Red eye & Retinal disorders Flashcards

1
Q

What kind of tests can we do to inspect the retina? [6]

A
  • Direct Ophthalmoscope
  • Optical Coherence Tomography (OCT)
  • Fundus Fluorescein Angiography (FFA)
  • Electrical Physiology including Electroretinogram (ERG), Electroculogram (EOG) and Visually Evoked Potentials (VEP)
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2
Q

What is Optical Coherence Tomography? [1]

A

A cross sectional scan of the Fovea Centralis (Macula)

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3
Q

How does a Fundus Fluorescein Angiography work?

A

Fluorescein dye injected

  • > Binds to blood proteins
  • > Blue light shone in and excites the fluorescein
  • > Light returns and the yellow-green light is isolated with a filter
  • > Yellow-green light shows shines on a film
  • > Fluorescein filled vessels appear white

This will help you spot any blockages or bleeds from an optical artery

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4
Q

Name 3 of the 9 retinal layers

A

Layers 1,2 & 9
1 - Retinal Pigment Layer
2 - Layer of rods and cones
9 = Inner cell fiber layer

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5
Q

What is electrical physiology? [1]

Give 3 examples

A

Series of investigations recording electrical signals from the eye, optic nerve or brain in response to visual sitmuli [1]

Includes:

  • Electroretinogram (ERG)
  • Electrooculogram (EOG)
  • Visually Evoked Potentials (VEP)
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6
Q

What does an electroretinogram test? [3]

A

Action Potentials in the retina in order to measure retinal function

An A wave ERG tests photoreceptors
A B wave ERG tests Muller’s Cells (Retinal Glial cells)

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7
Q

What does an Electrooculogram test?

What does it measure? [2]

A

Function of retinal pigment epithelium and photoreceptors (Layers 9 & 8). [2]

It measures the Resting Potential in both layers and forms a ratio called the Arden Ratio (1.85 is normal)

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8
Q

What does a Visually Evoked Potentials (VEP) Test measure? [2]

A

They record optic nerve function [1] by measuring electrical activity in the visual cortex [1] in response to stimuli. (if optic nerve isnt working the visual cortex wont be active)

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9
Q

VEP test: state the clinical significance of each of these pathological signs:

  • Reduced amplitude [2]
  • Latency in signal [2]
A

A reduced amplitude in the signals means theres a reduced cell number. Most often due to Ischaemic or Traumatic Optic Neuropathy.

Latency in the signal means the cell function is reduced. Most often due to Optic Neuritis causing demyelination.

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10
Q

List some retinal disorders

A
  • Central Retinal Vein Occlusion
  • Central Retinal Artery Occlusion
  • Ischaemic Optic Neuropathy
  • Optic Neuritis
  • Retinal Detachment
  • Age Related Macular Degeneration
  • Diabetic Retinopathy
  • Hypertensive Retinopathy
  • Inherited Retinal Dystrophies
  • Drug Induced Retinopathy
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11
Q

What retinal disorders cause a gradual visual loss [4] and which a sudden visual loss [4]?

A

Gradual:

  • Age-related Macular Degeneration
  • Diabetic Retinopathy
  • Inherited Retinal Dystrophies
  • Drug Induced Retinopathy

Sudden:

  • Retinal Detachment
  • Optic Neuritis
  • Ischaemic Optic Neuropathy
  • Central Retinal Artery or Vein Occlusion
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12
Q

What causes Central Retinal Vein Occlusion [4]

What causes Central Retinal Arterial Occlusion [2]

A

CRVO:

  • Hypertension
  • Glaucoma
  • Hyperviscosity eg polycythemia
  • Inflammation eg DM

CRAO:

  • Emboli from atheromatous plaque, valve, dental abscess
  • Inflammation eg SLE, IVDU
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13
Q

How does the retina appear on Central Retinal Vein [3] /Artery Occlusions?

A
CRVO:
- The retina is darker
- Tortuous dilated and engorged veins
- Macular & Optic Disc Oedema
- Cheesy pizza! Flame shaped hemorrhages
All because of the back up of blood

CRAO:

  • Pale retina, cherry red spot at macula
  • Conspicuously lacking blood
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14
Q

What are the types of Ischaemic Optic Neuropathy? [3]

A

Arteritic (AION) - Usually caused by giant cell arteritis

Non-Arteritic (NAION) - Unknown cause

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15
Q

AION

  • Definition [2]
  • GCA presentation [6]
  • GCA investigations [2]
  • Treatment [2]
A
Optic nerve damage [1] when posterior ciliary arteries are blocked [1] by inflammation or atheroma
GCA presentation
- Headache
- Scalp Tenderness
- Jaw Claudication
- Neck Pain
- Nausea/Anorexia
- Visual Loss/Diplopia

Test for inflammatory markers & a Temporal Artery Biopsy
Carry out ix before steroids

Treatment

  • Prednisolone 80mg for 24h PO
  • Taper steroids as ESR and symptoms settle, may take >1y
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16
Q

What are the symptoms of optic neuritis [4] and its cause [1]?

