Dr. Khalid Alabdulwahhab

Objectives At the end of session student should be able to:  Describe assessment tools for urgent ocular complaints.  Discuss clinical presentation, emergency assessment and treatment for true ophthalmic injuries (chemical exposure, ruptured Globe, hyphema )  Discuss clinical presentation, emergency assessment and treatment for Sudden Blindness (Central Retinal Artery Occlusion, Central Retinal Venous Occlusion, Acute Closed Angel Glaucoma, Optic neuritis and Retinal Detachment).  Discuss serious eye infections (zoster ophthalmicus and orbital cellulitis)

 Caused by Human Herpes Virus 3 (HHV3)  Morphologically identical with HSV but differ antigenically and clinically.  Can present as Varicella ( Chicken Pox) or Zoster.  15% of zoster affects ophthalmic division then the condition is called Herpes Zoster Ophthalmicus  Very rarely the eye may be involved if maxillary nerve affected. Eye infections Herpes Zoster Ophthalmicus

 The eye frequently becomes involved when the cutaneous lesions include the tip of the nose (Hutchinson sign), which means that nasociliary branch is involved which happen in one third of HZO.  Over all about 50% of patients with HZO develop ocular lesions. Eye infections

Herpes Zoster Ophthalmicus Clinically HZO can be divided into:  Acute  Chronic  Relapsing Eye infections

Acute HZO  General Fever Malaise Headache then Neuralgia (itching, tingling, burning sensation or sever deep pain)  Skin Rash (Maculopapular  pustular  crsting ulcer  Ocular lesions Conjunctivitis, episcleritis, scleritis Keratitis ○ Punctate epithelial keratitis(occur in 50% pt, appear in 2 days) ○ Microdendrites ( in 4-6 days, no central epithelial erosion) ○ Nummular keratitis ( 33% of pt, in 10 days) ○ Disciform keratitis (50% of pt, in 3 weeks) Anterior Uveitis Herpes Zoster Ophthalmicus Eye infections

Treatment  Skin Systemic: Acyclovir 800 mg X5 for 7 days Topical: ○ Antiviral cream ○ Steroid- antibiotic preparations  Ocular: Self limited Steroid + antiviral in sever cases Cycloplegic agents in uveitis  Intravenous acyclovir: Considered if any intracranial symptoms are present Dosage 30 mg/kg per day divided in three doses if creatinine is below 2 mg/dL Herpes Zoster Ophthalmicus Eye infections

Orbital Cellulitis (Postseptal Cellulitis)  Orbital cellulitis is an infection of the soft tissue behind the orbital septum  It is a serious ocular infection that has the potential to be life-threatening  Polymicrobial infection is common  Staph.aureus and Streptococcus pneumonia are is the most common pathogen  H. influenzae should be considered in young children Eye infections

Types:  Sinus related: most common from ethmoidal sinus  From adjacent structure Dacryocystitis Dental infection  Post traumatic: hr post orbital septum penetration  Post surgical Retinal detachment surgery Strabismus Dacryocystorhinostomy Orbital surgery Orbital Cellulitis (Postseptal Cellulitis) Eye infections

Clinical Features:  Chemosis  Proptosis  Painful diplopia  Restricted painful eye movements  Decrease vision in severe cases Orbital Cellulitis (Postseptal Cellulitis) Eye infections

Complications  Brain Abscess Meningitis Cavernous sinus thrombosis  Subperiosteal abscess  Ocular complications Exposure keratopathy Increased IOP CRAO CRVO Orbital Cellulitis (Postseptal Cellulitis) Eye infections

Management  Admission  CT orbit, sinuses and brain  Blood culture  Treatment: IV Broad spectrum antibiotic to cover gram - positive and negative and anaerobic Orbital Cellulitis (Postseptal Cellulitis) Eye infections

