The Red Eye - Chapter 4 PDF

CHAPTER 4 THE RED EYE Having a red eye is often a disturbing symptom for the patient and an alarming sign for the physician. From a clinical standpoint, the complaint may be of acute onset and short duration or of chronic nature and long protracted or recurrent course. When the eye appears red, this...

CHAPTER 4 THE RED EYE Having a red eye is often a disturbing symptom for the patient and an alarming sign for the physician. From a clinical standpoint, the complaint may be of acute onset and short duration or of chronic nature and long protracted or recurrent course. When the eye appears red, this often means that the blood vessels in the conjunctiva, sclera, or episclera are dilated and engorged. This dilatation and engorgement is called injection. It is important to differentiate between two types of injection: conjunctival injection and ciliary injection (Table 4-1 & Fig. 7- 1, 7-2). Conjunctival injection is associated with conjunctival pathology especially conjunctivitis, whereas ciliary injection is more serious and indicates inflammation of the cornea, iris, or ciliary body.Chapter:7 The Red Eye ACUTE RED EYE Acute red eye can be caused by a rather simple disorder, such as subconjunctival hemorrhage which does not usually require any treatment, or mild infectious conjunctivitis that can be treated easily by the primary care provider, and in some cases, might even resolve spontaneously. On the other hand, the red eye can point to a much more serious condition leading to loss of sight or indicating an underlying systemic disease that must be attended to. It is important to recognize those cases that can be treated by the general physician and those that must be referred to an ophthalmologist without delay. CONJUNCTIVITIS Conjunctivitis is inflammation of the bulbar and/or palpebral conjunctiva. It can be caused by an infectious agent such as bacteria, viruses, or chlamydia. It can also be caused by an allergic situation such as phlyctenular conjunctivitis or vernal kerato conjunctivitis (spring catarrh). The hallmark of conjunctivitis is hyperemia and discharge. Classifying conjunctivitis according to the type of discharge can be helpful: Purulent or mucopurulent: bacterial or chlamydia infection. Mucoid: allergic disease or secondary to dry eye. Watery: viral conjunctivitis.Chapter:7 The Red Eye 1. Acute bacterial conjunctivitis Etiology: It is inflammation of the conjunctiva caused by gram-positive bacteria such as Staphylococci and Streptococcus pneumoniae and viridans and gram-negative bacteria such as Hemophilus influenzae, Neisseria gonorrhoeae, Pseudomonas aeruginosa, and Moraxella. Clinical Picture: Symptoms: 1. Lid edema. 2. Hyperemia of the conjunctiva (injection). 3. Mucopurulent or purulent discharge (Fig. 7-3). 4. Foreign body sensation Fate and complications: Spontaneous cure may occur within 1 or 2 weeks without treatment, and in a much shorter time with treatment. May tum into chronic bacterial conjunctivitis if untreated. Secondary keratitis with possible corneal ulceration (central, marginal or even ring ulcers). Management: A. Prevention: Bacterial conjunct1v1t1s 1s very contagious. Therefore, standard infection control measures should be followed. B. Treatment: 1. Antibiotics a. Broad spectrum antibiotic drops. Commonly used ones include the fol lowing: i. Norfloxacin and ciprofloxacin are quinolone antibiotics with broad-spectrum activity and low toxicity. ii. Other antibiotics include chloramphenicol, gentamycin, tobramycin, and neomyc1n. (It is noteworthy that some of the topical antibiotics that are not used systemically due to their extensive side effects are excellent choices for topical use due to their broad spectrum effectiveness and excellent tolerability). They are instilled 4-6 times daily (sometimes more frequently in the more severe situations with the additional benefit of a rinsing effect for the profuse discharge). b. Antibiotic ointments: ointments provide higher concentration of antibiotic for a longer period of time than drops, therefore they are used at bedtime.Chapter:7 The Red Eye c. Systemic antibiotics are indicated only in exceptional situations such as gonorrheal and chlamydia! infections. 2. Culture and sensitivity studies are not routinely requested in simple uncomplicated bacterial conjunctivitis. 2. Neonatal Conjunctivitis or Ophthalmia Neonatorum It is a preventable disease occurring in newborn babies (see chapter 1 0). 3. Acute viral conjunctivitis Etiology: The most common causative viral agents are adenoviruses. Viral infections are well known to occur in epidemics hence the name: epidemic keratoconjunctivitis (EKC). Herpes simplex and Herpes Zoster are the second most common causes. Other viral causes include acute viral fevers such as measles, mumps, chicken pox, and influenza. Clinical Picture: Symptoms: Often the patient presents with unilateral involvement at first. Hyperemia. Watery eye is the prominent symptom with either absent or scanty mucous discharge. Some cases present with sudden onset of subconjunctival hemorrhage (acute hemorrhagic conjunctivitis) Signs: Palpebral conjunctival follicles (Fig. 7-4). Punctate epithelial keratitis (Fig. 7 -5). Lid vesicles in herpetic cases (Fig. 7 -6).Chapter:7 The Red Eye Tender preauricular lymph nodes.Chapter:7 The Red Eye Fate: Self-limiting, resolving in 7-14 days. Involvement of the fellow eye often occurs. Management:. Prevention: Viral conjunctivitis is highly contagious and infection transmission precautions must be followed. Also, doctors must be cautious when examining a case of conjunctivitis, especially those suspected to be adenoviral, to avoid transmitting the disease from one patient to another. Treatment: No topical or systemic antivirals are known to be effective in adenoviral infections. Therefore, symptomatic treatment with cold compresses and artificial lubricants is often the only regimen. Also, mild topical corticosteroid eye drops may help decrease inflammation and relieve symptoms, but Herpes must be excluded first. 