Presentation on theme: "Case 1 56 year old man presents for routine examination and these are the fundus photos . L R L 10- 21mmHg normal range Subgroup <21 mmHg Primary open."— Presentation transcript:
1 Case 156 year old man presents for routine examination and these are the fundus photos .LRL10- 21mmHg normal rangeSubgroup <21 mmHgPrimary open angle glaucomaIOP in the 20’s to low 30’sAcute angle closure glaucomaIOP 40’s to 60’sWhen to refer:IOP greater than 21 mmHgDifference of IOP of greater than 5 mmHgC:D greater than 0.5; asymmetry between 2 eyesSx of acute angle closure
2 Case 2 65 year old female presents with monocular diplopia Over 1.4 million cases done per year in the USOver 70% of those over the age of 75 have cataract
3 Case 3 65 year old smoker male presents blurred vision centrally Leading cause of visual loss in patients over the age of 50It is estimated that over 500,000 Canadians have some form of this diseaseDryNo treatment for the dry type except VITAMINS (C,E, zinc, beta carotene)WetThermal laser photocoagulation of new blood vesselsOnly good if new blood vessels are away from the centre of vision (laser also destroys healthy tissue)Photodynamic therapy with visudyne consists of laser treatment after dye infusionCloses blood vessels in the centre of vision but requires numerous treatments (5-6 over a 2 year period)New Treatment Lucentis/AvastinIntravitreal injections; 95% vision stabilization; 35% improveMany injections
4 Case 465 year old diabetic male presents with blurred vision centrallyOne of leading causes of visual lossClassified as non-proliferative vs. proliferative (presence of new blood vessels on disc or retina)Main causes of visual loss include: macular edema, vitreous hemorrhage, macular ischemiaTreated with laser, intravitreal injections of anti-VEGF or steroids, and surgery
6 Case 165 year old male presents with sudden painful loss of vision. States it was preceded by nausea and vomiting.
7 Case 223 year old diabetic presents with sudden visual loss following being hit with a softball.
8 Case 357 year old man with 30 year history of DM presents with sudden onset of rapidly progressive acute visual loss.
9 Case 465 year old make presents with sudden painless loss of vision. Preceded by flashes of light and floaters.
10 Case 565 year old make presents with sudden painless loss of vision. No RAPD. Eye appears white.Amaurosis fugax- precursor to strokeCentral retinal artery occlusion (CRAO)Box-carring, retinal opacificationRetinal emergency as perfusion may be restored with aggressive techniquesMay be related to embolic disease; systemic evaluation consists of carotid doppler and cardiac echoThink of giant cell arteritis in patient with bilateral CRAO- EMERGENCY to get on steroids
11 Case 665 year old male presents with sudden painless loss of vision. No RAPD. Eye appears white. PMHX smoker, HTN and diabetes.
12 Case 777 year old make presents with sudden painless loss of vision. No RAPD. Eye appears white. Smoker, HTN (190/110).Disc swelling, venous congestion and intraretinal hemorrhageCan predispose to new blood vesselsMay require laser surgeryLinked to hypertension, smoking, aging, clottingInflow disease (ocular ischemic syndrome)mid peripheral bloodMost related to near occlusion of internal carotid artery
13 Case 877 year old make presents with new distortion. No RAPD. Eye appears white.
14 Case 988 year old make presents with sudden loss of vision and says that it hurts when she chews. RAPD present. Eye appears white.Ischemic optic neuropathySwelling of disc and decrease vision in elderly is more likely to be vascularPale swollen disc often accompanied with splinter hemorrhages and loss of acuity; field loss in superior or inferior field (altitudinal)Arteritic versus non-arteritic (diabetes, HTN…)Rule out giant cell arteritisHigh ESR- may need steroidsBiopsy of vessels to confirm diagnosis
15 Case 1025 year old female with rapid loss of vision and decreased colour vision in the right eye. RAPD present. Eye is white.Optic neuritisInflammation of nerve may or may not be related to MS; usually youngNerve is hyperemic and swollenMay benefit from steroids (systemic)May be retrobulbar in nature- so not visible signsRule out a mass lesion
16 Causes of a Red Eye Blepharitis/Styes Lid malpositions Cellulitis Conjunctival/Scleral CausesExtraocular CausesBlepharitis/StyesLid malpositionsEctropionEntropion7th Nerve PalsyCellulitisPreseptalOrbitalConjunctivitisViralBacterialAllergicSubconjunctival hemorrhagePinguecula/PterygiumEpiscleritis/Scleritis
17 Causes of a Red Eye Hypopyon Infectious keratitis Intraocular CausesCorneal CausesHypopyonIritisPost-operativeEndophthalmitisAcute angle closure glaucomaTraumaHyphemaInfectious keratitisViral (HSV)BacterialFungalTraumaForeign BodyAbrasionContact lens issues