TRAUMA  Blunt Trauma Blunt trauma can damage any structure of the globe The eyelids frequently are swollen shut Assess the patient's ○ Visual acuity ○ Integrity of the globe ○ Anterior chamber If ○ Eye is blind ○ Anterior chamber is flat ○ There is obvious full-thickness laceration ○ There is intraocular foreign body A ruptured globe is certain, and no further attempts to assess or manipulate the eye no IOP measurement should take place

HYPHEMA  Blood in the anterior chamber is referred to as a hyphema  Hyphemas classified as traumatic or spontaneous  Traumatic hyphemas The result of bleeding from a ruptured iris root vessel Blunt and penetrating trauma can cause hyphemas.  Spontaneous hyphemas Frequently are associated with sickle cell disease Blunt Trauma TRAUMA

ED management consists of  Assessing concomitant injury Ruptured globe Intraocular foreign body  The patient's head should be elevated  The pupil should be dilated using atropine 1%  Managing rises in IOP: Topical Medications (B-blockers, adrenergic agonists, carbonic anhydrase inhibitors …etc) Intravenous mannitol Oral or intravenous (CAIs) such as Diamox  In patients suspected sickle cell disease, carbonic anhydrase inhibitors should be strictly avoided.  Nonaspirin containing analgesics or NSAID  Topical steroid to avoid AC fibrinous reaction  Admission/ bed rest: Because of the variance in treatment, the emergency physician should not assume responsibility for disposition  All hyphemas, regardless of etiology, should be seen by an ophthalmologist HYPHEMA Blunt Trauma TRAUMA

 Penetrating ocular trauma can occur from numerous sources  Any projectile injury has the potential for penetrating the eye  Any lid laceration from a sharp object has the potential to have lacerated the globe  Clues to a ruptured globe or intraocular foreign body: Shallow anterior chamber Hyphema Irregular pupil Significant reduction in visual acuity Poor view of the optic nerve and posterior pole on direct Ophthalmoscopy Penetrating Trauma/Ruptured Globe

 A modified Seidel test is helpful in identifying wound leaks  Any penetrating injury is considered a ruptured globe and mandates an eye shield and ophthalmology consultation.  Tetanus status should be determined and intravenous cephalosporin administered.  Do not attempt to measure IOP if a ruptured globe is suspected.  A Waters view x-ray, orbital CT scans or ultrasonography can be helpful in locating and confirming the presence of orbital and intraocular foreign bodies TRAUMA

Chemical Trauma  A chemical injury to the eye is a true ocular emergency  Chemical injury requires immediate treatment in the field and by the triage nurse  Immediate intervention consists of copious irrigation for at least 30 min with NS or RL.  Topical anesthesia and placement of a Morgan lens allow the irrigation to be delivered effectively and directly to the corneal surface. TRAUMA

Chemical Trauma  Litmus paper or pH portion of a urine dipstick can be used to assess the pH of the tears after 5-10 min of stopping irrigation  Irrigation should continue until pH improves to 7.5 to 8  Both acid and alkali burns can be blinding however Acid burns tend to coagulate proteins, thereby limiting the depth of penetration. Alkali burns (lye, ammonia) can rapidly penetrate the cornea, and aqueous pH can rise within minutes of exposure, causing damage to intraocular structures TRAUMA

Chemical Trauma  When the pH close to normal the eye should be inspected for Any particulate matter Visual acuity should be assessed A topical cycloplegic agent should be used for pain reduction if an epithelial defect is present Erythromycin ophthalmic ointment if both eyes affected. If only one eye is affected and an epithelial defect is present, pressure patch for the first 12 to 24 h TRAUMA

Chemical Trauma  Patient with Corneal clouding Epithelial defect after irrigation should receive prompt ophthalmology referral  Patients with Chemosis (edema of the bulbar conjunctiva overlying the white sclera) No corneal or anterior chamber findings should be treated with antibiotic ointment and referred to an ophthalmologist in 48 h. TRAUMA

ACUTE VISUAL REDUCTION/LOSS  Typically occurs in a patient with no previous history of glaucoma  When the pupil becomes mid-dilated and the iris leaflet touches the lens, "pupillary block" develops  This prevents circulation of the aqueous humor from the posterior chamber through the pupil into the anterior chamber  Pressures as high as 50 mm Hg and greater are not uncommon ACUTE ANGLE-CLOSURE GLAUCOMA

