Introduction
Age related
macular degeneration (AMD) accounts for almost 50% of those registered
as blind or partially sighted. 1-4 The development of management
strategies is limited by the diverse nature of the age related changes
and a lack of a clear understanding of the process of visual loss in the
elderly. Effective treatment is limited to the management of sub-retinal
neovascularisation (SRNV) in selected cases). Despite early expectations
that laser treatment might provide significant benefit in preventing blindness
5-7 recurrent disease and progressive visual failure limit the final outcome.
8-9. Early recognition and prevention of potential disease is not as yet
applicable to disease other than that related to SRNV.
The
aim of management is to minimise visual loss and disability in order to
maintain independence. The provision of visual aids, advice about lighting
and support in the home and community, with registration as necessary,
remain the mainstay of management.
The
purpose of these guidelines is, therefore, to define our current understanding
of the condition and to outline a management strategy (Appendix 1) that
may be adopted or modified, depending on local needs and facilities, by
ophthalmic services in the UK.
Definition
Despite
attempts to derive a classification and grading system for the disease
there is no fully accepted definition of age related macular degeneration.
The International Epidemiological Study Group 10 defines Age
Related Maculopathy (ARM) as a disorder of the macular area, most often
clinically apparent after 50 years of age, characterised by:
-
discrete
whitish-yellow spots identified as drusen.
-
increased
pigment or hyperpigmentation associated with drusen.
-
sharply
demarcated areas of depigmentation or hypopigmentation of the retinal pigment
epithelium and associated drusen.
These
age related changes with progressive accumulation of debris under the retina
predispose to late stage ARM identified as Age Related Macular Degeneration
(AMD) 11,12 which may be 'wet or dry' and feature:
-
geographic
atrophy of the retinal pigment epithelium with visible underlying choroidal
vessels.
-
retinal
pigment epithelial detachment with or without neurosensory detachment.
-
sub-retinal
or sub-pigment epithelial neovascularisation.
-
fibroglial
scar tissue, haemorrhages and exudates.
These
changes lead to progressive visual loss and worsening function in the elderly.
Epidemiology
Demography
Between
13,000 and 14,000 people are registered each year as blind or partially
sighted in England and Wales4 but it is difficult to determine
the total number of visually disabled people in the United Kingdom. There
are approximately 150,000 people aged 16 years and over living in private
households who are registered as visually disabled. This probably significantly
underestimates the true number that may be up to 1,000,00013
and closer to the 2.2% of the population over 65 years identified in the
Framingham Study3 as blind in one or both eyes from AMD.
The
incidence and prevalence of severe visual loss increases with age. 1,14
In 1997-8 3.7 million ophthalmic consultations were undertaken in England
15 60% of which will have involved people aged 60 or over. 16
In one study 14.1% of all visits to ophthalmologists by those over 65 were
for retinal problems. 17 Macular degeneration accounted for
the biggest single group. With the population over the age of 60 set to
increase by 45% in the next 20-25 years the increased load on both the
Health and Social Services and personal costs to the quality of life of
individuals affected by macular degeneration is daunting.
Risk
Factors
It is
usually held that AMD is most prevalent in Indo-European societies, 18
but it may be increasing in other communities. 19-22 Genetic
and environmental factors appear to modify the risk of visual loss although
the relative importance of these remains unclear. 23-30. Cigarette
smoking has recently emerged as a reasonably consistent risk factor. 31,32
Vascular disease and hypertension are sometimes associated with macular
degeneration but other associations such as light exposure 33
are not established risk factors. Dietary carotinoids, vitamin levels and
antioxidant use has not to date been shown to modify risk.34, 37
Prognosis
and Natural History
Conclusions
relating to the natural history of any condition will be dependent on the
population studied. Hospital-based studies include a substantial proportion
of patients for whom symptoms have prompted presentation, and who consequently
may be at greater risk of visual loss. Community derived studies should
provide a better reflection of the true risk and prevalence involved.
Drusen
For those
with bilateral soft drusen (ARM) seen in hospital the risk of progressing
to AMD with loss of vision in one eye appears to be in the order of 8%
per year over a three year period. 38,39 This risk is highest
in those with confluent drusen, focal hyperpigmentation or slow choroidal
perfusion on angiography. 40
Unilateral
AMD
With AMD-related
visual loss affecting one eye the risk of losing vision in the fellow eye
increases to between 7 and 10% annually. 41-43 The five year
risk is lowest in the absence of large drusen or pigment hyperplasia but
increases with one of these risk factors to 30% or with both to over 50%.
44
The highest risk is for those with a pigment epithelial tear in one eye
for whom the annual risk of second eye involvement is closer to 40%. 45
Pigment
epithelial detachment.
Pigment
epithelial detachment in patients under the age of 55 years is not usually
associated with significant visual loss 46,47 but occurring
in those over 55 is likely to result in visual loss within 4 years in the
majority of patients. 48 Such loss may reflect the presence
of neovascularisation under the detachment.
Sub-retinal
neovascularisation.
Sub-retinal
neovascularisation can occur throughout the fundus but rarely gives rise
to complications save in the macular area where it is associated with visual
loss. Angiographically well defined neovascular systems lying away from
fixation may on occasions be modified by treatment. If untreated, visual
loss may be rapid with neovascular extension under fixation in 75% of cases
within a year 6,7 such that 60% develop severe visual loss within
3 years. 9 Less well defined neovascularisation is considered
untreatable and grows more slowly, but still 40% develop severe visual
loss within 2 years. 49, 50 Juxta papillary lesions tend to
extend towards the macula but do not invariably cause visual loss as they
grow more slowly and may involute spontaneously.
The
location and angiographic characteristics of neovascular systems are used
in determining the approach to management. Away from the macula they are
described as peripheral or juxtapapillary. In the macula,
but lying more than 200 microns from fixation, they are defined as extrafoveal.
They are juxtafoveal or subfoveal when immediately adjacent
to, or under, the foveola. Neovascular systems with well defined leakage
seen on fluorescein angiography are described as classical and those
with ill defined leakage are considered occult. Some complexes are
mixed
with both classical and occult components.
Polypoidal
choroidopathy.
A form
of vascular change that may be confused with AMD has recently been described
in which haemorrhagic pigment epithelial detachments are associated with
angiographic varicose complexes at a choroidal level. These are best seen
on indocyanine angiography. The lesions of polypoidal choroidopathy 51-54
were first described in black middle aged women but can occur in any racial
group. Lesions may subside spontaneously or be associated with recurrent
haemorrhages leading ultimately to severe visual loss.
Management
Pathway
Despite
a growing interest in AMD the options for treatment remain limited. Treatment
is mainly targeted at the neovascular form of the disease using laser photocoagulation.
As the course of AMD, as opposed to ARM, can be highly variable, and the
final outcome dependent on the treatment and support offered it is appropriate
for an ophthalmologist with a special interest and experience in the care
of AMD to be involved from an early stage.
For
the majority of patients the main management option remains the provision
of low vision aids by the hospital or optometric services and community
support with partial sighted or blind registration as appropriate. The
provision of low vision care has been addressed in a separate College report
published in 1998. 55
The
value of routine screening, given the lack of effective treatment, is unproven.
There may be a case for self assessment, using an Amsler Grid, in those
patients with high risk of neovascular disease which includes those with
large soft drusen and pigment hyperplasia and those with established exudative
AMD in one eye.
