Ophthalmology Flashcards
(129 cards)
1
Q
Define cataracts
A
Cataract is the opacification of the crystalline lens that results from the normal ageing process, trauma, metabolic disorders (hereditary or acquired), medications, or congenital problems. This topic mainly addresses acquired cataract.
The most common cause of curable blindness in the world.
Diagnosis is made by the detection of a decrease in visual acuity that cannot be corrected by refractive correction, and an eye examination that is otherwise normal apart from opacity in the crystalline lens.
Treatment is with surgery involving an incision into the eye and removal of the opacified crystalline lens. In most cases the cataract is replaced by an artificial lens made of polymethyl methacrylate, acrylic, or silicone.
If an implant lens is not used, or there is remaining refractive error (e.g., astigmatism that is uncorrected by the implant lens), the patient may need to wear either a contact lens or spectacles to achieve good postoperative vision. Adjunctive procedures may be done at the time of surgery or afterwards to correct residual refractive error.
Over time, some patients will develop an opacification of the posterior capsule behind the implant lens after the cataract has been removed. This condition is treated with the neodymium-doped yttrium aluminium garnet (Nd:YAG) laser, which creates an opening in the opacified membrane to restore vision.
2
Q
Epidemiology of cataracts
A
The WHO estimates that cataracts currently account for 51% of reversible blindness worldwide, which translates to about 20 million people.
There are estimates that by 2020, the number of people with moderate or severe vision impairment caused by cataracts could be as high as 57 million, with an estimated 13 million people blind because of cataracts.
The socio-economic impact of the effect of cataracts is particularly important in developing countries, since 1 blind person usually takes 2 people out of the workforce. While cataracts can be congenital or due to trauma or metabolic conditions, age-related cataracts are the most common, and therefore have the greatest impact.
The Beaver Dam Eye Study in the US found that 23.5% of women and 14.3% of men had a visually significant cataract by the age of 65 years
3
Q
Aetiology of cataracts
A
Changes in the lens proteins (crystallins) affect how the lens refracts light and reduce its clarity, therefore decreasing visual acuity. Chemical modification of these lens proteins leads to the change in lens colour. New cortical fibres are produced concentrically and lead to thickening and hardening of the lens in nuclear sclerosis, which often appears yellow and can increase the focusing power of the natural lens. Increasing myopia can also be evidence of a progressing nuclear sclerotic cataract.
Although the most common cause of cataract is the normal ageing process, other conditions that can contribute to opacification of the lens include trauma, certain metabolic or hereditary conditions, infections (e.g., rubella), or congenital problems; some types of medication may also have an effect. Smoking and exposure to UV radiation have also been indicated as factors that may cause cataract progression, especially nuclear sclerotic cataracts.
4
Q
RFs for cataracts
A
STRONG Age >65 Smoking Long term UV exposure DM Eye trauma Long term ocular corticosteroids Fix Uveitus
WEAK
Other hereditary / metabolic conditions:
These include galactosaemia, Wilson’s disease, Marfan’s syndrome, and myotonic dystrophy. They may be associated with particular types of cataract (e.g., Christmas tree cataract in people with myotonic dystrophy; sunflower cataract in people with Wilson’s disease). Strength of association varies depending on each condition.
5
Q
Sx of cataracts
A
COMMON Subjective decrease in vision Blurring/cloudig Glare Washed out colour vsion Reduced acuity Defects in red reflex Inadequate glasses prescription Disruption to ADLs
6
Q
Ix for cataracts
A
Dilated fungus examination - fundus and optic nerve normal
Measure IOP - normal, or may be elevated if associated glaucoma
Glare vision test - significant cataract: reduced visual acuity under the conditions of glare stress
Slit lamp of anterior chamber = cataract visible
7
Q
Rx of cataracts
A
No visual impairment = observe
With functional impairment = phacoemulsification + intra ocular lens implant AKA SURGERY
+/- refractive error correction AKA reassess acuity and give glasses/contacts
May need Nd:YAG laser therapy:
While the cataract has been removed, some lens epithelial cells do remain on the internal surface of the remaining capsular bag and will proliferate. In a high percentage of patients this proliferation of remaining lens epithelial cells may result in a gradual opacification of the posterior capsule that can reduce the patient’s vision (termed a secondary cataract).
8
Q
Prognosis of cataracts
A
Most patients do well after cataract surgery provided they adhere to postoperative instructions and medication regimens. Regular eye examination will detect any cataract development in the other eye. Many patients receiving a monofocal lens need a spectacle correction to achieve their best acuity following cataract surgery. A high percentage of patients may develop a gradual opacification of the posterior capsule that can reduce the patient’s vision (secondary cataract). If the visual reduction is significant, an opening can be made in the capsule with a neodymium-doped yttrium aluminium garnet (Nd:YAG) laser. Once a capsular opening has been made, the capsule will not regenerate and a second treatment is rarely necessary. Various lens edge designs try to inhibit this process.
9
Q
Complications of cataracts
A
IO haemorrhage Corneal oedema Raised IOP Blindness Infection Cystoid macular oedema Posterior capsular tear Dysphotopsia Retinal detachment
10
Q
A 27-year-old man presents following an incident where he was struck in the left eye with a paint ball. He notices a sudden decrease in vision in the left eye, from 20/20 before the accident, to counting-fingers vision after the accident. On examination, the left pupil appears whitish, and visual acuity is greatly decreased. The patient does not have any history of other medical problems. On dilated eye examination, the lens in the left eye appears whitish anteriorly, with a spoke-like pattern. On direct ophthalmoscopy, the red reflex is diminished and retinal details are indistinct.
A
cataracts
A patient with a progressing nuclear sclerotic cataract may complain of an inadequate glasses prescription. The thickening of the lens can cause an increase in refractive power and make the patient appear to be increasingly myopic (near-sighted).
11
Q
A 27-year-old man presents following an incident where he was struck in the left eye with a paint ball. He notices a sudden decrease in vision in the left eye, from 20/20 before the accident, to counting-fingers vision after the accident. On examination, the left pupil appears whitish, and visual acuity is greatly decreased. The patient does not have any history of other medical problems. On dilated eye examination, the lens in the left eye appears whitish anteriorly, with a spoke-like pattern. On direct ophthalmoscopy, the red reflex is diminished and retinal details are indistinct.
A
cataracts
A patient with a progressing nuclear sclerotic cataract may complain of an inadequate glasses prescription. The thickening of the lens can cause an increase in refractive power and make the patient appear to be increasingly myopic (near-sighted).
12
Q
Define retinal vein occlusion
A
Retinal vein occlusion (RVO) is an interruption of the normal venous drainage from the retinal tissue. Either the central vein (CRVO) or one of its branches (BRVO) can become occluded. Uncommonly, the occlusion can occur in a vein that drains half of the retina. This is referred to as a hemiretinal vein occlusion (HRVO). Characteristically, in the retina proximal to the occlusion, the affected venous system is tortuous and dilated, and there are several intra-retinal haemorrhages and retinal oedema. RVOs are usually painless, sudden, and unilateral causes of vision loss.
Hypertension, diabetes mellitus, atherosclerosis, and glaucoma are major risk factors for the development of central retinal vein occlusion (CRVO) or branch retinal vein occlusion (BRVO) in older patients.
Hypercoagulability and vasculitis are important risk factors for the development of CRVO or BRVO in younger patients.
Treatment is focused on vision-threatening complications such as macular oedema and neovascularisation.
Several randomised clinical trials support the use of vascular endothelial growth factor (VEGF) inhibitors and intravitreal corticosteroids for the treatment of macular oedema in CRVO and BRVO.
13
Q
Epidemiology of retinal vein occlusion
A
The prevalence of RVO, regardless of type, has been reported to be between 0.7% and 1.6% in studies in the US and Australia.
Central retinal vein occlusion (CRVO) usually occurs in people >65 years of age, and the incidence is equal in men and women.
The prevalence of CRVO is between 0.1% and 0.4%.
Branch retinal vein occlusion (BRVO) also occurs primarily in people >65 years and does not have a sex preference.
Of patients with CRVO in one eye, 1% per year will develop an RVO of any type in the fellow eye, and 7% will develop another CRVO in the fellow eye in a 5-year period.
Similarly, 10% of patients with BRVO in one eye may experience an RVO of any type in a 3-year period.
14
Q
Aetiology of retinal vein occlusion
A
Central retinal vein occlusions (CRVOs) are caused by blockages of venous drainage in the region of the lamina cribrosa. Specifically, thrombus formation in the lumen of the central retinal vein interrupts blood flow.