20 Case 6 Episcleritis – inflammation of the episclera Scleritis – inflammation of the sclera
21 Case 7Viral keratitis – HSV – viral infection of the cornea usually in acharacteristic dendritic pattern
22 Case 8 Bacterial keratitis – bacterial infection of the cornea Fungal keratitis – fungal infection of the cornea
23 Case 9Corneal Abrasion – loss of the surface epithelium of thecornea
24 Case 11 Hypopyon – finding on exam - variety of causes – infection, inflammation- collection of WBC in the inferior aspect of theanterior chamber
25 Case12 Endophthalmitis – inflammatory condition of the intraocular cavities (AC/vitreous) usually caused byinfection
26 Basic Ocular Anatomy Extraocular Muscles - LR6SO4 Inferior Oblique Up and inCN IIISuperior RectusUp and outCN IIIMedial RectusMediallyCN IIILateral RectusLaterallyCN VISuperior ObliqueDown and inCN IVInferior RectusDown and outCN III
27 Diplopia Monocular = refractive or retinal Dx: disappears when affected eye is covered but persists when unaffected eye is coveredBinocular = ocular misalignmentDx: cover test reveals strabismus.Disappears if either eye is covered
29 Strabismus - diagnosis Upper 3 photos show comitant strabismusRight gazePrimary gazeLeft gazeStrabismus - diagnosisLower 3 photos show incomitant strabismus
30 Restrictive Strabismus Orbital fracture - Hx of traumaGrave’s disease – Hx of hyperthyroidism, proptosisOrbital inflammation – red eye, proptosis, painOrbital tumor – loss of vision, proptosis, usually no pain or redness
31 A 24 year old man complains of vertical diplopia worsening over the past 2-3 years. He notes he can lessen the problem by tipping his head to his left side. Cover test shows a small right hypertropia. The right eye does not depress in adduction as well as the left eye does in abduction. Review motility photos. What is the diagnosis?
32 Superior oblique function in various positions of gaze Primary positionadductionabduction
33 Trochlear (4th n.) Palsy Etiology Children – trauma, congenital Adults – trauma, vascular, (tumor)What is the time course of the diplopia?If acute, then more likely vascularWhat other problems does patient have?Trauma, diabetes, BP, headache, vomiting
37 Abducens (6th n.) Palsy Etiology Children – trauma, post-viral, otitis, tumorAdults – vascular, trauma, tumor, ICPWhat is the time course of the diplopia?If acute, then more likely vascularWhat other problems does patient have?Trauma, diabetes, BP, headache, vomiting
38 Pupils Pupillary Pathways Pupillary Light Reflex Pupillary Size CN II CN IIIPupillary SizeSympathetic system - dilationParasympathetic system – constrictionPupillary light reflex
39 Pupil Size Pathways 2 processes take place with iris dilatation Discussion in groups for 5 minutesPUPILLARY CONSTRICTION-Described by pupillary light reflex – previous slidePUPILLARY DILATATION2 processes take place with iris dilatation1. Iris sphincter relaxesAccomplished by SUPRANUCLEAR inhibition of the Edinger-Westphal nucleus – thereby reducing the parasympathetic output – relaxing the iris sphincter causing dilatation. This inhibition is inactive during with sleep, narcotics, anesthesia resulting in iris sphincter contraction and pupil constriction with these states.Reduced light decreases the excitatory impulses to the E-W nucleus, resulting in iris sphincter relaxing and dilation.2. Iris dilator contractsIncrease in output of the sympathetic nervous system which innervates the iris dilator muscleThink of the sympathetic nervous system as a ‘turbocharger’ for pupillary dilatation – that is parasympathetic inhibition alone can cause dilatation to some extent – but sympathetic stimulation enhances the speed and size of dilatation (some of the drops we use are sympathomimetic at the postganglionic neuron)Sympathetic pathway – 1st order neuron originates in the hypothalamus and descends through the brain stem into the lateral column of the spinal cord – it synapses with the 2nd order neuron at the level of C7-T2 (ciliospinal centre of Budge) and then leaves the spinal cord, travels over the apical pleura of the lung (why pts with Pancoast’s lung tumours get Horner’s syndrome) and into the neck to synapse at the superior cervical ganglion – the 3rd order neuron (postganglionic neuron) travels along the internal carotid artery (why pts with carotid dissection can get a Horner’s syndrome) into the head to the orbit (via the cavernous sinus)Pupil Size Pathways
40 Approach to Anisocoria 1st Question?Which pupil is the abN pupil?2nd Question?What tests will I do on exam to figure that out?Pupil Size in Bright LightPupil Size in Dim LightPupillary Light Reaction