4. Acute Non-infective Conjunctivitis Acute allergic conjunctivitis Etiology: Allergic conjunctivitis is an eye inflammation caused by an allergic reaction to an exogenous antigen like pollen, dust, mites, contact lens solution, or topical medications. It often occurs in people with a strong personal or family history of allergies. When the eyes are exposed to an inciting substance, the response is a release of histamine and other active mediators by mast cells, which stimulate the dilation of blood vessels, cause irritation of nerve endings, and increase the secretion of tears (Type I hypersensitivity).Chapter:7 The Red Eye Clinical picture: (minutes after exposure): Symptoms Itching is the most typical symptom of ocular allergy. Redness, lid puffiness (edema) and conjunctival edema. Tearing or mucoid discharge. Signs  Conjunctival papillae are found on examination of the palpebral conjunctiva (Fig. 7 -7). Prevention strategies: A voiding or limiting exposure to the environmental factors that cause allergic conjunctivitis if known. Treatment: Cold compresses are usually beneficial. Decongestant eye drops provide symptomatic relief. Antihistamines such as diphenhydramine and chlorpheniramine eye drops can attenuate allergic symptoms by about 40-5 0%. Mast cell stabilizers such as disodium cromoglycate eye drops. More severe cases require topical corticosteroids. However, long-term use of the more potent steroids can result in secondary glaucoma in predisposed persons. Non-steroidal anti-inflammatory eye drops (NSAIDs) are safe and sometimes effective. Allergen immunotherapy treatment may be tried. It involves administering certain small doses of allergens for desensitization. Phlyctenular Keratoconjunctivitis Etiology: This occurs commonly in children and young adults as a result of type IV hypersensitivity to microbial antigens (most commonly Staphylococcus aureus but Chapter:7 The Red Eye also Mycobacterium tuberculosis in endemic areas).e.g. tonsillitis, T.B. and intestinal parasites. Symptoms: The patient presents with watering, redness, and photophobia. Signs: Phlyctens are single or multiple greyish-yellow elevated inflammatory lesions at the limbus or Fig. 7-8: Phlyctenular Keratoconjunctivitis conjunctiva surrounded by intense injection of blood vessels (Fig. 7 -8). The lesion ulcerates and then heals with vascularization in the involved area over 2-3 weeks. Recurrences can occur at the edge and may rarely progress toward the center of the cornea. Treatment: Dark glasses may help alleviate the symptoms. Treatment of the cause of allergy if an infection is identified. Topical steroids are usually very effective but should not be used for long time. Corneal Ulcer & Keratitis A corneal abrasion means loss of epithelium. A corneal ulcer means loss of epithelium with involvement of the stroma (may be infectious or non-infectious). Keratitis means infiltration of the cornea with leucocytes which may be ulcerative or non-ulcerative. Bacterial keratitis: Etiology: The common causative bacterial organisms of corneal ulcer are as follows: Chapter:7 The Red Eye i. Gram-positive: Staphylococcus aureus, Staph. a/bus, Streptococcus hemolyticus, Staph. pneumoniae (Pneumococcus). ii. Gram-negative: Neisseria gonorrhoeae (gonococcus), N. meningitidis (meningococcus), Pseudomonas aeruginosa, Proteus. Predisposing factors: 1. Epithelial damage due to trauma, e.g. foreign body or misdirected eyelash. 2. Poor general resistance (such as in immune-compromised patients). 3. Xerosis (vitamin A deficiency). 4. Corneal edema may lead to desquamation of epithelium. 5. Neuroparalytic keratitis, e.g. herpes zoster, leprosy. 6. Exposure of the cornea due to proptosis or lagophthalmos. The course of a corneal ulcer depends on the virulence of the infecting agent, the host defense mechanism and the treatment received. Clinical picture: Symptoms: 1. Pain and photophobia (caused by mechanical and chemical irritation of the exposed nerve endings). 2. Foreign body sensation and reflex lacrimation (occur due to mechanical friction by the lids). 3. Blurred vision (results from corneal haze). 4. Redness of the eyes (occurs due to the injection of circumcorneal vessels). Signs 1. Lid edema. 2. Conjunctival chemosis. 3. Ciliary injection. 4. The corneal ulcer itself appears as an epithelial defect seen on slit lamp examination and confirmed by the fluorescein test (see box). The epithelial defect is often associated with greyish-white infiltration and/or edema (Fig. 7-9). Fluorescein Test Topical fluorescein is a water-soluble dye that can be used to stain corneal epithelial defects and ulcers. Fluorescein does not stain the intact corneal epithelium because the normal epithelial cell walls are hydrophobic. Areas of denuded epithelium allow the water soluble fluorescein to diffuse into the stroma thus highlighting the extent of the ulceration. After it is instilled in the eye, fluorescein stained areas appear as a green fluorescence when it is observed by blue light.Chapter:7 The Red Eye 5. Some degree of secondary iritis may follow resulting in varying degrees of anterior chamber reaction flare, cells, or even pus in severe cases. The latter is described as "hypopyon ulcer". Complications of corneal ulcer: In its acute phase, the most dreaded complication of a corneal ulcer is perforation (Fig. 7-1 0). Referral of any aggressive or persistent ulcer to an ophthalmologist is a necessity as many complications can follow if corneal perforation occurs. The most serious complications are endophthalmitis and secondary glaucoma. Microbiological investigations: A scraping: a smear is taken for bacteriological examinations. This is often essential to identify the causative organism, confirm the diagnosis, and guide the treatment.Chapter:7 The Red Eye Treatment of corneal ulcer: A bacterial corneal ulcer is a vision-threatening condition that demands prompt treatment by eradication of the causative bacteria. 