Branch retinal vein occlusions (BRVOs) most commonly occur at arteriovenous crossings, where an adventitial sheath is shared. Arterial disease is therefore a common aetiology for BRVO.
In both central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO), increased venous pressure can cause venous tortuosity, intra-retinal haemorrhage, and oedema in the affected region of the retina. Furthermore, as a result of ischaemia, local elevation of growth factors such as vascular endothelial growth factor (VEGF) may cause macular oedema and neovascularisation.
15
Q
RFs for retinal vein occlusion
A
STRONG Atherosclerosis HTN DM Hyperlipidaemia Hx smoking CV disease Glaucoma Increased BMI at 20 Increased serum a2 globulin Short axial length Age >65
WEAK Activated protein C resistance Va leiden Protein S deficiency Hypercoagulable state Protein S deficiency Antithrombin III deficiency Hyperhomocysteinaemia Vasculitis
16
Q
Sx of retinal vein occlusion
A
COMMON Sudden painless vision loss Optic nerve head oedema Intra-retinal haemorrhage Venous tortuosity and dilation Neovascularisation Vitreous haemorrhage Macular oedema
UNCOMMON Floaters Painful red eye Visual acuity - ischaemic RAPD Elevated IOP
17
Q
Ix for retinal vein occlusion
A
Fluorescein angiogram - delayed venous filling during transit phase; areas of blocked fluorescence
18
Q
Rx of retinal vein occlusion
A
Uncomplicated - RF modification
Retinal vein occlusion with macular oedema = intravitreal injection of a VEGF inhibitor such as ranibizumab, aflibercept, or bevacizumab
Retinal vein occlusion with neovascularisation = pan-retinal photocoagulation + RF modification
19
Q
Prognosis of retinal vein occlusion
A
Of patients with central retinal vein occlusion (CRVO) in one eye, 1% per year will develop an RVO of any type in the fellow eye, and 7% will develop another CRVO in the fellow eye in a 5-year period. Similarly, 10% of patients with branch retinal vein occlusion (BRVO) in one eye may experience an RVO of any type in a 3-year period.
20
Q
Complications of retinal vein occlusion
A
Loss of vision
Vitreous haemorrhage
21
Q
Define keratitis
A
Infectious keratitis refers to microbial invasion of the cornea causing inflammation and damage to the corneal epithelium, stroma, or endothelium. Non-infectious keratitis is, for the most part, rare.
This disorder is an ocular emergency and remains one of the major causes of blindness around the world.
Main risk factors include corneal trauma, contact lens wear, and breakdown of the corneal epithelium.
The diagnosis depends on a careful history, slit-lamp examination, and corneal scraping cultures.
Treatment consists of topical antimicrobial agents that may be supplemented by pupil-dilating agents, analgesics, corticosteroids, and systemic antimicrobials as needed.
Complications include corneal scarring, perforation, and endophthalmitis.
22
Q
Epidemiology of keratitis
A
The annual incidence of infectious keratitis in the developed world has been increasing due to higher rates of contact lens use, and is now 2 to 11 per 100,000 per year.
Among contact lens wearers, most patients present between 20 to 29 years of age, reflecting the age distribution of contact lens users.
Non-infectious keratitides are heterogeneous and their incidence depends on the underlying aetiology. Peripheral ulcerative keratitis (a type of autoimmune keratitis) associated with systemic autoimmune diseases is of special concern to primary care physicians. Peripheral ulcerative keratitis has an incidence of 3 cases per million per year according to one study from England
23
Q
Aetiology of keratitis
A
A key underlying predisposing factor for bacterial, fungal, Acanthamoeba, and viral keratitis is a compromised corneal epithelium. This can happen after overt ocular trauma, especially if a foreign body containing vegetable matter becomes lodged in the cornea.
A compromised epithelium can also be caused by severe dry eyes, trichiasis (ingrown eye lashes), or corneal exposure from poor lid function. Epithelial erosions, such as those found in recurrent erosion syndrome or in various hereditary corneal dystrophies, also predispose to corneal infections. Blepharitis and conjunctivitis may increase contact with microbes and predispose to keratitis.
Corneal ulcers and infiltrates are generally assumed to be bacterial, unless a high index of suspicion exists for another aetiology. Pseudomonas aeruginosa, S aureus, S epidermidis, S pneumoniae, H influenza, and Moraxella catarrhalis are the most common pathogens.
Viral keratitis is attributed to Herpes viride. H simplex and H zoster represent the main causes, although CMV and EBV have also been implicated.
Exposure keratitis that is due to dryness of the cornea caused by incomplete or inadequate eye-lid closure.
Photokeratitis is due to intense ultraviolet radiation exposure (e.g., snow blindness or welder’s arc eye.)
Allergic keratitis is a severe allergic response that may lead to corneal inflammation and ulceration (i.e., vernal keratoconjunctivitis).
Neurotrophic keratitis is characterised by absence of corneal sensitivity that renders the corneal surface vulnerable to occult injury and decreased reflex tearing.
Mooren’s ulcer is a rare inflammatory disorder of presumed autoimmune aetiology consisting of peripheral corneal ulceration with a variable clinical course. It is a diagnosis of exclusion.
Thygeson’s superficial punctate keratitis is characterised by a coarse punctate epithelial keratitis with little or no hyperaemia of the bulbar or palpebral conjunctiva of unknown aetiology.
Autoimmune keratitis is most commonly peripheral ulcerative keratitis associated with systemic autoimmune disease (e.g., rheumatoid arthritis, systemic lupus erythematosus, polyarteritis nodosa, Wegener’s granulomatosis, relapsing polychondritis, Behcet’s disease, sarcoidosis, inflammatory bowel disease, or rosacea).
24
Q
RFs for keratitis
A
STRONG Contacts Corneal trauma Corneal abrasions/erosions Immunocompromised Hx AI
WEAK Trichiasis Blepharitis Dry eye Poor eyelid function Previous herpetic disease Exposure keratitis Contaminated water exposure Topical corticosteroid use Topical anaesthetic use Hx eye surgery
25
Sx of keratitis
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Corneal infiltrate
Corneal ulcer
Denditic or geographical epithelial lesion (HSV)
Redness
Pain
Increased lacrimation
Lid oedema
Discharge
Decreased acuity
Photophobia
Raised IOP (HSV)
```
26
Ix for keratitis
Corneal MC+S
Gram stain: bacteria, fungi; Giemsa stain: bacteria, fungi, Acanthamoeba species; Gomori methenamine silver stain: fungi; acid-fast stain: Mycobacteria, Nocardia species; calcofluor white stain (fluorescent microscope): Acanthamoeba species
blood agar: most bacteria; chocolate agar: Haemophilus species, Neisseria species; non-nutrient agar with Escherichia coli overlay: Acanthamoeba species; Lowenstein-Jensen's medium: Mycobacteria species, Nocardia species; thioglycolate broth: aerobic and anaerobic bacteria
27
Rx of keratitis
Topical combination ABx or quinolone if bacterial
Antiviral if herpetic - ganciclovir or acyclovir
If fungal = topical or systemic anti fungal
Hyoscine = Cycloplegic drops paralyse the ciliary muscles thus dilating the eye, provide pain relief by preventing ciliary spasm and prevent posterior synechiae in cases of severe anterior chamber reaction.
Pain relief
If non-infectious keratitis = refer
Topical corticosteroids may minimise corneal scarring that occurs due to stromal inflammation once the infection is controlled, in a small subgroup of patients.
28
Prognosis of keratitis
Outcome in ophthalmology is generally measured in terms of final visual acuity, although cosmetic appearance, secondary eye problems such as glaucoma, and the need for surgery such as in penetrating keratoplasty are also important. A large study of microbial keratitis from Australia found that 22% of patients exhibited >2 Snellen lines of vision loss, and 2% lost ≥10 lines of vision.
29
Complications of keratitis
```
Small or large corneal perforation
Endopthalmitis - Spread of the infection to the intraocular cavities is a rare and dreaded complication of infectious keratitis that requires emergency intravitreal antimicrobial injection and/or vitrectomy. Visual prognosis is poor.