41 Horner’s Syndrome - DDx Damage to the sympathetic pathway resulting in a relatively small pupilCongenitalAcquired1st order neuron – central lesions (hypothalamospinal pathway)Stroke, tumour, MS, cervical spinal cord lesions2 nd order neuron - pre-ganglionic lesionsAdult-Tumour apex of the lung (Pancoast)Child- Neuroblastoma3rd order neuron – post-ganglionic (internal carotid)Internal carotid artery dissection, cavernous sinus thrombosis, prolactinoma
42 Horner’s Syndrome - Ix Generally - neuroimaging CT/MRI brain and neck CTA or head/neck or Carotid doppler – carotid dissectionCT chest – Pancoast tumour suspected
43 3rd Nerve PalsyParasympathetic fibres are involved when pupil unable to constrictPupillary fibres run along the outside of the 3rd CNPupil involved +/- oculomotor dysfunctionCompressive lesions are more likelyAneurysm, tumour, uncal herniationMotor fibres are more central in 3rd CNOculomotor dysfunction of CN III AND pupil sparedIntrinsic lesions are more likelyIschemic lesionsSeen in DM, GCA
44 3rd Nerve Palsy - Ix Pupil involved +/- oculomotor dysfunction NeuroimagingCTA (CT angiogram)AngiogramOculomotor dysfunction of CN III + pupil sparedObservationShould resolve in 8-12 weeksIf not completely resolved at that point - neuroimaging
46 Bruckner testThe simultaneous comparison of the red reflex from both eyes using ophthalmoscope(note difference in red reflex between eyes)
47 Amblyopia – diagnosisIn verbal patient – measure acuity using the hardest test the child can doAllen picture chart (easy), tumbling E chart (harder), Snellen chart (hardest)
48 Amblyopia Definition Prevalence AmblyopiaDefinitionLoss of visual acuity not correctable by glasses in an otherwise healthy eye (generic definition)A maldevelopment or loss of vision caused by abnormal binocular interaction or form vision deprivation during visual maturation (patho-physiologic definition)Prevalence2 – 4 % of populationCauses more visual loss and “legal” blindness (20/200 acuity) under age 45 than all other causes combined
50 Amblyopia – treatmentOnly works during “sensitive period” (roughly 0 – 6 years)Success varies inversely with ageEliminate any causes first (glasses, ptosis repair, etc.)Occlusion therapy (patching) is the gold standard
51 Strabismus - prevalence 2 – 4% of population (same as amblyopia, since they are so closely related)
52 Strabismus - diagnosis Cover test is key (gold standard)
53 TROPIA / PHORIA CONSTANT TROPIA: INTERMITTENT TROPIA: PHORIA: Eye turn present all of the timeConstant esotropiaINTERMITTENT TROPIA:Eye turn present some of the timeIntermittent exotropiaPHORIA:Eye turn present only when fusion brokenEsophoria
54 Strabismus - definition Misalignment of the eyesTypes:EsotropiaExotropiaHyper/hypotropiaESOTROPIAHYPERTROPIA
55 Why is leukocoria important? Need to know about leukocoria – a presenting sign of retinoblastomaAmbient light reflecting off the tumor appears white or yellow-white within the pupilStrabismus is a common feature in retinoblastoma
63 Rules 5 Golden of eye trauma 1. Check vision 1st 2. Agent-of-injury is King ! consider FB3. severe hemorrhage ? open eye4. Stat irrigation for burns5. Multi-trauma: ! examine globe 1st
64 Eye Trauma – timing of Rx Immediate: chemical burn *Urgent (hrs): ruptured globe, intraocular foreign bodySemi-urgent (48h): lid & lacrimal repairLess urgent (1-2 weeks): orbital fractures
65 Focused history - Bedside eye exam - Details: how, when, where.. Prior vision, eye conditionTetanus statusTime of last food/drinkBedside eye exam -
66 Teaching point: Intraocular Foreign Body May have pain or NO painDecreased vision or normal vision (asymptomatic!)Signs: as ruptured globe or minimal entry wound or none !Hx: high index of suspicion (! agent-of-injury)1st Rx: as in ruptured globeUrgent referral for surgeryNB: always check visionConsider CT, X-ray
67 Teaching points: Ruptured Globe CC: trauma (blunt or sharp), pain, decreased vision, ‘agent-of- injury’Signs: conj swelling, Hb++ (3D), hyphema +/- extruded uvea, irregular pupil…1st Rx: protect eye with shield, NPO, bedrest, anti-nausea medsUrgent transfer to ophthalmologyCaution: do not press on lids during exam( vision –> shield –> refer )
68 What is your management ? Orders:shield over Left eyeBedrestNPOanti-nausea medication prn(antibiotics..)urgent referral to Ophthalmology
76 Slide #4Optic disc drusenLumpy bumpy appearanceVessels not obscured
77 Case: Jill’s Headaches Jill, 35 y.o has had headaches, nausea, and vomiting for the past monthShe experiences brief episodes of dimming vision lasting secondsShe also notices a pulsing noise in her head.