1. The specific treatment Topical antibiotics: Initial therapy (before results of culture and sensitivity are available) should be with combination therapy of broad-spectrum antibiotics to cover both gramnegative and gram-positive organisms. Systemic antibiotics are usually not required. This is because the cornea is avascular and therefore systemic antibiotics have very poor penetration to the ulcer area. 2. Non-specific treatment Cycloplegic drugs: Preferably 1% atropine eye ointment or drops should be used to reduce pain from ciliary spasm, and to prevent the formation of posterior synechiae from secondary iridocyclitis. Systemic analgesics and anti-inflammatory drugs such as paracetamol relieve the pain and decrease the edema. Vitamins (A, B-complex, and C) may help in early healing of ulcers. 3. Physical and general measures Patching of the eye with a corneal ulcer helps relieve the pain caused by extreme sensitivity of the corneal nerves when the epithelium is denuded, and facilitates healing by preventing repeated friction by the lids during blinking. Hot fomentation: local application of heat gives comfort, reduces pain and causes vasodilatation which helps to bring antibodies. Viral KeratitisChapter:7 The Red Eye Most of the viruses tend to affect the epithelium of both the conjunctiva and the cornea, hence the typical viral lesions are described as viral keratoconjunctivitis. Common viral infections include herpes simplex keratitis, herpes zoster ophthalmicus, and adenovirus keratitis. Herpes Simplex Keratitis Ocular infection with herpes simplex virus (HSV) is extremely common. It causes herpetic keratoconjunctivitis and/or iritis. Etiology : HSV is of two types: HSV type I which typically causes infection above the waist (herpes labialis) and HSV type II which causes infection below the waist (herpes genitalis ). The type that affects the eye is usually type I and rarely type II. Herpes simplex virus (HSV) is a neurotropic virus that resides in the Gasserian ganglion of the fifth nerve. Primary infection usually occurs in early childhood when the child comes in contact with an infected or carrier adult. It usually results in mild signs and symptoms such as vesicular skin lesions in the lids or periorbital area, follicular conjunctivitis, punctate keratitis, or dendritic ulcer. Ocular involvement by HSV occurs in two forms, primary and recurrent. Most herpetic ulcers seen in adult patients are of the recurrent type. The virus lies dormant in the trigeminal ganglion. If immunity decreases, it periodically reactivates and causes recurrent disease. Predisposing factors: Predisposing stressful stimuli which may trigger an attack of herpetic keratitis include: fever, flu, exposure to ultraviolet rays, general ill- health, emotional or physical exhaustion, mild trauma, as well as topical or systemic steroids. Sometimes even the stress of menstruation or exposure to direct sunlight may be the only association. Clinical picture: Symptoms: same as bacterial keratitis Signs: Ocular lesions of herpes simplex 1. Active epithelial keratitis i. Punctate epithelial keratitis. ii. Dendritic ulcer (Fig. 7- 1 1) This is the typical lesion of recurrent epithelial keratitis. The ulcer is of an irregular linear branching shape. The branches are generally knobbed at the ends. The floor of the ulcer stains with fluorescein and the virus-laden cells at the margin take up Rose Bengal (double staining). There is an associated marked diminution of corneal sensations. Chapter:7 The Red Eye iii. Geographic ulcer Sometimes, the branches of a dendritic ulcer enlarge and coalesce to form a large epithelial ulcer with a 'geographic' or 'amoeboid' configuration (Fig. 7- 1 2). 2. Stromal keratitis Disciform keratitis (a central disc of persistent corneal edema) 3. Herpetic iridocyclitis. Treatment: I. Specific treatment Topical antiviral, acyclovir 3% ointment 5 times/day, until epithelial healing occurs. This should normally be discontinued after 1 0-14 days in order to avoid toxic keratopathy. If there are signs of toxicity, an alternative to topical treatment is oral antiviral treatment. II. Non-specific supportive therapy and physical and general measures are the same as for bacterial corneal ulcers. Herpes Zoster Ophthalmicus Herpes Zoster Ophthalmicus is an infection of the Gasserian ganglion of the fifth cranial nerve by the varicella-zoster virus (VZV). Etiology: The varicella-zoster virus is neurotropic in nature. The infection is usually contracted in childhood, and may manifest as chickenpox. The virus then remains dormant in the sensory ganglion of the trigeminal nerve. It is thought that, with depressed cellular immunity, the virus reactivates. Clinical features: In herpes Zoster Ophthalmicus, the frontal nerve is more frequently affected than the lacrimal and nasociliary nerves.Chapter:7 The Red Eye Hutchinson's rule, implies that ocular involvement is frequent if the patient presents with vesicles on the side or tip of the nose (cutaneous involvement of nasociliary nerve). Lesions of herpes zoster are strictly limited to one side of the midline of the head Clinical phases of HZO are: i. Acute, which may totally resolve. ii. Chronic, which may persist for years. iii. Relapsing, where the acute or chronic lesions reappear years later. Symptoms: A. General features: the onset of illness is sudden with fever, malaise, and severe neuralgic pain along the course of the affected nerve. B. Cutaneous lesions in the area of distribution of the involved nerve. Redness is followed by vesicle formation and then pustules, which subsequently burst to become crusting ulcers. When crusts are shed, sometimes permanent pitted scars are left (Fig. 7-1 3). Signs: A. Ocular complications usually appear at the subsidence of skin eruptions and may present as a combination of two or more of the following lesions: 1. Conjunctivitis: shows features ofviral conjunctivitis. 