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Y4 Neuro and Special Senses > Opthalmology Conditions > Flashcards

Opthalmology Conditions Flashcards

1
Q

Name 8 causes of a Red Eye Presentation

A

Acute Angle Closure Glaucoma
Endopthalmitis
Orbital Cellulitis
Corneal Abrasion
Hyphaema
Anterior uveitis
Keratitis
Scleritis

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2
Q

Define Glaucoma

A

Progressive optic neuropathy in which raised intraocular pressure is a key factor. Raised intraoccular pressure is caused by blockage in aqueous humour draining from eye.

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3
Q

What are the three types of Glaucoma

A

Open Angle
Closed Angle
Ocular HTN (elevated IOP without the other changes seen in Glaucoma)

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4
Q

Angle Closure Glaucoma can be acute or chronic, what is the difference?

A

Acute - severe eye pain, visual loss, headache and is an Opthalmic emergency

Chronic - Normally asymptomatic and picked up on routine screening , vision preserved until late stage

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5
Q

Risk factors for Acute Angle Closure Glaucoma

A

Increased Age
Asian Ethnicity
F>M
FH
Hyperopia
Shallow anterior chamber

Anticholinergic meds
Adrenergic meds
Tricyclic antidepressants

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6
Q

Describe Primary Angle Closure Glaucoma

A

Anatomically predisposed

Lens sits forward and pushes against iris

Pressure increases in posterior chamber causing forwards compression

Scar tissue forms in trabecular meshwork reducing drainage

Can be acute, subacute or chronic

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7
Q

Describe Secondary Angle Closure Glaucoma

A

Results from other eye pathologies

Push the iris/ciliary body in (eg SOL)

Pull the iris (iris neovascularisation)

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8
Q

Name three investigations for suspected AACG

A

Tonometry (measures intraocular pressure)

Gonioscopy (allows visualisation of anterior chamber and drainage system)

Slit lamp/Opthalmascope - Optic disc cupping

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9
Q

Chronic Angle Closure Glaucoma is normally asymptomatic, how does Acute present?

A

severely painful red eye

blurred vision

halos around lights

associated headache, nausea and vomiting

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10
Q

what is seen on examination of somone with Acute Angle-Closure Glaucoma?

A

Red-eye

Teary

Hazy cornea

Decreased visual acuity

Dilation of affected pupil

Fixed pupil size

Firm eyeball on palpation

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11
Q

Describe the opportunistic testing for Glaucoma via NICE guidelines

A

Every 2y from 60-70y
Annually from 70y
From age of 40 if affected first degree relative
African heritage >40

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12
Q

How is acute angle closure glaucoma managed? (primary care)

A
  • lie on back without pillow
  • give pilocarpine eye drops
  • give acetazolamide 500mg oral
  • give analgesia and an antiemetic if required
  • REFER FOR SAME DAY OPTHALMOLOGY ASSESSMENT
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13
Q

What are the secondary care management options for AACG?

A
  • pilocarpine
  • acetazolamide iv or oral
  • hyperosmotic agesnts - glycerol or mannitol
  • timolol
  • dorzolamide
  • brimonidine
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14
Q

What is the definitive treatment of AACG?

A
  • Inital Oral Acetazolamide and Drops
  • Followed by laser peripheral iridotomy (creates opening in iris, allowing equalisation of flow)
  • Definitive treatment is advised prophylactically for other eye
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15
Q

Define Endopthalmitis

A

Severe inflammation of anterior and/or posterior chamber (can be sterile but normally due to infection and often following surgery)

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16
Q

Give 5 causes of Endopthalmitis

A

Trauma
Eye Surgery
VEGF injections
Endogenous seeding
Extension of Corneal infection

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17
Q

Describe the likely pathogens of Endopthalmitis with each cause

A

Surgery - Coag neg Staph (epidermis)
Trauma - bacillus cereus
Endogenous - S.Aureus,Klebsiella

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18
Q

How does Endopthalmitis present?

A

Acute eye pain
Reduced vision
Hypopyon
?swollen eyelid

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19
Q

Name four risk factors for Endopthalmitis

A

Poor surgical technique
Contaminated lens
Contact lens wear
Immunosupression

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20
Q

What are the three subtypes of Post Op Endopthalmitis?

A

Acute (one to several days post surgery)
Delayed (up to 9m later, minimal or no pain)
Bleb Associated (after trabeculotomy for Glaucoma)

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21
Q

Name two differentials for Endopthalmitis

A

Retained lens material
Raised IOP as a result of procedure

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22
Q

How would you investigate Endopthalmitis?

A

Slit Lamp - Vitreous infiltrates
Vitreous sample for microbiology (Abx cover)

Endogenous - full infection screen

USS eye if unsure

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23
Q

Endopthalmitis is an emergency, depending on the aetiology how is it managed?

A

Bacterial - Direct Abx injection into Vitreous, if severe then Vitrectomy

Fungal - Vitrectomy and Intravitreal Amphoterecin

Systemic - Systemic Abx

Non Infectious - Steroids

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24
Q

Define Orbital Cellulitis

A

Sight threatening Opthalmic emergency characterised by infections of the soft tissue behind the septum

