiotics, antivirals, antifungals and anti-parasitic agents, some of which are toxic and require lengthy treatment.

Orbital cellulitis 

Orbital cellulitis is an ophthalmic emergency. It is a sight-threatening condition which occurs when there is a bacterial infection of soft tissues posterior to the orbital septum. This differs from pre-septal cellulitis, where there is infection of the soft tissue anterior to the orbital septum without involvement of the globe or orbit. The infection frequently originates from the paranasal sinuses, pre-septal cellulitis, dental infection, dacryocystitis and trauma. Causative organisms include S.Pneumonaie and S.Aureus. It is more common in children and in immunocompromised states. Patients present with a painful swollen eye, change in vision, fever, malaise and less common features of intracranial spread such as meningism or neurological impairment. Typically, there is a history regarding the source of infection, such as recent dental work or upper respiratory tract infection. Examination shows reduced vision and/or signs of optic nerve dysfunction, eyelid swelling and erythema, conjunctival oedema and injection, proptosis, decreased eye movements associated with pain, and the patient is usually febrile. Patients should also be examined for any signs of intracranial spread, such as meningism or focal neurological signs, and if available, fundoscopy should be carried out.

Image Source: Wikimedia Commons (2011). Orbital cellulitis, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Orbital_cellulitis.jpg (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2011). RtmaxobitinfectteethCT, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:RtmaxobitinfectteethCT.png (Accessed on: 5  May 2022).

Investigations include blood tests to assess inflammatory markers, blood cultures if febrile and/or culture of the nasopharynx and conjunctiva -although the yield is low, and imaging (contrast enhanced CT scan of orbit, sinuses and brain). Patients presenting with pre-septal cellulitis will need thorough examination to rule out orbital cellulitis. The table below shows differentiating features between orbital cellulitis and pre-septal cellulitis.

Pre-septal cellulitis	Orbital cellulitis
White-eye	Conjuctival injection and oedema
Full painless extraocular movements	Painful and/or restricted extraocular movements
No proptosis	Proptosis
Normal vision	Impaired vision and/or signs of optic nerve dysfunction
Systemically well	Fever and/or malaise

Adapted from Kim HJ, Kersten R. Peri-orbital and orbital cellulitis – Symptoms, diagnosis and treatment | BMJ Best Practice, https://bestpractice.bmj.com/topics/en-gb/734 (accessed 31 May 2022).

Patients suspected of having orbital cellulitis need urgent hospital admission and initiation of empirical intravenous antibiotics, which can be tailored to any positive cultures. Antibiotics should cover for anaerobic infections and also have good penetrance of the CSF to cover for intracranial spread. Prompt imaging should be arranged to assess for any evidence of sinusitis, confirm diagnosis and also assess for intracranial spread or presence of abscesses. Children will be managed under paediatrics, and all patients will require ophthalmology input. If necessary, dental, max-fax or ENT input may also be sought. Complications can be localised to the orbit (optic neuropathy, endophthalmitis, central retinal artery occlusion, subperiosteal abscess, ocular empyema) or intracranial (meningitis, abscess and thrombosis).

References 

• Ryder EC, Benson S. Conjunctivitis. StatPearls, https://www.ncbi.nlm.nih.gov/books/NBK541034/ (2022, accessed 15 June 2022).
• Azari AA, Arabi A. Conjunctivitis: A Systematic Review. J Ophthalmic Vis Res 2020; 15: 372.
• Manasseh GSL, Amarakoon S, Photiou V, et al. Approach to conjunctivitis in newborns. BMJ; 376. Epub ahead of print 23 March 2022. DOI: 10.1136/BMJ-2021-068023.
• Bourcier T, Thomas F, Borderie V, et al. Bacterial keratitis: Predisposing factors, clinical and microbiological review of 300 cases. Br J Ophthalmol 2003; 87: 834–838.
• Lin A, Rhee MK, Akpek EK, et al. Bacterial Keratitis Preferred Practice Pattern®. Ophthalmology 2019; 126: P1–P55.
• Sibley D, Larkin DFP. Update on Herpes simplex keratitis management. Eye 2020 3412 2020; 34: 2219–2226.
• Herpetic Eye Disease Study Group. Predictors of Recurrent Herpes Simplex Virus Keratitis. Cornea: March 2001 – Volume 20 – Issue 2 – p 123-128
• Ting DSJ, Ghosh N, Ghosh S. Herpes zoster ophthalmicus. BMJ; 364. Epub ahead of print 2019. DOI: 10.1136/BMJ.K5234.
• Meduri A, Grenga PL, Kaufman SC. Herpes Zoster Ophthalmicus. Expert Rev Ophthalmol 2021; 4: 537–545.
• Lorenzo-Morales J, Khan NA, Walochnik J. An update on Acanthamoeba keratitis: diagnosis, pathogenesis and treatment. Parasite; 22. Epub ahead of print 2015. DOI: 10.1051/PARASITE/2015010.
• Adamson J, Waterfield T. Fifteen-minute consultation: Preseptal and orbital cellulitis. Arch Dis Child – Educ Pract 2019; 104: 79–83.
• Kim HJ, Kersten R. Peri-orbital and orbital cellulitis – Symptoms, diagnosis and treatment | BMJ Best Practice, https://bestpractice.bmj.com/topics/en-gb/734 (accessed 31 May 2022).

Non-infectious red eye 

Corneal abrasion

Up to 24% of patients presenting to an emergency department with an eye issue have a corneal abrasion. In primary care, they account for 2% of all visits. Corneal abrasions are one of the commonest form of anterior segment trauma. A cornea is abraded when there is removal or loss of the epithelium, leading to a defect in the affected area. Common causes of corneal abrasion are fingernails (usually accidental injury from a child), contact lenses, cosmetic brushes, occupational exposure in high-risk occupations (e.g. mining, metal work, welding), sport-related trauma and abrasions from subtarsal foreign bodies. Corneal epithelial defects can also occur due to a breakdown of the epithelial cells from disease processes such as exposure, dry eye syndromes and neurotrophic keratopathy. In hospital, high-risk patients include NICU patients and ventilated adults. Patients present with redness, pain, foreign body sensation, photophobia, watering and blurred vision. A careful history to identify, if possible, the cause of trauma is necessary. Injury from organic matter carries a higher risk of contamination and, in particular, fungal inoculation. The cornea should be stained with fluorescein to delineate the defect. A seidel test (observation of washing out of fluorescein from the cornea surface by aqueous fluid from the anterior chamber) should be performed to assess for any signs of leakage indicating penetrating eye injury. An abnormal pupil shape might be a sign of penetrating eye injury. Eyes with abrasion secondary to blunt trauma or evidence of trauma in other ocular tissues will require ophthalmological assessment. Eyes with hyphaemas or hypopyon also necessitate urgent ophthalmology referral.

