Diagnosing and Managing Ocular Emergencies and Urgencies - PowerPoint Presentation

Diagnosing and Managing Ocular Emergencies and Urgencies Blair Lonsberry, MS, OD, MEd., FAAODiplomate, American Board of OptometryClinic Director and Professor of OptometryPacific University College of Optometryblonsberry@pacificu.edu 1

Disclosures and Special RequestPaid consultant for:Alcon Pharmaceuticals, Bausch and Lomb, Carl Zeiss Meditec, NiCox, SucampoSpecial Request:Interactive remotes don’t work on your TV, so please don’t take them home!  Commitment to change: - write down three things that you “learned” from this presentation that you can incorporate into your practice to improve patient care

What Classifies an Emergency?Any condition in which the patient has the potential for: vision loss, currently experiencing vision loss, permanent structural damage, pain or discomfort, or is an “emergency” for the patient.It is important to be able to triage a walk-in patient and, more importantly, a call-in patient.

What questions to ask? Onsetsuddenly noticed or sudden onset? Visual Lossany loss of vision?loss vs. blurry vision one eye or both part of visual field or all transient vs. permanent Pain is there pain? constant? scale (1-10) Redness is there any redness? location? Associated Factors contact lens wear? trauma? discharge? photophobia? medical history (eg. DM)

Common Types of Ocular EmergenciesVision Loss:Gradual vs. sudden onsetVision loss with or without painTrauma Red eyes

Visual LossVisual loss varies greatly in meaning from patient to patientranging from blur to complete blindness and may affect one or both eyesComponents include: acuity, visual field, color and brightness may be affected jointly or separatelyDetailed history and extent of vision loss crucial

Profound Loss of Vision Referring to a complete or greatly diminished vision affecting the whole fieldCommon causes of severe vision loss: Vascularcentral retinal vein occlusion, central retinal artery occlusion, vitreous hemeInflammatory optic neuritis Infiltrative optic neuropathy Mechanical retinal detachment

Monocular vs. BinocularOcular or optic nerve pathology causes monocular vision losslesion at or posterior to chiasm causes binocular vision lossVF defects become more congruous the further back in the visual pathwayHomonymous VF defects noted posterior to chiasm Difference between mono vs. bino usually straightforward, keeping the following in mind:Patients occasionally mistake homonymous hemianopsia (similar loss of visual field in both eyes) for a monocular loss

Visual Defects

MonocularDifferentiate between eyes that have lost all useful vision and those that have blurred visionBlurring of vision is not localized and may be caused by pathology anywhere from cornea to optic nerveNeed to get anatomical diagnosis first before considering the cause

General AppearanceLevel of consciousnessWhen introducing yourself be aware of the patient’s gross level of consciousness? Is the patient awake, alert and responsive?Personal Hygiene and DressIs it appropriate for the environment, temperature, age and social status of the patient?Is the patient malodorous or disheveled?

General AppearancePosture and Motor controlWhat posture does patient assume while sitting in the exam chairAre there any signs of involuntary motor activity such as tremorsE.g. damage to the cerebellum may produce a tremor that usually worsens with movement of the affected limb

Case Example48 yr old white female presented for diabetic eye exam on referral from her PCPShe was scheduled 2 weeks previously but had fallen and was unable to make that appointmentShe reports that her vision in her right eye seems to be getting worse over the past several weeks.Was diagnosed with diabetes 1.5 years ago BS control has been erratic with range between 120-240Last A1C: 9.1

Blood SugarThroughout a 24 hour period blood sugar typically maintained between 3.9-7.8 mmol/L (70-140 mg/dL) Diabetes is diagnosed with a fasting BS of > 7.0 mmol/L (126 mg/dL) or an A1c value of > 6.5Hypoglycemia is typically defined as plasma glucose 3.9 mmol/L (70 mg/dL) or lesspatients typically become symptomatic of hypoglycemia at 2.8 mmol/L (50 mg/dL) or less[A1c (%) x 1.59] – 2.59 = average Blood Glucose (in mmol/L)