Most commonly seen in Children, spreading from local infection

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25
Name five sources of infection for Orbital Cellulitis
Extension from periorbital structures Extension from presentation structures Direct Inoculation Post Surgery Haematogenous
26
Name four common pathogens and one rare for Orbital Cellulitis
Common - H.Influenza, Strep Pneumoniae, S.Aureus, S.Pyogenes Rare - mucormycosis (rare fungal associated with DKA and Neutropenic Sepsis)
27
how does orbital cellulitis present?
* Redness and swelling around the eye * Severe ocular pain * Visual disturbance * Proptosis * Ophthalmoplegia/pain with eye movements * Eyelid oedema and ptosis * Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare)
28
Orbital Cellulitis is generally a clinical diagnosis. What investigations could you do, and what would they show?
FBC - leukocytosis + raised inflammatory markers Blood cultures - negative LP (if focal signs) Swabs CT sinus and orbit with contrast - extension
29
Orbital Cellulitis is an emergency and requires urgent antibiotics and four hourly monitoring. What are the Abx of choice?
1) Co Amoxiclav If pen allergic - Clindamycin and Metronidazole MRSA - Vancomycin
30
When would you consider surgery in Orbital Cellulitis?
Resistant to antibiotics Reduced visual acuity CT evidence of orbital collection
31
Name four complications of Orbital Cellulitis
Endopthalmitis Meningitis Orbital Abscess Subperiosteal Abscess
32
Corneal injuries can be physical, chemical or environmental. What makes a corneal abrasion (partial thickness) more likely?
If the eye doesn’t shut properly
33
Other than corneal abrasions, what other corneal injuries are common?
Superficial Keratitis Foreign Bodies
34
If there is no clear mechanism of injury but you suspect damage to the cornea, what should you cosncier
HSV infection
35
How does a superficial corneal abrasion present?
Redness Pain Watering Foreign Body Sensation Photophobia
36
How does a penetration corneal injury present?
Distorted globe Hyphaema Conjunctival laceration Red and watering
37
Name some functional and general features you are looking for on observation of corneal injury
Functional - Diplopia, Abnormal visual fields, RAPD General - raised IOP, infection
38
How can the Cornea be examined in suspected corneal injury?
Seidles Test - 10% Fluorescine and slit lamp to look for corneal leak (yellow/orange) Abrasion with dilute fluorosciene
39
Name three red flags for corneal injury
Deep lid laceration Subconjunctival haemorrhage Pupils/Iris/Fundus abnormality
40
How would you manage a Corneal Abrasion?
Pain relief (topical NSAIDs or Oral Abx) Topical chloramphenicol to prevent secondary infection Tetanus prophylaxis where necessary Avoid contact lenses for 2 weeks
41
How are Corneal Foreign Bodies managed?
Topical anaesthetic Eye irrigation and removal with damp cotton bud After removal treat as corneal abrasion
42
How can rust rings be removed?
A sterile rotating burr
43
How should a penetrating corneal injury be managed?
Cover with rigid eye patch and refer immediately for emergency surgery
44
Give two examples of how chemical corneal injuries can be managed?
CA gas - blown off the eye using a hairdryer Pepper spray and chlorine gas - copiously irrigated
45
Define Hyphaema
When blood enters anterior chamber between cornea and iris
46
How does a Hyphaema present?
Decrease/ Loss of vision (may improve as gravity pulls the blood down) Red tinge to eye
47
Name 5 causes of a Hyphaema
Intraocular Surgery Blunt trauma Lacerating Trauma Leukaemia Retinoblastoma
48
How are Hyphaemas managed?
Small - Outpatient basis, antifibrinolytics, corticosteroids, mitotics, asparin Non resolving - surgical clean out Pain relief - avoid aspirin and NSAIDs due to platelet interaction
49
Name two complications of Hyphaema
Haemosiderosis Raised IOP
50
What is the grading system for chemical injury of the eye?
Roper Hall
51
What is the immediate management for Ocular Chemical Injury?
1) Check pH with universal indicator 2) Administer topical anaesthetic and remove contact lenses 3) 1L saline irrigation continued until pH is 7 4) Rechecked every 15 minutes
52
If the Chemical Injury of the eye was moderate or severe, how would it be managed?
Dexamethasone 1-2 hourly Vitamin C (topically and orally) Citrate and Tetracyclines
53
Conjunctivitis is inflammation of the conjunctiva. How does Bacterial Conjunctivitis present?
Purulent discharge Worse in the morning Inflamed conjunctiva Starts in one eye and spreads to the other
54
How does Viral Conjunctivitis present?
Clear discharge Other symptoms of viral infection (URTI) Preauricular lymph nodes
55
What advice should you give patients with conjunctivitis?
Usually resolves without treatment in 1-2 weeks Maintain good hygiene (avoid sharing towels, rubbing eyes) Avoid contact lenses Clean with cooled boiled water and cotton wool
56
How can bacterial conjunctivitis be managed?
Chloramphenicol (contraindicated if pregnant or breast feeding) Fusidic Acid
57
How does Allergic Conjuncitivitis present?
Swelling of conjunctival sac and eyelid Watery discharge Itch
58
How is Allergic Conjunctivitis managed?
Antihistamines (Oral or topical) Topical mast cell stabilisers used for several weeks if chronic symptoms
59
Name four causes of Anterior Uveitis
Autoimmune Infection Trauma Ischaemia
60
Anterior Uveitis can be Acute or chronic . How do they differ ?
Chronic is more Granulomatous, less severe, longer symptom duration (often \>3m)
61
Name three associations of Anterior Uveitis and Chronic Anterior Uveitis respectively
acute: HLA B27 related conditions - Anklyosing Spondylitis, IBD, Reactive Arthritis Sarcoidosis, Syphilis, TB, Lyme disease, herpes virus
62
How does Anterior Uveitis present?
* Spontaneous unilateral symptoms * Dull aching * Red Eye * Ciliary Flush (ring of red from cornea outwards) * Reduced visual acuity * Flashers and floaters
63
what are some signs seen on examination of anterior uveitis?
64
What causes floaters in Anterior Uveitis?
Inflammation and immune cells in the anterior chamber
65
What is Posterior Synechiae? Give an association
Adhesions that can cause disruption to pupillary shape Anterior Uveitis
66
If a GP suspects a sight threatening opthalmological condition, what should they do?
Same day assessment by ophthalmologist Slit lamp examination and IOP measurement
67
How would you manage Anterior Uveitis?
Steroids - oral, topical, IV Cytoplegic (paralysing ciliary muscles) /Mydriatic (dilating pupils) medication Immunosupressants Severe - Laser therapy, Cryotherapy
68