Image Source: Wikimedia Commons (2017). Corneal Abrasion with Fluorescein Staining, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Corneal_Abrasion_with_Fluorescein_Staining.jpg (Accessed on: 5  May 2022).

Small epithelial defects heal quickly, and the principle of treatment is to prevent infection during this healing process. Topical antibacterials such as chloramphenicol are usually sufficient. In patients with suspected exposure to fungal matter, appropriate prophylaxis might be necessary. Oral analgesia can be used for simple pain relief. Contact lens users should discontinue contact lens use during treatment. Larger defects and deeper defects take longer to heal and can be complicated by infection. Corneal abrasions increase the risk of developing recurrent corneal erosions where there is spontaneous breakdown of the epithelium. This is because of a dysfunctional adherence of the epithelial cells post-trauma. Persistent epithelial defects or recurrent corneal erosions will need specialist treatment such as tarsorrhaphy, amniotic membrane graft, micro-puncture, etc.

Foreign bodies 

In this section, discussion of foreign bodies will be limited to those on the ocular surface (conjunctiva and cornea). Materials can become embedded on the ocular surface, particularly if sharp or moving at a high velocity. Corneal or conjunctival foreign bodies tend to occur as occupational hazards. Foreign bodies can slip between the gaps in the frame, even in those who use safety glasses. It is important to ascertain the velocity and size of the foreign body as this informs the risk of a penetrating eye injury or intraocular or intraorbital foreign body.

Foreign bodies can be organic or inorganic, and organic matter carries a higher risk of infection due to the presence of microbes. Patients present with a history of redness, watering and foreign body sensation. Examination should include eversion of the lid to look for subtarsal foreign bodies and the fornices should be swept and examined.

Image Source: Wikimedia Commons (2007). Foreign body in eye, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Foreign_body_in_eye.jpg (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2018). Foreign body on cornea, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Foreign_body_on_cornea.png (Accessed on: 5  May 2022).

Iron and copper are toxic to cells and induce inflammation. Foreign bodies not deeply embedded need removal. Iron and copper foreign bodies leave a rust ring on removal, and this should also be removed as it induces inflammation and is toxic. On detection of a foreign body, attempt to remove it with a swab or irrigate it. Prophylactic topical antibiotic such as chloramphenicol should be given after removal to prevent bacterial infection. If there is suspicion of a penetrating eye injury, a shield should be placed over the eye, and urgent ophthalmology assessment sought, as should also be the case when there are unsuccessful attempts or inadequate removal of foreign body. Protective eyewear significantly decreases the risk of foreign bodies.

Allergic eye disease 

Allergic eye disease covers a spectrum of disease. This section covers the forms of allergic conjunctivitis. Allergic conjunctivitis is an umbrella term for a spectrum of disorders where conjunctivitis results typically from Type I hypersensitivity reaction to an allergen. It is estimated to affect up to 40% of the population and is usually seasonal. Allergic conjunctivitis can be classified as shown below. Allergic conjunctivitis is particularly common during the spring season, but only a proportion of individuals will experience symptoms severe enough to seek medical treatment.

Image source: Adapted from La Rosa M, Lionetti E, Reibaldi M, et al. Allergic conjunctivitis: a comprehensive review of the literature. Ital J Pediatr 2013; 39: 18.

Allergic conjunctivitis without corneal involvement occurs on secondary contact with an allergen. It is due to a type I hypersensitivity reaction with subsequent mast cell degranulation. Allergic conjunctivitis with corneal involvement is a lesser-understood process with both type I and type IV hypersensitivity reaction and changes in T cell signalling. The accompanying changes in T cell behaviour confer chronicity.

Allergic conjunctivitis without corneal involvement (simple allergic conjunctivitis) tends to occur in response to allergens present on the ocular surface. In this form, only the conjunctiva is involved. Incidence decreases with increasing age.

Seasonal

This occurs in response to allergens which are more abundant in certain seasons, such as pollen or grass. Sufferers tend to have a history of hay fever.

Perennial

This is a form of simple allergic conjunctivitis which occurs all year round and is triggered by environmental allergens such as dust mites or animal dander.

Acute

A term loosely used to describe an acute onset of simple allergic conjunctivitis as opposed to an episode persisting throughout the spring and summer or all year round.

Simple allergic conjunctivitis typically presents with bilateral watering eyes, itching, conjunctival swelling, and eyelid swelling. Pain is rarely a feature.

Image Source: Wikimedia Commons (2013). Allergicconjunctivitis, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Allergicconjunctivitis.jpg (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2017). Pterygium (conjunctiva), Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Pterygium_(conjunctiva).jpg (Accessed on: 5  May 2022).

Atopic Keratoconjunctivitis (AKC)

This tends to occur in patients with a history of atopy, and incidence decreases with age. It arises from allergen exposure in an individual with a genetic predisposition to atopy. Patients typically have a history of dermatitis, usually around the eyelids. Symptoms are usually present all year around and will include corneal symptoms. It is a chronic disease and persists for several years. Chronic unchecked inflammation can lead to corneal scarring and vascularisation with resultant decrease in vision.

Vernal Keratoconjunctivitis (VKC)

VKC occurs due to an immune-mediated response to both allergens and other factors in the environment, such as climate. It is more common in hot, arid environments. There is a male preponderance, and patients typically have a history of atopy and asthma. It usually resolves after adolescence. Symptoms are typically worse in springtime. Patients present with itching, watering (thick discharge secondary to goblet cell hyperplasia), pain and corneal symptoms. Foreign body sensation is a common symptom. Distinguishing features for VKC include giant papillae in the tarsal conjunctiva, which can present in a cobblestone pattern and perilimbal Horner-Trantas dots, which are aggregates of epithelial debris and eosinophils.

