Presentation on theme: "Diagnosing and Managing Ocular Emergencies and Urgencies"— Presentation transcript:
1 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 Optometry
2 Disclosures and Special Request Paid 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
3 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.
4 What questions to ask? Onset Visual Loss Pain Redness suddenly noticed or sudden onset?Visual Lossany loss of vision?loss vs. blurry visionone eye or bothpart of visual field or alltransient vs. permanentPainis there pain? constant? scale (1-10)Rednessis there any redness? location?Associated Factorscontact lens wear? trauma? discharge?photophobia? medical history (eg. DM)
5 Common Types of Ocular Emergencies Vision Loss:Gradual vs. sudden onsetVision loss with or without painTraumaRed eyes
6 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
7 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 hemeInflammatoryoptic neuritisInfiltrativeoptic neuropathyMechanicalretinal detachment
8 Monocular vs. Binocular Ocular 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 chiasmDifference 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
10 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
11 General Appearance Level of consciousness When 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?
12 General Appearance Posture and Motor control What 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
13 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 agoBS control has been erratic with range betweenLast A1C: 9.1
14 Blood SugarThroughout a 24 hour period blood sugar typically maintained between mmol/L ( 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)
16 Entrance Skills/Health Assessment VA: OD: finger count OS: 20/40 (6/12) CVF: OD: unable to assess OS: temporal hemianopsia Pupils: sluggish reactivity with a 2+ RAPD OD SLE: corneal arcus noted, no other significant findings IOP: 16, 16 mmHG OD, OS DFE: see photosNote: not patient photos
17 Physical Presentation Upon 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
18 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
19 Imaging/Surgery Referral MRI revealed large mass in her brainPatient was diagnosed with a CraniopharyngiomaShe was referred for immediate surgeryNeurosurgeon reported that she removed a tangerine sized Craniopharyngiomawas the largest tumor she has ever removedNote: not patient MRI
20 Craniopharyngioma Craniopharyngioma: slow-growing,epithelial-squamous origin,calcified cystic tumorarises from remnants of the craniopharyngeal ductCraniopharyngiomas have a benign histology but malignant behaviorthey have a tendency to invade surrounding structures and recur after what was thought to be total resection
21 CraniopharyngiomaVisual field examination may reveal various patterns of visual lossmost frequently bitemporal hemianopsiasuggestive of compression of the optic chiasma and/or tracts
22 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 shuntShe subsequently developed an infection post surgicallyShe 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
23 Neurological Screening: Cerebrum Frontal lobeEmotions, drive, affect, self-awareness, and responses related to emotional statesMotor cortex associated with voluntary skeletal movement and speech formation (Broca)
24 Right vs Left Brain Injury So 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.“
25 Right vs Left Brain Injury The 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.
26 Gradual Onset: Cataracts The 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)
27 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 andlow grade fever.
28 Preseptal Cellulitis Treatment Mild:Keflex or Ceclor mg QID for 5-7 daysAugmentin 500 mg TIDor 875 mg BID for 5-7 daysModerate to severe:IM Rocephin (ceftriaxone) 1-2 grams/day orIV Fortaz (ceftazidime) 1-2 g q8h.
29 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
30 QuestionActinic keratosis if left untreated has a 20% chance of converting to which of the following?1234
31 Pre-Malignant Eyelid Lesions: Keratoacanthoma Appears 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
32 Pre-Malignant Eyelid Lesions: Keratoacanthoma Lesion 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 SCCComplete excision is recommended as there are invasive variants
33 Pre-Malignant Eyelid Lesions: Actinic Keratosis Also 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)
34 Pre-Malignant Eyelid Lesions: Actinic Keratosis Appear 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)
35 Orbital Blowout Fracture Signs & Sx’s:EnophthalmosDiplopiaImpairment of eye movement 20 to EOM entrapment, orbital hemorrhage or nerve damageInfraorbital n. anesthesiaCT should include axial and coronal cuts
36 Orbital blowout fracture Disposition - 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.
37 Case 20 year old male presents with a red painful eye complains about red/painful right eyeStarted that morning when he woke upreports a watery discharge, no itching, and is not a contact lens wearerSLE:See attached image with NaFl stain
38 Herpes Simplex Keratitis: Clinical Features Characterized by primary outbreak and subsequent reactivationPrimary outbreak is typically mild or subclinicalAfter primary infection, the virus becomes latent in the trigeminal ganglion or corneaStress, UV radiation, and hormonal changes can reactivate the virusLesions are common in the immunocompromised (i.e. recent organ transplant or HIV patients)38
42 Herpes Simplex Keratitis Topical:Viroptic (trifluridine) q 2h until epi healed then taper down for 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
43 Prophylaxis?? Pitfalls to 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.
44 Case27 year old pharmacy student presents to the clinic on emergent basiscomplains about red/painful eyes for the past 2 daysstarted 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 allergieshas taken Visine 4-5 times/day since eyes became red but hasn’t helped much
45 QuestionWhich of the following best represents your patient?1234
47 Viral ConjunctivitisMost common infectious keratitis presenting on emergent basis62% caused by adenovirusTwo major types:Pharyngoconjunctival feverEpidemic keratoconjunctivitis
48 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
50 Interpreting the results NEGATIVE RESULTOnly a BLUE line appears in the control zone.A negative result is indicative of an absence of Adenovirus Antigens.POSITIVE RESULTThe 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.