What is the role of Cytoplegic/Mydriatic Medication in Anterior Uveitis? and give some examples.
cyclopentolate or atropine eye drops - antimuscarinic that block actions of iris sphincter muscles and ciliary body, dilate pupil and reduce pain associated with ciliary spasm by stopping action of ciliary body cycloplegic = Paralyses ciliary muscles mydriatic = dilate pupil
69
Keratitis is inflammation of the cornea, give some causes
viral - herpes simplex bacterial - pseudomonas, staphylococcus fungal - candida or aspergillus caonact lens acute red eye (CLARE) exposure keratitis - indequate eyelid coverage
70
Describe the pathophysiology of Bacterial Keratitis
Infection of one or more layers of the Cornea, normally once the epithelial layer has been breached (eg corneal abrasion) Risks - Diabetes, contact lens, corneal trauma
71
Name four presenting features of Keratitis
Redness Pain Photophobia Reduced acuity
72
What can be seen on examination of a Keratitic eye?
Oedema White cell infiltration Epithelial defect
73
How is Keratitis managed?
Intensive topical antibiotics - Ofloxacin for Pseudomonas cover (with or without cycloplegics) ?Steroids Stop contact lens use
74
Herpes Simplex Keratitis is the most common, and only normally affects epithelial layer. What could distinguish it from other causes of Keratitis?
Vesicles around the eye
75
What would Fluorescein staining of a HSV Keratitis eye show?
Dendritic corneal ulcer (branching and spreading)
76
How is HSV Keratitis managed?
Acyclovir (topical or oral) Ganciclovir eye gel Topical steroids
77
Define Scleritis
Inflammation of full thickness of the sclera Normally not caused by infection
78
What is the most severe form of Scleritis?
Necrotising Scleritis Visual impairment but not pain Can lead to Scleral perforation
79
Name four associated conditions with scleritis
SLE IBD RA Sarcoidosis
80
How does Scleritis present?
50% bilateral Pain (especially on eye movement) Photophobia Reduced acuity Abnormal pupillary response
81
How is Scleritis managed?
Underlying condition NSAIDs and Steroids
82
Name five causes of Gradual Visual Deterioration
Cataracts Open Angle Glaucoma ARMD Diabetic Retinopathy Presbyopia
83
What are Cataracts?
Opacification of the Lens Major cause of treatable blindness worldwide
84
Cataracts can be age related or non age related. Give three causes of non age related
Trauma Steroids Uveitis
85
What are the three classifications of Paediatric Cataracts
1/3 Inherited (Autosomal Dominant) 1/3 Systemic (Rubella, Fabrys) 1/3 Idiopathic
86
Cataracts can be classified depending on the location of lens affected. What are the three classifications
Nuclear Cortical Posterior Subcapsular
87
How do Nuclear Cataracts present?
Loss of colour vision Slow progression
88
How do Cortical Cataracts present?
Less visual degradation Slow progression
89
How to Posterior Subcapsular Cataracts present?
Disabling glare to bright lights Quick progression Links to DM and Steroids
90
Describe the pathophysiology of Cataracts
Lens is normally a highly organised structure to maintain transparency Lack of blood supply and inability to shed non viable cells leaves the lens succeptible to insult Results in loss of transparency, nodular sclerosis, inability to refract light
91
Give 6 presenting features of Cataracts
Painless loss of vision Halls around lights Sensitivity to light and glare Polyopia Myopic shift (improved near sighted) Loss of red reflex
92
Cataracts are a clinical diagnosis. What features will be seen on Opthalmoscope/Slit Lamp?
Loss of red reflex Opacification Obscuration of ocular detail
93
Surgery is carried out for Cataracts when they have a significant impact on ADLs. What are the two techniques called?
Phacoemulsification Extracapsular Cataract Extraction
94
Name two differences between the Cataract surgical techniques
PE - breaks up diseases lens and aspirates contents, small incision ECE- Whole removal of diseased nucleus, larger incision
95
Name three immediate and three delayed features of Cataract Surgery
Immediate - Endopthalmitis, Lens Malposition, Toxic Anterior Segment Syndrome Delayed - retinal detachment, macular degeneration, Posterior capsule opacification \* \*proliferation of lens remnants, treated with laser
96
Describe the four layers of the Macula
Choroid Bruch’s Membrane Retinal Pigment Epithelium Photoreceptors
97
ARMD is the leading cause of blindness in the UK, what are the two types?
Dry - 90% Wet - 10%
98
Describe Dry ARMD
Progressive atrophy Doesn’t exude Late - Geographic Atrophy (large well demarcated sections of retina stop functioning)
99
Describe Wet ARMD
Worse prognosis Development of new vessels from choroid layer into retina (via VEGF) Vessels leak - Oedema
100
Drusen are characteristic of ARMD. What are they?
Yellow deposits of protein/lipids between retinal pigment epithelium and Bruchs Can be normal Larger and greater numbers can be an early sign
101
Give four risk factors for ARMD
Age Smoking Chinese Ethnicity FH
102
How does ARMD present?
Gradually worsening central visual loss Reduced acuity Crooked appearance to lines Wet - more acute and rapid
103
Name four investigations (other than Snellen) for ARMD and what you would see
Amsler Grid Test - Straight Line Distortion Fundoscopy - Drusen OCT - cross sectional retinal view (wet) Fluorescein Angiography- Oedema and Neovascularisation
104
How is Dry ARMD managed?
No treatment just lifestyle means urges to slow progression (smoking cessation, BP control, Vitamins)
105
How is Wet ARMD managed?
Anti VEGF Vitreous injections (Ranibizumab) Started within three months
106
Give four risk factors for Open Angle Glaucoma
Age Afrocaribbean ethnicity Diabetes Myopia
107
Open Angle Glaucoma can be primary or secondary. What is primary?
Unknown aetiology Unsure if increased production or decreased drainage May be predisposed by microcirculatory factors and genetic damage
108
Open Angle Glaucoma can be primary or secondary. What is secondary?
Reduced drainage and increased IOP 5 subtypes : Neovascular (DM), Pseuodoexfoliative, Uveitis, Glucocorticoid Induced, Pigmentary
109
How does Open Angle Glaucoma present?
Largely asymptomatic until late stages Central vision relatively preserved until late - tunnel vision and bumping into things
110
Name five investigations for Open Angle Glaucoma
- Opthalmoscope (progressive cupping) - Humphrey visual field analyser - Goldman Applanation Tonometry - Gonioscopy - Corneal thickness (contextualises IOP)
111
There are a variety of drug classes that act on humour production and are used to treat OAG. What is the first line? Give two contraindications and two side effects