Image Source: Wikimedia Commons (2006). Vernal, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Vernal.jpg (Accessed on: 5  May 2022).

Giant Papillary Conjunctivitis (GPC)

GPC results from an immune hyperactivity reaction to chronic exposure to a foreign object. Chronic micro-trauma from the foreign object also facilitates entry of the allergen. This is typically seen in cases with contact lens use, prosthesis, or sutures. Patients typically experience itching, thick discharge, pain and foreign body sensation. Examination reveals features such as conjunctival hyperaemia and chemosis, as well as papillae in the tarsal conjunctiva.

Itching is a hallmark feature of allergic eye disease, and symptoms tend to be bilateral, although they may be asymmetrical. Patients also present with redness, watering, conjunctival chemosis, eyelid swelling and skin changes (if there is periorbital dermatitis). In patients with corneal involvement, accompanying symptoms will include pain, photophobia, blurred vision and foreign body sensation. Patients have a history of recurrent episodes of symptoms which may be seasonal or worsen in certain situations. Examination shows evidence of allergic conjunctivitis such as conjunctival hyperaemia, chemosis, papillae, corneal epithelial defects or punctate staining in patients with corneal involvement – these patients can also have ulcers with infiltrate in cases of infection. Diagnosis is clinical. Red flag features in the history or examination (according to NICE guidelines) should prompt referral for urgent ophthalmology assessment. Refractory cases with no red flag features can be referred routinely.

Adapted from NICE Conjunctivitis guidance, the following are red flag features in allergic conjunctivitis necessitating ophthalmology referral:

• Reduced visual acuity
• Marked eye pain, headache or photophobia
• Inability to open the eye or keep it open
• Red sticky eye in a neonate (within 30 days of birth)
• History of trauma (mechanical, chemical or ultraviolet) or possible foreign body
• Copious rapidly progressive discharge
• Possible infection with a herpes virus:
• Herpes simplex — may present as unilateral red eye with vesicular lesions on the eyelid
• Herpes zoster
• Soft contact lens use with corneal symptoms
• Recent intraocular surgery
• Systemic disease or immunosuppressed
• Suspected periorbital or orbital cellulitis

Treatment focuses on symptomatic relief, reducing inflammation and immunomodulation if necessary. Treatment Box 1 shows the ladder of treatment in patients with allergic eye disease.

Image source: Adapted from La Rosa M, Lionetti E, Reibaldi M, et al. Allergic conjunctivitis: a comprehensive review of the literature. Ital J Pediatr 2013; 39: 18.

Initial treatment for all forms of allergic conjunctivitis are similar, and further therapies are targeted to complications or response to treatment, as shown in treatment box 1. Corneal involvement requires more aggressive treatment than patients in whom the conjunctiva only is affected, and these patients require ophthalmology referral.

Simple therapies include:

• avoiding the allergen if possible
• cool compresses (these induce local vasoconstriction and provide symptomatic relief)
• lubricating eye drops and short courses of over-the-counter topical antihistamines

Topical mast cell stabilisers and antihistamines are effective in refractory cases, and a short course of steroids can break the cycle of inflammation. Topical calcineurin inhibitors are used in severe or refractory disease, usually with corneal involvement and are initiated by specialists. Superimposed bacterial infection can be treated with anti-bacterials.

Management in primary care should include:

• patient education (discourage patient from eye rubbing as this increases the risk of corneal ectasias)
• topical antihistamines and/or mast cell stabilisers (combination preparations are available)
• monitoring with prompt referral if necessary
• referring patients with multi-system disease to an allergy specialist

VKC and AKC will include treatment for simple allergic conjunctivitis as well as topical mast cell stabilisers. Acute flares might require treatment with topical corticosteroids, and this should be initiated by an ophthalmologist. Cases refractory to steroid therapy or who are difficult to wean off steroids will require treatment with steroid-sparing agents such as topical ciclosporin or tacrolimus. Patients with periocular dermatitis will require control of this and, if severe, will need dermatological input.

In GPC, first-line treatment will include removal of the offending foreign object. Chronic inflammation affecting the cornea can lead to corneal scarring and vascularisation with subsequent visual loss. This is particularly important in young children who can develop amblyopia deprived of visual stimuli.

Uveitis

Uveitis is an umbrella term for a heterogenous group of disorders causing inflammation of the uvea (iris, ciliary body and choroid). Classification of uveitis has been standardised by the International Uveitis Study Group. It is primarily classified anatomically, as shown in the illustrative table below.

Classification	Primary site	Disorders included	Aetiology
Anterior	Anterior chamber	Iritis, iridocyclitis, anterior cyclitis	Systemic disorders such as spondyloarthropathies, non-systemic such as Fuch’s heterochromic Iridocyclitis and infectious causes such as HSV
Intermediate	Vitreous	Pars planitis, Posterior cyclitis, Hyalitis	Systemic disorders such as sarcoidosis, non-systemic such as undifferentiated intermediate uveitis and infections such as syphilis
Posterior	Retina and choroid	Focal or diffuse choroiditis, chorioretinitis, Retinitis, retinochoroiditis, Neuroretinitis	Systemic disorders such as sarcoidosis, non-systemic such as birdshot chorioretinopathy and infections such as toxoplasma retinitis
Panuveitis	Anterior chamber, vitreous, retina and/or choroid		Systemic disorders such as Behcet disease, non-systemic such as sympathetic ophthalmia and infections such as syphilis

Source: Adapted from Deschenes J, Murray PI, Rao NA, et al. International Uveitis Study Group (IUSG) Clinical Classification of Uveitis. http://dx.doi.org/101080/09273940801899822 2009; 16: 1–2. (accessed 31 May 2022)

Uveitis can also be characterised by laterality, onset of symptoms, duration (limited or persistent), and course (acute -usually resolves within 3 months, recurrent, repeated episodes separated by periods of inactivity;  and chronic – persisting for longer than 3 months). The most common presentation of uveitis is acute anterior uveitis (AAU), accounting for up to 90% of cases in primary care settings22 and will be the focus of this section. In anterior uveitis, the anterior uvea – iris and ciliary body – are affected by inflammation. The peak age of presentation is between 30 and 40 years.