Corneal scarring
Cataract
Glaucoma
```
30
A 22-year-old university student presents with 3 days of right-eye pain, redness, photophobia, and a progressive decrease in his vision. He complains of yellowish discharge and mild right-lid swelling. The patient is a contact lens wearer and upon further questioning admits to falling asleep and wearing his contact lenses overnight 4 days ago while studying for a final examination (bacterial keratitis).
keratitis
31
An 81-year-old woman is brought in by her carer. One week ago the carer noted red scaly lesions on the left side of the patient's forehead and nose. The skin lesions do not cross the midline. Two days ago the left eye became red and teary. The patient has been complaining of decreased vision and discomfort in the left eye, as well as itching and tingling of her left forehead and scalp (V zoster virus keratitis).
keratitis
32
Define age-related macular degeneration
Potentially progressive maculopathy.
Sudden-onset of blurring or distortion of vision is often the presenting symptom.
Characterised by drusen formation, macular pigmentary changes, geographic atrophy, and neovascularisation of the choriocapillaris with exudation.
Leading cause of adult blindness in industrialised nations.
Typically affects white people aged >55 years.
Diagnosis and treatment are highly specialised and involve consultation with a retinal consultant.
33
Epidemiology of age-related macular degeneration
According to the World Health Organization (WHO), AMD is the third cause of visual impairment and is associated with a worldwide blindness prevalence of almost 9%
34
Aetiology of age-related macular degeneration
Pathogenesis is thought to involve a combination of oxidative stress and inflammation, although the precise role of these processes in the initiation and progression of the condition remains unclear. Accumulation of iron, which is a known trigger of oxidative stress, within cells of the retinal pigment epithelium (RPE) could be involved in cellular damage.
35
RFs for age-related macular degeneration
```
STRONG
Increasing age
Smoking
FHx
HTN
Fat intake
High cholesterol
```
36
Sx of age-related macular degeneration
COMMON
SO blurring or distortion of vision
Drusen = yellow deposits under the retina
Macular pigmentary changes
Choroidal neovascularisation
Pigment epithelial detachment
Progressive loss of vision in 1 or both eyes
Blurred or no vision in the center of the visual field
Slow recovery of visual function after exposure to bright light (photostress test)
37
Ix for age-related macular degeneration
Ampler grid - focal area of distortion
Optical coherence tomography - intraretinal fluid; subretinal fluid; pigment epithelial detachment; loss of normal retinal pigment epithelium and photoreceptor architecture; hyper-reflective scar
38
Rx of age-related macular degeneration
Early stage = observation and RFs
Intermediate = AREDS formulation - 2 tablets daily
(antioxidant)
+ specialist referral
SEVERE = intravitreal injection with VEGF inhibitor
+ AREDS antioxidant supplement
OR photodynamic therapy (verteporfin)
OR Thermal laser photocoagulation
39
Complications of age-related macular degeneration
Progression or development in the other eye
Photosensitivity reaction post photodynamic therapy
Traumatic injury post intravitreal injection
Retinal detachment post intravitreal injection
40
A 75-year-old woman presents with new-onset distortion in one eye. Vision is 20/80 in the involved eye. She has a family history of AMD and has smoked 20 cigarettes a day for most of her adult life.
age-related macular degeneration
41
Define peri-orbital and orbital cellulitis
Peri-orbital (also known as pre-septal) cellulitis is inflammation and infection of the superficial eyelid, usually from a superficial source. The inflammation remains confined to the soft tissue layers superficial to the orbital septum and ocular function remains intact.
Orbital cellulitis is an infection within the orbital soft tissues with associated ocular dysfunction and is usually due to underlying bacterial sinusitis. Orbital cellulitis is a far more serious condition and warrants hospital admission. It has much higher morbidity than peri-orbital cellulitis, and warrants urgent imaging and surgical evaluation by oculoplastic as well as a head-and-neck consultant.
Peri-orbital cellulitis is of concern in children because it may be secondary to occult underlying bacterial sinusitis or, rarely, due to bacteraemic spread from a primary infection (e.g., pneumonia), and may rapidly progress to orbital cellulitis in children.
Complications include sub-periosteal abscess, cavernous sinus thrombosis, intracranial abscess, and subsequent loss of vision and/or death.
42
Epidemiology of peri-orbital and orbital cellulitis
No racial or gender predilection exists for adults. However, children are twice as likely as adults to develop this condition. In children, males are twice as likely to develop the condition as females.
43
Aetiology of peri-orbital and orbital cellulitis
Organisms involved include Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus species, and anaerobes. Fungal infections (mucormycosis or invasive aspergillosis) have been seen in people with diabetic ketoacidosis or immunosuppression and recipients of organ transplantation, and are typically very aggressive and often fatal.
In the majority of pre-septal cellulitis in adults, the infection occurs from a superficial site of inoculation (e.g., insect bite, chalazion, epidermal inclusion cyst, folliculitis). In children, pre-septal cellulitis may reflect an underlying sinusitis. In all ages, orbital cellulitis most often reflects local spread of an upper respiratory tract infection, usually sinusitis. Less common sources of orbital cellulitis are orbital injury, fracture, dacryocystitis, endophthalmitis ('panophthalmitis'), or underlying dental infections. More rarely, infection may spread haematogenously.
44
RFs for peri-orbital and orbital cellulitis
```
STRONG
Sinusitis
Young age
Male sex
Lack of Hip vaccine
```
45
Sx of peri-orbital and orbital cellulitis
```
COMMON
Recent sinus infection
Recent eyelid injury
Redness and swelling of eye
Ocular pain
Decreased vision
Proptosis
Eyelid oedema
Insect bite on eyelid
Stye or chalazion
Skin infection
Chemosis
Tenderness around eye
Fever
Eyelid erythema
Elevated IOP
Headache
Malaise
Orbital fracture
Foreign body in eye or orbit
Drowsiness
N+V
Nasal discharge
```
46
Ix for peri-orbital and orbital cellulitis
Clinical examination
CT sinus + orbits with contrast
WBC count - elevated with left shift
Consider blood culture + swabs
Consider LP
47
Rx of peri-orbital and orbital cellulitis
Empirical ABx
Cefazolin OR
Cefuroxime + metro
If suspect MRSA - require hospitalisation
If present, a peri-ocular abscess should be incised and drained, and a swab of contents sent for culture and sensitivities.
+/- anti fungal therapy
Ephedrine nasal decongestion
IF really high orbital pressure, may need a lateral canthotomy and cantholysis
ALWAYS switch to targeted therapy
48
Prognosis of peri-orbital and orbital cellulitis
Peri-orbital cellulitis
Clinical improvement is usually seen within 24 to 48 hours. Prognosis is excellent, with full resolution in almost all cases.
Orbital cellulitis
A lag time of 24 to 48 hours commonly occurs between initiation of antibiotics and clinical response. If there is no improvement or if new signs such as decreased vision or afferent papillary defect appear, repeat CT scan and suspect abscess formation or resistant organisms. Prognosis depends on any underlying risk factors (i.e., patient is immunocompromised) or findings (i.e., abscess). Prompt and proper antibiotic treatment and drainage of sinusitis is critical to avoid progression to sub-periosteal orbital abscess, epidural abscess, and meningitis.
49
Complications of peri-orbital and orbital cellulitis
```
Sub-periosteal abscess
Ocular empyema
Meningitis
Orbital abscess
Epidural abscess
Ocular compartment syndrome
Death
```
50
A 9-year-old boy is brought to the emergency department with redness and swelling around his eye that has been present for 1 day. His left eyelid is red, tender to touch, and swollen. It will not open fully and he has a slightly decreased confrontational visual field in the left eye superiorly. He is afebrile and vital signs are normal. He denies any decrease in vision or double vision and his examination is significant for best corrected vision of 20/25 (right eye) and 20/25 (left eye). He has full motility of both eyes, has no afferent pupillary defect, and has eye pressures of 16 mmHg (right eye) and 18 mmHg (left eye). His conjunctiva and sclera are within healthy limits and the anterior chamber is deep and quiet. Fundus findings are normal in the left eye and the rest of his examination is within healthy limits. No masses are palpable. CT of orbits and sinus revealed absence of orbital fat stranding and sub-periosteal abscess. Patient had opacified ethmoid and frontoethmoidal recess on the left side.
peri-orbital and orbital cellulitis
51
Define retinal detachment
An acute or progressive condition in which the neuroretina separates from the retinal pigment epithelium with accumulation of sub-retinal fluid and loss of retinal function.
May be primary (rhegmatogenous retinal detachment), secondary to traction, or exudative in nature.
In rhegmatogenous retinal detachment, retinal discontinuity promotes retinal detachment.
Diagnosis is by indirect ophthalmoscopy or slit-lamp examination. In case of media opacity, B-scan ultrasonography is necessary.