2. Zoster keratitis: Fine or coarse punctate epithelial keratitis. Microdendritic epithelial ulcers. Unlike dendritic ulcers of herpes simplex, these are usually peripheral and stellate rather than exactly dendritic in shape. They have tapered ends, (not bulbs) (Fig. 7- 1 4). Nummular or disciform keratitis (multiple discrete spots of corneal infiltrations) (Fig. 7- 1 5). Diminution of corneal sensation is more severe than that of HSV. Neuroparalytic ulceration may occur.Chapter:7 The Red Eye Treatment: Contrary to Herpes Simplex where local therapies are the main line of treatment, systemic therapy for Herpes Zoster virus is the treatment of choice. 1. Oral antiviral drugs: the treatlnent should be started imtnediately after the onset of the rash Acyclovir is given in a dose of 800 mg 5 times/ day for 10 days. 2. Analgesics. 3. Systemic steroids may be given under the cover of systemic antivirals. The rationale is that they help to inhibit the development of post-herpetic neuralgia when given in high doses. II. Local therapy for ocular lesions a) Topical acyclovir 3% eye ointment 5 times /day for about 2 weeks. b) Topical steroid eye drops 4 times/day. c) Cycloplegics such as cyclopentolate eyedrops or atropine eye oinhnent tnay be given. Topical antibiotics are only used to prevent secondary infections. Fungal Corneal Ulcer Etiology: 1. Causative fungi: May be filamentous fungi such as Fusarium or yeast-like fungi such as Candida. 2. Modes of infection i. Injury by plant material such as a crop leaf or a branch of a tree. ii. Secondary fungal ulcers are common in patients who are immunosuppressed. Clinical features: Chapter:7 The Red Eye Symptoms are similar to the central bacterial corneal ulcer but less marked. Usually, a big hypopyon is present even if the ulcer is very small. Perforation in mycotic ulcers is rare. Corneal vascularization is absent (Fig. 7 -16). Laboratory investigations are required for confirmation of the diagnosis. Treatment: Topical antifungal eye drops should be used for a long period (6 to 8 weeks). Protozoal Keratitis (Acanthamoeba) Etiology: Acanthamoeba IS a free-living amoeba found In soil and fresh water. Swimming pools are particularly important. Mode of infection: Corneal infection with acanthamoeba results from direct corneal contact with any material or water contaminated with the organism. Contact lens wearers who do not observe strict hygienic rules, or use home-made saline (from contaminated tap water and saline tablets) are the group at highest risk for acanthamoeba infection. Clinical picture: Symptoms: Very severe relentless pain which is out of proportion to the degree of inflammation in a contact lens wearer is the hallmark of acanthamoeba infection. Signs: Usually, it is a central ring-shaped lesion with stromal infiltrates, and an overlying epithelial defect with radial perineuritis (Figs. 7-1 7, 7-1 8). Treatment: It is very resistant to treatment. Propamidine isethionate (Brolene) drops for up to one year. Penetrating keratoplasty is frequently required in non-responsive cases. Chapter:7 The Red Eye Episcleritis Episcleritis is an inflammation (often sectoral) of the episclera (the vascular layer between the conjunctiva and the sclera). The condition is uncommon and has the following features: no discharge, non-threatening to vision, and often shows tenderness over the inflamed area. If recurrent, it may be associated with an underlying systemic inflammatory or autoimmune disease (Fig. 7 -19). Scleritis Scleritis is inflammation of the sclera. It can occur with or without associated autoimmune diseases (e.g., rheumatoid arthritis, granulomatosis with polyangiitis). Scleritis can be localized or diffuse. It is uncommon, often protracted, and usually accompanied by pain that may be severe. A violaceous hue of sclera may indicate serious systemic disease such as a collagen vascular disorder (Fig. 7-20). Scleritis and episcleritis can be manifestations of chronic inflammatory or autoimmune disease. Photophthalmia It is inflammation of the cornea and conjunctiva due to exposure to intense light of short wavelength as in exposure to an ultraviolet lamp or arc welding. Symptoms (typically after a few hours): Chapter:7 The Red Eye Severe burning or aching pain. Watery or mucoid discharge. Photophobia and blepharospasm. Signs Hyperemia. Punctate corneal erosions may be seen. Treatment: Cold compresses. Application of a pad and bandage (without antibiotic drops) for 24 hours heals most of the cases. Oral analgesics if pain is intolerable. Topical anesthetic drops may be needed once or 'twice for temporary pain relief. This is to be used by the physician only and never by the patient. Acute Angle Closure Glaucoma Acute angle closure is an ophthalmic emergency, because, if left untreated, it can result in irreversible visual loss within hours due to the high level of lOP. Pathophysiology Mechanism of angle closure: (Fig. 7-2 1) Iris bombe 1s the usual underlying mechanism. The pupil is considered the bottle neck in the route of aqueous circulation from the posterior chamber to the anterior chamber. This relative narrowing is called relative pupillary block. The pressure in the posterior chamber (PC) rises in comparison to that of the anterior chamber (AC). In the mid-dilated state, the iris becomes redundant enough to bow forwards in an anterior curve called- iris bombe. The result can be contact between the peripheral iris and the periphery of the cornea with resultant acute closure of the anterior chamber angle. When the angle of the AC is thus closed, the lOP rises to very high levels. Predisposing (risk) factors for angle closure include having a small (hypermetropic) eye with shallowing of the anterior chamber which occurs towards the middle life (due to lens growth). Females are more prone to ACG. One of the precipitating factors is moderate pupillary dilation during emotional excitement, staying in the dark, or application of mydriatics for fundus examination. For the first 24-48 hours, the iris is adherent to the cornea with simple apposition or loose fibrin, so the situation can be reversible with medical treatment. Longer contact between the iris and the cornea may result in adhesions between the iris and the cornea (called peripheral anterior synechia) and will require surgery. Clinical picture: Chapter:7 The Red Eye Symptoms: Acute pain (due to stretching of ocular coats). Strong headache referred along the trigeminal nerve. Rapid drop of vision due to severe corneal eden1a. Colored haloes are seen around lights.  