Aetiology

AAU may occur as a response to systemic disease, non-systemic disease, or infection. Disorders associated with anterior uveitis ae shown below. In most cases of uveitis, there is no known cause.

Adapted from ‘Uveitis for the non-ophthalmologist’, the following are common conditions associated with uveitis:

Systemic

• Spondyloarthropathies – associated with the HLA B27 genotype
• Inflammatory bowel disease
• Sarcoidosis
• Behcet disease
• Vasculitides
• Interstitial nephritis
• Systemic Lupus Erythematosus

Non-systemic

• Fuch’s heterochromic Iridocyclitis

Infection 

• Herpes Simplex
• Varicella Zoster
• Tuberculosis
• Syphillis
• Lyme disease

Symptoms and signs

AAU typically presents with sudden onset (1-2 days) pain, redness, photophobia, watering and change in vision. It can affect all age groups. Some causes of anterior uveitis may present sub-acutely (1-2 weeks). Evidence of inflammation can be seen in the anterior chamber and sometimes just behind the lens in the anterior vitreous (usually the case in iridocyclitis). The hallmark features of anterior uveitis which may be present on examination with a slit lamp are listed below.

Adapted from ‘Uveitis Straight to the point of care’, the following are examination findings which may be present in anterior uveitis:

• Cells in the aqueous (visible in the anterior chamber)
• Flare (due to proteinaceous exudate)
• Fibrin in the anterior chamber
• Keratic precipitate (aggregate of inflammatory cells on corneal endothelium, can be granulomatous)
• Hypopyon
• Posterior synechiae (sticking of the iris to the lens capsule)
• Iris nodules (uncommon)
• Iris atrophy (associated with HSV and VZV)
• Cells in the anterior vitreous

Patients have a visibly red eye and with cases of posterior synechiae an irregular pupil. The pattern of redness is typically ciliary – a ring-like pattern of dilated vessels around the cornea due to involvement of the branches of the anterior ciliary arteries supplying the cornea, iris and ciliary body.

Image Source: Wikimedia Commons (2019). Fig-1-Photograph-showed-non-granulomatous-anterior-uveitis-with-nuclear-cataract-and-ciliary-injection-in-the-right-eye, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Fig-1-Photograph-showed-non-granulomatous-anterior-uveitis-with-nuclear-cataract-and-ciliary-injection-in-the-right-eye.gif (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2013). Anterior-uveitis, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Anterior-uveitis.jpg (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2013). Keratic-precipitates, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Keratic-precipitates.jpg (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (no date). Manual_of_ophthalmology_(1917)_(14592285118), Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Manual_of_ophthalmology_(1917)_(14592285118).jpg (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2006). Hypopyon, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Hypopyon.jpg (Accessed on: 5  May 2022).

Diagnosis

Patients suspected of having uveitis should be referred for urgent ophthalmology assessment, usually within 24 hours. Once a provisional diagnosis of AAU is made clinically, a uveitis screen should be carried out to determine the aetiology (if possible, although this is typically done in recurrent cases). Blood tests should include serum ACE, T-spot test, syphilis, ANA, ANCA and rheumatoid factor. CXR to assess for evidence of tuberculosis or bilateral hilar lymphadenopathy to suggest sarcoidosis. The ophthalmologist might carry out further investigations, such as OCT scanning.

Management

Principles of treatment are to treat inflammation and prevent complications, and in patients with chronic disease, to prevent relapses. First-line treatment is topical corticosteroids, and intensity of drops is tailored to the degree of inflammation according to the standardised grading system. Cycloplegics can also be given to relieve pain from ciliary spasm and to break or prevent formation of posterior synechiae by dilating the iris. Episodes refractory to topical treatment or those which are severe enough may require subconjunctival/intravitreal steroids or oral therapy. Raised intraocular pressure is treated with anti-glaucoma medication. Infectious uveitis will require treatment of the infection itself. Treatment should be initiated urgently in infectious cases as it tends to progress rapidly, is more aggressive and can lead to blindness. Long-term use of steroids increases the risk of cataracts and glaucoma. Steroid-sparing agents may be used in select patients with chronic uveitis, and biologics are an emerging successful therapy in refractory cases. Uveitis tends to recur. Patients with chronic disease have no overt signs such as redness or pain, even with ongoing inflammation. Typically, inflammation recurs when treatment is stopped or tapered. Early and prompt treatment can reduce morbidity and prevent blindness. Complications include posterior synechiae, which becomes permanent due to scarring, secondary glaucoma, band keratopathy, chronic macular oedema and cataracts.

Episcleritis

Episcleritis is inflammation of the episcleral tissue. It is usually self-limiting. It is classified as nodular or simple episcleritis. Simple episcleritis, where there is injection of the episcleral vessels without a nodule is more common. In the nodular form, there is injection over an underlying nodule, which commonly occurs within the interpalpebral fissure. It is a benign condition which tends to recur. There is a female preponderance, and occurs in middle age. Although frequently idiopathic, associations have been found with autoimmune and inflammatory diseases. Patients present typically with acute onset sectoral or diffuse redness and may experience mild discomfort in the area. There are no visual changes, and there may have been previous episodes. Examination shows injected vessels which are mobile over the underlying sclera, even in the nodular form. Diagnosis is clinical and can be confirmed by the application of 2.5% phenylephrine with the episcleral vessels blanching. Laboratory tests may be required in patients who have no systemic disease presenting with recurrent episodes.

Duration of each episode ranges from 2-3 days up to 3 weeks. The nodular form presents sub-acutely and has a prolonged course. As this is a self-limiting condition, treatment is not usually required in mild cases. Cool compresses and refrigerated tears may help. In moderate to severe cases, oral NSAIDS such as Ibuprofen can be given, and topical week topical steroids for 1-2 weeks can be administered. Treatment is tailored to the severity of inflammation. The prognosis for episcleritis is good.