Left untreated, rhegmatogenous retinal detachment typically results in blindness.
Surgical treatment is aimed at preventing fluid access to the sub-retinal space through the break and eliminating the traction causing the break.
If treated, prognosis is generally good. The most common cause of failure is scarring due to proliferative vitreoretinopathy.
52
Epidemiology of retinal detachment
12.9/100,000
The incidence of rhegmatogenous RD increases with age.
53
Aetiology of retinal detachment
Several factors can contribute to the structural change of the vitreous gel. These include:
```
Age
Myopia
Trauma
Cataract surgery
Ocular inflammation.
```
The development of rhegmatogenous RD is a consequence of vitreoretinal traction (such as a posterior vitreous detachment) leading to the development of one or more breaks in the retina. Fluid can then pass from the vitreous cavity through these retinal breaks into the sub-retinal space, which extends the detachment once the amount of incoming fluid exceeds the removal capacity of the retinal pigment epithelium (RPE). Detachment of the posterior vitreous is considered a major factor in the pathogenesis of rhegmatogenous RD. However, no preoperative diagnostic technique can accurately distinguish between a posterior vitreous detachment and a posterior vitreoschisis.
In eyes with tractional RD, the membranes on either surface of the retina are 1) attached to the retina, and 2) contractile. As the membranes contract, the retina detaches from the RPE. Accumulation of the sub-retinal fluid is a secondary event; as part of the normal fluid transport from the vitreous to the choroid, the fluid simply fills the space created by the elevated retina.
54
RFs for retinal detachment
```
STRONG
Posterior vitreous detachment
Increasing age
Myopia
Hx cataract surgery
Trauma
Intraocular tumour
Vitreous haemorrhage
DM
```
WEAK
Ocular inflammation/infection
Anatomical abnormality
Age related macular degeneration
55
Sx of retinal detachment
COMMON
RFs
Loss or deterioration of central vision:
For eyes with non-rhegmatogenous RD, visual loss may be sudden or more gradual; in case of an exudative RD, the central vision may remain very good for a long time despite the presence of sub-macular fluid. For eyes with a haemorrhagic RD, a sharply circumscribed central scotoma presents acutely.
Flashes of light - Preceding symptoms such as flashes of light may be elicited on questioning. The flashes are typically seen in the temporal visual field, and they are easiest to notice in a dark environment.
Loss of peripheral field
Floaters:
Indicate vitreous opacity. Floaters are common as a consequence of vitreous ageing. However, certain presentations may suggest retinal pathology.
Sudden onset of a large central floater suggests posterior vitreous detachment and presence of an operculum.
Numerous small floaters are suggestive of retinal haemorrhage.
56
Ix for retinal detachment
Acuity - impairment (Visual acuity may not be reduced if the detachment is peripherally located)
Slit lamp exam - retinal detachment; retinal break; vitreoretinal pathology (traction or presence of pigment)
Opthalmoscopy - retinal detachment; retinal break; vitreoretinal pathology (traction or presence of pigment)
57
Rx of retinal detachment
Asymptomatic retinal breaks without detachment may be monitored. Proper prophylactic treatment such as laser cerclage dramatically reduces the risk of subsequent detachment.
In symptomatic patients, the breaks are sealed using cryopexy or laser retinopexy.
Either scleral buckle or vitrectomy may be performed, or the procedures may be performed together. The breaks are sealed using cryopexy or laser retinopexy.
In eyes with haemorrhagic RD, the thickness of the sub-macular blood is a crucial factor in the decision-making; delay may lead to irreversible damage.
In mild haemorrhage, blood may be drained or evacuated through a retinotomy.
If the clot is large, retinal inversion may also be performed.
58
Prognosis of retinal detachment
Untreated rhegmatogenous RD has a grim prognosis, due to the development of proliferative vitreoretinopathy (PVR) and irreversible photoreceptor damage. However, with treatment, about 75% to 80% of patients have successful retinal reattachment with the first surgery, provided that the detachment was fresh, the treatment option was properly selected, and surgery was expertly performed.
Typically, the retina is attached either during surgery (almost always during vitrectomy, variably during scleral buckling, rarely during pneumatic retinopexy) or shortly after surgery and remains attached. In the minority of cases, the retina re-detaches, which must be treated with a second operation. The first operation has the highest chance of success, and every additional operation increases the risk of post-surgical PVR. This is true for all RD types.
Eyes with non-rhegmatogenous RD have a varied prognosis depending on the aetiology, extent, and duration of the condition.
59
Complications of retinal detachment
```
Endopthalmitis
Permanent loss of vision
Fellow eye detachment
Myopia
Cataract
Recurrence
Proliferative vitreoretinopathy
Post-scleral buckling / vitrectomy / pneumatic retinopexy complications
```
60
A 67-year-old man presents with a 2-day history of sudden visual loss in his right eye. He is slightly myopic and had successful cataract extraction with intraocular lens implantation 3 years earlier. He does not remember this eye ever having been injured. No pain was associated with the vision loss, and his blood pressure is normal with medication. The patient describes the loss of vision as a veil covering the visual field.
retinal detachment
61
A 71-year-old woman presents after accidentally discovering that she has no vision in her left eye. She covered her right eye as she was scratching her eyelid, and noticed that the left eye was 'blind'. She has been moderately myopic (-5 D) for decades but has no other significant history.
retinal detachment
62
Define amblyopia
A reduction of best corrected visual acuity that is not attributable to a structural abnormality of the eye or to visual pathways. For the brain to learn to see with each eye, and to develop the capacity for binocular vision, each eye must have a clear and focused retinal image, and the 2 eyes must be aligned. Research has demonstrated that there are critical periods for the development of normal vision, and that amblyopia is associated with structural changes in the primary visual cortex
A visual impairment resulting from abnormal visual stimulation during early childhood, the prevalence of which ranges from 1% to 4%.
Can result from strabismus, form deprivation (e.g., due to congenital cataracts or corneal opacities), and various types of refractive error. These errors include anisometropia (unequal refractive error between the 2 eyes), isoametropia (high but similar refractive error in the 2 eyes), and high astigmatism in 1 or both eyes.
Amblyopia due to strabismus with or without refractive error is commonly treated with initial optical correction, and subsequent patching or atropine penalisation of the better-seeing eye. Amblyopia due to refractive error alone frequently responds to optical correction alone.
Amblyopia due to form deprivation is treated initially with early surgery, to remove the visual obstruction. In unilateral or asymmetric cases, patching of the better-seeing eye is necessary after surgery.
Treatment is highly successful when instituted during infancy and pre-school years, although some children as old as 13 to 17 years respond to treatment, particularly if there has been no prior therapy.
63
Define strabismus
Strabismus refers to a misalignment of the eyes. If strabismus develops in adults, it can cause diplopia (double vision) and visual confusion (seeing different objects in the same location), and it is an important cause of amblyopia in children. Whereas normally both eyes fixate (look at) the object of interest, in strabismus one eye fixates and the other (non-fixating eye) is deviated.
Misalignment of the visual axes of the eyes; may be latent or manifest and, if manifest, it may be constant or intermittent.
Common cause of diplopia (double vision) and visual confusion (seeing different objects in the same place) in adults.
Important cause for amblyopia (decreased vision in an anatomically normal eye caused by suppression) in children.
May be aesthetically obvious to the patient and others, resulting in psychosocial problems.
Evaluation involves a detailed medical history, including a complete ocular history, followed by thorough neurological and ophthalmic examinations.
Treatment is directed at restoring and maintaining ocular alignment, eliminating diplopia or visual confusion, enabling binocular vision, and restoring normal appearance.
If strabismus is secondary to an underlying cause (e.g., abducens nerve [cranial nerve VI] palsy causing esotropia), treatment of this condition is necessary.
64
Epidemiology of strabismus
The prevalence of strabismus is higher in those with intellectual disabilities (44.1%) compared with the general population.
The prevalence in white people is 2% to 4%
65
Aetiology of strabismus
The aetiology of strabismus varies by type.
The aetiology of most infantile and paediatric forms of strabismus is poorly understood. Comitant (concomitant) strabismus seems to be a complex genetic trait, with the involvement of more than one gene. Twin studies have revealed a concordance rate of 73% to 82% among monozygotic twins and 35% to 47% among dizygotic twins.[10] The rate for dizygotic twins is higher than the concordance for siblings, indicating that environmental factors are likely to be involved. No modifiable risk factors have been identified for most forms of comitant strabismus.