Treatment Pressure reduction  Suppressants of aqueous humor production ○ Topical (B-blockers, Alpha-adrenergic agonists..) ○ Oral or intravenous CAIs (acetazolamide) ○ Intravenous mannitol ○ Pilocarpine : frequently will not cause the iris to constrict during the acute attack until the pressure is reduced. This maneuver will help protect against recurrence until an ophthalmologist can perform the definitive treatment procedure of creating a peripheral laser iridectomy ACUTE VISUAL REDUCTION/LOSS ACUTE ANGLE- CLOSURE GLAUCOMA

OPTIC NEURITIS  Is an inflammatory or demyelinated disorder of optic nerve  Types: Papilltis: optic disc is swollen and edematous Retrobulbar neuritis: If the optic nerve head is normal Neuroretinitis: optic papilltis and macular star ACUTE VISUAL REDUCTION/LOSS

 Reduction of vision is rapid and frequently painful (especially with eye movement).  An afferent pupillary defect is commonly present  Visual acuity can range from mildly reduced to no light perception (NLP).  Color vision is affected commonly more than visual acuity. The red desaturation test is helpful in identifying optic neuropathies ACUTE VISUAL REDUCTION/LOSS OPTIC NEURITIS

The Optic Neuritis Treatment Trial (ONTT) showed that:  1 year after an attack of optic neuritis, there was no difference in visual outcome between the patients treated with intravenous steroids and those given a placebo.  Treatment with intravenous steroids was associated with a slightly lower 2-year risk of subsequent development of multiple sclerosis, especially in patients whose MRI showed periventricular white matter lesions  Initial treatment with oral steroids is contraindicated and, for unexplained reasons, had the least favorable outcome ACUTE VISUAL REDUCTION/LOSS OPTIC NEURITIS

CENTRAL RETINAL ARTERY OCCLUSION  The first branch off the internal carotid artery is the ophthalmic artery, which supplies the central retinal artery, which in turn, provides the blood supply to the inner retina.  If the central retinal artery becomes occluded, the retina will infarct and become pale less transparent, and edematous  Sudden, profound, painless, monocular loss of vision  An APD is a common finding  Causes include: Embolus (carotid and cardiac) Thrombosis Giant cell arteritis Vasculitis (lupus) Sickle cell disease Trauma ACUTE VISUAL REDUCTION/LOSS

CENTRAL RETINAL ARTERY OCCLUSION  The retina will sustain irreversible damage within 90 min of total occlusion which is rare, but treatment should begin immediately  Treatment in embolic cases (the majority) is aimed at trying to convert a CRAO into a branch retinal artery occlusion Maneuvers include: Lie flat Digital massage 15X15 IOP-lowering drugs Vasodilation techniques (breathing into a paper bag to increase Paco2) ACUTE VISUAL REDUCTION/LOSS

CENTRAL RETINAL VEIN OCCLUSION  Thrombosis of the central retinal vein causes retinal venous stasis, edema, and hemorrhage  Loss of vision is variable, painless, monocular, and rapid  Funduscopic examination typically reveals optic disc edema and diffuse retinal hemorrhages in all quadrants ACUTE VISUAL REDUCTION/LOSS

Predisposing factors:  Old age  Hypertension  Hypercoagulable disorders  Vasculitis  Glaucoma  Hyperopia Treatment:  No specific treatment is available  Aspirin 60 to 325 mg daily  Referrer to an ophthalmologist for CENTRAL RETINAL VEIN OCCLUSION ACUTE VISUAL REDUCTION/LOSS

retinal detachment  The separation of the sensory retina from the retinal pigment epithelium by subretinal fluid  Types: Rhegmatogenous Tractional Exudative  Symptoms: Flashes( Photopsia) Floaters Dark veil or curtain  Emergent condition need retina specialist to manage ACUTE VISUAL REDUCTION/LOSS