Image Source: Wikimedia Commons (2017). Episcleritis, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Episcleritis.jpg (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2013). Episcleritiseye, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Episcleritiseye.jpg (Accessed on: 5  May 2022).

Scleritis 

Scleritis is an uncommon, potentially blinding condition characterised by inflammation of the scleral tissue. Scleritis may be categorised by anatomical location, pathogenesis, or presence of necrosis. The image below shows the common classification of scleritis.

Image source: Adapted from Sims J. Scleritis: presentations, disease associations and management. Postgrad Med J 2012; 88: 713–718.

The most common form of scleritis is anterior scleritis, where there is inflammation anterior to the recti muscles. This presents as a painful red eye with or without associated loss of vision. There are different forms of anterior scleritis. Pathophysiologically, there is oedema and cellular infiltration of the entire thickness of the sclera. Commonly, inflammation begins in a focal area and then spreads over the anterior segment. Inflammation can be granulomatous (histologically epitheloid cells and multinucleate giant cells) or non-granulomatous (histologically plasma cells, macrophages and lymphocytes).

Non-necrotising

This can be diffuse or nodular. In diffuse non-necrotising scleritis, there is diffuse inflammation of the affected portion of the sclera. In nodular, there is a distinct nodule(s) of inflamed sclera. The nodular form is more common in patients who have a previous history of Herpes Zoster Ophthalmicus. The nodules, in this case, are immobile compared to nodular episcleritis. In the non-necrotising form, the sclera becomes translucent due to rearrangement of scleral collagen following inflammation.

Necrotising with inflammation

This is the most severe form with tissue necrosis. It is characterised by severe pain and scleral tenderness and is often bilateral. Necrosis of the sclera leads to exposure of the underlying choroid. The vaso-occlusive form is more common in rheumatoid arthritis with patches of scleral oedema, which eventually coalesce and necrose. Granulomatous scleritis can occur in medium vessel vasculitis. Surgically induced scleritis can occur after repeated ocular surgery and commonly presents within 1-month post-procedure. It is more common in surgical procedures involving the ocular surface and with administration of mitomycin C. The inflammation is usually localised to the surgical wound, although it might spread. Here, the sclera thins out and exposes the underlying uvea.

Scleromalacia perforans

This a form of necrotising scleritis where there is progressive, painless thinning of the sclera in the absence of inflammation. It is more common in older patients with a long history of rheumatoid arthritis. Scleral perforation rarely occurs due to scarring.

There is an association with systemic diseases such as rheumatoid arthritis, vasculitis and connective tissue disorders, particularly in necrotising disease. There is a female preponderance, and it typically presents between the fifth and sixth decades. The presentation of scleritis is varied depending on disease course. It can present as an acute episode, a relapsing-remitting illness or as a chronic process. Patients can present with gradual onset, severe boring pain, which wakes them up at night. It is worse in the morning and improves during the course of the day, and may radiate to the temples. The eye may be diffusely red and tender or localised to an area, and there may be associated visual loss.

Image Source: Wikimedia Commons (2012). Lederhaut MUC0367xxk, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Lederhaut_MUC0367xxk.jpg (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2017). Recurrent scleritis, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Recurrent_scleritis.jpg (Accessed on: 5  May 2022).

On examination, there is an area of diffusely swollen sclera with injection of the scleral vessels. It typically has a violaceous hue, and the inflamed vessels are deep and cannot be moved with a cotton bud. The globe is tender to touch, and application of 2.5% Phenylephrine distinguishes scleritis (non-blanching) from episcleritis (blanching). They may be associated keratitis or uveitis. Areas of necrosis appear thinned out with visibility of the underlying choroid. Patients can also be examined for features of associated systemic disease. Diagnosis is clinical, but investigations can be carried out to confirm diagnosis (in cases of uncertainty) or to test for underlying or associated diseases. Ocular imaging can include B-Scan ultrasonography and MRI to detect cases of posterior scleritis with more generalised imaging to look for conditions such as sarcoidosis or tuberculosis. Laboratory tests should screen for associated conditions. The principle of treatment is to control inflammation and, therefore, decrease damage to ocular structures. Treatment summary for scleritis is shown in treatment box 2.

Image source: Adapted from Sims J. Scleritis: presentations, disease associations and management. Postgrad Med J 2012; 88: 713–718.

Patients suspected of having scleritis need urgent same-day ophthalmology assessment. In patients with associated diseases, multi-disciplinary management is required. Complications of scleritis include keratitis, uveitis, glaucoma, cataract formation, rarely scleral perforation and loss of vision.

Acute Angle Closure (AAC) 

Angle closure is an ophthalmological emergency where a sudden occlusion of aqueous outflow leads to an acute rise in intraocular pressure, which in turn can cause irreversible damage to the optic nerve (glaucoma).

Overview

In angle closure, the trabecular meshwork is occluded by the peripheral iris (irido-trabecular contact). This obstructs the outflow of aqueous humour through the iridocorneal angle, leading to an acute rise in intraocular pressure. These patients will have a normal optic disc. When there is evidence of optic nerve damaged, it is then termed angle closure glaucoma. Angle closure can be classified as primary or secondary. Primary angle closure occurs in an eye with a shallow angle configuration. Secondary angle closure due to a local or systemic factor occurs in an eye with a normal angle configuration. Acute angle closure is sudden onset occlusion of the angle.

Pathophysiology

The mechanisms by which angle closure arises includes relative pupillary block, non-pupillary block and lens-induced angle closure. In relative pupillary block, decreased outflow through the pupil creates a pressure gradient/accumulation of aqueous in the posterior chamber, resulting in the anterior bowing of the iris, which then acutely occludes the angle. In non-pupillary block, there is an abnormal iris configuration. In the lens-induced form, a bulkier lens or a lens that has moved anteriorly decreases aqueous outflow. There is often a mixture of mechanisms.

Image Source: Wikimedia Commons (2006). UBM Angle closure glaucoma, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:UBM_Angle_closure_glaucoma.jpg (Accessed on: 5  May 2022).