Latanoprost Pregnancy and Breast Feeding Brown Iris pigmentation and pigmentation of surrounding skin (also lash thickening, irritation)
112
What is the surgical management for Open Angle Glaucoma?
Lasted trabeculoplasty Soft laser ‘wakes up meshwork’ Or Trabeculectomy Can cause iritis and blebitis
113
Describe the pathophysiology of Diabetic Retinopathy
Vessels in the retina are damaged by prolonged hyperglycaemia, leading to increased vascular permeability
114
Describe 6 features of Diabetic Retinopathy as seen on an Opthalmoscope
Blot Haemorrhages and Hard Exudates (leakage) Microaneurysms (weakness) Venous Beading Cotton Wool Spots (nerve damage) Neovascularisation (local GF release)
115
Diabetic Retinopathy can be non proliferative, proliferative or a maculopathy. Describe non proliferative
Mild - Microaneurysms Moderate - Microaneurysms, Blot Haemorrhages, Hard Exudates, Cotton Wool Spots, Venous Beading Severe - Blot Haemorrhages and Microaneurysms in four quadrants, beading in \>2 quadrants, IMRA in any quadrant
116
Diabetic Retinopathy can be non proliferative, proliferative or a maculopathy. Describe proliferative
Neovascularisation Vitreous Haemorrhage
117
Diabetic Retinopathy can be non proliferative, proliferative or a maculopathy. Describe Maculopathy
Macular Oedema Ischaemic Maculopathy Can be focal/diffuse/central involving
118
Name four complications of Diabetic Retinopathy
Rubeosis Iridis (new BV formation in iris) Retinal detachment Vitreous Haemorrhage Cataracts
119
How is Diabetic Retinpathy managed?
Anti VEGF Laser Photocoagulation Severe - keyhole vitreoretinal Surgery Optimise DM control
120
Name three requirements of the accommodation reflex
Eyes converging Pupil size reducing Lens changing shape and pattern
121
What is Presbyopia?
Gradual loss of accommodation response due to decline in elasticity, becoming apparent when amplitude is insufficient to carry out near tasks
122
How does Presbyopia present?
Difficulty carrying out near tasks Accommodative lag (from distance to near vice versa) Tiring with continuous close work
123
How is Presbyopia treated?
OTC glasses are normally sufficient If pre-existing refractive error - prescription glasses
124
If Presbyopia happens prematurely, what is the likely cause?
Accommodative Insufficiency (Associated with encephalitis and enclosed head trauma) Inability to maintain binocular enlargment as object becomes closer (aka eye strain)
125
Name six causes of sudden visual loss
CRAO Anterior Ischaemic Optic Neuropathy Vitreous Haemorrhage Retinal Vein Occlusion Retinal Detachment Optic Neuritis
126
What are the five broad causes of Central Retinal Artery Occlusion?
CVS Disease (carotid atherosclerosis, AF) Vascular disease (dissection, fabrys) Inflammatory (GCA) Haematological Rare (toxoplasmosis, Surgery)
127
Describe the arterial division and supply to the Retina
First branch of internal carotid - Opthalmic Opthalmic gives off retinal and ciliary (supplying outer retina) Retinal splits into superior and inferior and then temporal and nasal
128
How does CRAO present?
Sudden onset painless loss of vision Due to potential supply from cilioretinal it can have a central area of visual sparing RAPD Pale Retina Cheery Red Spot (Anastamotic supply)
129
How can CRAO be confirmed?
Fluorosciene Angiography Slowed flow/filling defect
130
CRAO just be managed within 6 hours (if GCA - immediate steroids). What are the management options?
Intra-arterial thrombolysis - catheter directed delivery of tPA via Opthalmic Artery Anterior Chamber Paracentesis (if not a candidate for Thrombolysis,reduces IOP to dislodge) Ocular massage Hyperbaric O2 Vasodilator
131
Define Anterior Ischaemic Optic Neuropathy
Loss of vision as a result of damage to optic nerve from ischaemia Involves the 1mm head of optic nerve (AKA disc)
132
Anterior Ischaemic Optic Neuropathy can be Arteritic or Non Arteritic. Describe the Arteritic
5-10% Inflammation and thrombosis of short posterior ciliary arteries resulting in ischaemia of optic nerve head
133
How does Arteritic Anterior Ischaemic Optic Neuropathy present?
Rapid onset unilateral visual loss and decreased acuity Chalky white pallor of optic disc Amaurosis fugax? GCA signs?
134
How is Arteritic Ischaemic Optic Neuropathy investigated?
GCA - ESR/CRP, Temporal Artery Biopsy MRI/USS - between Arteritic and non OCT
135
Describe the management options for Arteritic Anterior Ischaemic Optic Neuropathy
IV Methylpred for 3 days (switch to oral and taper) MAB against IL6 (Tocilizumab) Methotrexate
136
Anterior Ischaemic Optic Neuropathy can be Arteritic or Non Arteritic. Describe the Non Arteritic
Majority idiopathic reduces blood flow Crowded optic disc Associated with - sleep apnoea, sildenafil, drusen
137
How does Non Arteritic AION present?
Acute painless visual loss RAPD Optic disc oedema and peripapillary splinter haemorrhages
138
How is Non Arteritic AION managed?
Exclude arteritic Large doses of steroid
139
Vitreous haemorrhage is one of the most common causes of sudden painless visual loss. Describe the possible aetiologies
Proliferative diabetic retinopathy (fragile vessels) Posterior vitreous detachment Ocular Trauma
140
How does Vitreous Haemorrhage present?
- Sudden painless visual loss - Red Hue (may turn green after breakdown) - New onset floaters/cobwebs - May be worse in the morning if blood settles during sleep
141
Name four investigations for Vitreous Haemorrhage
IOP Slit Lamp - Red Cells in anterior vitreous Rule out retinal detachment USS
142
Describe the general management of Vitreous Haemorrhage
Exclude retinal detachment Rest with head elevated and re- evaluate in 3-7 days for source
143
Name four definitive treatment options for Vitreous Haemorrhage
Laser Photocoagulation (for proliferative vasculopathies) Anterior Retinal Cryotherapy Vitrectomy VEGF
144
Name three complications of Vitreous Haemorrhage
Haemosiderosis Bulbi Retinal Detachment Ghost cell glaucoma (rigid cells with denatured Hb)
145
Describe the pathophysiology of Retinal Vein Occlusion
- Thrombus forms in retinal veins and blocks drainage - Pooling of blood in retina - Leakage causing macula oedema and retinal haemorrhages - VEGF release
146
How does Retinal Vein Occlusion present?
Sudden painless loss of vision
147
Name four features of fundoscopy for Retinal Vein Occlusion
Flame Haemorrhages Blot Haemorrhages Optic Disc Oedema Macula Oedema
148
Name three bloods you would like to do in Retinal Vein Occlusion
FBC - Leukaemia ESR - inflammatory disorders Glucose - Diabetes
149
How is Retinal Vein Occlusion managed?