Mild
low risk disease (ARM) requires no special management and, coming on slowly,
can be managed in the community. Optometrists would seem to be well placed
to carry out routine examinations and offer advice about the value of magnification
and lighting. Optometrists can reassure patients with minimal symptoms
or signs of ARM and should not refer further. Referral from the primary
sector usually occurs when visual impairment begins to interfere with normal
lifestyle. Referral is indicated when:
-
There
is rapidly developing visual failure but still reasonable vision suggestive
of exudative disease that might benefit from urgent assessment and laser
treatment.
-
There
is significant visual loss needing accurate diagnosis.
-
There
is significant visual loss needing partially sighted or blind registration.
General
practitioners and optometrists need to be aware of the urgent nature of
referrals for patients with recent onset of distortion and visual loss
(less than a month) and who still have reasonably good vision (6/12 or
better). 56 Such patients may still have treatable disease and
should be referred urgently to either the ophthalmic casualty department
or to the outpatient clinic following discussion with the local ophthalmologist.
This is particularly true for the second eye when the other eye is already
involved. In the elderly population with AMD concurrent ophthalmic disease,
such as cataract and glaucoma, may also frequently occur and needs to be
identified and treated appropriately.
The
management pathway will involve the following stages and it is important
that the resources and personnel to achieve these are properly funded:
-
Diagnosis
and assessment of macular disease including angiography and exclusion of
other treatable causes of visual failure.
-
Treatment
by laser photocoagulation or otherwise as appropriate.
-
Rehabilitation
including:
a) provision
of suitable optical aids in the primary or secondary sector and training
in their use.
b)
Completion when appropriate of the form BD8 (BP1 in Scotland, A 655 in
Northern Ireland) and referral to Social Services (Appendix 2).
c)
Counselling and rehabilitation within the hospital and statutory or voluntary
services in the community.
Diagnosis
and assessment
History
Pointers
to macular degeneration include recent change in visual function particularly
affecting reading, face recognition and difficulties with change of lighting.
A dark patch that rapidly fades may also be recognised on waking. Distortion
is a feature of macular disease in contrast to the ghosting, doubling or
multiplication of images associated with cataract. If the change is recent
and rapid, sub retinal fluid associated with neovascularisation is often
the basis for the disturbance. This is in contrast to the gradual decline
that reflects developing atrophy.
Examination
Snellen
distance acuity and near vision should be recorded. The corrected Snellen
acuity does not normally improve with the use of a pin hole in macular
disease. Amsler grid examination reflects change lying within the upper
and lower temporal arcade vessels, identifies the areas of involvement
and establishes a base line for future comparison. Slit lamp fundus examination
of both eyes, usually with an indirect or contact lens, confirms the diagnosis
and provides clues as to the location of any neovascularisation. Such clues
will include small areas of sub-retinal fluid, exudate, haemorrhage or
pigment epithelial elevation. The presence of co-existing conditions such
as cataract, glaucoma and corneal disease should be sought.
Angiography
and colour photography.
Fluorescein
angiography, which is available in 96.4% (189 out of 196) of UK eye departments
recently surveyed, 57 will confirm the findings and provide
the basis for subsequent management. it is usually performed by a trained
ophthalmic photographer. Whilst colour photography alone may suffice as
a clinical record intravenous fluorescein angiography is indicated when:
-
There
is a need to confirm the diagnosis of exudative macular degeneration as
suggested by the symptoms and clinical findings.
-
There
is a need to define the exact location of any neovascular tissue and, if
well defined (classical), to determine the precise area to be treated by
laser photocoagulation.
-
There
is a need to detect persistent or recurrent neovascular tissue following
previous laser treatment. Sometimes this may be needed to reassure an anxious
patient fearing further neovascular growth.
-
There
is unexplained visual loss requiring further evaluation.
Angiography
may also be justified to provide permanent records and for teaching or
research but should only be undertaken with fully informed consent and
due consideration of the risks.
The
risks of fluorescein angiography 58 should be borne in mind,
particularly when assessing individuals with a history of atopy or a previous
reaction to the dye. Apart from the yellowing of the skin and urine, about
one in ten suffer some nausea and retching. The more serious complications
of anaphylaxis and collapse are much rarer occurring in less than 1 in
2,000. Death, whilst extremely rare, is reported in one in 1-200,000. Staff
should be trained in basic life support and emergency drugs should be readily
available in the photography department.
It
is appropriate that information is available to patients undergoing angiography
preferably in accessible leaflet form (currently available in 123 departments
or 68%). An example is seen in Appendix 3. Whilst the provision of information
is probably more important, the issue of signed consent (obtained in 1998
in 118 UK departments or 62.4%/)57 must be considered and agreed
with the Trust concerned.
Intravenous
fluorescein injection can be done by anyone designated to do so, subject
to certification of competence, provided the ophthalmologist is responsible
for ordering the test and for ensuring that all reasonable safety precautions
are observed. The use of nurses may provide opportunities to streamline
an angiographic service making it more accessible and effective. Nurse
led fluorescein administration was performed in 57 departments in 1998
(30.1%).
Angiography
should be available with a minimum of delay particularly given the rapid
growth potential of any neovascular lesion. As the angiographic features
may progress rapidly, laser treatment should be undertaken within 48 hours
of the latest angiogram if at all possible. Time savings in obtaining an
early angiogram for study will be achieved by the use of digital rather
than conventional angiography (available in 35 UK departments in 1998).
Whilst the capital outlay may be higher, the saving on photographic time
and consumables will be considerable and there is the added advantage that
angiograms are immediately available. Such a digital system will also attract
other uses for research and teaching, and may be adapted for indocyanine
angiography.
Indocyanine
angiography has a role in the assessment of vascular systems under the
pigment epithelium which may be ill defined on fluorescein angiograph,
and in the assessment of the particular condition of polypoidal choroidopathy.59
How far it results in benefit in terms of management remains controversial.60
If an iodine based dye is used allergy to iodine and shellfish should be
excluded before its use.
It
is normal to photograph the central 30 degrees centred on the macula, and
all angiography should include views of the second eye. This will allow
for comparison in respect of the disease involved and help to exclude other
unidentified problems. Stereo photography offers a definite advantage in
the clinical information gained and can be achieved by the use of a stereo
separator or by displacing the camera from side to side during the study.
Colour
photography is routinely undertaken with angiography. It helps to determine
the nature of changes seen of the angiogram particularly in defining exudative
change and the cause of blocked fluorescence due to haemorrhage, pigment
or other cause. Drusen are sometimes much more visible on angiography than
colour photography and vice versa.
ii.
Treatment
Choroidal
neovascularisation is a major cause of visual loss in AMD and one that,
when well defined, may be amenable to treatment. Effective treatment protocols
for laser photocoagulation have been published 5-7 but treatment can be
difficult and better undertaken by an ophthalmologist who has a special
interest and experience in managing such lesions. Pending the confirmed
results of the current prospective treatment trials of radiation and photodynamic
therapy (PDT), and their approval for use if appropriate, the mainstay
of interventional treatment is that of laser photocoagulation. When first
seen, unfortunately, most eyes with choroidal neovascularisation have poorly
defined complexes and are untreatable.49,61 Argon, or equivalent lasers,
are almost universally available in UK eye departments (98.9%). The green
argon wavelength (514mu) or yellow (577nm) is used to avoid unnecessary
lutein uptake and retinal damage. Yellow light has the advantage of being
transmitted more predictably through a nuclear sclerotic lens.