Risk factors

• Age (commonest around ages 55-65)
• Female preponderance
• Ethnicity – commoner in people of Asian heritage, particularly far eastern
• Shorter eyes
• Hypermetropia

Presentation

It is typically precipitated by events causing pupil dilatation or ciliary body effusion, such as watching television in a dark room or waking up at night and turning on the lights, iatrogenic (pharmacological) or emotional stress. Common symptoms and signs of acute angle closure are shown below.

Adapted from ‘Angle-closure Glaucoma Straight to the point of care’, the following are common presenting features of acute angle closure:

• Intermittent or constant:
• Unilateral severe ocular or periocular pain with headache
• Nausea and vomiting
• Blurred vision
• Seeing haloes around bright objects such as lights due to corneal oedema
• Decreased VA due to corneal oedema
• Unilateral red eye
• Hazy cornea due to cornea oedema
• Fixed mid-dilated pupil
• Unilateral raised intraocular pressure (usually in the 50s)
• Shallow anterior chamber
• The contralateral eye usually has an occludable angle

Patients typically present acutely and may have a history of episodes of intermittent angle closure, which spontaneously resolves.

Image Source: Wikimedia Commons (2020). Acute angle closure glaucoma, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Acute_angle_closure_glaucoma.JPG (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2011). Acute Angle Closure-glaucoma, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Acute_Angle_Closure-glaucoma.jpg (Accessed on: 5  May 2022).

Diagnosis

Acute angle closure is diagnosed clinically. Angle closure is diagnosed through examination using a set criteria and clinically as set out below.

• Presence of at least 2 of the following symptoms: ocular or periocular pain, nausea and/or vomiting, an antecedent history of intermittent blurring of vision with haloes.
• Presenting intra-ocular pressure (IOP) >21 mmHg.
• Presence of at least 3 of the following signs: conjunctival injection, corneal epithelial oedema, mid- dilated unreactive pupil and shallow anterior chamber.

Ultrasound or OCT of the anterior segment may be utilised in patients suspected to have angle closure or with abnormal iris configuration to confirm diagnosis. Imaging to assess the health of the optic nerve head will also be utilised.

Management

Suspected acute angle closure should be referred urgently same day to ophthalmology or urgent eye service. Acutely, treatments aim to lower the intraocular pressure. Patients should be encouraged to lie in a supine position. First line treatment will include topical treatment such as prostanglandin analogues, oral or IV carbonic anhydrase inhibitors, miotics, and beta blockers. Second-line options in refractory cases can involve medical treatment such as IV mannitol or surgical treatment such as anterior chamber paracentesis. In patients with a clear cornea after successful control of intraocular pressure, laser peripheral iridotomy can be performed as soon as possible. Clear lens extraction is a procedure also considered in primary angle closure. Long-term treatment will include preventative measures such as a laser or surgical peripheral iridotomy.

Chemical or thermal injury 

Ocular burns can result from either chemical or thermal contact. Chemical injuries represent up to 22% of ocular trauma.

Chemical injuries require immediate assessment and initiation of appropriate treatment. They frequently occur in households, at workplaces with handling of industrial-grade chemicals and sometimes in crimes. Acids cause damage by precipitating tissue protein, leading to coagulation. The proteins on the ocular surface form a coagulum with acid molecules, and this forms a barrier to further penetration; the exception to this is hydrofluoric acid, which rapidly penetrates the eye. Alkalis cause proteolysis, hydrolysis of GAGs, and as they are lipophilic, rapidly cross cell membranes. Caustic alkalis have the potential to cause more severe damage than acidic substances as a result. Chemicals can cause damage to conjunctival epithelium, limbal stem cells, cornea and anterior segment dependent on extent of penetration and hence lead to sight-threatening long-term ocular surface problems, which are difficult to manage. It is important to take a detailed history and determine what chemical has come in contact with the eye.

The eye should immediately be copiously irrigated with 0.9% sodium chloride/Hartmann’s or water and pH checked using litmus paper prior to and after irrigation. The normal surface pH of the eye can be determined by checking the pH of the unaffected eye or if both eyes are affected, using an average reference of 7.4. The patient needs urgent same-day ophthalmological assessment and management. Treatment will focus on promoting healing, reducing inflammation and prevention/managing complications.

Image Source: Wikimedia Commons (2009). Chemical burn injury, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Chemical_burn_injury..jpg (Accessed on: 5  May 2022).

Thermal injuries occur when the ocular surface is directly exposed to heat, such as cooking oils. This causes coagulation of ocular surface proteins. Principles of treatment for thermal injuries are similar to those for chemical injuries. The main aim is to remove the offending agent and cool the eye. The eye should be copiously irrigated with 0.9% sodium chloride/Hartmann’s or water. Urgent ophthalmology opinion should be sought.

Dry eyes 

Dry eye is a collective term for disease processes leading to deficient tear volume or excessive evaporation, creating a diseased ocular surface which is often inflamed. It is a multifactorial disease, and prevalence ranges from 5-35% depending on the age group. The tear film has three components: a mucin layer (mainly secreted by goblet cells), an aqueous layer (mainly secreted by the lacrimal glands) and a lipid layer (secreted by meibomian glands). Dry eye occurs from an interaction of mechanisms: tear instability, tear hyperosmolarity, inflammation and ocular surface damage. Inflammation is a key component which is present in the majority of patients with dry eyes. Dry eyes are classified according to the 2007 dry eyes workshop (DEWS).

The following illustrates the classification of dry eyes according to the dry eyes workshop:

Aqueous deficient dry eye

• Sjogren syndrome (primary and secondary)
• Non-Sjogren syndrome
• Lacrimal deficiency
• Lacrimal gland obstruction
• Circatrizing conjunctivitis
• Reflex hyposecretion
• Systemic drugs

Evaporative dry eye

• Intrinsic
• Meibomian gland disease
• Lid disorders
• Low blink rate
• Drug-induced
• Vitamin A deficiencies
• Extrinsic
• Contact lens use
• Ocular surface disease
• Topical drugs preservatives

Common symptoms include redness, pain and discomfort, sensation of dryness, foreign body sensation, photosensitivity, burning sensation, stringy discharge, intermittent or constant blurred vision and reflex watering. Symptoms worsen over the course of the day and are exacerbated by conditions which increase evaporation (outside on a windy day) or decrease blink rate (staring at a screen). Patients might complain of other symptoms of associated disease, such as a dry mouth in Sjogren’s syndrome. Examination may reveal lid margin disease or evidence of contributing disorders, conjunctival hypereamia, decreased tear break-up time, mucous debris, decreased tear film column and punctate epithelial erosions. According to the DEWS, dry eyes can be graded in terms of severity on a scale of 1 to 4 (see table below).