51 Interpreting the results Invalid 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
52 JOURNEY OF THE “RED EYE” Patient has “Red Eye”“Red Eye” ProtocolFront Office IDs & Isolate the “Red Eye”Patient is taken to “Red Eye Room”“Red Eye” Patient history & work upTech performs AdenoPlus™ test to rule out AdenovirusDr. starts clinical evaluation with Adenoviral conjunctivitis confirmed, or rule outDr. proceeds with evidence based treatment
53 History Signs Symptoms Pink eye exposure, spread from one eye to the other, recent upper respiratory symptomsItching, burning, foreign body sensation, tearing, discharge, eyelash mattingPre-auricular adenopathy, chemosisNo significant pain, light sensitivity, or visual lossAdenoPlusPOSITIVENEGATIVEEducation: hygiene and hand washingSupportive care: artificial tears, cool compresses and antihistaminesAntiviral medicationNo antibioticsConsider topical antibiotics or antihistamines
54 Viral Conjunctivitis: Signs and Symptoms Pseudomembranes in severe casesSubconjunctival hemesGritty sensationWatery dischargeSticky in morningsFollicular responseChemosisInjectionSPKInfiltrates possiblePositive lymph nodes
55 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
56 Management Betadine (Melton-Thomas Protocol): Proparacaine4-5 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.
57 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.
58 Sinusitis Red Eye With a sinus infection or inflammation the 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
59 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 daysBecause of increasing resistance to the antibiotic amoxicillin — the current standard of care — the ISDA recommends AugmentinAugmentin 250/500 TID for 5-7 days for adults, days for childrenAlternative is Keflex 500 mg QID
60 Flashes and FloatersPatients often present complaining of “spots” or “cobwebs” in front of their eyesCauses 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
64 Flashes and FloatersSudden onset typically means a PVD, retinal tear or hemeIf the spots appear after flashing light, then retinal tear must be eliminatedMyopes 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
65 Flashes and Floaters: Management A 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
66 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
67 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
68 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
69 Acquired Lid Nevi Acquired 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 pedunculatedcompound (involving both dermis and epidermis) tend to be dome shaped
70 Corneal UlcersInfective bacterial and fungal corneal lesions cause severe pain and loss of visionSigns and Symptoms:Pain, photophobia, tearingMucopurulent 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
74 Corneal Ulcers The 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
75 Corneal UlcersInfective bacterial and fungal corneal lesions cause severe pain and loss of visionS and S:Pain, photophobia, tearingMucopurulent 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
76 Associated FactorsContact lens wear, especially soft and extended wear lensRecent history of corneal traumaTopical steroid useHistory of exposure to vegetative matter (fungal etiology)
77 Protein Synthesis Inhibitors These 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
78 TetracyclinesNonresistant strains concentrate this antibiotic intracellularly resulting in inhibition of protein synthesis.Broad spectrum, bacteriostatic,effective against gram (+) and (-) bacteria and against non-bacterial organismswidespread 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.
79 Tetracyclines This group includes: Tetracycline (250mg mg cap BID-QID) needs to be taken 1 hour before or 2 hours after a meal.Minocycline (100 mg cap BID)Doxycycline (20mg mg cap or tab BID)
80 Tetracyclines: Acne 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) ortetracycline 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
83 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
84 Epidemiology Nonarteritic: usually seen in younger patients Fellow eye involved in 25-40% of casesAssociated with hypertension and diabetes
85 EpidemiologyArteritic: usually seen in >55 yrs old (mostly over 70)fellow eye involved in 75% of cases within 2 weeks without treatment
86 Symptoms Acute 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.
87 Ocular SignsSudden, unilateral, painless decreased vision and color visionPositive RAPDAltitudinal visual field defect (usually inferior and large)Swollen optic discFellow nerve often crowded with small or absent cup (“disc at risk”)
88 Additional Testing Lab tests: Check blood pressure STAT ESR (rule out arteritic form)CBC (low hematocrit, high platelets)Fasting blood sugarC reactive protein,VDRL/FTA-ABSANACheck blood pressure
89 Management Arteritic: Non-arteritic: Systemic steroids to prevent fellow eye involvementmethylprednisolone 1 g IV qd in divided doses for 3 days then,prednisone mg po qd with a slow taperCheck PPD, blood glc and chest radiographs before starting systemic steroidsNon-arteritic:Consider daily aspirin
90 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
91 TIA’sStroke is 3rd leading cause of mortality in developed countries and most common cause of neurological disability15-20% 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
92 TIA’sRisk of stroke after TIA has traditionally been considered relatively low, butnew 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.
93 TIA’s: High Risk Factors Five (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!
94 TIA: Early TreatmentSeveral treatments are likely to be effective in preventing stroke in the acute phase after a TIA:AspirinAnticoagulantsStatinsEndarterectomy (for >50% carotid stenosis)Further research needed for:Lowering blood pressure acutely after TIAProphylactic use of neuroprotective drugs
95 Amaurosis Fugax:TMB Most common cause is: thromboembolic disease (eg carotid artery disease throwing emboli) orvasospasmDescribed 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
96 Alkali Chemical Burns Alkali exposure results in: Loss of corneal and conjunctival epi, stromal keratocytes and endotheliumLoss of clarity is secondary to stromal hydrationDamage to the vascular endothelium of conjunctival and episcleral vesselsIntraocular structures such as iris, lens and ciliary body are rapidly damaged if alkali penetrates cornea.
97 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
98 Chemical Burn Treatment Immediate 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)
99 Chemical Burn Treatment Water 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.
100 Chemical Burn Treatment Effectiveness 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.
101 Chemical Burn Treatment Severe 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.