Nausea and vomiting that may simulate acute abdomen due to reflex vagal stimulation. There may be a history of previous intermittent episodes of pain and blurred vision (intermittent or subacute angle closure). Signs: Red eye characterized by ciliary injection. A marked increase in lOP. Severe corneal edema and haze. Very shallow AC (Fig. 7-22). Semi-dilated irreactive (fixed) pupil that is frequently vertically oval (Fig. 7-22). Rapid drop of vision (down to PL in so1ne cases). The optic disc may not be visualized due to loss of corneal clarity (corneal edema). Gonioscope examination of the fellow eye is essential to look for an occludable angle (Fig. 7-23)Chapter:7 The Red Eye The fate of the attack: If medically treated early enough (before the development of peripheral anterior synechiae), the pressure drops, the pupil constricts and the angle opens again. If left untreated, the optic nerve rapidly atrophies and vision is pennanently lost (absolute glaucoma). Treatment: The definitive treatment of acute angle-closure glaucoma (AACG) is surgical. Initial medical treatment aims at lOP reduction, suppression of inflammation, and reversal of angle closure to provide favorable conditions for surgery. 1 - Hospitalization. 2- Hyperosmotic agents: Mode of action - These agents increase the plasma tonicity or osmolality. This helps to draw water out of the eyes with subsequent lowering of the intraocular pressure. The most commonly used is intravenous mannitol (20%) 1 -2 g/kg body weight. A 20% solution is given over 3 0-40 minutes. 3- Carbonic anhydrase inhibitors: as oral tablets or intravenous injection. 4- Topical miotics: Pilocarpine 2-4% every 15 minutes initially then every 30 minutes until the pupil constricts. Thereafter, it is used four times daily till surgery. This is effective in pulling the iris away from the angle and opening the drainage channels. Miotics also increase the aqueous outflow. It is to be noted that miotics, though very effective, are not expected to act unless the lOP is initially reduced by hyperosmotic agents. This is because very high lOP results in ischemic paralysis of the constrictor muscle. Chapter:7 The Red Eye 5- Topical B-blockers to reduce the aqueous formation. 6- Topical steroids to relieve the inflammation. 7- Analgesics and anti-emetics. Gonioscopy must be done after medical control of the acute attack to see the presence and extent of such adhesions: i. If the attack is aborted within 24 hours and the angle closure by PAS is not extensive (50% or more of the angle is open), then laser iridotomy or surgical iridectomy should be sufficient. ii. If the angle closure by PAS is more than 50% (occurs tn longer attacks), a filtration operation, e.g. trabeculectomy is needed (See chapter 6). iii. Cataract extraction (see Box) There is a recent trend of performing phacoemulsification and IOL implantation as soon as the lOP is reduced medically. This is expected to relieve the pupillary block permanently, deepen the AC and bring long-term better lOP control. The Other Eye Laser peripheral iridotomy is indicated in the fellow eye if gonioscopy has revealed an occludable angle. Acute Iridocyclitis (Anterior Uveitis) Uveitis is defined as inflammation of the uveal tract, which is further subdivided into anterior, intermediate, and posterior components (Fig.7-25). The anterior part is composed of the iris and ciliary body. Uveitis may be triggered by genetic, trautnatic, immune, or infectious mechanisms. However, it is cotnmonly idiopathic (in more than 50% of cases). Inflammatory cells, exudates, and/or toxins pour into the narrow spaces of the eye: anterior chamber, posterior chamber, retrolental space, and anterior vitreous causing Chapter:7 The Red Eye the clinical picture and complications. Etiology: Non-infectious 1) Idiopathic (most common). 2) Juvenile idiopathic arthritis (JIA). 3) Sarcoidosis causes granulomatous uveitis. 4) Behcet's disease: an autoimmune disease commonly seen in young and middle aged males. It is associated with orogenital ulcers, arthritis, and thrombophlebitis in addition to ocular inflammation (anterior and posterior uveitis with possible hypopyon, vitritis, retinal vasculitis, and papillopathy) (Figs. 7-26, 7 -27).Chapter:7 The Red Eye Vogt Koyanagi Harada (VKH) syndrome: a multisystem disorder with panuveitis, exudative retinal detachment, vitiligo, pol iosis, and neurological manifestations including headache and possible deafness (Fig. 7 -28) 6) Secondary to some ocular causes such as traumatic or hypermature cataract, retinal detachment and some intraocular tumors. InfectiousChapter:7 The Red Eye Viral: HSV (herpes simplex virus) and HZV (herpes zoster virus) Bacterial: Tuberculosis, syphilis, or Lyme disease can cause granulomatous uveitis. Fungal. Symptoms: Symptoms are those of acute inflammation: Neuralgic pain is a prominent symptom. Redness, photophobia, increased lacrimation.. Defective vision occurs due to: Corneal epithelial edema with increased lOP. Precipitation of inflammatory cells on the back of the cornea ( keratic precipitates or K.Ps) (Fig. 7- 29). Turbidity of aqueous by plasma proteins (aqueous flare). Miosis and spasm of ciliary muscle that may cause induced myopia. Macular edema due to posterior diffusion of inflammatory toxins (Fig. 7 - 30). Chapter:7 The Red Eye Aqueous