Diabetic retinopathy in pregnancy1. R M BEST, 2. U
CHAKRAVARTHY
+ Author Affiliations 1. Department of Ophthalmology, Queens
University of Belfast 2. Royal Victoria Hospital, Belfast BT12 6BA
Diabetic retinopathy is one of the major causes of preventable
blindness in the UK and USA in those aged between 24 and 64 years.1
For a proportion of diabetic women, the first half of this period
coincides with peak fertility and childbearing years. Diabetic eye
disease may develop for the first time during pregnancy, and visual
loss at this stage has serious implications for both the patient
and her family. In the past, the prognosis for pregnancy in
diabetic women with microvascular disease was so poor that many
physicians advised avoidance or termination of pregnancy.2With the
recognition that the level of glycaemia during pregnancy is
directly related to the incidence of congenital malformations, the
emphasis on the management of diabetic pregnancy has been one of
meticulous control of blood sugar and this has undoubtedly resulted
in lower rates of fetal malformations. However, intensive control
of glycaemia may carry risks to diabetic mothers particularly to
those with established microvascular diseases such as retinopathy
and nephropathy. Studies on the influence of pregnancy on the
natural history of diabetic retinopathy have shown that
deterioration is frequently observed.3 4 Until recently there has
been controversy as to whether the progression of retinopathy which
occurs in such women is due to the natural tendency of diabetic
retinopathy to worsen or to unique factors operative during
pregnancy. Several major studies have gone some way towards
explaining the mechanisms underlying progression of retinopathy
during pregnancy. Klein et al performed a prospective study on a
large series of individuals, comprising 171 pregnant and 298
non-pregnant insulin dependent diabetic women.5 The level of
diabetic retinopathy in the first trimester was assessed using
standard retinal photographs and compared with postpartum
photographs. After adjusting for duration of diabetes, glycaemic
control, and blood pressure current pregnancy was [Full text of
this article] http://bjo.bmj.com/content/81/3/249.extract6. Dibble
CM, Kochenour NK, Worley RJ, Tyler FH, Schwartz M. Effect of
pregnancy on diabetic retinopathy. Obstet Gynaecol. 59: 699-704;
1982 7. Soubrane G, Canivet J, Coscas G. Influence of pregnancy on
the evolution of background retinopathy. Int Ophthalmol Clin. 8:
249-255; 1985 8. The Diabetes Control and Complications Trial
Research Group. Effect of pregnancy on microvascular complications
in the Diabetes Control and Complications Trial. Diabetes Care 23:
1084-1091; 2000 9. Axer-Siegel R, Hod M, Fink-Cohen S, Kramer M,
Weinberger D, Schindel B, Yassur Y. Diabetic retinopathy during
pregnancy.
Ophthalmology 103(11): 1815-1819; 1996 10. MMWR. Blindness
caused by diabetes-Massachusetts, 19871994. MMWR-Morbidity &
Mortality Weekly Report 45: 937941; 1996 11. Trautner C, Icks A,
Haastert B et al. Incidence of blindness in relation to diabetes. A
population-based study. Diabetes Care 20: 1147-1153; 1997 12. Dinn
RB, Harris A, Marcus PS. Ocular changes in pregnancy. Obstet
Gynecol Surv. Feb 58(2):137-44; 2003 13. Klein R, Klein BEK, Magli
YL, Brothers RJ, Meuer SM, Moss SE, David MD. An alternative method
of grading diabetic retinopathy. Ophthalmology 93: 1183-1187; 1986
14. Lapolla A, Cardone C, Negrin P, Midena E, Marini S, Gardellin
C, Bruttomesso D, Fedele D. Pregnancy does not induce or worsen
retinal and peripheral nerve dysfunction in insulindependent
diabetic women. J Diabetes Complications 12: 74-80; 1998 15.
Lovestam-Adrian M, Agardh CD, Aberg A, Agardh E. Preeclampsia is a
potent risk factor for deterioration of retinopathy during
pregnancy in type I diabetic patients. Diabet Med. 14: 1059-1065;
1997 16. Chen HC, Newsom RS, Patel V, Cassar J, Mather H, Kohner
EM. Retinal blood flow changes during pregnancy in women with
diabetes. Invest Ophthalmol Vis Sci. 35(8): 3199-3208; 1994 17.