Laser Photocoagulation Intravitreal Steroids Anti VEGF therapies
150
Retinal detachment is where the neuro sensory layer separates from the pigmented. What are the two classifications?
Rhegmatous - following retinal break, normally after posterior vitreous detachment Non Rhegmatous - Exudative (retinal drainage fluid between subretinal space) or tractional (fibres in vitreous contract, pulling retina away)
151
Myopia is a risk factor for all classifications of retinal detachment (longer and thinner). Give two risk factors for each classification
Rhegmatogenous - Age, Marfans Tractional - Diabetic Retinopathy, Retinal Vein Occlusion Exudative - inflammatory, vascular disease
152
How does Retinal Detachment present?
Painless Peripheral vision loss (shadow coming across vision) Flashes and floaters
153
How would you examine suspected retinal detachment?
-Pupillary Reflexes (?RAPD) -Visual Acuity and Fields -Dilated fundal exam (if large - sheet of sensory retina towards centre of globe) Slit lamp - cells in anterior chamber, tobacco dust
154
How are Retinal Tears managed?
Laser therapy or Cryotherapy Created adhesions between retina and choroid to prevent detachment
155
How is retinal detachment managed?
- Vitrectomy (replacement with oil/gas) - Scleral buckling (pressure on sclera to bring choroid in) - Pneumatic Retinopexy (gas bubble in vitreous to push against retinal layers)
156
Define Optic Neuritis
Inflammation of optic nerve characterised by the triad: reduced vision, eye pain and impaired colour vision
157
There are many causes of Optic Neuritis. Name 6
GCA Autoimmune diseases Post infectious TB B12 Deficiency Drugs (Ethambutol, Isoniazid)
158
Give three signs on examination of Optic Neuritis
RAPD Altitudinal field defects Scotoma
159
How could you consider managing Optic Neuritis?
IV Methylpred to speed healing
160
What is Devics Disease?
Inflammatory demyelinating and necrotising Disease mainly involving the spinal cord and optic nerve Appears like MS on scans Cause of Optic Neuritis Treated with steroids and plasma exchange
161
What is Acute Demyelinating Optic Neuritis?
Demyelination and atonal loss likely secondary to inflammatory process and delayed hypersensitivity
162
Name three presenting features of Acute Demyelinating Optic Neuritis
Photopsia Uhthoff Phenomenon - increase in symptoms with increase in body temp Pulfrichs Phenomenon - objects moving straight appear curved
163
Diplopia can be monocular or binocular, what is the difference?
Monocular - doesn’t disappear with one eye closed, likely opthalmological aetiology Binocular - with one eye closed it disappears, likely neurological aetiology
164
Describe the anatomical course of CNIII
Emerges from midbrain Travels close to PCA Pierces dura near tentorium cerebelli Lateral cavernous sinus Superior orbital fissure
165
Name four causes of Oculomotor nerve lesions
Diabetes GCA Raised ICP PCA Aneurysm
166
How do Oculomotor nerve lesions present?
Fixed dilated pupil that doesn’t accommodate Ptosis Unopposed lateral deviation Intortion on looking down Microvascular - pupil sparing
167
How do Oculomotor nerve lesions present (sympathetics involved)?
Pupil will be fixed but not dilated
168
Trochlear Nerve lesions are rare, give three causes
Orbital trauma Diabetes Infarction secondary to hypertension
169
Name 6 causes of Diplopia
CNIII lesion CNIV lesion CNVI lesion Orbital Blow Out # Thyroid Eye Disease MG
170
How do Trochlear Nerve Lesions present?
Vertical Diplopia Weakness of downward and intortion Compensatory head tilt away from affected side
171
How does a CNVI lesion appear?
Inability to look laterally
172
Give three causes of a CNVI lesion
MS Pontine Cerebrovascular incident Raised ICP (due to long course)
173
Describe the pathophysiology of an Orbital Blow Out Fracture
Usually from an object \<5cm Force transmits along rim and into orbital floor Force is transmitted into three buttresses (infraorbital, displacement of zygomaticofrontal suture, fracture of zygomatic arch)
174
Name five clinical features of Orbital Blow Out Fractures
Periorbital bruising Surgical Emphysema Vertical Diplopia (worse on looking up) Endopthalmos Infraorbital Paraesthesia
175
What investigations should you do for a suspected Orbital Blow Out?
Plain XRay - Facial, Occipitomental, Submentovertical (droplet sign in maxillary sinus) CT
176
How are Orbital Blow Out Fractures managed?
Don’t blow nose for 10 days Some can be managed with just broad spec abx Surgery
177
What Orbital Blow Out Fractures require surgery?
- White eye blow out - Symptomatic Exopthalmos of \>2mm - \>50% orbital floor involved - Non resolving Diplopia after 2-3 weeks
178
What is Thyroid Eye Disease?
Most common extrathyroidal manifestation of Graves Can also be hypothyroid or euthyroid Due to cross reactivityof autoantibodies
179
The onset of Thyroid Eye Disease is normally within 18 months of diagnosis. Describe the pathophysiology
Initial inflammatory phase lasting 6-24 months (expansion of extraocular muscles and orbital fat resulting in proptosis and optic neuropathy) Followed by inactive fibrotic phase Infiltration of lymphocytes stimulate cytokine release and polysaccharide release from fibroblasts - leads to oedema
180
What are the important receptors in Thyroid Eye Disease?
TSH IGF1
181
Name four risk factors for Thyroid Eye Disease
Current smoker Female Middle Aged Radioiodine therapy
182
How does Thyroid Eye Disease present?
Ocular irritation Ache behind eye Lid oedema and lateral flare Circumferential white eye Lid lag Progressive optic neuropathy - blurred vision, reduced acuity
183
How would you investigate Thyroid Eye Disease?
Thyroid levels CT (soft tissue)/MRI (bone view pre op) Visual acuity CXR and TPMT (pre med)
184
How is Thyroid Eye Disease staged?
Clinical activity scoring and severity Dolor, Rubor, Calor, Tumor, Functio Laesa (Mourits)
185
Describe some general management points for Thyroid Eye Disease
Joint endocrine ophthalmology clinic Smoking cessation Maintain Euthyroid State Prescribe ocular lubricants
186
Describe the more definite management of Thyroid Eye Disease
Prisms to control Diplopia Botox to reduce upper lid swelling Pulsed IV Methylprednisolone and Azathioprine Orbital Radiotherapy Orbital decompression if steroids don’t work
187
When does Thyroid Eye Disease require management?
Mourits\>4 DON/RAPD/Field Defect
188
What is Myasthenia Gravis?
Autoimmune disease where antibodies destroy neuromuscular connections Affects voluntary muscles of the body
189
Describe the pathophysiology of Myasthenia Gravis