A
  • Pain on eye movements
    • acute onset Loss of vision (central scotoma)
  • Relevant Afferent Pupil Defect
  • Swollen Optic Disc

MS!

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17
Q

Define scotoma

A

Loss of visual acuity [1] in a specific area of vision [1]

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18
Q

What are the risk factors for age related macular degeneration? [3]
ARMD nature of vision loss [3]

What are the types of Age Related Macular Degeneration and explain differences in pattern of vision loss?

A

Age
Smoking
Poor Diet (B12 def)

Progressive loss of the central vision with distortion (metamorphopsia). Quiet eye.

Wet (20%) - sudden
Dry (80%)- slow onset, gradual

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19
Q

Wet AMD pathogenesis [2]
Dry ARMD description [2]
Fundal signs [4]

A

Wet AMD occurs when aberrant vessels grow from the choroid into neuro-sensory retina and leak

Dry ARMD- drusen and degenerative changes at the macula

Ophthalmoscope:

  • Optic disc edge is made irregular by lumpy, yellow matter
  • Optic cup absent
  • Vessels show abnormal branching patterns
  • Disciform scar - as blood vessels grow subretinally and bleed, blood reabsorbs with subsequent fibrosis and raised sub retinal scar is left
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20
Q

Diabetic retinopathy
What is the main first step in microvascular disease of diabetes in the eye?
Ocular changes can be classified into 2
Ocular changes can also be staged into 2

A

Microvascular disease leads to ocular ischemia and hypoxia, increased VEGF

Ocular changes can be classified into

  • Structural changes
  • Retinopathy

Stages:

  1. Non-proliferative diabetic retinopathy
  2. Proliferative diabetic retinopathy
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21
Q

What are Retinal Dystrophies? [3]

A

A large number of inherited disorders [1] which affect photoreceptor function [1] leading to Progressive Visual Loss [1]

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22
Q

What are the types of retinal Dystrophies? [4]

A

Photoreceptor Dystrophies e.g. Retinitis Pigmentosa
RPE-Dystrophies (Retinal Pigment Epithelium) e.g. Stargardt Macular Dystrophy
Choroidal Dystrophies
Vitreoretinal Dystrophies

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23
Q

What is retinitis Pigmentosa [2] and its inheritance [1]

Symptoms [2]

A

Causes severe degeneration [1] of the Rod photoreceptors [1]

Can be Autosomal dominant, recessive or x-linked. [1]

Night blindness
Tunnel vision loss (loss of peripheral retina)

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24
Q

Name some drugs that cause drug-induced retinopathy? [3]

Pattern of loss of vision in drug-induced retinopathy [1]