Loukovaara S, Harju M, Kaaja R, Immonen I. Retinal capillary blood
flow in diabetic and nondiabetic women during pregnancy and
postpartum period. Invest Ophthalmol Vis Sci. 44(4):14861491; 2003
18. Schocket LS, Grunwald JE, Tsang AF, DuPont J. The effect of
pregnancy on retinal hemodynamics in diabetic versus nondiabetic
mothers. Am J Ophthalmol. 128(4): 477-484; 1999 19. Klein BE, Moss
SE, Klein R. Effect of pregnancy on progression of diabetic
retinopathy. Diabetes Care 13(1): 34-40; 1990 20. Lauszus F, Klebe
JG, Bek T. Diabetic retinopathy in pregnancy during tight metabolic
control. Acta Obstet Gynecol Scand. 79(5): 367-370; 2000 21. Chew
EY, Mills JL, Metzger BE, Remaley NA, JovanovicPeterson L, Knopp
RH, Conley M, Rand L, Simpson JL, Holmes LB et al. Metabolic
control and progression of retinopathy. The Diabetes in Early
Pregnancy Study. National Institute of Child Health and Human
Development Diabetes in Early Pregnancy Study. Diabetes Care 18(5):
631-637; 1995 22. Shamoon H, Duffy H, Fleischer N, Engel S, et al.
The effect of intensive treatment of diabetes on the development
and progression of long-term complications in insulin-dependent
diabetes mellitus. N Engl J Med. 329(14): 977; 1993 23. Wang PH,
Lau J, Chalmers TC. Meta-analysis of effects of intensive
blood-glucose control on late complications of type I diabetes.
Lancet 341(8856): 1306-1309; 1993 24. McCulloch DK. Pathogenesis
and natural history of diabetic retinopathy. Up-To-Date Online
V11.3. 2002
148 McGill Journal of Medicine 200525. Sharp PS, Fallon TJ,
Brazier OJ, Sandler L, Joplin GF, Kohner EM. Long-term follow-up of
patients who underwent yttrium-90 pituitary implantation for
treatment of proliferative diabetic retinopathy. Diabetologia
30(4): 199-207; 1987 26. Rosenn B, Miodovnik M, Kranias G, Khoury
J, Combs CA, Mimouni F, Siddiqi TA, Lipman MJ. Progression of
diabetic retinopathy in pregnancy: association with hypertension in
pregnancy. Am J Obstet Gynaecol. 166(4): 1214-1218; 1992 27. Sheth
BP. Does pregnancy accelerate the rate of progression of diabetic
retinopathy? Current Diabetes Reports 2(4): 327-330; 2002 28.
Diabetic Retinopathy. Preferred Practice Patterns (pamphlet).
San Francisco, CA: The American Academy of Ophthalmology 13: 28;
1998 29. Aiello LP, Gardner TW, King GL, Blankenship G, Cavallerano
JD, Ferris FL 3rd, Klein R. Diabetic retinopathy. American Diabetes
Association: Position Statement. Diabetes Care 23: S73-S76; 2000
30. Anonymous. Effect of pregnancy on microvascular complications
in the Diabetes Control and Complications Trial. Diabetes Care 23:
1084-1091; 2000
Jeff Van Impe, MD, will be attending McMaster University for his
first year of residency in Psychiatry. His research interests have
shifted from Ophthalmology to substance abuse and addiction.
Effect of Pregnancy on Diabetic Nephropathy and RetinopathyJ
Coll Physicians Surg Pak Feb 2004;14(2):75-8.Bahawal Victoria
Hospital, Bahawalpur
Objective: To determine whether pregnancy worsens renal function
in women with diabetic nephropathy and the effect of pregnancy on
diabetic retinopathy. Design: Cross-sectional analytical study.
Place and Duration of Study: The study was conducted in OPD,
Bahawal Victoria Hospital, Bahawalpur from September 1997 to June
2003. Subjects and Methods: Thirty-five patients (aged 20-36 years
) identified with diabetic nephropathy and moderate to severe renal
dysfunction(creatinine {Cr} > 1.4 mg/dl) at pregnancy onset by
retrospective chart review. Alterations in glomerular filtration
rate (GFR) were estimated. An equal number of non-pregnant
premenopausal type I diabetic women with similar degrees of renal
dysfunction served as controls for non-pregnant rate of decline of
renal function and potential contributing factors. Student`s t-test
and repeated measures analysis of variance were analyzed. Results:
Mean serum Cr rose from 1.8 mg/dl prepregnancy to 2.5 mg/dl in the
third trimester. Renal function was stable in 27%, showed transient
worsening in pregnancy in 27%, and demonstrated a permanent decline
in 45%. Proteinuria increased in pregnancy in 79%.Exacerbation of
hypertension or pre-eclampsia occurred in 73% and 71% of these
showed acceleration of disease during the pregnancy. All the
patients had diabetic retinopathy, though proliferative retinopathy
was diagnosed and treated in only 54.5.% prepregnancy. The
retinopathy progressed, requiring laser therapy, in 45.4%. Macular
edema was noted in 6 of the patients. Other diabetic complications
included peripheral and autonomic neuropathy in 8 patients.