- Receptor sites at NMJ are destroyed - Not enough stimulation to trigger action potential - Increased fatiguability with use (reduced ACh) and improvement with rest
190
Name some signs of Myasthenia Gravis
Ptosis Cogan Lid Twitch (down gaze followed by up gaze, eye saccades and lid overshoots) Incomitant strabismus Raised eyebrows Pupils never involved
191
Name three diagnostic tests for MG
Tensilon Test (inhibits AChesterase, only useful when they have measurable findings) Repetitive Nerve Stimulation Test (decline in compound muscle action potentials within the first 4-5 stimuli) Single Fibre EMG
192
Name two laboratory tests for MG
Serum Anti ACh Receptor Titre Serum Anti Muscle Specific Kinase AB titre
193
What is the main differential for MG?
Lambert Eaton Syndrome Improvement of symptoms with repeated stimulation
194
Describe the management of MG
Med - Steroids, Pyridostigmine, Immunomodulators (if refractory) Surgery - Removal of thymus
195
Give three causes of Transient Visual Symptoms
Amaurosis Fugax Papilledema Migraine
196
What is Amaurosis Fugax?
Hypoperfusion of optic nerve, normally secondary to carotid artery atherosclerosis and secondary thromboemboli Precedes stroke so urgent investigations required
197
Other than carotid pathology, give three causes of Amaurosis Fugax
GCA Retinal Migraine Papilledema
198
How does Amaurosis Fugax present?
Curtain descending down over vision If provoked by gaze - optical lesion
199
How is Amaurosis Fugax investigated?
Inflammatory markers Carotid imaging and cardiac evaluation MRI/MRA
200
How is Amaurosis Fugax managed?
TIA - stroke work up GCA - Emperic steroids and temporal artery biopsy Antiplatelets/Anticoag
201
What is Papilledema?
Optic disc swelling secondary to raised ICP Oedema, continued pressure and optic nerve atrophy
202
Name five causes of raised ICP
Skull is too small for brain Brain volume is too large Obstruction of CSF flow Increased CSF production Decreased CSF drainage
203
Name three investigations you would do to define the underlying cause of Papilledema
BP CT/MRI LP with opening pressure
204
What is the Dandy Criteria for Idiopathic Intracranial Hypertension?
Papilledema Normal neuro exam Normal MRI imaging Normal CSF composition Elevated LP opening pressure
205
The fundoscopy of Papilloedema is graded by the Frisen scale. What is this?
0 - Normal Optic Disc 1 -C shaped Halo of disc oedema 2 - Circumferential halo of disc oedema 3 - Obscuration of one or more segments of major blood vessels leaving disc 4 - partial obstruction of a segment of blood vessels on disc 5 - partial or total obstruction of all vessels on disc
206
Name three ways Papilloedema can present
Asymptomatic Signs of raised ICP Abducens Palsy
207
The gold standard management for Papilloedema is to treat underlying cause and reduced ICP. How should IIH be managed?
Weight reduction Acetazolamide ?CSF Shunt, Duran Venous Stenting
208
Define Migraine
Primary headache disorder characterised by severe unilateral throbbing pain, associated with nausea, photophobia, phonophobia and preceding aura Typically lasting 4-72hrs
209
What is Photophobia?
Light sensitivity, ocular discomfort and headache exacerbated by light Always bilateral (differentiates from trigeminal issues - unilateral)
210
What are the five types of migraine with neuro- opthalmological symptoms
- Aura without headache (eg TIA) - Basilar Type (dizziness, ataxia, tinnitus) - Retinal (headache, scotoma, scintillation#) - Migraine with binocular blindness - Migrainous infarction (ischaemic brain lesions)
211
Blepharitis is inflammation of the eyelid margin, and can be anterior or posterior. What are the three main aetiologies?
``` Staph Infection Seborrhoeic Dermatitis (ant) Meibomian Gland Dysfunction (post) ```
212
What are the symptoms of Blepharitis?
Gritty/Itching/Burning Bilateral symptoms Lids stuck together upon waking Associated - dry eye, Seborrhoeic dermatitis, rosacea
213
What are the signs of each of the underlying causes of Blepharitis?
Staph - Telangiectasia, eyelash deformity Seborrhoeic- greasy lid margin, eyelashes stuck together Meibomian - oil globules, Chalazia
214
Give three differentials of Blepharitis
BCC/SCC of eyelid Contact/Atopic dermatitis Impetigo
215
How should you manage Blepharitis?
Inform it’s a chronic condition but can be managed Avoid contact lenses Warm compress/lid massage/ cleansing Chloramphenicol is infection
216
Dry eyes can be hyposecretive or evaporative. Give some causes of hyposecretion
Sjögren Lacrimal gland insufficiency Lacrimal gland obstruction Antihistamines TCA
217
Dry eyes can be hyposecretive or evaporative. Give some causes of evaporation
Meibomian gland dysfunction (Blepharitis) Blink disorder (Parkinson’s Thyroid Allergies Prolonged computer use
218
Dry eyes can cause a gritty, foreign body sensation worse at the end of the day. What are some red flags?
Severe eye pain Significant visual loss Photophobia
219
Name three investigations for dry eyes
Slit lamp Schirmers (measure amount of eye wetting after five minutes) Tear break uptime (time between last blink and first appearance of fluorosciene stained tear)
220
What are some general managements for dry eyes?
Review medications Smoking cessation Regular breaks
221
Name three tear substitutes
Drops (Hypermellose) Gels (Viscotears, less frequent application) Ointments (Coat cornea and reduce evaporation)
222
Define Chalazion
Focus of granulomatous inflammation in eyelid arising from blocked meibomian
223
How do Meibomian Cysts/Chalazions present?
Gradually enlarging round firm lesion Generally painless once inflammation has settled Blurred vision if compressing cornea Yellowish swelling on underside of lid
224
How would you manage Chalazia
BD warm compress Massage Clean with baby shampoo
225
You would only investigate chalazia if it was recurrent or atypical. When would you refer?
Large and persistent Visual problems Low threshold in young children (amblyopia)
226
What is the most common periocular malignancy? Give three risk factors
BCC of the eye Older age, Male, UV exposure
227
How does Periocular BCC present?
Slow developing non resolving lesion of the eyelid On lower lid or medial canthus most commonly May lose eyelashes
228
How are Periocular BCCs managed?
Advise on sun protection Mohs micrographic Surgery ?Radiotherapy
229
What is Herpes Zoster Opthalmaticus (ie Shingles of Eye)?
Viral disease characterised by painful vesicular rash in one or more dermatomal distributions by trigeminal nerve Due to reactivation of VZV within sensory ganglion
230
How does Herpes Zoster Opthalmaticus present?