Acquired paralytic strabismus is related to malfunction of one or more of the 3 cranial nerves - oculomotor (cranial nerve III), trochlear (cranial nerve IV), and abducens (cranial nerve VI) - providing motor supply to the extraocular muscles.
Restrictive strabismus results from mechanical restriction of eye movements caused by such conditions as Graves' disease and orbital fractures.
Sensory strabismus is caused by reduced visual acuity in one eye.
Craniofacial and cranial dysinnervation syndromes and craniosynostosis may also lead to the development of strabismus.
In recurrent strabismus the abnormality recurs following initially successful treatment for the same kind of strabismus, while in consecutive strabismus the abnormality occurs following treatment for a different kind of strabismus, and residual strabismus denotes strabismus that remains after partially successful treatment.
Strabismus may also be associated with myasthenia gravis (myasthenia strabismus) and supranuclear palsies (supranuclear strabismus).
Acute-onset strabismus may be caused by an intra-cranial process such as a mass lesion, raised intra-cranial pressure, central nervous system (CNS) infarction, or inflammation in the CNS.
Strabismus is more common in children with global CNS problems, such as cerebral palsy or developmental delay.
66
RFs for strabismus
STRONG
FHx
Prematurity: The frequency of strabismus is higher in patients with a history of ROP - a condition of the retina in preterm babies that affects the development of the retinal vasculature, potentially resulting in poor structural and visual outcome. Increasing severity of ROP is a further risk factor for strabismus. The presence of neurological complications in preterm babies also increases the risk of strabismus
WEAK
Refractive error
67
Sx of strabismus
```
STRONG
Diplopia
Eye-misalignment
Amblyopia
Abnormal eye movements
Visual confusion
Asthenopia
Intermittent closure of one eye
Cranial nerve palsy
```
68
Ix for strabismus
Cover test - Both eyes fixate an object and one eye is covered. If the fellow eye makes a re-fixation movement, manifest strabismus is present, but if the fellow eye makes no movement, no manifest strabismus is present. The direction of the re-fixation movement is opposite to the direction of the deviation (e.g., if the fellow eye makes an outward movement when the other eye is covered, it was deviated inwards, and an esotropia is diagnosed).
A positive cover test denotes the presence of a manifest strabismus, and a negative cover test denotes the absence of a manifest strabismus.
Result
positive: manifest strabismus present; negative: manifest strabismus absent
If the cover test is negative (i.e., absence of a manifest strabismus), the presence of a latent strabismus is indicated by a positive UCT.
First the cover test is performed, and if this is negative, the cover is removed. If the uncovered eye makes a re-fixation movement, latent strabismus (also known as phoria) is present.
Result
positive: latent strabismus present
69
Rx of strabismus
Correct refractive error
Extra-ocular muscle surgery
Chemodenervation with botox
Rx any related amblyopia (with patches) or diplopia with prisms
70
Complications of strabismus
Amblyopia
Red binocular vision
Psychosocial
71
A 4-month-old healthy girl with normal antenatal and birth history is brought in by her parents, who note that both her eyes are looking toward the nose. Examination shows a large-angle esotropia with freely alternating fixation (i.e., each eye fixates objects, with no preference for either eye). No significant refractive error is present, and the remainder of the eye examination is normal. The infant is diagnosed with infantile esotropia.
strabismus
If strabismus occurs acutely, and it does not meet the criteria for primary strabismus, the patient must be urgently referred to an ophthalmologist for a thorough evaluation. This may represent an intra-cranial process, such as a mass lesion, aneurysm, raised intra-cranial pressure, central nervous system (CNS) infarction, or inflammation in the CNS.
72
A 34-year-old man complains of double vision after recovering from facial trauma that included a fracture of the left orbital floor. He describes the double vision as manifesting with one image on top of the other. The patient complains that he is unable to function unless he closes one eye. Examination shows hypotropia of the left eye, which becomes larger when the patient tries to look up. The remainder of the ocular examination is normal. A CT scan of the orbits demonstrates orbital tissue herniating through a fracture in the floor of the left orbit, and the patient is diagnosed with restrictive incomitant left hypotropia.
strabismus
If strabismus occurs acutely, and it does not meet the criteria for primary strabismus, the patient must be urgently referred to an ophthalmologist for a thorough evaluation. This may represent an intra-cranial process, such as a mass lesion, aneurysm, raised intra-cranial pressure, central nervous system (CNS) infarction, or inflammation in the CNS.
73
Define uveitis
Uveitis is an inflammation of one or all parts of the uvea, or the vascular area between the retina and sclera of the eye. The anterior uvea is composed of the iris and ciliary body; an irritation of this segment, or anterior uveitis, leads to acute painful symptoms and photophobia. Inflammation of the posterior uvea, including the choroid, retina, and retinal vasculature, carries a risk of painless visual loss. Uveitis of all types affects children and adults, and the aetiology is most commonly idiopathic.
Anterior uveitis involves inflammation of the iris and ciliary body. Intermediate uveitis involves the posterior ciliary body and pars plana. Posterior uveitis involves the posterior vitreous, retina, choroid, retinal vasculature, and optic nerve. Panuveitis involves inflammation in the anterior, intermediate, and posterior segments of the eye.
All types of uveitis are potentially blinding conditions and should be referred to and managed by an experienced ophthalmologist.
Diagnosis is clinical. Acute anterior uveitis may be idiopathic, or associated with HLA-B27-related disease or viral eye disease. Posterior uveitis is associated with localised infections or systemic infection, or systemic inflammatory disease. Diagnosis of underlying disease may require investigation. In the clinical setting of multiple recurrences or strong suspicion based on history and review of systems, a targeted work-up should be undertaken to rule out an underlying infectious cause or co-existent autoimmune disease. Rarely, uveitis can be caused by a previous eye injury or underlying neoplasm.
Even after full laboratory and diagnostic work-up and treatment, aetiology may not be determined.
Treatment for systemic disease causing uveitis must be given in conjunction with uveitis therapy.
Topical corticosteroids are usually adequate for acute non-infectious anterior uveitis, but intermediate and posterior uveitis usually requires injected local corticosteroids or systemic steroids, or other immunosuppression.
74
Epidemiology of uveitis
In the US, incidence is about 15 cases per 100,000 person-years
The peak age of presentation of uveitis is between ages 30 and 40 years
Anterior uveitis, specifically iritis, is the most common form, representing about 75% of cases.
75
Aetiology of uveitis
Aetiology can be divided into idiopathic, infectious, and non-infectious causes. Infectious causes include herpes simplex virus (HSV), herpes zoster virus, CMV, HIV, Lyme disease, toxoplasmosis, TB, syphilis, and histoplasmosis.
Non-infectious causes include seronegative arthropathies, inflammatory bowel disease, autoimmune disorders, sarcoidosis, multiple sclerosis, and eye trauma.
Acute anterior uveitis may be idiopathic, or associated with HLA-B27-related disease or viral eye disease. One study found that 49.4% of patients with anterior uveitis tested positive for the HLA-B27 antigen. Posterior uveitis is associated with localised infections or systemic infection, or systemic inflammatory disease. Rarely, uveitis can be caused by a previous eye injury or underlying neoplasm.
76
RFs of uveitis
STRONG
Inflammatory diseases
HLA-B27
Ocular trauma
WEAK
30-40
77
Sx of uveitis
```
COMMON
Pain
Dec vision
Synechiae
Flare
Keratic precipitates
Tearing
Photophobia
Floaters
Eye-redness WO discharge
Constricted or non-reactive pupil
Decreased IOP
Retinal exudates
Macular oedema
Optic disc swelling
Retinal haemorrhages
Ciliary flush
Corneal oedema
Cataract
```
78
Ix for uveitis
Clinical diagnosis
79
Rx of uveitis
1. Corticosteroid eye-drops
+ periocular or intraocular corticosteroid injection
2. Oral corticosteroid
Cycloplegics can be used if the inflammation is causing synechiae or the uveitis is fibrinous in nature, as can happen with HLA-B27-related uveitis or various granulomatous uveitic conditions.
eg atropine ophthalmic: (1% solution) 1 drop into the affected eye(s) twice daily
Uveitis may be idiopathic, or associated with HLA-B27-related disease or systemic inflammatory disease, viral eye disease or other localised infections, or systemic infection. Diagnosis of underlying disease may require investigation.
In patients with a first-episode unilateral, non-granulomatous uveitis without symptoms or systemic manifestations, no further evaluation is warranted. This is also true for patients with a recent history of trauma or surgery or with clinical signs of HSV or herpes zoster virus infection.