A

Antimalarials
Phenothiazines
Tamoxifen

All can lead to gradual loss of vision

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25
List some modern treatments for retinal diseases? [2]
Gene Therapy Bionic Eye
26
How does Gene Therapy work for retinal disorders? [3]
- Disorder due to a defective or missing gene (E.g. Choroideraemia) - Viral vector inserts replacement gene - Replacement gene synthesises protein
27
CRAO Presentation [2] Signs [3]
Presentation - Dramatic visual loss within seconds of occlusion - Episodes of amaurosis fugax Signs: - Afferent pupil defect + cherry red spot (fovea) - retina appears pale - may see emboli inside arteries
28
CRVO Compare pattern of visual loss to CRAO and explain this difference [2] State 2 types of CRVO
Pattern of visual loss - Sudden painless visual loss - Less sudden than CRAO why? - Mechanism of visual loss due to development of ischemia and macular edema Non-ischemic, ischemic CRVO
29
``` CRVO Investigation What is the treatment given and why [2] Prognosis [2] What should you aim to prevent long term [1] and how [4] ```
Fundus fluorescein angiogram - Determines degree of ischemia Treatment - Pan-retinal photocoagulation [1] prevents and treats neovascularisation [1] - Aim to prevent rubeotic glaucoma and painful eye - Give beracizumab for macular edema - dexamethasone intravitreal implants Prognosis - visual prognosis is poor [1] even if macular edema resolves anatomically [1]
30
BRVO - presentation [1] - explain difference [2]
Presentation - Asymptomatic if macula not affected - Unilateral visual loss - Visual field defect corresponds to affected area Only a portion of retina is affected as opposed to the whole retina in central retinal a/v occlusion But otherwise same predisposing factors as CRVO
31
Explain how retinal ischemia can cause macular edema [4]
- Retinal ischemia leads to release of VEGF [1] - neovascularisation [1] - fragile and leaky blood vessels [1] - prone to hemorrhage [1] - macular edema
32
Explain how drusen is formed in pathogenesis of dry ARMD [4]
Drusen signify optic nerve head axonal degenration [1] Abnormal axonal metabolism leads to intracellular mitochondrial calcification [1] Some axons rupture and mitochondria are extruded [1] into extra-cellular space Calcium is deposited here and drusen form [1] This causes the optic disc head to become irregular and lumpy and the optic cup to become absent with abnormal branching vessels
33
AMD risk factors [4] Symptoms [5] Signs [3]
RF: - increasing age, smoking, CV RFs, FHx Sy: - initially no deterioration in visual acuity but difficulty making out images - difficulty reading and making out faces - difficulty with night vision and changing light conditions (specifically changes in Amsler grid self-evaluation and trouble with reading) - visual fluctuation, metamorphsia (distortion of central vision) - central vision loss Si: - poor visual acuity (especially near vision early in disease) - full peripheral field - quiet eye
34
``` Diabetic retinopathy Classification Mild NPDR Moderate NPDR [5] Severe NPDR [3] Proliferative diabetic retinopathy features ``` Structural changes - Age-related cataracts (AGE) - Ocular ischemia causing neovasculargenesis (rubeosis) - Glaucoma
Mild NPDR - 1 or more microaneurysm Moderate NPDR - microaneurysms - blot haemorrhages - hard exudates - cotton wool spots, venous beading/looping - intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR Severe NPDR: - blot haemorrhages and microaneurysms in 4 quadrants - venous beading in at least 2 quadrants - IRMA in at least 1 quadrant Stage 1: hyperglycemia damages pericytes but eye exam normal Proliferative: - hypoxia causes increased VEGF > neovascularisation - fragile leaky capillaries are prone to bleeding - Vitreous hemorrhage > increased risk of RD due to fibrosis causing traction - Maculopathy - leakage from vessels near macula cause edema
35
Name 3 types of hemorrhages you would see on PDR Name 3 conditions that accelerate development of DM retinopathy Treatment modalities [4]
Types of hemorrhages: blot, flame shaped, vitreous Conditions that accelerate DM retinopathy: - Pregnancy - Dyslipidemia, high BP - Renal disease, smoking, anemia Treatment - Good glycemic control - Laser photocoagulation for maculopathy and proliferative retinopathy - Triamcinolone, anti-VEGF (intravitreal) - Vitrectomy if big VH
36
Describe the outcomes laser photocoagulation [2]