VEGF and DME

Entrance Skills/Health AssessmentVA: OD: finger count OS: 20/40 (6/12)CVF: OD: unable to assess OS: temporal hemianopsiaPupils: sluggish reactivity with a 2+ RAPD ODSLE: corneal arcus noted, no other significant findingsIOP: 16, 16 mmHG OD, OSDFE: see photos Note: not patient photoshttp://content.lib.utah.edu /cdm4/ item_viewer.php?CISOROOT =/EHSL-WFH&CISOPTR=159

Physical PresentationUpon entering the room I noted that her right hand was twitchingI asked her how long that had been going on and she said about 2-3 weeksI asked her if she experienced headaches, to which she said she had bad headaches that even woke her up at night

ReferralContacted her PCP who reported that she had examined the patient 3 weeks prior and had not noted any of these findingsReferred the patient for an immediate MRIwasn’t able to be scheduled until the next day

Imaging/Surgery ReferralMRI revealed large mass in her brainPatient was diagnosed with a Craniopharyngioma She was referred for immediate surgery Neurosurgeon reported that she removed a tangerine sized Craniopharyngiomawas the largest tumor she has ever removed Note: not patient MRIhttp://neurosurgery.ucla.edu/images/Pituitary%20Program/Craniopharyngioma/Cranio_Sag_Preop_fullylabeled.jpg

CraniopharyngiomaCraniopharyngioma:slow-growing, epithelial-squamous origin, calcified cystic tumor arises from remnants of the craniopharyngeal duct Craniopharyngiomas have a benign histology but malignant behaviorthey have a tendency to invade surrounding structures and recur after what was thought to be total resection

CraniopharyngiomaVisual field examination may reveal various patterns of visual lossmost frequently bitemporal hemianopsiasuggestive of compression of the optic chiasma and/or tracts

Our PatientPatient had a complete resection of the tumor in addition to radiation therapyShe developed several significant perioperative complications:Leakage of CSF which resulted in her having to have a shunt She subsequently developed an infection post surgically She is NLP in her right eye, but did regain 20/40 vision in her left eyeRetains a temporal hemianopsia OSDiabetes control became erratic and was put on several hormone replacement medications

Neurological Screening: CerebrumFrontal lobeEmotions, drive, affect, self-awareness, and responses related to emotional statesMotor cortex associated with voluntary skeletal movement and speech formation (Broca)

Right vs Left Brain InjurySo what happens if one side of the brain is injured? People who have an injury to the right side of the brain "don't put things together" and fail to process important information. As a result, they often develop a "denial syndrome" and say "there's nothing wrong with me.“

Right vs Left Brain InjuryThe left side of the brain deals more with language and helps to analyze information given to the brain. If you injure the left side of the brain, you're aware that things aren't working (the right hemisphere is doing its job) but are unable to solve complex problems or do a complex activity. People with left hemisphere injuries tend to be more depressed, have more organizational problems, and have problems using language.

Gradual Onset:CataractsThe decreased acuity must correlate with the severity of the cataract…ie if cataract doesn’ t correlate with the amount of vision loss (or afferent pupillary defect present) then you need to find another reason for the vision (or other test results)

Preseptal Cellulitisinfection and inflammation anterior to the orbital septum and limited to the superficial periorbital tissues and eyelids. Signs and Symptoms include:eyelid swelling, redness, ptosis, pain and low grade fever.

Preseptal Cellulitis TreatmentTreatment: Mild: Keflex or Ceclor 250-500mg QID for 5-7 daysAugmentin 500 mg TID or 875 mg BID for 5-7 days Moderate to severe: IM Rocephin (ceftriaxone) 1-2 grams/day or IV Fortaz (ceftazidime) 1-2 g q8h.