Conclusion: Pregnancy induced progression is seen in the decline of
renal functions. Patients with diabetic nephropathy were found to
have a > 40% chance of accelerated progression of their disease
as a result of pregnancy. Forty-five percent of the patients had
permanent decline in GFR in association with pregnancy. Category:
Obstetrics and Gynecology Keywords: Diabetes Mellitus. Pregnancy.
Diabetic Complications. Diabetic Nephropathy. Diabetic Retinopathy.
Nephropathy. Retinopathy. Click here for Full Text Article
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DIABETIC RETINOPATHYWhat is diabetic retinopathy? Diabetic
retinopathy is a complication of diabetes and a leading cause of
blindness. It occurs when diabetes damages the tiny blood vessels
inside the retina, the light-sensitive tissue at the back of the
eye. A healthy retina is necessary for good vision. If you have
diabetic retinopathy, at first you may notice no changes to your
vision. But over time, diabetic retinopathy can get worse and cause
vision loss. Diabetic retinopathy usually affects both eyes.What
are the stages of diabetic retinopathy?
Diabetic retinopathy has four stages:1. Mild Nonproliferative
Retinopathy. At this earliest stage, microaneurysms occur. They are
small areas of balloon-like swelling in the retina's tiny blood
vessels.
2. Moderate Nonproliferative Retinopathy. As the disease
progresses, some blood vessels that nourish the retina are
blocked.
3. Severe Nonproliferative Retinopathy. Many more blood vessels
are blocked, depriving several areas of the retina with their blood
supply. These areas of the retina send signals to the body to grow
new blood vessels for nourishment.
4. Proliferative Retinopathy. At this advanced stage, the
signals sent by the retina for nourishment trigger the growth of
new blood vessels. This condition is called proliferative
retinopathy. These new blood vessels are abnormal and fragile. They
grow along the retina and along the surface of the clear, vitreous
gel that fills the inside of the eye.
By themselves, these blood vessels do not cause symptoms or
vision loss. However, they have thin, fragile walls. If they leak
blood, severe vision loss and even blindness can result.Who is at
risk for diabetic retinopathy?
All people with diabetes--both type 1 and type 2--are at risk.
That's why everyone with diabetes should get a comprehensive
dilated eye exam at least once a year. Between 40 to 45 percent of
Americans diagnosed with diabetes have some stage of diabetic
retinopathy. If you have diabetic retinopathy, your doctor can
recommend treatment to help prevent its progression. During
pregnancy, diabetic retinopathy may be a problem for women with
diabetes. To protect vision, every pregnant woman with diabetes
should have a comprehensive dilated eye exam as soon as possible.
Your doctor may recommend additional exams during your
pregnancy.How does diabetic retinopathy cause vision loss?
Blood vessels damaged from diabetic retinopathy can cause vision
loss in two ways:1. Fragile, abnormal blood vessels can develop and
leak blood into the center of the eye, blurring vision. This is
proliferative retinopathy and is the fourth and most advanced stage
of the disease.
2. Fluid can leak into the center of the macula, the part of the
eye where sharp, straight-ahead vision occurs. The fluid makes the
macula swell, blurring vision. This condition is called macular
oedema. It can occur at any stage of diabetic retinopathy, although
it is more likely to occur as the disease progresses. About half of
the people with proliferative retinopathy also have macular oedema
Does diabetic retinopathy have any symptoms?
Diabetic retinopathy often has no early warning signs. Don't
wait for symptoms. Be sure to have a comprehensive dilated eye exam
at least once a year.What are the symptoms of proliferative
retinopathy if bleeding occurs?
At first, you will see a few specks of blood, or spots,
"floating" in your vision. If spots occur, see your eye care
professional as soon as possible. You may need treatment before
more serious bleeding occurs. Haemorrhages tend to happen more than
once, often during sleep. Sometimes, without treatment, the spots
clear, and you will see better. However, bleeding can reoccur and
cause severely blurred vision. You need to be examined by your eye
care professional at the first sign of blurred vision, before more
bleeding occurs. If left untreated, proliferative retinopathy can
cause severe vision loss and even blindness. Also, the earlier you
receive treatment, the more likely treatment will be effective.How
are macular oedema and diabetic retinopathy detected?