Outcome of laser photocoagulation: - Will not improve vision - Aim to prevent blindness
37
CRAO Ax [3]
Ax: • Carotids: atheromatous disease causes fibrin-platelet emboli; often gives rise to amaurosis fugax • Heart: calcifications from aortic valves, endocarditis or SLE vegetation, mural thrombus (AF), atrial myxoma • Vasculitis: vaso-occlusion due to GCA, PAN or SLE
38
CRAO Mx [5] | Long term plan
* **form of stroke; mx according to local stroke protocols*** - If seen within 6h of onset, aim is to increase retinal blood flow by reducing IOP by ocular massage - Hyperbaric oxygen, inhaled carbon - Identify and treat CV risk factors - Surgical: Anterior chamber paracentesis (of aqueous humor) - Infusion of tPA in opthalmic artery o Long term: primary prevention of CVS RFs to minimise further events
39
CRVO RF [5]
- increasing age, HTN, DM - open angled glaucoma - hypercholesterolemia - hyper viscosity (polycythaemia, leukaemia, Waldenstrom’s macroglobulinaemia) - inflammatory (sarcoidosis, Bechet’s disease)
40
CRVO Mx | 3 modalities
Manage 3 areas: - Vision loss - Retinal neovascularisation: photocoagulation - Prevent rubeotic glaucoma and painful eye
41
CRVO Rx Vision loss [2] Prevent rubeotic glaucoma and pain fun eye [2]
• Vision loss: - intra-vitreal anti-VEGF - DEXAMETHASONE implants or intravitreal TRIAMCINOLONE ACETONIDE • Prevention of rubeotic glaucoma and painful eye: - RANIBUZUMAB for macular oedema, lasers - intravitreal DEXAMETHASONE implants
42
Retinitis pigmentosa Fundoscopy [2] Ix [4]
Fundoscopy: - black bone spicule shaped pigmentation in peripheral retinal - mottling of retinal pigment epithelium Ix: - slit lamp examination - genetic testing - electro retinopathy - visual field perimetry - optical coherence tomography
43
Retinitis pigmentosa | Mx [2]
Mx: - incurable but vitamin A - mx of any co-existing cataracts or glaucoma can help slow progression
44
Vitreous haemorrhage | Ax [8]
- proliferative diabetic retinopathy (50%) - branch or central retinal vein occlusion - sickle cell anaemia - retinal hole or retinal tear formation - wet disciform macular degeneration - posterior vitreous detachment - Valsalva phenomenon - posterior uveitis
45
Vitreous haemorrhage Symptoms [4] Signs apparent on large hemorrhage [4]
- sudden, painless loss of vision or haze - red hue in vision - floater - shadows or dark spots in vision Signs: - reduced visual acuity, absent red reflex - retina cannot be seen - visual field defect
46
Vitreous haemorrhage Ix [3] Prognosis
Ix: - dilated fundscopy (vitreous haemorrhage) - slit-lamp (RBC in anterior vitreous) - B-scan USS to identify cause Prognosis: usually spontaneously absorbs
47
Vitreous haemorrhage Mx - Dense VH [1] - DM patients with previous photocoagulation and recurrent VH
Vitrectomy to remove blood for dense VH DM patients with previous photocoagulation and recurrent VH: acceptable to wait 3m for resolution
48
Mx of AMD Dry [3] Wet [3]
Dry AMD: • Glasses and visual aids - magnifiers • Social support including blind registration if required - zinc and anti-oxidant vitamins A, C and E may reduce progression Wet AMD: • Argon laser photocoagulation may be helpful in early neovascular macular degeneration, to ablate membrane of new vessels and prevent bleeding • Intravitreal anti-VEGF (Avastine, Lucentis) monoclonal antibodies treatment • Cold laser + Verteporfin to ablate membrane of new vessels and prevent bleeding
49
Fundoscopy of AMD features of: Dry [3] Wet [3] 2 other investigations
o Dry: - drusen (colloid bodies) - retina appears dry with areas of hyperpigmentation - prominent choroidal vessels o Wet: - fluid exudates - localised detachment of pigment - disciform scar (subretinal blood vessels grow and bleed and blood is reabsorbed with subsequent fibrosis and a raised subretinal scar) Ix: slit lamp, fluorescein angiography (if considering laser)
50
AMD prognosis
wet carries worse prognosis (progresses more rapidly) but dry is less treatable
51
How do we diagnose the cause of Acute Red Eye?
We base it on pain, redness, discharge & vision
52
What are the causes of acute red eye? [4]
- Uveitis - Conjunctivitis (Bacterial, viral, chlamydial, allergic) - Scleritis - Acute (closed angle) Glaucoma - Keratitis/Corneal Ulcer - Orbital Cellulitis
53
What are the types of conjunctivitis? [2]
Bulbar - affects conjunctiva over the sclera Palpebral - affects conjunctiva on inside of lids (Can be both)
54