QuestionA 65 year old white male patient presents with this lesion on his forehead. States it is “itchy” and is flaky in appearance. What is this?Seborrheic keratosisKeratoacanthomaBasal cell carcinomaActinic keratosis

QuestionActinic keratosis if left untreated has a 20% chance of converting to which of the following? 1234

Pre-Malignant Eyelid Lesions: KeratoacanthomaAppears as a solitary, rapidly growing nodule on sun exposed areas of middle-aged and older individualsNodule is usually umbilicated with a distinctive crater filled with keratinLesion develops over weeks and undergoes spontaneous involution within 6 mo to leave an atrophic scar

Pre-Malignant Eyelid Lesions: KeratoacanthomaLesion on the eyelids may produce mechanical problems such as ectropion or ptosis.Differential SCC, BCC, verruca vulgaris and molluscumMany pathologists consider it a type of low grade SCC Complete excision is recommended as there are invasive variants

Pre-Malignant Eyelid Lesions: Actinic KeratosisAlso known as solar or senile keratosisMost common pre-malignant skin lesionDevelops on sun-exposed areas and commonly affect the face, hands and scalp (less commonly the eyelids)

Pre-Malignant Eyelid Lesions: Actinic KeratosisAppear as multiple, flat-topped papules with an adherent white scale.Development of SCC in untreated lesions as high as 20%Management is surgical excision or cryotherapy (following biopsy)

Orbital Blowout FractureSigns & Sx’s: EnophthalmosDiplopiaImpairment of eye movement 20 to EOM entrapment, orbital hemorrhage or nerve damageInfraorbital n. anesthesiaCT should include axial and coronal cuts

Orbital blowout fractureDisposition - If no diplopia, minimal displacement, and no muscle entrapment, discharge with follow up within a week.Consider Surgery - For enophthalmos, muscle entrapment, or visual loss.Management: Ice packs beginning in clinic and for 48 hrs will help decrease swelling associated with injury.Elevate head of bed (decrease swelling).If sinuses have been injured, give prophylactic antibiotics and instruct patient not to blow nose.Treat nausea/vomiting with antiemetics.

Case20 year old male presents with a red painful eyecomplains about red/painful right eye Started that morning when he woke up reports a watery discharge, no itching, and is not a contact lens wearerSLE:See attached image with NaFl stain

Herpes Simplex Keratitis: Clinical FeaturesCharacterized by primary outbreak and subsequent reactivationPrimary outbreak is typically mild or subclinicalAfter primary infection, the virus becomes latent in the trigeminal ganglion or cornea Stress, UV radiation, and hormonal changes can reactivate the virusLesions are common in the immunocompromised (i.e. recent organ transplant or HIV patients)

Dendritic Ulcers 39

Herpes Simplex KeratitisTopical:Viroptic (trifluridine ) q 2h until epi healed then taper down for 10-14 days. Viroptic is toxic to the cornea.Zirgan (ganciclovir) available in USA, use 5 times a day until epi healed then 3 times for a weekOral acyclovir (2 g/day) has been reported to be as effective as topical antivirals without the toxicityValtrex (valcyclovir)) 500 mg TID for 7-10 daysFamvir (famciclovir) 250 mg TID for 7-10 daysIf stomal keratitis present, after epi defect has healed, add Pred Forte QID until inflammation reduced and then slowly taper

Prophylaxis??Prophylaxis of 400 mg acyclovir BID vs placebo for 1 year resulted in a lower recurrence in the treatment arm (19% vs 32%)Valtrex 500 mg qd was found to be equivalent to acyclovir BIDPitfalls to Prophylaxis :Reduction of recurrence does not persist once drug stoppedResistance????van Velzen, et. al., (2013) demonstrated that long-term ACV prophylaxis predisposes to ACV-refractory disease due to the emergence of corneal ACVR HSV-1.

Case27 year old pharmacy student presents to the clinic on emergent basiscomplains about red/painful eyes for the past 2 days started OD then transferred to OSreports a watery discharge, no itching, and is not a contact lens wearerreports that others in his class have had a similar red eyeno seasonal, food or drug allergies has taken Visine 4-5 times/day since eyes became red but hasn’t helped much

Question 1 2 3 4 Which of the following best represents your patient?