Laser
photocoagulation.
In 1982
three studies showed treatment benefit from argon laser photocoagulation
when a well defined neovascular complex lay outside 200 microns from fixation.
5-7
This is most likely to be the case when the visual acuity is still good
(6/12 or better) and the duration of symptoms short (less than a month).56
Such situations are, however, rare and occur in only 5-10% of those seen.
61 Despite the initial hopes of treatment it is now recognised
that continued growth of the membrane and recurrent disease are major limiting
factors for success and occur in about 50% within 5 years after initial
successful treatment. 8,9,56
Some
patients with juxta and sub foveal membranes may benefit from treatment
62-64
Sub foveal treatment produces a marginal benefit at 12 months and a maximal
one at 24 months. As treatment destroys the fovea there is an immediate
fall in visual acuity that often makes this treatment unacceptable. Any
benefit from treating juxtafoveal lesions is limited by their tendency
to continue growing. Polypoidal choroidopathy may benefit from treatment
and the recurrence of haemorrhage leading to visual loss may be prevented.
Any of these treatments should, therefore, only be carried out after careful
consideration, detailed explanation and counselling.
Pigment
epithelial detachments do not usually benefit from laser treatment 65
Treatment is frequently complicated by rapid visual loss associated with
a pigment epithelial tear or rapid progression of an unrecognised neovascular
response. A few neovascular lesions outside the detachment itself or within
the 'notch' have been shown to respond favourably to focal laser treatment.66
Pigment epithelial detachments occurring in patients under the age of 55
do not require treatment as the prognosis is good.46, 47
Neovascularisation
can progress with great rapidity resulting in significant visual loss even
within a few days.67 If, on the basis of new symptoms or clinical
examination, choroidal neovascularisation is suspected fluorescein angiography
should be performed urgently and interpreted with a minimum of delay to
avoid the risk of irreversible damage and a lost opportunity for laser
treatment. 67,68 Well defined extrafoveal neovascularisation
should be photocoagulated following careful explanation of the implications
and expectations of treatment that, it is hoped, will reduce, but not eliminate,
the risk of severe visual loss. The treatment scotoma produced and possibility
of further visual loss should be discussed.
There
is evidence from controlled trials that lesions with the characteristics
below can benefit from treatment:
-
Classic
extraffiveal neovascularisation located 200 microns from fixation.
-
Sub foveal
complexes of less than 1 disc area and with vision of less than 6/24. As
any treatment benefit is only fully achieved at 24 months, most ophthalmologists
feel that treatment is not justified given the immediate loss of vision
produced.
Some juxtapapillary
complexes and lesions of polypoidal choroidopathy may also benefit from
treatment. juxtafoveal and sub foveal lesions are treated only after careful
consideration.
The
recommended treatment protocol usually involves:
-
Heavy
confluent laser photocoagulation (514nm or 577nm) covering the whole of
the angiographic lesion and a margin of 100 microns around it.
-
Laser
power setting and duration to achieve an intense white coagulum.
-
A planned
sequence of burns around and onto the lesion avoiding other structures.
-
Location
of the initial burns to minimise the risk of movement causing an exclamation
mark burn up to fixation .
Treatment
may require long burns and at a high power level to ablate the membrane
adequately. Retrobulbar anaesthesia to reduce extraneous movement is not
usually needed and may require the presence of an anaesthetist. Injection
complications which, whilst rare, can be serious.69 Monitoring
by pulse oximetry and intravenous access are necessary in view of the low
but significant risk of cardio-respiratory collapse70.
Recurrent
disease remains the main obstacle to successful management with figures
of 10% at 1-2 months, 21% at 3 months increasing to 42% at a year and 53%
at 3 years being reported.8,9 The optimal review interval following
laser treatment is uncertain but the first visit usually occurs at two
to three weeks. Clinical examination and angiography are performed at this
visit with further treatment if necessary although the best results occur
when the first treatment is successful. Thereafter the review intervals
increase provided the situation is stable (e.g. 6 and 12 weeks and 3 monthly
thereafter). Repeat angiograms are needed if membrane persistence or recurrence
is suspected.
Patients
should be made aware of the risk of recurrent disease particularly in the
first year. A patient's observation of subjective change or on the Amsler
Grid should not be overlooked as it may indicate recurrence.71
Patients should have easy return access to the ophthalmologist both for
their treated eye but also for the other eye which is at significant risk41,43
of similar disease. Patients are also more likely to present earlier should
disease in the second eye occur at which stage a developing lesion may
be more amenable to treatment. Patients and all staff should be aware of
this and direct access may be needed to avoid missed treatment opportunities.
Newer
treatments.
More recently
a number of alternative managements have been proposed and have or are
being subjected to clinical trial. These include:
-
Alpha
interferon which was not shown to be beneficial in a controlled study.
72-76
-
Photodynamic
therapy using a photosensitising dye has been subject to a multicentre
prospective study.77-82 The findings imply some improvement
in visual outcome at one year if more than 50% of the neovascular complex
is classical. The high costs of this treatment may not prove generally
acceptable and will be subject to considerable further discussion.
-
Ionising
radiation by external beam application is the subject of several studies.
83-86
-
Surgical
removal may have some value in idiopathic disease and that associated with
the presumed histoplasmosis syndrome but much less so for membranes associated
with AMD.87-90 Although some authors have reported benefit from
surgery good reading facility is rarely achieved.
-
Surgical
translocation of the central retina with simultaneous membrane ablation
is subject to ongoing study.
-
Vitamin
and dietary supplements including the use of zinc and selenium that have
not proved helpful. 36,37,91,92
-
Prophylactic
laser treatment causes the disappearance of drusen but has also been shown
to provoke neovascular complications.93-100 It is undergoing
further evaluation in multicentre clinical trials.
Management
of co-existing disease.
Macular
degeneration may co-exist with other conditions. Studies have shown that
both AMD and cataract are common in the elderly each being present in almost
half of those over the age of 75.101 It is not surprising that
for about a quarter of the population both coexist. Given the changes in
threshold for cataract surgery 102 such surgery is not always
contraindicated in the presence of macular degeneration. The improved clarity
and illumination can be significant even if central acuity remains affected.
There is, however, a small risk of the neovascular process being accelerated
by surgery that should be kept in mind.103
Similarly
aggressive glaucoma treatment may be justified to forestall peripheral
field loss adding to the central failure. The constraints of clinical governance
should not prevent surgery being offered with each clinical situation being
judged and managed on its own merits.
iii)
Rehabilitation
All patients
losing vision due to AMD will suffer significant loss of independence
be it through the inability to drive, to read or to manage their own affairs.
The early provision of advice and support will encourage independence and
minimise the socio economic isolation that AMD causes. Care in the community
involving the family, statutory social services, patient or disease centred
voluntary services is, therefore, vital. Often but, not invariably, this
is triggered by visual handicap registration. The pattern of help available
around the country is very variable and the attention given to sight loss
in community care plans diverse.104 There is a need for greater
public awareness of AMD and a more uniform standard of care in which ophthalmologists
must have a central role working with the statutory and voluntary sectors
to achieve this.
Provision
of low vision aids.