SEVERITY	1	2	3	4
Discomfort, severity and frequency	Mild and/or episodic, occurs under environmental stress	Moderate, episodic or chronic stress or no stress	Severe, frequent or constant without stress	Severe and/or disabling and constant
Visual symptoms	None or episodic mild fatigue	Annoying and/or activity-limiting episodic	Annoying, chronic and/or limiting activity	Constant and/or possibly disabling
Conjunctival injection	None to mild	None to mild	+/-	+/++
Conjunctival staining	None to mild	Variable	Moderate to marked	marked
Corneal staining	None to mild	Variable	Marked/central	Severe punctate erosions
Corneal/tear signs	None to mild	Mild debris, meniscus	Filamentary keratitis, mucus clumping, tear debris	Filamentary keratitis, mucus clumping, tear debris, ulceration
Lid/meibomian glands	MGD variably present	MGD variably present	Frequent	Trichiasis, keratinization, symblepharon
Fluorescein tear break up time	Variable	≤10sec	≤5secs	immediate
Schirmer score	Variable	≤10mm/5min	≤5mm/5min	≤2mm/5min

Source: Adapted from Lemp MA, Baudouin C, Baum J, et al. The definition and classification of dry eye disease: Report of the definition and classification subcommittee of the international Dry Eye WorkShop (2007). In: Ocular Surface. 2007, pp. 75–92.

Diagnosis of dry eyes is clinical. Investigations include measurement of the tear break-up time, Schirmer’s test to assess the extent of tear production and ocular surface staining. Laboratory tests can be carried out in cases such as Sjogren’s syndrome to test for specific autoantibodies. Management aims to control symptoms and prevent complications. Treatment options are shown in treatment box 3 and are based on the severity of dry eye according to the grading system. Management should also be tailored according to the aetiology of dry eyes and should include treatment of the underlying disease process.

Treatment box 3
Grade 4	Grade 3 therapy and Systemic anti-inflammatories Surgical intervention
Grade 3	Grade 2 therapy and Serum eye drops Bandage contact lenses Permanent punctal occlusion
Grade 1	Patient education Lifestyle modification Environmental modification Modification of contact lens wear Medication review Lid therapy for blepharitis Artificial tears Manage associated ocular and systemic conditions
Grade 2	Grade 1 therapy and Topical anti-inflammatories Essential fatty acids Oral antibiotics (macrolide and tetracyline derivatives) Punctal plugs

Source: Adapted from Lin H, Yiu SC. Dry eye disease: A review of diagnostic approaches and treatments. Saudi J Ophthalmol 2014; 28: 173–181.

Grade 1 disease can be successfully managed in primary care settings, but Grade 2 and above will need specialist ophthalmic input. Children with dry eyes who have corneal changes should be referred urgently to ophthalmology. Patients suspected of having a systemic condition, persistent symptoms after 12 weeks or having abnormal eyelid structure of function should be referred to ophthalmology.  Complications of dry eyes include bacterial keratitis, corneal melt, corneal vascularisation, and corneal scarring.

Blepharitis

Blepharitis is inflammation of the eyelid margin. It is commonly a chronic condition with acute episodes of marked inflammation. Blepharitis is common; up to 37% of patients seen by ophthalmologists have been reported to have blepharitis. Blepharitis is a multifactorial disease and various interacting mechanisms such as chronic low-grade bacterial infection, inflamed skin from conditions such as eczema or acne rosacea and parasitic infestations. Blepharitis can be classified anatomically, although patients may have an overlap of different types.

The following is a classification system for blepharitis, adapted from ‘Blepharitis’:

• Anterior blepharitis
• Staphylococcal blepharitis
• Seborrheic blepharitis
• Posterior blepharitis/ Meibomian Gland Dysfunction
• Mixed blepharitis with elements of anterior and posterior disease

Anterior blepharitis occurs when there is disease around the eyelashes. It can be staphylococcal or seborrheic. In staphylococcal blepharitis, there is chronic low-grade infection around the base of the eyelashes with an immune response to the bacteria. It is more likely to occur in patients with a history of atopic dermatitis; clinically, there are often hard scales and collarettes around the base of the eyelashes. In seborrheic blepharitis, there is less inflammation than in staphylococcal cases, and there are soft, greasy scales with surrounding skin around the eyes and nasolabial folds greasy, in keeping with seborrheic dermatitis.

Posterior blepharitis can occur in patients with acne and seborrheic dermatitis but can also occur in patients without evidence of a skin condition. It is primarily a disease of the meibomian glands with meibomian gland dysfunction leading to dilatation and obstruction of the glands. The sebum normally acts as a surfactant, but with obstructed glands and decreased expression, the tears evaporate and tear film breaks up easily. Some patients also develop an immune response to the mite Demodex commonly found in hair follicles and sebaceous glands, and this causes blepharitis.

Symptoms are due to irritation of the lid and dry eyes. They include itching of the eyelids, burning sensation, foreign body sensation, watering, intermittent blurred vision, mild photophobia and crusting, particularly in the morning. Patients may also describe episodes of eyelid swelling and redness or give a history of chalazions and styes. Symptoms are commonly bilateral, although one eye may be more affected than the other and present in a relapsing and remitting course.

Examination may reveal scaling of the eyelashes, telangiectasia in the lid margin, eyelid redness and/or swelling and dilated and/or obstructed meibomian glands. Mild conjunctival hypereamia is common in flares. Tear break-up time may be decreased, and the corneal may have evidence of dryness and inflammation, such as punctate epithelial erosions. The patient may have a chalazion, and in those with long-standing disease, there may be notching and scarring of the lid margin and disorders of the eyelashes, such as depigmentation and misdirection.