Conjunctivitis Bacterial Conjunctivitis Allergic Conjunctivitis Viral Conjunctivitis Blepharo-conjunctivitis

Viral ConjunctivitisMost common infectious keratitis presenting on emergent basis 62% caused by adenovirusTwo major types:Pharyngoconjunctival feverEpidemic keratoconjunctivitis

Viral ConjunctivitisPCF: history of recent/current upper respiratory infectionEKC: highly contagious with a history of coming in contact with someone having a red eye.Adenovirus 8 common variant leading to “rule of 8’s”First 8 days red eye with fine SPKNext 8 days deeper focal epithelial lesionsFollowing 8 potential development of infiltratesResolutionRPS Adeno Detector available to use for adenoviral confirmationAdenoPlus is currently being marketed and distributed by NiCox

AdenoPlusHave you heard about this? www.nicox.com

Interpreting the resultsNEGATIVE RESULT Only a BLUE line appears in the control zone. A negative result is indicative of an absence of Adenovirus Antigens.POSITIVE RESULT The presence of both a BLUE line in the control zone and a RED line in the result zone indicates a positive result. Even if the RED line is faint in color, incomplete over the width of the test strip, or uneven in color, it must be interpreted as positive. A positive result indicates the presence of Adenovirus antigens. www.rpsdetectors.com

Interpreting the resultsInvalid ResultIf a BLUE line does not appear, the test may be invalid. Reimmerse the absorbent tip into the buffer vial for an additional 10 seconds.If a BLUE line still does not appear after 10 minutes, the test must be discarded and the subject retested by resampling the eye using a new AdenoPlus test kit www.rpsdetectors.com

Patient has “Red Eye” “Red Eye” ProtocolJOURNEY OF THE “RED EYE” Patient is taken to “ Red Eye Room ” Dr. proceeds with evidence based treatment “ Red Eye ” Patient history & work up Dr. starts clinical evaluation with Adenoviral conjunctivitis confirmed, or rule out Front Office IDs & Isolate the “ Red Eye ” Tech performs AdenoPlus™ test to rule out Adenovirus

POSITIVE Education: hygiene and hand washing Supportive care: artificial tears, cool compresses and antihistaminesAntiviral medicationNo antibiotics NEGATIVE Consider topical antibiotics or antihistamines History Signs Symptoms  Pink eye exposure, spread from one eye to the other, recent upper respiratory symptoms  Itching, burning, foreign body sensation, tearing, discharge, eyelash matting  Pre-auricular adenopathy, chemosis  No significant pain, light sensitivity, or visual loss AdenoPlus

Viral Conjunctivitis: Signs and SymptomsGritty sensationWatery discharge Sticky in morningsFollicular responseChemosisInjectionSPKInfiltrates possiblePositive lymph nodes Pseudomembranes in severe casesSubconjunctival hemes

ManagementConsider the use of anti-inflammatory treatment to relieve patient symptoms and improve comfortAlrex QID OULotemax QID OUFML QID OUEKC patients are typically very uncomfortable and would benefit from anti-inflammatory treatmentespecially if infiltrates or pseudomembrane present

ManagementBetadine (Melton-Thomas Protocol):Proparacaine 4-5 drops of Betadine 5%Get patient to close eye and gently roll them aroundAfter one minute, lavage the eyeLotemax/FML 4 times a day for 4 daysAlternative: Betadine swabsticks. 5% Betadine solution only comes in 30 ml bottles cost $14.00. Case of 200 Betadine swabsticks apprx. 45 dollars.

ManagementAntivirals used in HSV keratitis are ineffective in treatment of viral conjunctivitisNew Update: in conversation with several colleagues, Zirgan 4-5 times/day has shown significant improvement in patients over a 7-10 time period. Important to stress limited contact with others, frequent hand washing, not sharing of towels, etc.