Macular oedema and diabetic retinopathy are detected during a
comprehensive eye exam that includes:
Visual acuity test. This eye chart test measures how well you
see at various distances.
Dilated eye exam. Drops are placed in your eyes to widen, or
dilate, the pupils. Your eye care professional uses a special
magnifying lens to examine your retina and optic nerve for signs of
damage and other eye problems. After the exam, your close-up vision
may remain blurred for several hours.
Tonometry. An instrument measures the pressure inside the eye.
Numbing drops may be applied to your eye for this test.
Your eye care professional checks your retina for early signs of
the disease, including:
Leaking blood vessels.
Retinal swelling (macular oedema).
Pale, fatty deposits on the retina--signs of leaking blood
vessels.
Damaged nerve tissue.
Any changes to the blood vessels.
If your eye care professional believes you need treatment for
macular oedema, he or she may suggest a fluorescein angiogram. In
this test, a special dye is injected into your arm. Pictures are
taken as the dye passes through the blood vessels in your retina.
The test allows your eye care professional to identify any leaking
blood vessels and recommend treatment.How is a macular oedema
treated?
Macular oedema is treated with laser surgery. This procedure is
called focal laser treatment. Your doctor places up to several
hundred small laser burns in the areas of retinal leakage
surrounding the
macula. These burns slow the leakage of fluid and reduce the
amount of fluid in the retina. The surgery is usually completed in
one session. Further treatment may be needed. A patient may need
focal laser surgery more than once to control the leaking fluid. If
you have macular oedema in both eyes and require laser surgery,
generally only one eye will be treated at a time, usually several
weeks apart. Focal laser treatment stabilizes vision. In fact,
focal laser treatment reduces the risk of vision loss by 50
percent. In a small number of cases, if vision is lost, it can be
improved. Contact your eye care professional if you have vision
loss.How is diabetic retinopathy treated?
During the first three stages of diabetic retinopathy, no
treatment is needed, unless you have macular oedema. To prevent
progression of diabetic retinopathy, people with diabetes should
control their levels of blood sugar, blood pressure, and blood
cholesterol. Proliferative retinopathy is treated with laser
surgery. This procedure is called scatter laser treatment. Scatter
laser treatment helps to shrink the abnormal blood vessels. Your
doctor places 1,000 to 2,000 laser burns in the areas of the retina
away from the macula, causing the abnormal blood vessels to shrink.
Because a high number of laser burns are necessary, two or more
sessions usually are required to complete treatment. Although you
may notice some loss of your side vision, scatter laser treatment
can save the rest of your sight. Scatter laser treatment may
slightly reduce your colour vision and night vision. Scatter laser
treatment works better before the fragile, new blood vessels have
started to bleed. That is why it is important to have regular,
comprehensive dilated eye exams. Even if bleeding has started,
scatter laser treatment may still be possible, depending on the
amount of bleeding. If the bleeding is severe, you may need a
surgical procedure called a vitrectomy. During a vitrectomy, blood
is removed from the center of your eye.What happens during laser
treatment?
Both focal and scatter laser treatment are performed in your
doctor's office or eye clinic. Before the surgery, your doctor will
dilate your pupil and apply drops to numb the eye. The area behind
your eye also may be numbed to prevent discomfort. The lights in
the office will be dim. As you sit facing the laser machine, your
doctor will hold a special lens to your eye. During the procedure,
you may see flashes of light. These flashes eventually may create a
stinging sensation that can be uncomfortable. You will need someone
to drive you home after surgery. Because your pupil will remain
dilated for a few hours, you should bring a pair of sunglasses.
For the rest of the day, your vision will probably be a little
blurry. If your eye hurts, your doctor can suggest treatment.What
is a vitrectomy?
If you have a lot of blood in the center of the eye (vitreous
gel), you may need a vitrectomy to restore your sight. If you need
vitrectomies in both eyes, they are usually done several weeks
apart. A vitrectomy is performed under either local or general
anaesthesia. Your doctor makes a tiny incision in your eye. Next, a
small instrument is used to remove the vitreous gel that is clouded
with blood. The vitreous gel is replaced with a salt solution.
Because the vitreous gel is mostly water, you will notice no change
between the salt solution and the original vitreous gel. You will
probably be able to return home after the vitrectomy. Some people
stay in the hospital overnight. Your eye will be red and sensitive.