Arrangements
for the provision of low vision aids and initiation of rehabilitation should
be integral to the advice and care provided by an ophthalmologist. The
recent College document55 on the provision of low vision care
has defined a person with low vision as someone 'who with a normal correction
is not able to perform those visual tasks needed for vocational, avocational
and social needs'. Almost all patients suffering visual loss due to AMD
may be helped by visual aids. Optical aids involve high powered reading
additions, magnifiers, illuminated magnifiers and telescopes. Electronic
aids include closed circuit television or specialised adaptations of existing
systems e.g. computer software. Non-optical aids include lights and typoscopes.
Different
models of low vision aid provision exist around the country involving ophthalmologists,
optometrists and low vision therapists?55 In 1998 178 eye units
in the United Kingdom (90.8%) had some form of low vision aid service.
The remainder had access to local providers. Nationally the availability
of LVA services in general was very uneven when surveyed in 1999.105,106
Patient acceptance and improved ability in the use of aids has been demonstrated
when full support and training are given. A range of aids may be needed
to meet specific tasks. It is not adequate to issue a patient with a magnifying
aid and not provide sufficient after care.
Patients
trained in eccentric fixation and the use of better lighting can greatly
improve their reading ability. 107
Specialist
low vision centres, within or outside hospitals, will be staffed by a multidisciplinary
team to assess the low vision and the daily living skills needed. A simpler
hospital service involves a visiting low vision therapist who will provide
and explain the use of low vision aids and advise on eccentric viewing
and lighting. The problems of daily living skills and rehabilitation can
also be addressed in a limited fashion. Optometrists in high street practice
and some social service and voluntary organisations offer similar provision
and advice about aids which will depend on local organisation, interest
and skills.
Recently
a framework document from the Low Vision Services Working Group108
has
proposed the establishment of Low Vision Services Committees at a local
level to address the fragmentation of current services and stimulate multi-disciplinary
working to improve communication and differences in care.
Visual
handicap registration.
The number
of blind people in Britain has been counted since 1851 starting with a
simple declaration of blindness on census returns. Ophthalmologists now
have a vital role in identifying those with visual handicap (Appendix 2)
and initiating the process of visual handicap registration by social services
leading to access to the statutory services and allowances available. The
form BD8 in England and Wales, BP1 in Scotland and A655 in Northern Ireland
also provide the basis for analysis of the causes, incidence and prevalence
of visual handicap across the country.
The
social and economic benefit to society must be substantial if independence
is maintained. When treatment has not proved possible or effective, there
are two aspects to rehabilitation. These consist of firstly maximising
the residual vision, often employing low vision aids, and secondly providing
education and training to enable the patient to lead as normal a life as
possible within the limits of the disease. No firm data, however, exist
as to the costs and benefits of good management.
Training
and coping strategies.
Coming
to terms with chronic visual disability either as a result of untreatable
disease or following unsuccessful treatment is a depressing and arduous
process. Patients with severe visual loss due to AMD often have unrealistic
expectations and some patients never adjust to their disability.
Explaining
the management of AMD requires patience and sympathy. Patients with AMD
greatly benefit from continuing support and information about their condition
and all patients losing vision need hope and encouragement. When no specific
treatment is available it should be emphasised from the beginning that
peripheral vision will be maintained and that there is no harm in using
the eyes. Advice with regard to the future prognosis should be an integral
part of the management. Often great anxiety with its attendant risk of
depression can be relieved by understanding that complete blindness does
not occur as a result of AMD.
Utilisation
of existing vision can be greatly enhanced by ensuring that objects are
bigger, brighter and bolder and that contrast is increased. This may be
achieved by such devices as angle poise lamps, larger print and the use
of felt tipped, rather than ball point, pens. Liquid level indicators,
markers for cooker dials, free directory enquiries, enlarged telephone
dial numbers are available as are large print books, bank statements, talking
books, newspapers and clocks.
Mobility
is aided with the use of either symbol or guide canes and can improve confidence
outside the patient's home. Guide dogs are rarely of benefit for patients
with AMD although they are entitled to apply for one. A home visit from
a low vision therapist will often provide the basis for useful advice.
Statutory
and voluntary support services in the community.
The changes
associated with care in the community and boundary changes have altered
the role of the statutory social services. They and the new primary care
groups or their equivalent now have a greater role as the purchasers of
care. Training and rehabilitation courses for those recently registered
as visually handicapped and others with vision difficulties are provided
by social services and blind associations . Such courses will include the
elements of a low vision rehabilitation service.
Further
support and advice are available in information documents, tapes and large
print material from the national organisations such as the Royal National
Institute for the Blind or from local charitable blind associations. Disease
focused societies such as the Macular Disease Society provide a useful
source of information for those affected by AMD. A list of a number of
these bodies is in the appendix 4. With the predicted increase in the older
population over the next 20 years the effect of macular degeneration remains
daunting. The greater co-operation developing between all those involved
provides the hope of a more focused and effective service in the future.
Appendix
1
Goals
and objectives for the management of macular degeneration
The
development of clinical guidelines and good practice statements provide
a basis for clinical governance and for measurement of practice and its
audit.
The
following should be the national aim of an effective service.
-
Good patient
data with regard to risk factors and disease characteristics.
-
Recognition
by the purchasers of service (Primary Care Groups or their equivalent)
of the significance of sight loss and its amelioration by treatment and
support.
-
An improved
patient and public awareness of macular degeneration and the pointers to
its development.
-
Even access
to care across the country~ Such care should enable the early recognition
of impending disease within the primary sector and its early referral to
achieve optimal treatment benefit.
-
Timely
response within the ophthalmic community to minimise the visual morbidity
resultant from macular degeneration. This may, in turn, demand concentration
of resources both in terms of equipment and ophthalmic and other personnel.
The following
should be objectives for the management of an individual patient and could
provide the basis for audit.
Suspicion
of developing AMD:
-
Urgent
referral if there is recent onset of distortion and dropping vision. A
telephone call may be needed to determine urgency in individual cases.
A patient at risk should be seen as soon as possible and preferably within
a week if a neovascular membrane that might be treatable is suspected.
-
Referral
resulting in ophthalmic assessment within 3 months for non urgent cases
with the identification of any other disease or specific risk factors.
Management
of a treatable neovascular complex:
-
Examination
by an ophthalmologist with knowledge and experience in the care of patients
with AMD.
-
Fluorescein
angiography to be reviewed and used as the basis for treatment.
-
Careful
explanation and counselling.
-
Laser
treatment within 48 hours of the angiogram, if at all possible. Delay after
this time may necessitate further angiography to exclude progression.
-
Review
2 - 3 weeks following laser treatment with repeat anglogram and if needed
re-treatment. Review thereafter is as appropriate.
Management
of untreatable AMD in one eye or following unsuccessful treatment:
-
Careful
explanation by the ophthalmologist at the time of diagnosis as to the nature
of the problem.
-
Advice
and counselling about risks for the other eye and how to identify developing
disease.
-
Indication
as to how to obtain further information and how to seek urgent help should
the second eye become involved.
Management
of bilateral untreatable AMD:
-
Careful
explanation by the ophthalmologist at the time of diagnosis as to the nature
of the problem.
-
Advice
and counselling about future visual function and an indication as to how
to obtain further information.
-
Early
visual handicap registration and referral for low vision aid assessment
within 13 weeks or earlier as appropriate.
-
Provision
of advice and support in the community at an early stage in keeping with
local arrangements. This should follow an initial contact or visit being
made by Social Services, or voluntary agency for the blind, within a month.
It is
essential that a full assessment of need is undertaken and the appropriate
support provided. It is likely that the patient will need to be seen and
visited at home to achieve this.