If the patient presents with bilateral, recurrent, or granulomatous uveitis, further evaluation is needed. CBC, angiotensin-converting enzyme (ACE) level (elevated in sarcoidosis), syphilis serology, and HLA-B27 help to identify a related systemic disease. Testing for rheumatoid factor and anticyclic citrullinated peptide (anti-CCP) antibodies should be done in the setting of suspected rheumatoid arthritis. Antidouble-stranded DNA levels and complement levels may be elevated in SLE. Other HLA antigens may point to the presence of specific disorders. Elevated levels of antineutrophil cytoplasmic antibodies point to the presence of a vasculitic condition.
80
Prognosis of uveitis
The prognosis is variable and depends upon the aetiology, location, and severity of uveitis. Panuveitis, intermediate uveitis, and posterior uveitis resulting in retinal, choroidal, or optic nerve damage tend to result in a worse outcome than anterior uveitis. In a large study of uveitis patients, 35% had visual loss of >20/60 in at least one eye, whereas 22% became unilaterally or bilaterally blind.
81
Complications of uveitis
```
Synechia
Retinal scarring
Cataract
Band keratopathy
Macular oedema
Glaucoma
Choroidal neovascularistion
Retinal detachment
```
82
A 40-year-old man presents to the emergency department complaining of red eye without purulent discharge. He also has pain, photophobia, blurred vision, and tearing. On slit-lamp examination, the attending ophthalmologist notices a small irregular pupil, conjunctival injection around the corneal limbus, and WBCs in the anterior chamber.
uveitis
83
A 30-year-old woman presents with onset of bilateral decreased vision associated with floaters. Slit-lamp examination of the anterior segment shows no abnormality. However, on dilated fundoscopic examination, vitreous cells and a choroiditis are apparent.
uveitis
84
Define conjunctivitis
Conjunctivitis is the inflammation of the lining of the eyelids and eyeball caused by bacteria, viruses, allergic or immunological reactions, mechanical irritation, or medicines.
Symptoms include an irritated red eye with a watery or purulent discharge.
Allergic conjunctivitis is usually bilateral with watery discharge and itching.
Treatment for allergic conjunctivitis includes topical mast cell stabilisers and antihistamines; bacterial conjunctivitis treatment includes topical antibiotics; viral conjunctivitis requires symptomatic treatment.
Bacterial and viral conjunctivitis is highly contagious; measures to prevent spread of infection should be considered.
85
Epidemiology of conjunctivitis
Conjunctivitis commonly affects males and females of all ages.
It is usually treated by general practitioners and is estimated to account for almost 1% of all primary care consultations
In England there are 13-14 cases in 1000 people per year
86
Aetiology of conjunctivitis
The most common bacterial pathogens in infective conjunctivitis include Pneumococcus, Staphylococcus aureus, Moraxella catarrhalis, and Haemophilus influenzae.
Rarely, Neisseria gonorrhoeae causes a hyperacute purulent conjunctivitis; the organism is transmitted from the genitalia to the hands and then to the eyes.
Chlamydia is a common cause of persistent conjunctivitis.
Viral conjunctivitis can be caused by adenovirus, herpes simplex, Epstein-Barr, varicella zoster, molluscum contagiosum, coxsackie, and enteroviruses.
Adenoviral conjunctivitis usually causes epidemic keratoconjunctivitis, follicular conjunctivitis, and non-specific conjunctivitis
Contact lens wear may lead to a keratoconjunctivitis or giant cell papillary conjunctivitis secondary to infrequent lens replacement, prolonged wearing time, poor lens hygiene, allergenic contact lens solutions, ionic nature or high water content, or poor fit of contact lenses.
Mechanical conjunctivitis can be caused by chronic conjunctival irritation, especially while sleeping. It is often caused by floppy eyelid syndrome, which is associated with obesity, sleep apnoea, upper eyelid laxity, and lid imbrication (upper eyelid excursion over lower eyelid).
Toxic/chemical conjunctivitis results from irritation of the conjunctiva by environmental exposure to chemicals (including acids and bases). Some eye preparations, such as glaucoma medicines, antibiotics, and antivirals, often contain preservatives such as benzalkonium chloride that may accumulate in the conjunctiva after frequent administration; these preservatives can be a causative factor.
Ocular cicatricial pemphigoid may develop from a genetic predisposition or in response to certain topical medicines such as idoxuridine, pilocarpine, epinephrine (adrenaline), timolol, and echothiophate.
Neoplastic conjunctivitis is caused by a sebaceous gland carcinoma; secondary radiotherapy may also induce a chronic conjunctivitis.
87
RFs for conjunctivitis
```
STRONG
Exposure to infected person
Environmental irritants
Allergen exposure
Swimming pools
Asian or mediterranean young male
Atopy
Contacts
Ocular prosthesis
Mechanical irritation
```
```
WEAK
Asthma
Hayfever
Topical eye medicine
Sebacious gland carcinoma
Hx rheum disease
```
88
Sx of conjunctivitis
Watery discharge - More common in viral than allergic or bacterial infection.
Mucoid discharge - more common in allergic than viral or bacterial infection
Purulent discharge - More common in bacterial than viral infection.
Itching - More common in allergic than viral infection
Eyelids stuck together in morning - Occurs with both bacterial and viral infection
Pre-auricular lymphadenopathy = More common in viral than bacterial infection
Conjunctival follicles
Superficial punctate keratopathy
Unilateral disease - More common in bacterial than viral infection
Corneal sub epithelial infiltrates
Corneal pannus
Vesicular skin rash - May indicate herpes zoster infection.
89
Ix for conjunctivitis
Clinical
90
Rx of conjunctivitis
Allergic
1. Tears
2. Cool compress
3. Mast cell stabilisers
4. Antihistamines
5. Topical NSAIDS
6. Topical corticosteroids
7. Topical ciclosporin
Bacterial
BS ABx
Viral
Ganciclovir topical
91
Prognosis of conjunctivitis
Allergic conjunctivitis
Most patients respond to treatment but may experience seasonal exacerbations.
Bacterial conjunctivitis
Generally self-limiting over 5 to 10 days; no significant long-term complications. Contact lens wearers and immunocompromised patients are at most risk of complications.
Viral conjunctivitis
Most cases are self-limiting; approximately 30% to 50% of patients with the form of adenovirus that causes epidemic keratoconjunctivitis may develop subepithelial infiltrates, which may lead to persistent visual loss and light sensitivity.
Non-infectious conjunctivitis
Most patients recover well after discontinuation of the cause.
92
Complications of conjunctivitis
```
Dry eyes
Keratitis
Corneal inflitrates
Lacrimal drainage problems
Symblepharon - Scarring of the conjunctiva may lead to eyelid malposition and secondary tearing or eyelash problems
```
93
A 6-year-old girl with no significant past medical history presents 4 days after developing a red, irritated left eye. Her mother states that she has been wiping thick whitish-yellow discharge from her eye, and the eye is matted shut in the morning. She denies any exposure to an infected person, upper respiratory tract symptoms, or contact lens use. She also denies any significant pain or light sensitivity. On examination, the patient's pupils are equal and reactive. She does not have a tender pre-auricular lymph node. Penlight examination does not reveal any corneal opacity, but thick, whitish discharge is seen.
conjunctivitis
94
A 14-year-old boy with no significant past medical history presents 3 days after developing a red, irritated right eye that spread to the left eye today. He has watery discharge from both eyes and they are stuck shut in the morning. He reports recent upper respiratory tract symptoms and that several children at his day camp recently had pink eye. He denies significant pain or light sensitivity and does not wear contact lenses. On examination, his pupils are equal and reactive and he has a right-sided, tender pre-auricular lymph node. Penlight examination does not reveal any corneal opacity.
conjunctivitis
95
Define angle-closure glaucoma
Angle-closure glaucoma (ACG) is a group of diseases in which there is reversible (appositional) or adhesional (synechial) closure of the anterior-chamber angle resulting in elevation of the intra-ocular pressure (IOP). The angle closure may occur in an acute or chronic form. In the acute form, the IOP rises rapidly as a result of relatively sudden blockage of the trabecular meshwork by the iris, via the pupillary block mechanism (mechanism that pushes iris from behind leading to angle closure). The chronic form may develop after acute angle closure where synechial closure of the angle persists. It may also develop over time, as the angle closes from prolonged or repeated contact between the peripheral iris and the trabecular meshwork, which often leads to peripheral anterior synechiae (PAS) and functional damage to the angle.