You will need to wear an eye patch for a few days or weeks to
protect your eye. You also will need to use medicated eyedrops to
protect against infection.Are scatter laser treatment and
vitrectomy effective in treating proliferative retinopathy?
Yes. Both treatments are very effective in reducing vision loss.
People with proliferative retinopathy have less than a five percent
chance of becoming blind within five years when they get timely and
appropriate treatment. Although both treatments have high success
rates, they do not cure diabetic retinopathy. Once you have
proliferative retinopathy, you always will be at risk for new
bleeding. You may need treatment more than once to protect your
sight.What can I do if I already have lost some vision from
diabetic retinopathy?
If you have lost some sight from diabetic retinopathy, ask your
eye care professional about low vision services and devices that
may help you make the most of your remaining vision. Ask for a
referral to a specialist in low vision. Many community
organisations and agencies offer information about low vision
counselling, training, and other special services for people with
visual impairments. A nearby school of medicine or optometry may
provide low vision services.What can I do to protect my vision?
The NEI urges everyone with diabetes to have a comprehensive
dilated eye exam at least once a year. If you have diabetic
retinopathy, you may need an eye exam more often. People with
proliferative retinopathy can reduce their risk of blindness by 95
percent with timely treatment and appropriate followup care. A
major study has shown that better control of blood sugar levels
slows the onset and progression of retinopathy. The people with
diabetes who kept their blood sugar levels as close to normal
as
possible also had much less kidney and nerve disease. Better
control also reduces the need for sight-saving laser surgery. This
level of blood sugar control may not be best for everyone,
including some elderly patients, children under age 13, or people
with heart disease. Be sure to ask your doctor if such a control
programme is right for you. Other studies have shown that
controlling elevated blood pressure and cholesterol can reduce the
risk of vision loss. Controlling these will help your overall
health as well as help protect your vision.What should I ask my eye
care professional?
You can protect yourself against vision loss by working in
partnership with your eye care professional. Ask questions and get
the information you need to take care of yourself and your
family.
What are some questions to ask? About my eye disease or
disorder...
What is my diagnosis? What caused my condition? Can my condition
be treated? How will this condition affect my vision now and in the
future? Should I watch for any particular symptoms and notify you
if they occur? Should I make any lifestyle changes?
About my treatment...
What is the treatment for my condition? When will the treatment
start and how long will it last? What are the benefits of this
treatment and how successful is it? What are the risks and side
effects associated with this treatment? Are there foods, drugs, or
activities I should avoid while I'm on this treatment? If my
treatment includes taking medicine, what should I do if I miss a
dose? Are other treatments available?
About my tests...
What kinds of tests will I have? What can I expect to find out
from these tests? When will I know the results? Do I have to do
anything special to prepare for any of the tests? Do these tests
have any side effects or risks? Will I need more tests later?
Other suggestions
If you don't understand your eye care professional's responses,
ask questions until you do understand. Take notes or get a friend
or family member to take notes for you. Or, bring a tape recorder
to help you remember the discussion. Ask your eye care professional
to write down his or her instructions to you. Ask your eye care
professional for printed material about your condition. If you
still have trouble understanding your eye care professional's
answers, ask where you can go for more information. Other members
of your health care team, such as nurses and pharmacists, can be
good sources of information. Talk to them, too.
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Diabetic retinopathyFrom Wikipedia, the free encyclopedia Jump
to: navigation, search Main article: Diabetes MellitusDiabetes
mellitusRelated articles
Types of diabetes
Prediabetes: Impaired fasting glycaemia Impaired glucose
tolerance Diabetes mellitus type 1 Diabetes mellitus type 2
Gestational diabetes
Blood tests
Blood sugar Glycosylated hemoglobin Glucose tolerance test
Fructosamine
Diabetes management
Diabetic diet Anti-diabetic drugs Insulin therapy Glossary of
diabetes
Complications
Cardiovascular disease Diabetic comas: Diabetic hypoglycemia
Diabetic ketoacidosis Nonketotic hyperosmolar Diabetic myonecrosis
Diabetic nephropathy Diabetic neuropathy Diabetic retinopathy
Diabetes and pregnancy
Diabetic retinopathyClassification and external resources H36.