Appendix
2
Criteria
for recommendation for partially sighted or blind registration 109
Partially
sighted:
There
is no legal definition of partial sight. The guidelines are that a person
can be certified as partially sighted if they are:
Substantially
and permanently handicapped by defective vision caused by congenital defect
or illness or injury.
As
a general guide this will apply when the following apply:
-
3/60 to
6/60 Snellen with a full field.
-
Up to
6/24 Snellen with moderate contraction of the field, opacities in media
or aphakia.
-
6/18 Snellen
or better if there is a gross field defect, for example hemianopia, or
if there is marked contraction of the visual field, for example in retinitis
pigmentosa or glaucoma.
Blindness:
The
National Assistance Act 1948 says that a person can be certified as blind
if they are: So blind that they cannot do any work for which eyesight
is essential.
This
will generally apply when:
-
The visual
acuity is below 3/60.
-
The visual
acuity is between 3/60 and below 6/60 when there is a very contracted visual
field.
-
The vision
is 6/60 or better when there is a very contracted visual field especially
if the contraction is in the lower part of the field.
Other
points to consider relate to how recently the person's eyesight has failed
and the person's age at which the eyesight failed.
Appendix
3
The following
is a suggested outline describing fluorescein angiography, Headings should
be boxed. The text should be in a font size of 16 and in bold to facilitate
reading.
What
is fluorescein angiography?
This
is a simple test to give your doctor more information about the condition
of the back of your eye. It helps decide the best form of treatment or
management.
What
does the test involve?
When
you arrive at the out-patient department your eyes will be tested. You
will be asked a few questions about your general health. Drops will be
put into both eyes to dilate your pupils. The drops may blur your vision
for a short time. It is, therefore, advisable that you do not drive yourself
for the appointment. It is important that you let us know if you have any
allergies, or if you have had an unwanted reaction to fluorescein before,
Once
your pupils are dilated you will be taken into the Angiography room. Photos
will be taken of the back of your eye using a special camera. Then a small
amount of dye will be injected into a vein in your arm. Within seconds
the dye travels in your blood to the blood vessels in your eye. Your eye
is then is photographed to give more information about the condition of
the back of your eye. No X-rays or radioactive substances are used. The
eye is not touched during the test. The actual test takes about 10 to 15
minutes. Following the test we ask you to stay in the department for about
1/2hour to check that you do not have any side effects and are all right
to go home. If you are elderly or have a long way to come it is advisable
to bring someone with you.
Would
it be all right to have the test if 1 am on tablets?
Yes,
it is all right to take any tablets or medicines as usual on the day of
the test.
Is
it all right to eat and drink before the test?
Yes,
you can cat or drink what you like before the test.
Are
there any side effects?
The
dye will give your skin a yellow tinge and your urine will be bright yellow
for one or two days. There may be some blurring of vision caused by the
drops and some dazzle from the camera flash. One in ten patients feels
slightly sick or short of breath but the feeling rarely lasts more than
a few seconds. If, in rare cases, patients have severe breathing or circulatory
difficulties the emergency team will be called. Although extremely rare,
a few deaths have been reported in the past.
When
will 1 know the results?
You
may not be given the results of the test straight away. The results will
be given to you at your next appointment. Please check that you know when
your next appointment is. Staff in the department will be happy to assist
you.
Appendix
4
Some useful
addresses:
Local
Blind Associations.
Addresses
should be obtainable locally or through the RNIB
Royal
National Institute for the Blind,
224,
Great Portland Street,
London,
WIN LAA
0207
388 1266
The
Guide Dogs for the Blind Association.
Hillfields,
Burghfield,
Reading, Berks, RG7 3YG
01734
835555
The
Macular Disease Society,
13a
Bridge Street,
Andover,
Hampshire, SP10 1BE
0845
241 2041
The
Partially Sighted Society,
Queens
Road,
Doncaster,
South Yorkshire, DN1 2NX
01302
323132
National
Association for the Education, Training and Support of Blind and Partially
Sighted People (OPSIS).
Court
Oak Road,
Harborne,
Birmingham, B17 9TG
0121
428 5037
Talking
Newspaper Association of the UK,
National
Recording Centre,
Heathfield,
East Sussex, TN21 8D13
01435
866102
Calibre,
Aylesbury,
Bucks,
HP22 5XQ
01296
432339
RNIB
Talking Book Service
Mount
Pleasant
Wembley,
Middx HAO I RR
0208
903 6666
A list
of the independent services available for the blind and visually impaired
is available from the Royal College of Ophthalmologists.
Appendix
5
Glossary
of terms:
Age
Related Maculopathy (ARM):
A
disorder of the macular area, most often clinically apparent after 50 years
of age, and characterised by:
-
discrete
whitish-yellow spots identified as drusen.
-
increased
pigmentation or hyperpigmentation associated with drusen.
-
sharply
demarcated areas of depigmentation or hypopigmentation of the retinal pigment
epithelium and associated drusen.
Age-Related
Macular Degeneration AMD (ARMD):
There
is no universally accepted definition of this term. The late stages of
ARM are identified as Age Related Macular Degeneration (AMD) which may
be 'wet or dry' and feature:
-
geographic
atrophy with visible underlying choroidal vessels.
-
pigment
epithelial detachment with or without neurosensory detachment.
-
sub-retinal
or sub pigment epithelial neovascularisation.
-
fibroglial
scar tissue, haemorrhages and exudates.
These
changes lead to progressive central visual loss and worsening function
in the elderly.
Disciform
Scar:
Sub-retinal
fibrovascular tissue, often part of the healing response following choroidal
neovascularisation.
Drusen:
Yellowish
excrescences external to the retinal pigment epithelium that are well defined
small deposits (hard drusen) or ill defined deposits (soft drusen) lying
between the basement membrane of the retinal pigment epithelium and Bruch's
membrane. Drusen are the ophthalmoscopic and histological hallmark of age-related
change at the level of Bruch's membrane. They may be discrete, sub-confluent
or confluent in configuration.
Extrafoveal
Choroidal Neovascularisation:
Choroidal
neovascularisation that is no closer than 200 microns from the centre of
the foveal avascular zone as judged by fluorescein angiography.
Exudative
Macular Degeneration:
Manifestations
of choroidal neovascularisation and/or pigment epithelial detachment in
a patient with AMD and may be referred to as being 'wet'.
Geographic
Atrophy:
One
or several areas of well demarcated zones of apparent atrophy of retinal
pigment epithelium. Drusen are usually present as well and are often crystalline.
Juxtafoveal
Neovascularisation:
Choroidal
neovascularisation that is closer than 200 microns from the centre of the
foveal avascular zone but that does not reach the centre of the foveal
avascular zone.
Macular
Photocoagulation Study (MPS):
A
series of ongoing multicentre clinical trials funded by the National Eye
Institute that are investigating the value of laser photocoagulation for
patients with exudative AMD.
Non-exudative
Macular Degeneration:
Macular
changes characterised by drusen, pigment changes and atrophy but not serous
elevation of the neuroretina associated with choroidal neovascularisation
or pigment epithelial detachment.
Pigment
Epithelial Detachment:
Accumulation
of fluid ('serous pigment epithelial detachment') or blood ('haemorrhagic
pigment epithelial detachment') beneath the retinal pigment epithelium.
Associated choroidal neovascularisation is usually present in older patients.