Acute angle-closure glaucoma is an urgent but uncommon, dramatic symptomatic event with blurring of vision, painful red eye, headache, nausea, and vomiting.
Diagnosis is made by noting high intra-ocular pressure, corneal oedema, shallow anterior chamber, and a closed angle on gonioscopy.
Medical or surgical therapy is directed at widening the angle and preventing further angle closure.
If glaucoma has developed it is treated with therapies to lower intra-ocular pressure.
Chronic angle-closure glaucoma is diagnosed by noting peripheral anterior synechiae on gonioscopy, as well as progressive damage to the optic nerve and characteristic visual field loss. It is treated with therapies to lower intra-ocular pressure.
96
Epidemiology of angle-closure glaucoma
The number of people affected by glaucoma in the world is approximately 45 million.
One third are from primary angle-closure glaucoma (PACG). Half of cases leading to blindness are estimated to result from PACG.
97
Aetiology of angle-closure glaucoma
Angle closure can be primary, secondary to another eye disease, or drug-induced.
Eye diseases that can cause ACG include a thick cataractous lens (phacomorphic glaucoma); ectopic lens (e.g., in settings of trauma, as well as Marfan’s or Weill-Marchesani syndrome); neovascularisation of the angle secondary to diabetic retinopathy or ocular ischaemia; and tumours.
Sulfa-containing drugs can cause ACG by causing supraciliary body effusions. This form of ACG has a distinctly different aetiology and is not treated in the same fashion as primary angle-closure glaucoma. It is unresponsive to laser peripheral iridotomy and is treated with topical corticosteroids and discontinuation of the causative drug, as well as topical and systemic intraocular pressure lowering drugs
98
RFs for angle-closure glaucoma
```
STRONG
Female
Hyperopia
Shallow peripheral anterior chamber
Inuit/asian
```
WEAK
Age
FHx
Sulfa containing medications + anticholinergics - Anticholinergic topical pupil dilators (e.g., cyclopentolate or atropine) or systemic medication (e.g., sulfonamides, topiramate, phenothiazines).
99
Sx of angle-closure glaucoma
```
COMMON
Halos around lights
Aching eye / brow
Headache
N+V
Eye redness
Reduced acuity
```
Raised IOP - In healthy eyes, IOP is generally 10 to 21 mmHg. In acute attacks, IOP rises rapidly to relatively high levels, typically above 40 mmHg. In chronic ACG, the IOP may be variably elevated depending on the extent of angle closure.
Corneal oedema
Fixed dilated pupil
Incidental finding - In chronic disease, most patients are asymptomatic and ACG is incidentally detected as part of an ophthalmic examination.
Blurred vision/change in vision
100
Ix for angle-closure glaucoma
Gonioscopy - trabecular meshwork is not visible in angle closure, because the peripheral iris is in contact with it
Slit lamp - shallow anterior chamber; and signs of glaucoma: large optic cup, narrowing of the neuroretinal rim, splinter haemorrhage, nerve fibre loss
Automatic static perimetry - visual field defects
101
Rx of angle-closure glaucoma
1. Carbonic anhydrase inhibitors decrease aqueous humour formation and are used commonly as first-line therapy in combination with beta-blockers and alpha-2 agonists.
2. pilocarpine ophthalmic: (1-2%) 1 drop into the affected eye(s) up to four times daily
When ACG is suspected to be secondary to pupillary block or plateau iris syndrome and once intra-ocular pressure (IOP) is <40 mmHg, these agents may be incorporated.
These agents cause pupil constriction with thinning of the iris and its pulling away from the inner eye wall and trabecular meshwork, thus opening the angle.
3. Mannitol
If there is failure of initial medical treatment or intra-ocular pressure (IOP) is greater than 50 mmHg, hyperosmotic agents are used to control acute episodes of elevated IOP.
DEFINITIVE - laser peripheral iridotomy after corneal oedema resolves
An untreated fellow eye has a 40% to 80% risk of developing an acute attack. Therefore, it is recommended that the contralateral eye be treated prophylactically with laser peripheral iridotomy if the chamber angle is found to be anatomically narrow.
102
Complications of angle-closure glaucoma
```
Retinal vein occlusion
Loss of vision
Iridotomy SEs
Fellow eye attack
Permanent reduction in acuity
```
103
Prognosis of angle-closure glaucoma
The prognosis following an episode of acute angle-closure glaucoma is favourable if the intra-ocular pressure (IOP) can be controlled. IOP is reported to be controlled with laser peripheral iridotomy alone in 42% to 72%, and in white people more often than in Asians
Greater extent of PAS, a higher presenting IOP, and a larger cup-to-disc ratio are all predictors of poor pressure control following iridotomy.
104
A 64-year-old woman presents to the emergency department with severe pain around her right eye of 4-hour duration, accompanied by blurred vision in that eye. She is also nauseated. Examination shows a red right eye with oedematous cornea and a wide pupil that is unresponsive to light. Intra-ocular pressure is extremely elevated (60 mmHg), only in the right eye. The anterior chamber angle is closed in both eyes.
angle-closure glaucoma
Patients may present with spontaneously resolving symptoms of intermittent ache and/or blurred vision with haloes around lights seen from one eye. Patients may also notice a change in vision, which may represent long-standing chronic progressive visual field loss.
105
Define open-angle glaucoma
Glaucoma is a neurodegenerative condition primarily due to dysfunction in outflow of the nutrient-rich fluid, aqueous humour that constantly flows through the eye. Aqueous humour, created in the ciliary body, passes through the pupil into the small area between the iris and the cornea, called the anterior chamber. The fluid then flows into the periphery of the chamber known as the anterior chamber angle. This angle is where the fluid travels through the trabecular meshwork and into blood vessels. Open-angle glaucoma is characterised by an anatomically open angle but with an obstructed and slowed drainage system outflow. The mechanism of blockage is unclear. A rise in increased intra-ocular pressure results, characterised by retinal ganglion cell damage, then peripheral vision loss in early disease and central vision loss in late disease.
Glaucoma is the second leading cause of blindness in the world, with open-angle glaucoma being the most common type.
Frequently presents asymptomatically and may be identified on routine ophthalmic examination.
Intra-ocular pressure is most often elevated, but may be normal in some cases.
Optic disc cupping is diagnostic.
May lead to irreversible loss of peripheral vision and, later, of central vision if untreated.
106
Epidemiology of open-angle glaucoma
Glaucoma is the second leading cause of blindness in the world, causing permanent vision loss.[2] Primary open-angle glaucoma is the most common type of glaucoma, accounting for around 70% of cases.[3] One study estimated that by 2020 around 59 million people worldwide will have primary open-angle glaucoma, with 5.9 million of these people having bilateral blindness.[3] Open-angle glaucoma is the main irreversible cause of blindness in black people.[3][4] In the US, around 2.2 million people have open-angle glaucoma, with a threefold higher prevalence in African-American people compared with non-Hispanic white people.