(E10.3 E11.3 E12.3 E13.3 E14.3) 250.5
ICD-10
ICD-9
DiseasesDB 29372 MedlinePlu s eMedicine MeSH
000494 001212
oph/414 oph/415 D003930
Diabetic retinopathy is retinopathy (damage to the retina)
caused by complications of diabetes mellitus, which can eventually
lead to blindness. It is an ocular manifestation of systemic
disease
which affects up to 80% of all patients who have had diabetes
for 10 years or more[1]. Despite these intimidating statistics,
research indicates that at least 90% of these new cases could be
reduced if there was proper and vigilant treatment and monitoring
of the eyes[2].
Normal vision. Courtesy NIH National Eye Institute
The same view with diabetic retinopathy.
Contents[hide]
1 2 3 4 5
Signs and symptoms Pathogenesis Risk factors Diagnosis
Management o 5.1 Laser photocoagulation o 5.2 Panretinal
photocoagulation o 5.3 Intravitreal Triamcinolone acetonide o 5.4
Vitrectomy 6 Experimental treatments o 6.1 C-peptide o 6.2 Pine
bark extract 7 References 8 See also 9 External links
[edit] Signs and symptomsDiabetic retinopathy often has no early
warning signs. Even macular edema, which may cause vision loss more
rapidly, may not have any warning signs for some time. In general,
however, a person with macular edema is likely to have blurred
vision, making it hard to do things like read or drive. In some
cases, the vision will get better or worse during the day. As new
blood vessels form at the back of the eye as a part of
proliferative diabetic retinopathy (PDR), they can bleed
(hemorrhage) and blur vision. The first time this happens, it may
not be very severe. In most cases, it will leave just a few specks
of blood, or spots, floating in a person's visual field, though the
spots often go away after a few hours. These spots are often
followed within a few days or weeks by a much greater leakage of
blood, which blurs vision. In extreme cases, a person will only be
able to tell light from dark in that eye. It may take the blood
anywhere from a few days to months or even years to clear from the
inside of the eye, and in some cases the blood will not clear.
These types of large hemorrhages tend to happen more than once,
often during sleep. On funduscopic exam, a doctor will see cotton
wool spots, flame hemorrhages (similar leisons are also caused by
the alpha-toxin of Clostridium novyi), and dot-blot
hemorrhages.
[edit] PathogenesisDiabetic retinopathy is the result of
microvascular retinal changes. Hyperglycemia-induced intramural
pericyte death and thickening of the basement membrane lead to
incompetence of the
vascular walls. These damages change the formation of the
blood-retinal barrier and also make the retinal blood vessels
become more permeable.[3] The pericyte death is due to the
"hyperglycemia persistently activates protein kinase C- (PKC-,
encoded by Prkcd) and p38 mitogen-activated protein kinase (MAPK)
to increase the expression of a previously unknown target of PKC-
signaling, Src homology-2 domaincontaining phosphatase1 (SHP-1), a
protein tyrosine phosphatase. This signaling cascade leads to PDGF
receptordephosphorylation and a reduction in downstream signaling
from this receptor, resulting in pericyte apoptosis..."[4] Small
blood vessels such as those in the eye are especially vulnerable to
poor blood sugar (blood glucose) control. An overaccumulation of
glucose and/or fructose damages the tiny blood vessels in the
retina. During the initial stage, called nonproliferative diabetic
retinopathy (NPDR), most people do not notice any change in their
vision. Some people develop a condition called macular edema. It
occurs when the damaged blood vessels leak fluid and lipids onto
the macula, the part of the retina that lets us see detail. The
fluid makes the macula swell, which blurs vision. As the disease
progresses, severe nonproliferative diabetic retinopathy enters an
advanced, or proliferative, stage. The lack of oxygen in the retina
causes fragile, new, blood vessels to grow along the retina and in
the clear, gel-like vitreous humour that fills the inside of the
eye. Without timely treatment, these new blood vessels can bleed,
cloud vision, and destroy the retina. Fibrovascular proliferation
can also cause tractional retinal detachment. The new blood vessels
can also grow into the angle of the anterior chamber of the eye and
cause neovascular glaucoma. Nonproliferative diabetic retinopathy
shows up as cotton wool spots, or microvascular abnormalities or as
superficial retinal hemorrhages. Even so, the advanced
proliferative diabetic retinopathy (PDR) can remain asymptomatic
for a very long time, and so should be monitored closely with
regular checkups.