Prodrome Acute painful vesicular rash Hutchinsons Sign - lesions at side/root of nose which is a strong predictor of ocular inflammation
231
Name four investigations for Herpes Zoster Opthalmaticus
Test corneal sensation Culture for VZV specific IgM Slit lamp Fluorosciene (Rule out corneal damage)
232
How is Herpes Zoster Opthalmaticus managed?
If skin rash is only symptom - Aciclovir and topical steroids If any sign of intraocular pathology - systemic steroids WHO ladder for pain relief May require corneal transplant or glaucoma surgery in future
233
What is a Subconjunctival Haemorrhage? Give four causes
Bleeding of the conjunctival vessels into subconjunctival space Valsalva HTN Contact lenses Drugs
234
How do Subconjunctival Haemorrhages present?
Unilateral red eye Red patch with sharply defined edges Otherwise normal eye exam If no posterior margin - intracranial bleed
235
What advice should you give someone with Subconjunctival Haemorrhages?
Self limiting Eye drops for dry eyes Discourage Aspirin and NSAIDs
236
What is Posterior Vitreous Detachment?
Vitreous gel comes away from retina Very common, especially in older patients
237
How does Posterior Vitreous Detachment present?
Painless condition May be completely asymptomatic Slight Vision loss, floaters, flashing lights
238
How is Posterior Vitreous Detatchment managed?
No treatment necessary, over time brain adjusts Can predispose to retinal tears/detachment so monitor
239
What is Retinitis Pigmentosa?
Congenital inherited condition where there is degeneration of rods and cones Rods degenerate more than cones (night time blindness)
240
How does Retinitis Pigmentosa present?
Symptoms usually start in childhood Night blindness Peripheral vision lost before central
241
What would be seen on fundoscopy of Retinitis Pigmentosa?
Bony spicule pigmentation (most concentrated around mid peripheral area)
242
Name two diseases associated with Retinitis Pigmentosa
``` Ushers Syndrome (+ hearing loss) Bassen Kornzweig ```
243
Describe the management of Retinitis Pigmentosa
Genetic counselling Visual aids Driving limitations Slow progression - vitamins, antioxidants, anti vegf, steroids
244
Give five causes of an abnormally shaped pupil
Trauma to muscles Anterior uveitis (scar tissue) AACG (Ischaemic damage - oval) Coloboma (holes in iris) Tadpole (spasm in part of pupil, migraines)
245
Name four causes of a dilated pupil
Oculomotor nerve palsy Raised ICP Cocaine Adie/Tonic Pupil
246
What is a Tonic Pupil?
Damage to post ganglion parasympathetic May be viral Dilated and sluggish to light
247
Name four causes of a constricted pupil
Horners Argyll Robertson (Neurosyphilis) Opiates Pilocarpine
248
Describe the features of Horners Syndrome
Ptosis Miosis Anhidrosis Enopthalmos Light and Accomodation reflexes unaffected
249
Name the four central lesions that can cause Horners Syndrome (4S’s). What is characteristic?
Stroke Multiple Sclerosis Swelling Syringomyelia Anhidrosis of arm and trunk as well as face
250
Name the four preganglionic lesions that can cause Horners Syndrome (4Ts). What is characteristic?
Tumour Trauma Thyroidectomy Top Rib Anhidrosis of race
251
Name the four post ganglionic lesions that can cause Horners Syndrome (4Cs). What is characteristic?
Carotid aneurysm Carotid artery dissection Cavernous sinus thrombosis Cluster headache No anhidrosis
252
What is associated with Congenital Horners?
Heterochromia
253
Name two ways Horner’s Syndrome can be diagnosed
Cocaine Eye Drops - blocks NA uptake, normal eye dilated but no effect on other eye Adrenaline Eye Drops - Won’t dilate a normal pupil but will in Horners
254
Name five features on fundoscopy of Hypertensive Retinopathy
Silver/copper wiring (thickened and sclerosed) AV nipping (sclerosis where they cross) Cotton wool spots Hard exudate Retinal haemorrhages
255
Name three risk factors for Choroidal Melanoma
Light iris Sunlight exposure Positive FH
256
How does Choroidal Melanoma present?
Tends to be asymptomatic May have blurred vision, paracentral scotoma, floaters and flashes
257
How does a Choroidal Melnaoma appear on Fundoscopy?
Nodular dome shaped lesion
258
Name two non surgical and two surgical managements of Choroidal Melanoma
Laser Photocoagulation, Sterotactic Radiotherapy Block excision, Enucleation
259
What is Amblyopia?
Decreased vision arising from dysfunctional processing of visual information Due to degradation of retinal image during critical development Can be functional or organic (irreversible)
260
Name three common causes of Amblyopia
Constant Strabismus Asymmetric refractive errors Orbital pathology affecting growth/clarity (eg strawberry naevus)
261
Describe the period in which Amblyopia can be reversed
In first 2-3 years it develops rapidly Develops more slowly until 7/8y If halted and then restored before the age of around 8 it can be reversed
262
Amblyopia normally has a significant difference in acuity between eyes. How is this defined?
Two or more Snellen/LogMAR differences
263
How can Amblyopia be managed?
Modifying visual input into affected eye Correcting refractive error Obscuring visual input to other eye(patching, drops)
264
Define Strabismus
Misalignment of the Eyes resulting in non corresponding retinal images Often idiopathic or secondary to hydroceph/SOL/cerebral palsy/trauma
265
What is the terminology for Strabismus?
Eso - inward Exo - outward Hypo - down Hyper - up Manifested - tropia Latent - Phonia
266
How can Strabismus be classified?
Congenital or acquired Right/Left/Alternating Permanent or intermittent Manifest or latent Concomitant (non paralytic) or incomitant
267
What is a non paralytic strabismus?
Size of deviation doesn’t vary with direction of gaze Usually congenital Extraocular muscles and nerves are normal Compensatory head tilt
268
How does Esotropia present?
Inward turning squint Can be on accommodation
269
How does Exotropia present?
Outward squint Begins intermittently with daydreaming/tiredness and progresses
270
How does Hyper/Hypotropia present?
Vertical Strabismus Changes in head posture SO paresis
271
What is the Hirschberg test for Strabismus?
Hold a pen torch in front of patients eyes and observe where reflection lies Outer margin - Esotropia Inner Margin - Exotropia
272
Other than the Hirschberg test, name three other investigations for Strabismus
Cover uncover - observe movement Alternate cover - shows latent Orthoptic Assessment
273
How is Strabismus managed?
Correcting refractive errors Prisms ?Surgical intervention ?Chemodenervation
274
What is Paralytic Strabismus?
Damag to extraocular muscles/nerves
275
What is Myopia?