What is the presentation of Conjunctivitis? [5] Explain how discharge can guide ddx [3] Causes [5] Rx [3]
- Red/pink conjunctiva - Eyelids stick together - Vision unaffected, no pain - +/- photophobia - Purulent (bacteria) ``` Bacterial = Pus Viral = Watery Allergic = Mucous ``` Causes: adenoviruses - small lymphoid aggregates appear as follicles on conjunctiva, bacterial or allergic, chlamydial infection, ophthalmia neonatorum Rx - Chloramphenicol 4-6h - Allergic, give emedastine, sodium cromoglicate, steroids
55
What is uveitis? [3] | What is the anterior uvea [2]
Inflammation of the middle vascular layer of the eye (ciliary body, iris & choroid) Anterior uvea - iris and ciliary body
56
How does anterior uveitis present? [4] Describe what happens to the pupil with the natural history of anterior uveitis [2] What diagnostic test is used in suspected anterior uveitis [2]
- None/mild irritation - Pericorneal Redness - No Discharge - Blurred Vision Fixed constricted pupil Small pupil initially from iris spasm [1] Pupil may become irregular/dilate due to adhesions between lens and iris (synechiae) [1] Talbot's test - pain increases as the eyes converge [1] and pupils constrict ( ask the patient to watch their finger approach their nose) [1]
57
What are the types of Uveitis? [4] | Ix [2]
Ant - Iris Intermediate - Ciliary Body Post - Choroid Panuveitis Slit lamp Ocular imaging
58
Slit lamp appearance in: - Anterior uveitis [2] - Intermediate uveitis [2]
Anterior - Inflammatory cells leak from iris into Aqueous humor - > Hazy cell filled Ant chamber [1] and Hypopyon (cells settled inferiorly in ant chamber) [1] Intermediate - Inflammatory cells leak from ciliary body in Vitreous Humour [1] - > Patient has hazy vision or "floaters" [1]
59
Causes of Uveitis: - Anterior [4] - Intermediate [3] - Posterior & panuveitis [4]
Anterior: - AS, Still's - Sarcoid, Behcets - Crohn's, Reiter's - Herpes, TB, syphilis, HIV Intermediate - MS - Lymphoma - Sarcoid Posterior & Panuveitis - HSV, toxoplasmosis, TB, CMV, endophthalmitis - Lymphoma, sarcoidosis - Behcets
60
Treatment of uveitis [3] | Complications [4]
1) 0.5%-1% prednisolone 2h 2) cyclophenolate 1%/8h to keep pupil dilated, preventing adhesions between lens and iris (synechiae) 3) Monitoring Complications: - prolonged inflammation causes disruption to aqueous flow and glaucoma +/- adhesions - also get cystoid macular oedema, cataracts, chorioretinal scarring, retinal detachment and vitreous opacities
61
What is scleritis [2] How does scleritis present [4] Ix [2] Mx
Generalised inflammation with edema of conjunctiva [1] and scleral thinning [1] - Severe boring type headache, photophobia, pain on eye movement - Diffuse redness, tender eye - Normal vision - No discharge - Visual acuity may be decreased Ix - ESR, ANCA (for anti-neutrophil cytoplasmic antibody-assoc vasculitis) - Slit lamp examination Mx - Refer to specialist urgently
62
Corneal ulcer symptoms [3] RF Ix Mx [2]
- Eye pain - photophobia - Eye watering RF: contact lens users Ix: fluorescein staining Mx: remove contact lenses, abx or antifungal drops
63
What are the types of eye cellulitis? [2]
Preseptal | Orbital
64
What causes both types of cellulitis? [2]
Preseptal cellulitis: - Lid cyst or insect bite Orbital Cellulitis - Sinusitis & Dental Infection
65
How do the types of cellulitis present? [6]
``` Severe Pain Redness Lid Swelling Decreased eye mobility Diplopia, blurred vision Exophthalmos ```
66
Causative organisms of orbital cellulitis
Staphs Strep pneomoniae Strep pyogenes
67
Orbital cellulitis management [4]
Admit for prompt CT, ENT and ophthalmic opinion Antibiotics Surgery - prevent extension of infection to meninges or cavernous sinus
68
Subconjunctival haemorrhage Causes [2] Tx [1]
Spontaneous esp if on anticoagulants Traumatic - local, basal skulll Tx: reassurance
69
Keratitits - inflammation of cornea | Causative organisms [3]
Causes: - HSV - Adenoviral - Bacterial
70
Keratitis: HSV Presentation Ix Tx [2]
Dendritic ulcer Stains with flourescein or rose bengal Treatment: topical acyclovir and immediate referral to an ophthalmologist
71
Keratitis: adenoviral Presentation [2] Tx
Punctate opacities of cornea, which may stain with fluorescein Preauricular Lymphadenopathy + history of viral illness/sore throat Treatment: supportive, refer if no improvement or excessive pain/loss of vision
72
Keratitis: Bacterial Presentation [3] Mx
- Infiltrate or ulcer on cornea (look for fluorescein staining) + presence of hypopyon + history of contact lens wear Treatment: refer urgently