Image Source: Wikimedia Commons (2017). Anterior Blepharitis, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Anterior_Blepharitis.jpg (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2012). Blepharitis, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Blepharitis.JPG (Accessed on: 5  May 2022).

Blepharitis is diagnosed clinically based on symptoms and slit lamp examination. It is a chronic condition, and as such, patient education is important. Treatment of blepharitis is usually lid therapy. Patients are advised to apply warm compresses (a microwaveable bag may be purchased) for 5-10 mins and then wash the eyelid gently with a cotton tip applicator with water or an additive such as sodium bicarbonate or tea tree oil if mite infestation. Patients with meibomian gland dysfunction or chalazions should massage the eyelids to express clogged ducts. Lid therapy can be practised a few times a week when stable and more frequently (a few times daily) in exacerbation of disease. Artificial tears can be used to treat dry eye symptoms. Topical antibiotics such as Fusidic acid or Erythromycin may be used to treat active folliculitis in anterior blepharitis. Patients, particularly those with meibomitis or rosacea, will benefit from a course of oral antibiotics (macrolides or tetracylines) to clear bacteria from the lid margin. In marked ocular inflammation, a short course of steroids will decrease inflammation and prevent complications related to this. Refer patients for same-day ophthalmology assessment if there are symptoms of corneal disease, there is rapid onset visual loss, orbital or pre-septal cellulitis is suspected and if the eye is red with red flag features. Chalazions are a common result of meibomian gland dysfunction, and treatment is as above. In patients with chalazions lasting several months despite optimal lid therapy, incision and curettage may be indicated.

Image Source: Wikimedia Commons (2010). Chalazion sup 02, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Chalazion_sup_02.jpg (Accessed on: 5  May 2022).

Image Source: Wikimedia Commons (2016). Chalazion2 01242005 (cropped), Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Chalazion2_01242005_(cropped).jpg (Accessed on: 5  May 2022).

Trichiasis

This occurs when individual eyelashes are misdirected posteriorly towards the conjunctiva and cornea. It is usually secondary to scarring from a previous inflammatory process, such as blepharitis or herpes zoster or secondary to trauma, which can be iatrogenic. Patients commonly complain of foreign body sensation, redness and discomfort, and in cases of corneal abrasions, corneal signs such as photophobia.

Image Source: Wikimedia Commons (2023). Trachoma 1, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Trachoma_1.png (Accessed on: 5  May 2022).

First line treatment is usually epilation of trichiatic lashes, and this usually lasts for a few weeks. It is temporary, and the lashes typically grow back, with patients requiring several sessions. Electrolysis of the affected area may be utilised, but this requires a few sessions to achieve a satisfactory result. Laser ablation, cryotherapy and surgical intervention are other applicable therapies.

References 

• Edwards RS. Ophthalmic emergencies in a district general hospital casualty department. Br J Ophthalmol 1987; 71: 938–942.
• Domingo E, Moshirfar M, Zabbo CP. Corneal Abrasion. Emerg Dep Analg An Evidence-Based Guide 2021; 184–187.
• La Rosa M, Lionetti E, Reibaldi M, et al. Allergic conjunctivitis: a comprehensive review of the literature. Ital J Pediatr 2013; 39: 18.
• Patel DS, Arunakirinathan M, Stuart A, et al. Allergic eye disease. BMJ 2017; 359: j4706.
• NICE. Conjunctivitis – allergic | Health topics A to Z | CKS | NICE, https://cks.nice.org.uk/topics/conjunctivitis-allergic/ (2020, accessed 23 May 2022).
• Deschenes J, Murray PI, Rao NA, et al. International Uveitis Study Group (IUSG) Clinical Classification of Uveitis. http://dx.doi.org/101080/09273940801899822 2009; 16: 1–2.
• NICE. Uveitis | Health topics A to Z | CKS | NICE, https://cks.nice.org.uk/topics/uveitis/ (accessed 24 May 2022).
• Huang J, Maxwell E. Uveitis Straight to the point of care. BMJ Best Pract 2022; 63.
• Burkholder BM, Jabs DA. Uveitis for the non-ophthalmologist. BMJ; 372. Epub ahead of print 3 February 2021. DOI: 10.1136/BMJ.M4979.
• Sainz De La Maza M, Molina N, Gonzalez-Gonzalez LA, et al. Clinical Characteristics of a Large Cohort of Patients with Scleritis and Episcleritis. Ophthalmology 2012; 119: 43–50.
• Sims J. Scleritis: presentations, disease associations and management. Postgrad Med J 2012; 88: 713–718.
• Friedman DS, Foster PJ, Aung T, et al. Angle closure and angle-closure glaucoma: what we are doing now and what we will be doing in the future. Clin Experiment Ophthalmol 2012; 40: 381–387.
• Khondkaryan A, Francis BA. Angle-closure Glaucoma Straight to the point of care. BMJ Best Pract 2019; 1–39.
• Said DG, Dua HS. Chemical burns acid or alkali, what’s the difference? Eye 2019 348 2019; 34: 1299–1300.
• Singh P, Tyagi M, Kumar Y, et al. Ocular chemical injuries and their management. Oman J Ophthalmol 2013; 6: 83.
• Lin H, Yiu SC. Dry eye disease: A review of diagnostic approaches and treatments. Saudi J Ophthalmol 2014; 28: 173–181.
• Lemp MA, Baudouin C, Baum J, et al. The definition and classification of dry eye disease: Report of the definition and classification subcommittee of the International Dry Eye WorkShop (2007). In: Ocular Surface. 2007, pp. 75–92.
• NICE. Scenario: Management | Management | Dry eye syndrome | CKS | NICE, https://cks.nice.org.uk/topics/dry-eye-syndrome/management/management/ (2017, accessed 15 June 2022).
• Eberhardt M, Rammohan G. Blepharitis. StatPearls, https://www.ncbi.nlm.nih.gov/books/NBK459305/ (2022, accessed 15 June 2022).
• NICE. Blepharitis | Health topics A to Z | CKS | NICE, https://cks.nice.org.uk/topics/blepharitis/ (2019, accessed 15 June 2022).