Flare Normally limited proteins are present in the aqueous due to the presence of a blood aqueous barrier, which prevents excessive plasma protein molecules from accumulating inside the aqueous and keeps it clear. During inflammation, as in uveitis, chemical mediators (such as cytokines) cause breakdown of the blood aqueous barrier resulting in excessive plasma protein leakage and accumulation inside the anterior chamber. This is clinically seen as "aqueous flare" and is a measure of active inflammation inside the eye. Signs: Red eye: often circumcorneal injection. Cornea: keratic precipitates (white blood cells) on the endothelium are a hallmark of iritis. They may be large, so-called mutton fat type seen in granulomatous uveitis (e.g. sarcoid, tuberculosis, syphilis, Lyme disease). Corneal edema may be present. Anterior chamber: cells and flare, fibrin, hypopyon. Iris: loss of normal iris pattern (muddy iris). Pupil: miosis, may be irregular due to posterior synechiae. lOP: may be low (ciliary body inflammation and failure), normal, or high. Dilated posterior segment examination: it is mandatory to exclude signs of posterior segment inflammation such as vitritis, retinal detachment, or tumor. Investigations: Routine extensive laboratory work up is NOT required in many cases of uveitis since idiopathic cases are the majority and most causes or associations can be diagnosed or suspected on clinical grounds only. Lab work, if needed, must be targeted toward the suspected clinically diagnosed etiology. Chapter:7 The Red Eye A nonspecific workup may be requested only if the history and the physical examination findings are unremarkable and/or in the presence of uveitis that is granulomatous or recurrent. The following tests may be of help: Complete blood cell (CBC) count. Erythrocyte sedimentation rate (ESR). Antinuclear antibody (ANA). Venereal disease research laboratory (VDRL) and Rapid plasma reagin test (RPR) for syphilis. Purified protein derivative (PPD) for T.B or better IGRA (Interferon Gamma Release Assay). Lyme antibody titre. HLA (such as B27 and B5) testing. Chest radiography (to assess for sarcoidosis or tuberculosis). Infectious workup (for HIV/toxoplasmosis), depending on the presentation. Complications: Uveitic glaucoma: cells and exudates in the anterior chamber can clog the angle. Posterior synechiae: fibrin will cause adhesions between the two adjacent surfaces (back of the iris and anterior lens surface). In early cases, the synechia can be broken by mydriatics but later on, fibrin becomes fibrous causing permanent adhesions (Fig. 7 -32). Ring synechia: adhesions between the back of the pupil and the anterior lens preventing the passage of aqueous from the posterior to the anterior chamber pushing the iris forward (iris bombe). The anterior surface of the iris is thus close to the back of the cornea at the periphery and peripheral anterior synechia (PAS) can close the angle permanently (Figs. 7- 33, 7-34, 7-3 5).Chapter:7 The Red Eye Other complications can occur as complicated cataract and cystoid macular eden1a and even atrophic globe (atrophia bulbi). Management: Treatment of anterior uveitis mms to alleviate the patient's symptoms, prevent, and treat complications. Initially 1. Cycloplegia relieves pmn and prevents posterior synechiae: cyclopentolate 1 °/o TDS or atropine 1 %. 2. Topical corticosteroid treatment: the great majority of cases will respond to topical corticosteroids drops (e.g. dexamethasone 0. 1% or prednisolone 1% ). They are given hourly by day and in ointment form at night. 3. Alternatives to topical treatment are subconjunctival delivery for severe cases. Periocular and systemic steroids are very rarely needed in anterior uveitis. Chapter:7 The Red Eye 4. Ocular hypotensive treatment: if necessary. 5. Appropriate antimicrobial treatment in infectious cases. Later Gradual tapering of topical steroid treatment is necessary to avoid recurrence/rebound of inflammation, four weeks taper may be suitable in most cases. Some cases require extended therapy with topical steroid eye drops once or twice daily. Secondary glaucoma in cases of uveitis can occur due to: 1) Cellular trabecular block, 2) Steroid response, 3) Acute angle closure due to iris bombe, 4) Synechia! angle closure and 5) Neovascularization in rubeosis.Chapter:7 The Red Eye Endophthalmitis Definition: Endophthalmitis is an inflammatory condition of the intraocular cavities (i.e., the aqueous and/or vitreous humor) usually caused by infection. Panophthalmitis is inflammation of all coats of the eye together with intraocular structures (Fig. 7 -36). Etiology: There are 2 types of endophthalmitis: endogenous (i.e., metastatic) and exogenous. Endogenous endophthalmitis results from the hematogenous spread of organisms from a distant source of infection (e.g. endocarditis). Exogenus endophthalmitis results from direct inoculation of an organism from the outside as a complication of ocular surgery, foreign bodies, and/or blunt or penetrating ocular trauma. Diagnosis: Endophthalmitis is a clinical diagnosis. It should be supported by a culture of intra ocular fluids, although a negative culture occurs in more than 30% of cases. The patient complains of decreased vision, red eye, and ocular pain. Patients may feel otherwise well and are usually afebrile. On physical examination, vision is decreased, the conjunctiva is injected, and a hypopyon is present in most cases. There are white blood cells in the aqueous humor and vitreous humor, so the view of the retina is hazy. The differential diagnosis of infectious endophthalmitis is sterile intra-ocular inflammation. The latter may occur as a reaction to surgery and is typically greatest on the first postoperative day, whereas infective endophthalmitis usually occurs on the second day or later. These cases are medical emergencies, as delay in treatment may result in permanent vision loss. Treatment: Systemic antibiotics alone are not effective in