Near sighted Excess optical power for axon length, light focuses in front of retina
276
Name three risk factors for Myopia
FH Close up work Marfans
277
Define Hypermetropia
Long sightedness Insufficient power for axonal length Light is focussed beyond retina
278
Name three risk factors for Hypermetropia
Corneal Dystrophy Congenital Cataracts Micropthalmia
279
Describe registering as visually impaired
Two levels: Severely sight impaired/Blind Loss of sight in one eye doesn’t qualify you unless you also have poor sight in the other
280
Name two benefits to officially registering as blind or partially
Blind persons income tax allowance, 50% reduction on TV licence Free NHS Sight Test, Glasses vouchers
281
Describe the DVLA visual requirements for driving
Able to read a car plate made after 1st September 2001 from 20 meters Visual Acuity of 6/12 Lorry/Bus have to have 6/7.5 Atleast in best eye
282
How can a LogMAR score be calculated from Snellen?
Snellen 6/10 Log10(10/6)
283
How can a LogMAR score be calculated?
0.1 + score of best line read - (0.02\* letters read)
284
Name three causes of generalised blurring
Presbyopia Dry Eyes Cataracts
285
Name two causes of central blurring
Diabetic Maculopathy Macular Degeneration
286
Name two causes of black spots/blobs
Does it move with eye? Y - Vitreous Disease N - Retinal Detachment
287
Name two causes of Photopsia
Detached Retina Migraine with Aura
288
Name three uses for Mydriatic/Cycloplegic drops
Dilation for retinal visualisation Amblyopia Refraction for children with glasses
289
Name three Mydriatic/Cycloplegic drops
Anticholinergic - Atropine, Cyclopentolate Sympathetic - Phenylephrine
290
Name three side effects of Mydriatic/a Cycloplegic drops
Eye whitening Face redness/warmth Can’t drive until worn off
291
Name a side effect of Fluoroscein
Staining
292
Define Retinoblastoma
Retinoblastomas are the most common primary intraocular malignancy in children. They are caused by sporadic or inherited mutations in the retinoblastoma gene (Rb)
293
What are the two types of Retinoblastoma
Sporadic (usually unilateral) Hereditary (normally bilateral and associated with other malignancies)
294
Describe the aetiology of Heritable Retinoblastoma
Two hit hypothesis of Rb gene Autosomal Dominant inheritance
295
How do Retinoblastomas present?
Leukocoria Strabismus
296
How is suspected Retinoblastoma investigated?
Fundoscopy Ultrasound of the orbit MRI (CT radiation could induce cancer in those with germline RB mutation)
297
How should Retinoblastomas be managed?
Salvageable - Cryotherapy, Brachytherapy, Chemotherapy Non Salvagable - Enucleation
298
Name three complications of Cataract surgery and how they’re minimised (if relevant)
Endopthalmitis - prophylactic abx Posterior Capsule Rupture Floppy Iris Syndrome
299
Name three causes of RAPD
Optic Neuritis Retinal Detachment CMV
300
What is Pilocarpine and how does it work?
* muscarinic cholinergic agonist * causes * constriction of the pupil - mitotic * ciliary muscle contraction * both of which open up pathway to trabecular meshwork
301
What are **Acetazolamide** and **Dorzolamide** and how do they work?
* Carbonic anhydrase inhibitor * reduces production of aqueous humour = reduces IOP
302
How do hyperosmotic agents such as glycerol and mannitol work?
increase the osmotic gradient between the blood and fluid in the eye
303
What is Timolol and how does it work?
* Beta blocker * reduces production of aqueous humour
304
What is Brimonidine and how does it work?
**sympathomimetic** that reduces the production of aqueous fluid and increase uveoscleral outflow
305
What is open-angle glaucome?
gradual increase in resistance through the trabecular meshwork making it more difficult for aqueous humour to flow through the meshwork and exit the eye. Therefore the pressure slowly builds within the eye and this gives a slow and chronic onset of glaucoma
306
what happens to the optic disc when IOP is raised?
* Cupping of the optic disc * small indent in the optic disc becomes larger as the pressure in the eye puts pressure on the indent making it wider and deeper * \>0.5 the size of the optic disc is abnormal
307
what are some risk factors for OAG?
* increasing age * FHx * black ethnic origin * Nearsightedness (myopia)
308
how does OAG present?
* often asymptomatic for a long time * diagnosed by routien screening * affects peripheral vision first which closes in until the pt experinces tunnel vision * gradual onset of fluctuating pain, headaches, blurred vision and halos aroud lights (more at night)
309
what are the 2 ways intraocular pressure can be measured?
**non-contact tonometry** - shooting a puff of air at the cornea and mesauring the corneal response to the air - less accurate **goldmann applanation tonometry** - gold standard, device mounted on a slit lamp that makes contact with cornea and applies different pressures to front of the cornea to get accurate measurement of the intraocular pressure
310
how is OAG diagnosed
* goldmann applanation tonometry - check pressure * fundoscopy - optic disc cupping and optic nerve health * visual field assessment - peripheral vision loss
311
What is the management of OAG? And when is treatment usually initiated?
* **1st line = latanoprost** (prostaglandin analogue which increases uveoscleral outflow) * other options: timolol, dorzolamide, brimonidine * trabeculectomy surgery can be performed when eyedrops are inefective
312
what are the 3 main side effects of latanoprost?
* eyelash growth * eyelid pigmentation * iris pigmentation / browning
313
what is trabeculectomy surgery and what is it used for?
used in OAG when eyedrops ineffective new channel created from the naterior chamber through the sclera to a location under conjunctiva. causes a bleb under the conjunctiva where the aqueous humour drains. resbsorbed into the general circulation from the bleb
314
what is preseptal/periorbital cellulitis? what commonly causes it?
an infection anterior to the orbital septum commonly caused by an infection in adjacent structures, dacryocystitis, insect bites, hordeolum, trauma
315
how does preseptal/periorbital cellulitis present?
inflammed eyelids but with white eyes and normal visual acuity painless eye movements no diplopia
316
how is periorbital/preseptal cellulitis managed?
Flucloxacillin 500mg QDS 7 days
317
how is preseptal/periorbital cellulitis differentiated from orbbital cellulitis?
reduced visual acuity, proptosis, ophthalmoplegia/painful eye movements not associated with preseptal cellulitis

Y4 Neuro and Special Senses (9 decks)

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