Sinusitis Red EyeWith a sinus infection or inflammationthe sinuses swell and mucus cannot properly drain. The increase in mucus and the narrow passage through which it tries to escape creates pressure in the sinuses that leads to pain. The sinuses surround the ocular regionpressure from sinuses may feel like eye pressure.swollen sinuses and nasal membranes can push against ocular nerves resulting in pain. Pooled mucus can result in infection that increases the pain in the sinus and ocular region even

Sinusitis TreatmentThe infection is likely bacterial and should be treated with antibiotics if:symptoms last for 10 days without improvement, orinclude fever of 102 degrees or higher, nasal discharge and facial pain lasting three to four days Because of increasing resistance to the antibiotic amoxicillin — the current standard of care — the ISDA recommends Augmentin Augmentin 250/500 TID for 5-7 days for adults, 10-14 days for childrenAlternative is Keflex 500 mg QID

Flashes and FloatersPatients often present complaining of “spots” or “cobwebs” in front of their eyes Causes of floaters include: posterior vitreous detachment (PVD), retinal tear, vitreous heme, uveitis.Since PVD and retinal tears present the same way, a RT has to be eliminatedAsk the patient whether spots move with eye and continue to move after the eye has stoppedLarge spots could be blood clots

Posterior Vitreous Detachment (PVD)

Vitreous Heme

Retinal Tear

Flashes and FloatersSudden onset typically means a PVD, retinal tear or hemeIf the spots appear after flashing light, then retinal tear must be eliminated Myopes tend to have floaters and will notice them for a long timeKey is to rule out potentially sight threatening condition for the floaters, ie retinal tear.Patients with retinal condition such as lattice degeneration and myopes need to be educated about S&S of RD (flashes and floaters)5-10% population has latticeRisk of RD with lattice is approx 1%30-50% of patients with a RD have lattice

Flashes and Floaters:ManagementA patient who presents with a sudden onset PVD without retinal breaks or hemorrhage requires repeat peripheral examination in six weeks, as the risk of retinal complications is highest within the six weeks following vitreous detachment. If no retinal breaks are seen at that point, routine yearly examination is all that is needed

Lid NeviLid nevi: congenital or acquiredoccur in the anterior lamella of the eyelid and can be visualized at the eyelid margin. The congenital eyelid nevus is a special category with implications for malignant transformation. With time, slow increased pigmentation and slight enlargement can occur.An acquired nevus generally becomes apparent between the ages of 5 and 10 years as a small, flat, lightly pigmented lesion

Congenital NevusThe nevus is generally well circumscribed and not associated with ulceration. The congenital nevus of the eyelids may present as a "kissing nevus" in which the melanocytes are present symmetrically on the upper and lower eyelids. Presumably this nevus was present prior to eyelid separation

Congenital NevusMost nevi of the skin are not considered to be at increased risk of malignancy. However, the large congenital melanocytic nevus appears to have an increased risk of malignant transformation of 4.6% during a 30 year period

Acquired Lid NeviAcquired nevi are classified as: junctional (involving the basal epidermis/dermis junction), typically flat in appearanceintradermal (involving only the dermis), tend to be dome shaped or pedunculated compound (involving both dermis and epidermis) tend to be dome shaped

Corneal Ulcers Infective bacterial and fungal corneal lesions cause severe pain and loss of visionSigns and Symptoms:Pain, photophobia, tearing Mucopurulent discharge with generalized conjunctival injectionDecreased VA (esp if on visual axis)Possible AC reaction and hypopyonDense infiltrateSatellite lesions around main lesion may indicate fungal infection

Sterile vs Infectious Infiltrates

Peripheral (Sterile) Corneal Ulcer

Infectious Corneal Ulcer

Corneal UlcersThe Steroids for Corneal Ulcers Trial (SCUT)Conclusions:  no overall difference in 3-month BSCVA and no safety concerns with adjunctive corticosteroid therapy for bacterial corneal ulcersresearchers did find significant vision improvement for one specific subgroup of the study by using steroid therapy on patients with severe ulcersApplication to Clinical Practice:  Adjunctive topical corticosteroid use does not improve 3-month vision in patients with bacterial corneal ulcers unless in the severe category