107
Aetiology of open-angle glaucoma
Open-angle glaucoma is a neurodegenerative process wherein retinal ganglion cells slowly degenerate. It has been linked to hereditary factors. A gene at the GLC1A locus is associated with adult- and juvenile-onset open-angle glaucoma. Myocilin mutations have been described in people with primary open-angle glaucoma
108
RFs for open-angle glaucoma
```
STRONG
IOP >23mmhg
>50yo
FHx
Black
```
WEAK
Myopia
DM
HTN
109
Sx of open-angle glaucoma
```
COMMON
Cup to disc ratio >0.4
Notching of optic nerve cup
Peripheral vision loss
Raised IOP
Scotomas
Loss of nerve fibre layer
```
UNCOMMON
Retinal haemorrhage
110
Ix for open-angle glaucoma
Tonometry - intra-ocular pressure elevated if above normal range: 10 mmHg and 21 mmHg
Direct opthalmoscopy - cup-to-disc ratio over 0.6 may be suspicious of glaucoma as is asymmetry of greater than 0.2 between the two eyes; visualisation of optic disc and retina quality; flame haemorrhages in late disease
Indirect ophthalmoscopy - cup-to-disc ratio over 0.6 may be suspicious of glaucoma as is asymmetry of greater than 0.2 between the two eyes; 3-dimensional view of retina and optic disc cupping
Slit-lamp biomicroscopy - cornea should be clear, anterior chamber should be deep, and drainage angle should be open
Visual field testing - scotomas indicating loss of the nerve fibre layer
111
Rx of open-angle glaucoma
1. Topical ophthalmic prostaglandin analogues
1. Topical BBs
1. Topical carbonic anhydrase inhibitors
1. Topical a2 adrenergic antagonists (apraclonidine)
2. Combination Rx
3. Topical cholinergic agonists
DEFINITIVE
Laser trabeculopathy
OR
Surgical intervention
112
Prognosis of open-angle glaucoma
Glaucoma is a slowly progressive, lifelong disease that may be slowed or halted with treatment.[2] Prognosis is based on the degree of disease at diagnosis, the response to treatment, the patient's adherence to treatment, and the patient's life expectancy. At diagnosis, 20% of people have already lost significant peripheral vision. If the condition is left untreated and intra-ocular pressure stays at ≥30 mmHg, blindness may occur in 3 years or less. Affected people will describe trouble in visually accommodating from bright to dark rooms, and in navigating street kerbs and objects in their periphery. Most people who adhere to, and respond well to, treatment can expect to maintain a functional level of vision for the remainder of their life
113
Complications of open-angle glaucoma
Vision loss
114
A 50-year-old man presents for a routine eye examination with no symptoms. He has elevated intra-ocular pressure of 25 mmHg in the right eye and 30 mmHg in the left eye. On dilated examination, the cup-to-disc ratio is 0.5 in the right eye and 0.8 in the left eye. Corneal thickness and gonioscopy are normal. Subsequent automated testing of visual fields demonstrates peripheral visual field loss greater in the left eye than in the right. Repeated automated visual field testing shows that the visual field defects are reproducible.
open-angle glaucoma
Primary open-angle glaucoma is usually symptomless. If it does cause symptoms, the disease is quite advanced. Symptoms would be painless visual loss in the form of visual field defects. Open-angle glaucoma may present with symptoms of unilateral vision loss with normal bilateral intra-ocular pressure: for example, walking into objects only on the right side. Corneal thickness measurements and gonioscopy may be normal and on dilated examination, the cup-to-disc ratio in the affected eye may be borderline to ≥0.4. Patients may also show an inferior notch in the cup with a flame-shaped haemorrhage. Automated testing of visual fields shows reproducible superior visual field defects in the affected eye.
115
A 50-year-old man presents for a routine eye examination with no symptoms. He has elevated intra-ocular pressure of 25 mmHg in the right eye and 30 mmHg in the left eye. On dilated examination, the cup-to-disc ratio is 0.5 in the right eye and 0.8 in the left eye. Corneal thickness and gonioscopy are normal. Subsequent automated testing of visual fields demonstrates peripheral visual field loss greater in the left eye than in the right. Repeated automated visual field testing shows that the visual field defects are reproducible.
open-angle glaucoma
Primary open-angle glaucoma is usually symptomless. If it does cause symptoms, the disease is quite advanced. Symptoms would be painless visual loss in the form of visual field defects. Open-angle glaucoma may present with symptoms of unilateral vision loss with normal bilateral intra-ocular pressure: for example, walking into objects only on the right side. Corneal thickness measurements and gonioscopy may be normal and on dilated examination, the cup-to-disc ratio in the affected eye may be borderline to ≥0.4. Patients may also show an inferior notch in the cup with a flame-shaped haemorrhage. Automated testing of visual fields shows reproducible superior visual field defects in the affected eye.
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Define vitreous haemorrhage
Vitreous hemorrhage is the extravasation, or leakage, of blood into the areas in and around the vitreous humor of the eye.The vitreous humor is the clear gel that fills the space between the lens and the retina of the eye. A variety of conditions can result in blood leaking into the vitreous humor, which can cause impaired vision, floaters, and photopsia.
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Aetiology of vitreous haemorrhage
Diabetic retinopathy
Trauma
Retinal detachment or tear
Posterios vitreous detachment
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Other causes:
Proliferative sickle cell Retinopathy
Macroaneurysms
Age-related macular degeneration
Terson syndrome
Retinal neovascularization as a result of branch or central retinal vein occlusion
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RFs for vitreous haemorrhage
Diabetic retinopathy
Trauma
Retinal detachment or tear
Posterios vitreous detachment
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Other causes:
Proliferative sickle cell Retinopathy
Macroaneurysms
Age-related macular degeneration
Terson syndrome
Retinal neovascularization as a result of branch or central retinal vein occlusion
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Sx of vitreous haemorrhage
Common symptoms of vitreous hemorrhage include:
Blurred vision
Floaters – faint cobweb-like apparitions floating through the field of vision
Reddish tint to vision
Photopsia – brief flashes of light in the peripheral vision
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Ix for vitreous haemorrhage
Vitreous hemorrhage is diagnosed by identifying symptoms, examining the eye, and performing tests to identify the cause. Some common tests include:
Examination of the eye with a microscope
Pupil dilation and examination
An ultrasound examination may be used if the doctor does not have a clear view of the back of the eye
Blood tests to check for specific causes such as diabetes
A CT scan to check for injury around the eye
Referral to a retinal specialist
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Rx of vitreous haemorrhage
In most cases, the patient is advised to rest with the head elevated 30–45°, and sometimes to put patches over the eyes to limit movement prior to treatment in order to allow the blood to settle. The patient is also advised to avoid taking medications that cause blood thinning (such as aspirin or similar medications).
The goal of the treatment is to fix the cause of the hemorrhage as quickly as possible. Retinal tears are closed by laser treatment or cryotherapy, and detached retinas are reattached surgically.
Even after treatment, it can take months for the body to clear all of the blood from the vitreous. In cases of vitreous hemorrhage due to detached retina, long-standing vitreous hemorrhage with a duration of more than 2–3 months, or cases associated with rubeosis iridis or glaucoma, a vitrectomy may be necessary to remove the standing blood in the vitreous.
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Define central retinal arterial occlusion
Central retinal artery occlusion (CRAO) is a disease of the eye where the flow of blood through the central retinal artery is blocked (occluded). There are several different causes of this occlusion; the most common is carotid artery atherosclerosis.
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Epidemiology of central retinal arterial occlusion
The incidence of CRAO is approximately 1 in 100,000 people in the general population
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Aetiology of central retinal arterial occlusion
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Atherosclerosis
Emboli
Giant cell arteritis
Dissecting aneurysms
Arterial spams
External eye compression (EG in spine surgeries in the prone position)
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RFs for central retinal arterial occlusion
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>50
Male
Smoking
HTN
DM
Dyslipidaemia
Angina
Valvular disease
Cancer
Hypercoagulable blood
FHx
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Additional risk factors include endocarditis, atrial myxoma, inflammatory diseases of the blood vessels, and predisposition to forming blood clots
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Causes:
Atherosclerosis
Emboli
Giant cell arteritis
Dissecting aneurysms
Arterial spams
External eye compression (EG in spine surgeries in the prone position)
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Sx of central retinal arterial occlusion
Central retinal artery occlusion is characterized by painless, acute vision loss in one eye
Upon fundoscopic exam, one would expect to find: cherry-red spot (90%) (a morphologic description in which the normally red background of the choroid is sharply outlined by the swollen opaque retina in the central retina), retinal opacity in the posterior pole (58%), pallor (39%), retinal arterial attenuation (32%), and optic disk edema (22%).
During later stages of onset, one may also find plaques, emboli, and optic atrophy.
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Ix for central retinal arterial occlusion
Upon fundoscopic exam, one would expect to find: cherry-red spot (90%) (a morphologic description in which the normally red background of the choroid is sharply outlined by the swollen opaque retina in the central retina), retinal opacity in the posterior pole (58%), pallor (39%), retinal arterial attenuation (32%), and optic disk edema (22%).
One diagnostic method for the confirmation of CRAO is Fluorescein angiography, it is used to examine the retinal artery filling time after the fluorescein dye is injected into the peripheral venous system.
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Rx of central retinal arterial occlusion
While no treatment has been clearly demonstrated to be benefit for CRAO in large systematic reviews of randomized clinical trials, many of the following are frequently used:
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Lowering intraocular pressure;
Dilating the CRA;
Increasing oxygenation;
Isovolemic hemodilution;
Anticoagulation;
Dislodging or fragmenting thrombus or embolus;
Thrombolysis; and
Hyperbaric oxygen.
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Prognosis of central retinal arterial occlusion
The artery can re-canalize over time and the edema can clear. However, optic atrophy leads to permanent loss of vision. Irreversible damage to neural tissue can occur after approximately 15 minutes of complete blockage to the central retinal artery, but this time may vary between people.