treating endophthalmitis because of poor intraocular penetration. Intravitreal antibiotics (vancomycin plus ceftazidime) are given after a sample of vitreous is taken. Whereas initial therapy is empirical, subsequent injections may be tailored according to culture results. Vitrectomy is the line of treatment resot1ed to in the more severe cases especially those with vision of HM or less Chapter:7 The Red Eye Orbital Cellulitis Definition: This is inflammation of the soft tissue posterior to the orbital septum. Symptoms: Patients may have proptosis, decreased ocular mobility, ocular pain, and tenderness in eye movement (Fig. 7-3 7). Typically, orbital cellulitis is not associated with a drop of vision unless the eye globe is involved. Fever and leukocytosis are usually present in children, but they may be absent in adult. Etiology: The greatest majority of cases occur secondary to pre-existing sinus infections (spread from the ethmoid is most common). Less common causes include orbital surgery, facial fractures, and dacrocystitis. Microbiology: streptococcus, staphylococcus, H. Influenza, and anaerobes. Investigations: should be confirmed with imaging (CT or MRI), to evaluate the extent of retroorbital involvement and if an orbital abscess has developed. Treatment: hospitalization, IV antibiotics (broad-spectrum coverage of staph, strep, and anaerobes). In case of abscess formation, an incision is done for drainage. Management should better be done in conjunction with ENT consultation. Chapter:7 The Red Eye Complications of orbital cellulitis can include localized abscesses, intracranial extension causing intracranial abscess, meningitis, or cavernous sinus thrombosis. Differential diagnosis of bacterial orbital cellulitis includes malignancy, invasive fungal disease (mucormycosis), and orbital pseudo tumor (an idiopathic cause of painful ophthalmoplegia with inflammatory proptosis) Cavernous Sinus Thrombosis Etiology: A rare condition in which blood clotting occurs inside the cavernous sinus. It is usually due to the spread of infection from sinusitis and orbital or preseptal cellulitis. It is a very dangerous condition with a high mortality rate. Symptoms: Features are of rapid onset and may include severe headache, malaise, nausea and vomiting, unilateral or bilateral proptosis and chemosis. Signs: Congestion of the facial, conjunctival, and retinal veins as well as reduced vision. In addition, there are signs of ocular muscle paresis resulting from compromised function of the third to sixth cranial nerves, which run through the cavernous sinus (Fig. 7-39). Investigations required include MRI and MRV to confirm the diagnosis. Differential diagnosis includes orbital cellulitis and carotid-cavernous fistula. Treatment consists of urgent hospitalization, parenteral antibiotics, anticoagulants, and rarely surgical intervention. Subconjunctival Hemorrhage Definition:Chapter:7 The Red Eye Subconjunctival hemorrhage is the accumulation of blood in the potential space between the conjunctiva and the sclera (Fig 7-40). Etiology: It is often spontaneous without an apparent cause. It Fig. 7-40: Subconjunctival hemorrhage may occur due to some Valsalva' s phenomenon (increase in venous pressure due to straining). It may infrequently indicate hypertension or a blood coagulation defect. Although this condition may look alarming, it is completely benign Subconjunctival hemorrhage can also occur due to skull base fracture following severe trauma (see later). II- CHRONIC RED EYE Keratoconjunctivitis sicca (KCS). Vernal keratoconjunctivitis (VKC). Trachoma. Pterygium. Toxic conjunctivitis. Thyroid eye disease (TED) (see chapter 3: Protective system of the eye). Keratoconjunctivitis sicca Keratoconjunctivitis sicca, commonly called dry eye, is a disorder resulting from tear deficiency or dysfunction. It causes ocular redness with discomfort, a burning sensation, sense of dryness, and in later stages, it may cause blurred vision (Fig. 7-41) (see chapter 3). Chapter:7 The Red Eye Vernal Keratoconjunctivitis (VKC) This condition is a bilateral chronic inflammation of the conjunctiva, often with secondary corneal involvement. Symptoms can occur all year round, but often have a marked seasonal component with exacerbations during the spring (vernal). It occurs more frequently In males (2: 1) who commonly have a personal or family history of atopy. Clinical picture: Symptoms: Severe itching and copious mucoid discharge. With corneal involvement, there may be photophobia and blurring of vision. Signs Limbal VKC There is a thickened, fleshy appearance to the limbus. Palpebral VKC. Conjunctival hyperemia and chemosis associated with diffuse papillary hypertrophy are more prominent on the upper tarsus. In more severe cases, the papillae can enlarge giving rise to giant 'cobblestone' papillae. These may cause mechanical ptosis. Both limbal and palpebral VKC can occur either in isolation or together (Fig. 7-42). Corneal involvement: Keratopathy includes the following: Punctate epithelial erosions are most common superiorly. Pannus and corneal vascularization. Chapter:7 The Red Eye Associations/complications: - Severe allergic conjunctivitis is associated with keratoconus. - Steroid-induced glaucoma may occur secondary to long-term topical steroid use. Management: Topical vasoconstrictors can provide temporary symptomatic relief. The mainstay of treatment is topical antihistamines, topical mast cell stabilizers, or drugs that have both effects such as olopatadine. It is important to start mast cell stabilizers prophylactically 2 weeks or more before the time when allergy normally occurs. Topical steroids are reserved for severe exacerbations. Oral antihistamines are useful, especially if associated with rhinitis. For more severe disease and in cases of significant corneal involvement, topical steroids should be administered initially at high frequency and then rapidly tapered. Topical cyclosporine 1 -2% may