Corneal Ulcers Infective bacterial and fungal corneal lesions cause severe pain and loss of visionS and S:Pain, photophobia, tearing Mucopurulent discharge with generalized conjunctival injectionDecreased VA (esp if on visual axis)Possible AC reaction and hypopyonDense infiltrateSatellite lesions around main lesion may indicate fungal infection

Associated FactorsContact lens wear, especially soft and extended wear lensRecent history of corneal traumaTopical steroid useHistory of exposure to vegetative matter (fungal etiology)

Protein Synthesis InhibitorsThese antibiotics work by targeting the bacterial ribosome. they are structurally different from mammalian ribosomes, in higher concentrations many of these antibiotics can cause toxic effects.This group includes: (a) tetracyclines, (b) aminoglycosides, (c) macrolides, (d) chloramphenicol, (e) clindamycin, (f) quinupristin/dalfopristin and (g) linezolid

TetracyclinesNonresistant strains concentrate this antibiotic intracellularly resulting in inhibition of protein synthesis.Broad spectrum, bacteriostatic, effective against gram (+) and (-) bacteria and against non-bacterial organisms widespread resistance has limited their use.Drug of choice for Rocky Mountain Spotted Fever, Cholera, Lyme disease, mycoplasma pneumonia, and chlamydial infections.Side effects include gastric discomfort, phototoxicity, effects on calcified tissues, vestibular problems, pseudotumor.

TetracyclinesThis group includes:Tetracycline (250mg - 500 mg cap BID-QID) needs to be taken 1 hour before or 2 hours after a meal.Minocycline (100 mg cap BID)Doxycycline (20mg - 100 mg cap or tab BID)

Tetracyclines: Acne RosaceaAcne rosacea: affects females>males after 30 with peak incidence 4-7th decade of Celtic/Northern European descent. Males more disfigured. 4 subtypes with classic signs of flushing, papules or pustules usually in crops, telangiectasia. secondary ocular complications (85% of patients) and often precede other skin manifestations include erythema, itching and burning.Mainstay oral Tx is Oracea (40 mg in morning) or tetracycline 500 mg po BID or doxycycline 100 mg po BID or minocycline 100 mg po BID for 4-12 wks.NOTE: Oracea is subantimicrobial therapy

Acne Rosacea Treatments Oral AntibioticsTopical Treatments Non-PrescriptionErythromycin metronidazole (Metrogel) Rosacea-Ltd III Tetracycline BenzaClin (Clindamycin 1% & benzoyl peroxide 5%) ZenMed Doxycycline BenzaMycin (Erythromycin 3% & benzoyl peroxide 5%) Neova Therapy Minocycline tretinoin (Retin-A) Kinerase Clindamycin 1% lotion/gel Rosacare Plexion Cleanser/Lotion (Sulfa 10% & sulfur 5%) www.internationalrosaceafoundation.org

Anti-inflammatory effects Degrade extracellular proteins Tetracyclines inhibit MMPsAnti-inflammatory

Question75 white female complains of sudden decreased vision left eye. From picture above what is most likely cause? 1. BRVO2. Ischemic optic neuropathy3. Papilledema4. Low tension glaucoma

EpidemiologyNonarteritic: usually seen in younger patientsFellow eye involved in 25-40% of casesAssociated with hypertension and diabetes

EpidemiologyArteritic: usually seen in >55 yrs old (mostly over 70) fellow eye involved in 75% of cases within 2 weeks without treatment

SymptomsAcute visual loss (arteritic>non)dyschromatopsia Arteritic may also have associated:Headache, fever, malaise, weight loss, scalp tenderness, jaw claudication, amaurosis fugax, diplopia, and eye pain.