Retinal
Pigment Epithelial Changes:
These
are either i) atrophic changes of the pigment epithelial-Bruch's membrane
complex that lead to an appearance of hypopigmentation, or ii) hyperplastic
changes of the retinal pigment epithelial-Bruch's membrane complex that
lead to an appearance of hyperpigmentation.
Soft
Drusen:
These
drusen are larger than hard drusen and usually have ill-defined, non-discrete
margins. Histologically, these represent diffuse deposits lying between
the basement membrane of the retinal pigment epithelium and Bruch's membrane.
They are often sub-confluent or confluent in their distibution.
Subfoveal
Choroidal Neovascularisation:
Choroidal
neovascularisation that involves the centre of the foveal vascular zone.
References
1. Grey
RHB, Burns-Cox CJ, Hughes A. Blind and partially sighted registration in
Avon. Br J Ophthalmol 1989: 73: 988-94.
2.
Thompson JR, Rosenthal AR. Recent trends in the registration of blindness
and partial sight in Leicester. Br J Ophthalmol 1989; 73: 95-9.
3.
Leibowitz HM et al: The Framingharn Eye Study Monograph; an ophthalmological
and epidemiological study of cataract, glaucoma, diabetic retinopathy,
macular degeneration, and visual acuity in a general population of 2631
adults, 1973-1975. Surv Ophthalmol (suppl) 1980; 24:335-610.
4.
Evans J. Causes of blindness and partial sight in England and Wales 1990-1991.
Studies on medical and population subjects No. 57. London, Her Majesty's
Stationery Office, 1995.
5.
Coscas G. Soubranne G. Photocoagulation des neovaisaux souretiensdlans
le degenerescence maculaire senile par laser a argon: resultas d'une etude
randomisee de 60 cas. Bull Mern Soc Fr Ophthalmol 1982; 88: 102- 6.
6.
Macular Photocoagulation Group. Argon laser photocoagulation for senile
macular degeneration: results of a randomised clinical trial. Arch Ophthalmol
1982; 100: 912-8.
7.
Moorfields Macular Study Group. Treatment of senile macular degeneration;
a single blind randomised trial by argon laser photocoagulation. Br J Ophthalmol
1982; 66: 745-53.
8.
Chisholm IFL The recurrence of neovascularisation and late visual failure
in senile disciform lesions. Trans Ophthalmol Soc UK 1983; 103: 354-9.
9.
Macular Photocoagulation Study Group: Argon laser photocoagulation for
neovascular maculopathy: three year results from randomised clinical trials.
Arch Ophthalmol 1986; 104: 694-701.
10.
The International ARM epidemiological Study Group. An International C Classification
and grading system for age-related maculopathy and age related macular
degeneration Surv. Ophthalmol. 1995 39 367-374
11
Gass JDM. Pathogenesis of disciform detachment of the neuro-epithelium.
3. Senile disciform macular degeneration. Am J Ophthalmol 1967; 63: 617-44.
12.
Sarks SH: Drusen and their relationship to senile macular degeneration.
Aus J Ophthalmol 1980; 8117-130.
13.
Bruce I. McKennell A. Walker E. Blind and partially sighted adults in Britain:
the RNIB Survey Vol 1 p 43-4. London HMSO 1991
14.
Gafour M, Allan D, Foulds WS. Common causes of blindness and visual handicap
in the West of Scotland Br J Ophthalmol 1983 67209-213
15.
Korner KH09 Out Patient Attendance Activity and Accident and Emergency
Services Activity. Published in Out Patient and Ward attendances, England.
Financial year 1997-8. Published by Department ofHealth, prepared by the
Government Statistical Services.
16.
Shaw DE, Gibson JM, Rosenthal R. A year in a general ophthalmic out-patient
department in England. Arch. Ophthalmology 1986 104 1843-46
17.
Ellwein LB, Friedlin V, McBean AM, Lee PP Use of Eye Care Services among
the 1991 Medicare population. Ophthalmology 1996 103 1732-43
18.
Gregor Z. Joffe L. Senile macular changes in the black African. Br J Ophthalmol
l978;62:547-550.
19.
Kubo N. Ohno Y. Yanagawa H. Yuzawa M, Matsui M, Uyama M. Annual estimated
number of patients with senile disciform macular degeneration in Japan.
Research committee on chorioretinal degenerations. The Ministry of Health
and Welfare of Japan.1989; 136-139.
20.
Kubo N. Ohno Y Yuzawa, M, et al. Report on Nationwide clinico-epidemiological
survey of senile disciform macular degeneration in Japan. Research committee
on chorioretinal degenerations. The Ministry of Health and Welfare of Japan.
1990, 121-124.
21.Yuzawa
M, Hagita K, Egawa T. Minato H. Matsui M. Macular lesions predisposing
to senile disciform macula degeneration. Jpn J Ophthalmol. 1991; 35, 87-95.
22.
Maruo T. Ikebukuro N. Kawanabe K, Kubota N. Changes in causes of visual
handicaps in Tokyo Jpn J Ophthalmol. 1991, 35, 268-272.
23.
Hyman
LG, Lilienfeld AM, Ferris FL, Fine SL. Senile macular degeneration: A case-control
study. Am J Epidemiol 1983; 118:213-27.
24.
Delancy W Oates R. Senile macular degeneration: A preliminary study. Aim
Ophthalmol 1982; 14:21-4.
25.
Kahn HA, Leibowitz MM, Ganley JP, Kini MM, Colton T. Nickerson RS, et al.
The Framingham Eye study.11. Association of ophthalmic pathology with single
variables previously measured in the Framingham Heart Study. Am J Epidemiol
1977; 106:33-4 1.
26.
Maltzman BA, Mulvihill MM, Greenbaum A. Senile macular degeneration and
risk factors: a case-control study. Am Ophthalmol 1979; 11: 1197-1201.
27.
Piguet B. Wells JA, Palmvang IB, Wormald R. Chisholm IH Bird AC. Age-related
Bruch's membrane change: a clinical study of the relative role of heredity
and environment. Br J Ophthalmol 1993; 77: 400-3.
28.
Heiba IM, Elston RC, Klein BEK, Klein R. Sibling correlations and segregation
analysis of age-related maculopathy: The Beaver Dam eye study. Genet Epidemiol.
1994; 11: 51 -67.
29.
Silvestri TG, Johnson PB, Hughes AE. Is genetic predisposition an important
risk factor in age-related macular disease? Eye 1994; 8: 564-568.
30.
Klein ML. Mauldin WM. Stoumbos VD. Heredity and age-related macular degeneration.
Observations in monozygotic twins. Arch Ophthalmol. 1994; 112: 932-937.
31.
Seddon JM, Willett WC, Speizer FE, Hackinson SE. A prospective study of
cigarette smoking and age-related macular disease in women. JAMA. 1996,
276: 1141-1146.
32.
Smith W Mitchell P Leeder SR. Smoking and age-related maculopathy. The
Blue Mountain eye study. Arch Ophthalmol. 1996; 114:1518-1523.
33.
Rozanowska, M, Jarvis-Evans J. Korytowski W Boulton, ME, Burke J.M, Sarna
T. Blue light-induced reactivity of retinal age pigment. In vitro generation
of oxygen-reactive species. J Bio Chem. 1995; 27: 18825-18830.
34.
Seddon JM, Ajam UA, Sperduto RD, et al. Dietary carotenoids, Vitamins A,C
and E and advanced age related macular degeneration. JAMA 1994; 272: 1413-1420.
35.