act as a steroid-sparing agent. Trachomatous Conjunctivitis (Egyptian Ophthalmia) Trachomatous conjunctivitis is a chronic inflammatory condition. Trachoma is the world's leading cause of preventable blindness of infectious origin. It is endemic in Egypt, especially among rural children. Etiology: Trachoma is a chronic keratoconjunctivitis caused by the gram-negative organism, Chlamydia trachomatis that contains both DNA and RNA. This micro-organism produces intracellular basophilic inclusion bodies in epithelial cells. It is susceptible to tetracycline, erythromycin, and sulfonamides. No solid immunity occurs, so recurrences are common. Pathology: Chapter:7 The Red Eye The organism is epitheliotropic. Two phases of the disease process exist. However, both phases may coexist in the same patient. Active phase: follicular or papillary conjunctivitis. Cicatricial (healing) phase: conjunctival scarring alone, if mild to moderate, tends to be asymptomatic. Severe scarring causes many complications. Clinical Picture: Symptoms: 1. Mild irritation and foreign body sensation is often present. 1. Mild chronic discharge. 2. In the chronic stage, the cornea is involved causing pain, lacrimation and photophobia. Signs: WHO classification: Trachomatous follicles TF: beginning of the infection with 5 or more follicles, on the inner surface of the upper palpebral conjunctiva, visible with magnification (Fig. 7-43). Trachomatous inflammation TI: the eye is irritated and highly infectious, with thickening or swelling of the upper eyelid. Papillary hypertrophy and inflammatory thickening of the upper tarsal conjunctiva obscuring more than half of the deep tarsal vessels. Trachomatous scarring TS: the presence of Fig. 7-43: Upper palpebral conjunctival follicles scarring in the tarsal conjunctiva which often appears as white lines when examined with magnification. Trachomatous trichiasis TT: lashes tum in to rub and scratch the cornea. Corneal opacity (CO): continual inflammation and scratching from rubbing lashes lead to clouding of the cornea with decreased vision. Conjunctival complications: Chapter:7 The Red Eye Post-trachomatous degenerations and concretions (PTDs & PTCs ). Posterior symblepharon: adhesions in the fornices. Xerosis: Goblet cell atrophy. Fibrosis of lacrimal ducts. Corneal complications (manifestations rather than complications): Limbal follicles or Herbert's rosettes are small rounded grayish areas in the upper cornea due to subepithelial lymphoid infiltrations. Pannus: superior superficial epithelial vascularization (Fig. 7-44) and cellular infiltration. Resolved limbal follicles may leave small gaps in the pannus (Herbert's Pits), which are typical of trachoma. Corneal ulcer: Typical: superficial, linear, horizontal ulcers at the lower edge of the pannus. Atypical (not related to pannus) occurring due to rubbing by trichiasis with superimposed bacterial infection. Corneal opacity or scarring due to healed corneal ulcers. This reflects the prevalence of vision loss and blindness resulting from trachoma Lid complications: Ptosis: either mechanical (heaviness due to cellular infiltration) or due to fibrosis and weakness of Muller's muscle. Trichiasis: due to local scarring around the lid margin. Cicatricial entropion: due to conjunctival shrinkage (Fig. 7 -45).Chapter:7 The Red Eye Lacrimal system complications: Obstruction of puncti by fibrosis. Chronic canaliculitis with epiphora. Chronic dacryocystitis or dacryoadenitis. Management: Prevention: Although trachoma was eliminated from most of the developed world in the 20th century, this disease persists in many parts of the developing world. The WHO has developed a strategy to prevent trachoma with the goal of eliminating it. The strategy, titled SAFE, involves: - Surgery to treat advanced forms of trachoma. - Antibiotics to treat and prevent the infection. - Facial cleanliness. - Environmental improvement in water, sanitation, and fly control. Treatment: Medical: Local sulfonamide or broad-spectrum antibiotic eye drops and ointment (tetracycline, erythromycin, chloramphenicol) used frequently for 6-12 weeks. Oral azithromycin, sulfonamide, tetracycline or broad-spectrum antibiotics. Surgical: Picking of PTDs. Surgery for complications such as trichiasis and entropion. Chapter:7 The Red Eye Pterygium Definition: Pterygium is an abnormal wedge-shaped growth of degenerated fibrovascular conjunctiva that extends progressively over the cornea, usually from the nasal side (Fig. 7 -46). Etiology: Usually occurs in patients living in hot climates with excessive exposure to ultraviolet rays from the sun. Symptoms It may be asymptomatic if small, but when it grows, patients complain of irritation, inflammation, visual disturbance (due to induced astigmatism or growth into the visual axis), and bad cosmetic appearance. Treatment is surgical excision if progressive or disfiguring. Symptoms of irritation may be temporarily relieved by topical lubricants, decongestants, and mild steroids. Toxic Conjunctivitis (Conjunctivitis Medicamentosa) Toxic conjunctivitis is not allergic in nature, but it is frequently confused with allergic ocular disease. It implies direct damage to ocular tissues from an offending agent, usually a preservative or medication. It occurs in patients on long-term therapy with multiple preservative-containing topical ocular medications, such as in glaucoma treatn1ent. Conjunctival hyperemia predominantly involving the inferior fornix is the most common manifestation. The eyelids and cornea may also be involved (eyelid hyperemia and /or corneal superficial punctate keratitis). Often the original eye condition for which the eye drops were used Improves upon initial treatment, but the eye irritation worsens with continued use. Treatment is by discontinuing the suspected offending agent(s) and switching to preservativefree topical therapies or even oral medications (when applicable) in cases where continued therapy is required