[edit] Risk factorsAll people with diabetes mellitus are at risk
those with Type I diabetes (juvenile onset) and those with Type II
diabetes (adult onset). The longer a person has diabetes, the
higher the risk of developing some ocular problem. Between 40 to 45
percent of Americans diagnosed with diabetes have some stage of
diabetic retinopathy. [5] After 20 years of diabetes, nearly all
patients with type 1 diabetes and >60% of patients with type 2
diabetes have some degree of retinopathy.[6] Prior studies had also
assumed a clear glycemic threshold between people at high and low
risk of diabetic retinopathy.[7][8] However, it has been shown that
the widely accepted WHO and American Diabetes Association
diagnostic cutoff for diabetes of a fasting plasma glucose 7.0
mmol/l (126 mg/dl) does not accurately identify diabetic
retinopathy among patients.[9] The cohort study included a
multi-ethnic, cross-sectional adult population sample in the US, as
well as two crosssectional adult populations in Australia. For the
US-based component of the study, the sensitivity was 34.7% and
specificity was 86.6%. For patients at similar risk to those in
this study (15.8% had
diabetic retinopathy), this leads to a positive predictive value
of 32.7% and negative predictive value of 87.6%. Published rates
vary between trials, the proposed explanation being differences in
study methods and reporting of prevalence rather than incidence
values.[10] During pregnancy, diabetic retinopathy may also be a
problem for women with diabetes. It is recommended that all
pregnant women with diabetes have dilated eye examinations each
trimester to protect their vision.[citation needed] People with
Down's syndrome, who have three copies of chromosome 21, almost
never acquire diabetic retinopathy. This protection appears to be
due to the elevated levels of endostatin[11], an anti-angiogenic
protein, derived from collagen XVIII. The collagen XVIII gene is
located on chromosome 21.
[edit] DiagnosisDiabetic retinopathy is detected during an eye
examination that includes:
Visual acuity test: This test uses an eye chart to measure how
well a person sees at various distances (i.e., visual acuity).
Pupil dilation: The eye care professional places drops into the eye
to widen the pupil. This allows him or her to see more of the
retina and look for signs of diabetic retinopathy. After the
examination, close-up vision may remain blurred for several hours.
Ophthalmoscopy: This is an examination of the retina in which the
eye care professional: (1) looks through a device with a special
magnifying lens that provides a narrow view of the retina, or (2)
wearing a headset with a bright light, looks through a special
magnifying glass and gains a wide view of the retina. Note that
hand-held ophthalmoscopy is insufficient to rule out significant
and treatable diabetic retinopathy. Optical coherence tomography
(OCT): This is an optical imaging modality based upon interference,
and analogous to ultrasound. It produces crosssectional images of
the retina (B-scans) which can be used to measure the thickness of
the retina and to resolve its major layers, allowing the
observation of swelling and or leakage. Digital Retinal Screening
Programs: Systematic programs for the early detection of eye
disease including diabetic retinopathy are becoming more common,
such as in the UK, where all people with diabetes mellitus are
offered retinal screening at least annually. This involves digital
image capture and transmission of the images to a digital reading
center for evaluation and treatment referral. See Vanderbilt
Ophthalmic Imaging Center [1] and the English National Screening
Programme for Diabetic Retinopathy [2] Slit Lamp Biomicroscopy
Retinal Screening Programs: Systematic programs for the early
detection of diabetic retinopathy using slit-lamp biomicroscopy.
These exist either as a standalone scheme or as part of the Digital
program (above) where the digital photograph was considered to lack
enough clarity for detection and/or diagnosis of any retinal
abnormality.
The eye care professional will look at the retina for early
signs of the disease, such as: (1) leaking blood vessels, (2)
retinal swelling, such as macular edema, (3) pale, fatty deposits
on the retina (exudates) signs of leaking blood vessels, (4)
damaged nerve tissue (neuropathy), and (5) any changes in the blood
vessels. Should the doctor suspect macular edema, he or she may
perform a test called fluorescein angiography. In this test, a
special dye is injected into the arm. Pictures are then taken as
the dye passes through the blood vessels in the retina. This test
allows the doctor to find the leaking blood vessels.