Mares Perlman JA, Brady WE, Wein R; et al. Scrum antioxidants and age-related
macular degeneration in a population based case-control study. Arch Ophthalmol.
1995; 113: 1518-1523.
36.
Evans JR. Antioxidant vitamin and mineral supplements for age related macular
degeneration (Cochrane Review). In The Cochrane Library; Issue 4 1999.
Oxford: Update Software.
37.
Evans JR, Henshaw K. Antioxidant vitamin and mineral supplementation for
preventing age related macular degeneration (Cochrane Review). In The Cochrane
Library, Issue 4 1999. Oxford Update Software.
38.
Smiddy WE, Fine SL: Prognosis of patients with bilateral macular drusen.
Ophthalmology 1984; 91:271-277.
39.
Holz FG, Wolfensberger TJ, Piguet B. Gross-Jendroska M, Wells JA, Minassian
DC, Chisholm IH, Bird AC. Bilateral macular drusen in age-related macular
degeneration: prognosis and risk factors. Ophthalmology 1994, 101: 1522-8.
40.
Piguet B. Palmvang IB, Chisholm 1H, Minassian D, Bird AC. Evolution of
age related macular degeneration with choroidal perfusion abnormality Am
J Ophthalmol 1992; 113:657-63
41.
Gregor Z. Bird AC, Chisholm IH: Senile disciform macular degeneration in
the second eye. Brj Ophthalmol 1977; 61:141-7.
42.
Bressler SB et al: Natural course of choroidal neovascular membranes within
the foveal avascular zone in senile macular degeneration. Am J Ophthalmol
1982; 93:157-163.
43.
Shrahlman E, Fine SL, Hillis A: The second eye of patients with senile
macular degeneration. Arch Ophthalmol 1983; 101: 1191-93.
44.
Bressler SB et al for the Macular Photocoagulation Study Group: Drusen
characteristics and risk of exudation in the fellow eye of argon SMD patients
in the Macular Photocoagulation Study. Invest Ophthalmol Vis Sci (suppl)
1989; 30:154.
45.
Schooppner G. Chuang EL, Bird AC. Retinal pigment epithelial tears: risk
to the second eye. Am J Ophthalmol 1989; 108: 683-85.
46.
Meredith TA, Braley RE, Aaberg TM. Natural history of serous detachments
of the retinal pigment epithelium Am J Ophthalmol 1979 88 643-51
47
Lewis MI Idiopathic serous detachment of the pigment epithelium. Arch Ophthalmol
1978 69 1-16
48.
Barondes MJ, Pagliarini S. Chisholm IH, Hamilton AM, Bird AC. Controlled
dial of laser photocoagulation of pigment epithelial detachments in the
elderly; a four year review. Br J Ophthalmol 1992; 76: 5-7
49.
Soubrane G. Coscas G. Koenig F. Francaus C. Natural history of occult
forms of SRNV. Doe Ophthalmol Proc Series 1987; 50: 219-23.
50.
Bressler NM et al: Natural course of poorly defined choroidal neovascularisation
associated with macular degeneration. Arch Ophthalmol 1988; 106 1537-42.
51.
Capone A, Wallace RT, Meredith TA. Symptomatic choroidal neovascularisation
in blacks. Arch Ophthalmol 1994, 112: 1091-7.
52.
Yannuzzi LA, Ciardella A, Spaide RF, Rabb M, Freund KB, Orlock DA. The
expanding clinical spectrum of idiopathic polypoidal choroidal vasculopathy.
Arch Ophthalmol 1997,115:478~85.
53.
Spaide RF, Yannuzzi LA, Slakter IS, Sorenson J. Orlach DA. Indocyanine
green video angiography of idiopathic polypoidal
choroidal
vasculopathy. Retina 1995, 15: 100-10.
54.
Spraul CW Grossniklaus HE, Lang GK. Idiopathische polypose choroidale Vaskulopathie
(1PCV).KEnische Monatsblatter fur Augenheilkunde. 1997, 210: 405-6.
55.
The Provision of Low Vision Care. The Royal College of Ophthalmologists
1998
56.
Grey RHB, Bird AC, Chisholm IH. Senile disciform macular degeneration:
features indicating suitability for photocoagulation. Br J Ophthalmol 1979;
63: 85-9,
57.
Reddy G., Chisholm IH. A review of fluorescein angiography services currently
available in the United Kingdom. Royal College of Ophthalmologist Annual
Meeting 1999 Poster.
58.
Yannuzzi LA et al: Fluorescein angiography complication survey. Ophthalmology
1986; 93:611-617.
59.Yanuzzi
LA. Slalkter JS, Sorensen JA, Guyer DR, Orlock DA. Digital indocyanine
green video angiography and choroidal angiography. Retina 1992; 12: 191-223.
60.
Bressler NM., Bressler SB. Indocyanine green angiography - can it help
preserve the vision of our patients? Arch Ophthalmol 1996,114, 747-49.
61.
Bressler NM, Bressler SB Gragoudas ES: Clinical characteristics of choroidal
neovascular membranes. Arch Ophthalmol 1987; 105:209-13.
62.
Macular Photocoagulation Study Group. Laser treatment of subfoveal recurrent
neovascular lesions in age-related macular degeneration Arch Ophthalmol
1991; 109: 1232-41.
63.
Macular Photocoagulation Study Group. Laser treatment of subfoveal neovascular
lesions in age-related macular degeneration Arch Ophthalmol 1991; 109:
1220-3 1. and 1242-57.
64.
Coscas G. Soubrane G, Ramahefasolo C, Fardeau C. Perifoveal laser treatment
for subfoveal choroidal new vessels in age related macular disease. Arch
Ophthalmol 1991, 109: 1258-65.
65
Moorfields Macular Study Group.Retinal pigment epithelial detachments in
the elderly: a controlled trial of laser Br J Ophthalmol 1979 63 85-89
66.
Maguire JI, Benson WE, Brown GC. Treatment of foveal pigment epithelial
detachments with contiguous extrafoveal choroidal neovascular membranes.
Am J Ophthalmol 199 1; 109: 523-29.
67.
Klein ML, Jorizzo PA, Watzke RC. Growth features of choroidal neovascular
membranes in age-related macular degeneration. Ophthalmology 1989; 96:1416-1421.
68.Vander
JF, Morgan CM, Schatz H. Growth rate of subretinal neovascularization in
age-related macular degeneration. Ophthalmology 1989; 96:1422-29.
69.Wittpenn
JR et al. Respiratory arrest following retrobulbar anaesthesia. Ophthalmology
1986; 93: 867-70.
70.
Royal College Guidelines on Ocular Anaesthesia. Revision in preparation.
71
Fine AM et al. Earliest symptoms caused by neovascular membranes in the
macula. Arch Ophthalmol 1986: 104:513-14.
72.
Fung W. Interferon alpha-2a for the treatment of age-related macular disease.
Am J Ophthalmol 1991, 112: 349-50
73.
Gillies MC, Sarks JP, Beaumont PE, Hunyor AB, McKay D, Kearns M, McClusky
PI, Sarks SH. Treatment of choroidal neovascularisation in age-related
macular degeneration with interferon alfa-2a and alfa-2b. Brj Ophthalmol
1993, 77 :759-65.
74.
Kirkpatrick JN, Dick AD, Forrester JY Clinical experience with interferon
alpha- 2a for exudative age-related macular degeneration Br J Ophthalmol
1993, 77:766-70.
75.