Ocular SignsSudden, unilateral, painless decreased vision and color visionPositive RAPDAltitudinal visual field defect (usually inferior and large)Swollen optic disc Fellow nerve often crowded with small or absent cup (“disc at risk”)

Additional TestingLab tests:STAT ESR (rule out arteritic form)CBC (low hematocrit, high platelets)Fasting blood sugarC reactive protein, VDRL/FTA-ABSANACheck blood pressure

ManagementArteritic:Systemic steroids to prevent fellow eye involvement methylprednisolone 1 g IV qd in divided doses for 3 days then, prednisone 60-100 mg po qd with a slow taperCheck PPD, blood glc and chest radiographs before starting systemic steroids Non-arteritic:Consider daily aspirin

Vision Loss Without Pain:TIA/TMB/Amaurosis Fugax Refers to temporary visual impairment of variable duration (seconds to hours)TIA: transient ischemic attack-can be cerebral or retinalTMB: transient monocular blindness secondary to a retinal TIAAmaurosis Fugax: same as TMBAbrupt onset, progression to involve all or part of visual field, sight usually returnsWithin affected area, visual acuity maybe dimmed or completely lost

TIA’s Stroke is 3rd leading cause of mortality in developed countries and most common cause of neurological disability 15-20% of patients with stroke have a preceding TIA, though guidelines for referral and evaluation are debatedTraditional guidelines suggested that assessment should be complete within 1 week of TIA

TIA’sRisk of stroke after TIA has traditionally been considered relatively low, but new studies indicate that the risk is much higher than previously thought and the time window for prevention is short.Effective secondary prevention depends on reliable identification of those at high risk and targeting treatment.

TIA’s: High Risk FactorsFive (5) risk factors are associated with a high risk (30%) of recurrent stroke at 3 months: Age over 60Symptom duration greater than 10 minutesMotor weaknessSpeech impairmentDiabetesIsolated sensory of visual symptoms were associated with low risk of stroke!

TIA: Early TreatmentSeveral treatments are likely to be effective in preventing stroke in the acute phase after a TIA:AspirinAnticoagulants StatinsEndarterectomy (for >50% carotid stenosis)Further research needed for:Lowering blood pressure acutely after TIAProphylactic use of neuroprotective drugs

Amaurosis Fugax:TMBMost common cause is:thromboembolic disease (eg carotid artery disease throwing emboli) or vasospasmDescribed as “curtain falling over vision”Risk of stroke or death is about 3-5%, which is significantly lower than for a cerebral TIA (15-20%)Px still require work-up to determine cause: e.g. carotid doppler

Alkali Chemical BurnsAlkali exposure results in:Loss of corneal and conjunctival epi, stromal keratocytes and endotheliumLoss of clarity is secondary to stromal hydration Damage to the vascular endothelium of conjunctival and episcleral vesselsIntraocular structures such as iris, lens and ciliary body are rapidly damaged if alkali penetrates cornea.

Acidic Chemical BurnsEpithelium provides effective barrier to weak acids. Stronger acids cause protein precipitation in epithelium and stroma which creates a barrier to further penetration.Very strong acids penetrate as quickly as alkalis

Chemical Burn TreatmentImmediate irrigation is of paramount importanceMost patients are disabled by severe blepharospasm and disorientation so require assistance away from harm and to initiate irrigation.Make sure to remove any solid particulate matter prior to beginning irrigationMinimum of 15 minutes constant irrigation (some recommend 30 minutes)

Chemical Burn TreatmentWater is commonly recommended however it is hypotonic to corneal tissue and can result in increased water intake into the corneal and subsequent diffusion of corrosive materials deeper into cornea.Recommend fluids of higher osmolarity such as sterile lactated Ringers and balanced saline solution.

Chemical Burn TreatmentEffectiveness of irrigation can be assessed using pH paper and continued as long as pH outside of the normal range.For grade I and II burns will typically heal without permanent damage. Topical steroid/antibiotic drops/ung recommended and daily follow up.Cycloplegia for pain and further reduction of inflammation.

Chemical Burn TreatmentSevere ocular burns are difficult to treat and may require months of healingBasic treatment of these eyes is to reduce inflammatory response caused by necrotic tissueCorticosteroid useProphylactic antibiotics (consider doxycycline as it inhibits proteinase activity) May require surgical intervention with debridement of necrotic tissue and possibly reconstructive surgery.