73
Foreign body management [3]
Visualise Remove with cotton bud if superficial Chloramphenicol drops for infection prevention
74
``` Radiation burn Define Ax [2] Symptoms [4] Ix Mx ```
``` UV light damages cornea Ax: arc welding, sunbeds Presentation: - Foreign body sensation - Blepharospasm - Watering - Intense pain 6-12h after exposure Ix: slit lamp Mx: same as corneal abrasion with topical anesthetics ```
75
``` Chemical burns Acid vs alkali burn Presentation [5] Ix Mx [7] ```
``` Alkali > acid Presentation: - Foreign body sensation - Blepharospasm - Watering - Intense pain - CORNEAL HAZE ``` ``` Ix: slit lamp Mx: - immediate referral - Remove all large particulate matter and wash out well with saline until pH of conjunctiva sac returns to 7 - Topical anesthetics: tetracaine 1% every 2 min until patient comfortable - Abx prophylaxis - Topical steroids - Systemic and topical vitamin C - Lubricants ```
76
Penetrating injury Ax [4] Presentation [5] Complications [4]
``` Ax: glass, hammer and chisel, pencils Presentation: - Pain - Lid margin tears - Lacrimal duct damage - Flat anterior chamber - Iris prolapse (distorted pupil) ``` Complications: - Cataract - Vitreous haemorrhage - Retinal detachment - Globe rupture
77
Penetrating injury How does globe rupture present? [3] Ix [3] Mx [3]
Globe rupture: - Loss of vision - RAPD - Low IOP Ix: - Slit lamp - XR for FB intraocular - XR skull for intracranial involvement Mx: - DO NOT remove large foreign object e.g. dart, knife - Support object with padding, transfer supine and pad unaffected eye to prevent damage from conjugate movement - Surgical correction
78
``` Blunt trauma Ax [3] What are 3 presentations? Ix Mx [2] ```
Ax: fist, shuttlecock, squash or football injury Presentation: - Intraocular hemorrhage - Secondary hemorrhage - Orbital blows Ix: CT head (depressed fracture of posterior orbital floor) Mx: surgical fracture reduction, muscle release
79
Blunt trauma: Intraocular hemorrhage presentation [2] Secondary haemorrhage presentation [5] Orbital blows [3]
Intraocular hemorrhage: - Reduced visual acuity - Hyphaemia (blood in anterior chamber) Secondary hemorrhage: - Within 5d of injury causes secondary glaucoma - Traumatic mydriasis - Vitreous haemorrhage - Optic nerve damage Orbital blows: - Sudden increase in intra-orbital pressure - Orbital contents herniate into maxillary sinus - Tethering of inferior rectus and IO > diplopia and restriction on upward gaze
80
When orbital contents herniate into maxillary sinus, how can this be confirmed on examination [2]
Loss of sensation | Infraorbital nerve injury
81
How does a blow out fracture occur? [2] | Explain how diplopia occurs [2]
The rim of the orbit is very strong so it tends not to fracture. On blunt force trauma (football), sudden increase in pressure within orbit [1] the force can be transmitted to the walls/floor of the orbit causing fractures of the weaker bones there [1] Diplopia and unable to elevate eye occurs due to tethering of inferior rectus and inferior oblique muscles [2]
82
Clinical test for blow-out fracture Investigations - what will it show [2] Management [2]
- Reduced sensation of the infra-orbital nerve coming out the infra-orbital foramen - test for loss of sensation over lower lid skin - CT may show depressed fracture of posterior orbital floor - Fracture reduction and muscle release
83
Management Scleritis [4]
* Non-necrotising anterior: NSAIDs and oral high dose PREDNISOLONE * Necrotising OR posterior: immunosuppression (CICLOSPORIN or RITUXIMAB and METHYLPREDNISLONE) * Refractory: INFLIXIMAB * Imminent globe perforation: surgery
84
Corneal ulcer | Ax [3]
Ax: bacterial (pseudomonas), herpetic (see keratitis), fungal (more likely if steroids)
85
Corneal abrasion Ax [3] Sx [4]
``` Epithelium of cornea is breached Ax: - trauma (cat scratch, baby finger nail, twig) - contact lenses, chemical injury - previous corneal disease ``` Sy/Si: - intense pain - photophobia - reduced visual acuity - lacrimation
86
Corneal abrasion Ix Mx [4]
Ix: blue light and stain with fluorescein (stain green) Mx: • Local anaesthetic drops: e.g. TETRACAINE 1% before examination • Send home with analgesics, CHLORAMPHENICOL ointment for copious lubrication and a pad with compression • If still foreign body sensation when pad removed after 24h, then re-examine with fluorescein • If abrasion still present after 48h, refer