Lewis ML, Davis J. Chuang E. Interferon alpha-2a in the treatment of exudative
age-related macular degeneration. Gracies Arch Clin Exp Ophthalmol 1993;
231: 615-8.
76.
Interferon study group. Interferon Alfa-2a is ineffective for patients
with choroidal neovascularisation secondary to age related macular degeneration:
results of a prospective randomised placebo controlled clinical trial.
Arch Ophthalmol 1997; 115: 865-72.
77.
Kramer M, Miller J-W Michaud N. et al. Liposomal benzoporphyrin derivative
verteporfin photodynamic therapy Selective treatment of choroidal neovascularisation
in monkeys. Ophthalmology 1996; 103: 427-38.
78.
Richter A, Wateffield E, Jain A, et al. Photosensitising potency of structural
analogues ofbeDzoporphyrin derivative (BPD) in a mouse model. Br J Cancer
1991; 63 87-93
79.
Gragoudas ES, Schmidt-Erfurth U. Sickenberg M, et al. Results and preliminary
dosimetry of photodynamic therapy for choroidal neovascularisation in age-related
macular degeneration. Invest Ophthalmol Vis Sci (Suppl) 1997; 38: 73.
80.
Schmidt-Erfurth U. Miller JW, Sickenberg M, et al. Photodynamic therapy
for choroidal neovascularisation in a phase VII study: preliminary results
of multiple treatments. Invest Ophthalmol Vis Sci(Suppl) 1997; 38: 74.
81.
Reinke MH, Canakis C, Husain D, et al. Photodynamic therapy (PDT) retreatment
of normal retina and choroid in the primate. Invest Ophthalmol Vis Sci(Suppl)
1997; 38: 75.
82.
TAP Study Group. Photodynamic Therapy of Subfoveal Choroidal Neovascularisation
in Age Related Macular Degeneration with Verteporfin. One year results
of 2 randomised clinical trials - TAP report 1. Arch Ophthalmol 117 1999;
1329-45
83.
Chakravathy U. Houston RF, Archer D13. Treatment of age-related subfoveal
membranes by teletherapy: a pilot study Br J Ophthalmol 1993, 77: 265-73.
84.
Bergink GJ, Deutman AF, van den Broek JF, van Daal WA, van der Maazen RW.
Radiation therapy for subfoveal choroidal neovascular membranes in age-related
macular degeneration A pilot study. Graefes Arch Clin Exp Ophthalmol 1994,
232:591-8.
85.
Finger PT, Berson A, Sherr D, Riley R. Balkin RA, Bosworth JL. Radiation
therapy for subretinal neovascularisation Ophthalmology 1996; 103: 878-89.
86.
Hollick ED, Goble M Knowles PI, Ramsey MC, Deutsch G. Casswell AG. Radiotherapy
treatment ofage-related subfoveal neovascular membranes in patients with
good vision. Eye 1996; 10, 609-16.
87.
Thomas M. Grand NIG. Williams DE Lee CM. Pesin SR. Lowe M. Surgical management
ofsubfoveal choroidal neovascularisation. Ophthalmology. 1992, 99:952-68.
88.
Lambert HM, Capone A, Aaberg TM, Stemberg P Mandell BA, Lopez P Surgical
excision ofsubfoveal neovascular membranes in age-related macular degeneration.
Am J Ophthatmol 1992; 113: 257-62.
89.
Thomas MA, Dickinson J13, Melberg NS, Ibanez HE, Dhaliwal RS. Visual results
after surgical removal of subfoveal choroidal neovascular membranes. Ophthalmology
1994; 101: 1384-96.
90.
Ormerod et al. Long term outcomes after surgical removal of advanced subfoveal
neovascular membranes in age related macular degeneration Ophthalmology
1994, 101; 1202-10.
91.
Newsome DA et al: Oral zinc in macular degeneration. Arch Ophthalmol 1988;
106: 192-8.
92.
Stur M, Tittl M, Reitner A, Meisinger V Oral zinc and the second eye in
age-related macular degeneration. Invest Ophthalmol Vis Sci. 1996; 37:
1225-35.
93.
Haut. Renard Y. Kraiem S. Bensoussan C, Moulin E Preventive treatmentusing
laser of age-related macular degeneration of the contralateral eye after
age-related macular degeneration in the first eye. J Ophthalmol. 1991;
14:473-6.
94.
Ruiz-Moreno JM, Alio JL. Direct perifoveal photocoagulation of soft drusen.
Am Acad Ophthalmol. 1993.
95.Weizig
PC. Treatment of drusen-related ageing macular degeneration byphotocoagulation.
Trans Am Ophthalmol Soc 1988;86:276-90.
96.
Sigelman J. Foveal drusen resorption one year after perifoveal laser photocoagulation.
Ophthalmology 1991 ;98: 1379-83.
97.
Figueroa MA, Regueras A, Bertrand J. Laser photocoagulation to treat macular
soft drusen in age related macular degeneration. Retina 1994; 14: 391-6.
98.
Guymer RH, Gross JM, Owens SL, Bird AC, Fitzke FW. Laser treatment in subjects
with high-risk clinical features of age related macular degeneration. Posterior
pole appearance and retinal function. Arch Ophthalmol 1997; 115: 595-603.
99.
Frennesson IC, Nilsson SE. Laser photocoagulation of soft drusen in early
age- related maculopathy (ARM). The one-year results of a prospective,
randomised trial. Eur J Ophthalmol 1996; 6:307-14.
100.
Choroidal neovascularization prevention trial research group. Laser treatment
in eyes with large drusen. Ophthalmology 1998; 105: 11-23.
101.GibsonjM,
Rosenthal AR, Lavery J. A study of the prevalence of eye disease in the
elderly in an English community Trans Ophthalmol See UK 1985.104 196-203
102.
College Cataract Guidelines, Royal College of Ophthalmologists, London
1995
103.
Pollack A, Marcovich A, Bukelman A, Oliver M. Age related macular degeneration
after extracapsular cataract extraction with intraocular lens implantation.
Ophthalmology 1996 103. 1546-54
104.
Lovelock R, Powel IJ, S Craggs, Shared Territory: Assessing the Social
Support needs of visual impaired people- CEDR Dept, Social Work Studies
University of Southampton. Joseph Rountree Foundation, York 1995
105.
Culharn L, Ryan B, Jackson J, Hill A, Jones B, Bird A.C. Identification
and location of low vision services in the United Kingdom. Invest Ophthalmol
Vis Sci (suppl) 1999 40, 1502.
106.
Fragmented Vision. RNIB London, 1999.
107.
Nilsson U1, Frennesson C, Nilsson S.E. Location and stability of newly
established eccentric retinal locus suitable for reading achieved through
training of patients with a dense central scotoma. Optom Vis Sci 1998 75
(12) 873-8.
108.
Low Vision Services. Recommendations for future service delivery in the
UK. Published on behalf of the Low Vision Services Consensus Group 1999
by the RNIB, London, 1999.
109.
Record of examination to certify a person as blind or partially sighted
(BD8 1990). Guidance notes. The Stationery Office, London.
Members
of the group responsible for the Guidelines
Mr I.H.
Chisholm Southampton Eye Unit (Chair)
Professor
A.C. Bird Institute of Ophthalmology, London.
Mr
R.H.B. Grey Bristol Eye Hospital.
Mr
J. Richardson Sunderland Eye Infirmary.
Dr
S. Roxburgh Ninewells Hospital, Dundee. |