[edit] ManagementThere are three major treatments for diabetic
retinopathy, which are very effective[citation needed] in reducing
vision loss from this disease. In fact, even people with advanced
retinopathy have a 90 percent chance of keeping their vision when
they get treatment before the retina is severely damaged. These
three treatments are laser surgery, injection of triamcinolone into
the eye and vitrectomy. It is important to note that although these
treatments are very successful, they do not cure diabetic
retinopathy. Caution should be exercised in treatment with laser
surgery since it causes a loss of retinal tissue. It is often more
prudent to inject triamcinolone. In some patients it results in a
marked increase of vision, especially if there is an edema of the
macula. Avoiding tobacco use and correction of associated
hypertension are important therapeutic measures in the management
of diabetic retinopathy. [12] The best way of addressing diabetic
retinopathy is to monitor it vigilantly. By 2008 there were other
drugs (eg kinase inhibitors and anti-VEGF) available.[13][edit]
Laser photocoagulation
Laser photocoagulation can be used in two scenarios for the
treatment of diabetic retinopathy. It is widely used for early
stages of proliferative retinopathy.[edit] Panretinal
photocoagulation
Panretinal photocoagulation, or PRP (also called scatter laser
treatment), is used to treat proliferative diabetic retinopathy
(PDR). The goal is to create 1,000 - 2,000 burns in the retina with
the hope of reducing the retina's oxygen demand, and hence the
possibility of ischemia. In treating advanced diabetic retinopathy,
the burns are used to destroy the abnormal blood vessels that form
in the retina. This has been shown to reduce the risk of severe
vision loss for eyes at risk by 50%.[14]
Before the laser, the ophthalmologist dilates the pupil and
applies anesthetic drops to numb the eye. In some cases, the doctor
also may numb the area behind the eye to prevent any
discomfort.
The patient sits facing the laser machine while the doctor holds
a special lens to the eye. The physician can use a single spot
laser or a pattern scan laser for two dimensional patterns such as
squares, rings and arcs. During the procedure, the patient may see
flashes of light. These flashes may eventually create an
uncomfortable stinging sensation for the patient. After the laser
treatment, patients should be advised not to drive for a few hours
while the pupils are still dilated. Vision may remain a little
blurry for the rest of the day, though there should not be much
pain in the eye. Patients may lose some of their peripheral vision
after this surgery, but the procedure saves the rest of the
patient's sight. Laser surgery may also slightly reduce colour and
night vision. A person with proliferative retinopathy will always
be at risk for new bleeding, as well as glaucoma, a complication
from the new blood vessels. This means that multiple treatments may
be required to protect vision.[edit] Intravitreal Triamcinolone
acetonide
Triamcinolone is a long acting steroid preparation. When
injected in the vitreous cavity, it decreases the macular edema
(thickening of the retina at the macula) caused due to diabetic
maculopathy, and results in an increase in visual acuity. The
effect of triamcinolone is transient, lasting up to three months,
which necessitates repeated injections for maintaining the
beneficial effect. Complications of intravitreal injection of
triamcinolone include cataract, steroid-induced glaucoma and
endophthalmitis.[edit] Vitrectomy
Instead of laser surgery, some people require a vitrectomy to
restore vision. A vitrectomy is performed when there is a lot of
blood in the vitreous. It involves removing the cloudy vitreous and
replacing it with a saline solution. Studies show that people who
have a vitrectomy soon after a large hemorrhage are more likely to
protect their vision than someone who waits to have the operation.
Early vitrectomy is especially effective in people with
insulin-dependent diabetes, who may be at greater risk of blindness
from a hemorrhage into the eye. Vitrectomy is often done under
local anesthesia. The doctor makes a tiny incision in the sclera,
or white of the eye. Next, a small instrument is placed into the
eye to remove the vitreous and insert the saline solution into the
eye. Patients may be able to return home soon after the vitrectomy,
or may be asked to stay in the hospital overnight. After the
operation, the eye will be red and sensitive, and patients usually
need to wear an eyepatch for a few days or weeks to protect the
eye. Medicated eye drops are also prescribed to protect against
infection.
[edit] Experimental treatments[edit] C-peptide
Though not yet commercially available, c-peptide has shown
promising results in treatment of diabetic complications incidental
to vascular degeneration. Once thought to be a useless byproduct of
insulin production, it helps to ameliorate and reverse many
symptoms of diabetes[15].[edit] Pine bark extract
A pine bark extract of oligomeric proanthocyanidins has been
shown to improve microcirculation, retinal edema and visual acuity
in the early stages of diabetic retinopathy[16].
[edit] References1. ^ PJ Kertes, TM Johnson Eds. Evidence Based
Eye Care (c) 2007 2. ^ Tapp, R. et al (2003) The prevalence of and
factors associated with diabetic retinopathy in the Australian
population. Diabetes care. 26(6), pg. 1371. 3. ^ Understanding
diabetic retinopathy by Pardianto G et al., in Mimbar Ilmiah
Oftalmologi Indonesia.2005;2: 65-6. 4. ^
http://www.nature.com/nm/journal/v15/n11/full/nm.2052.html
"Activation of PKC- and SHP-1 by hyperglycemia causes vascular cell
apoptosis and diabetic retinopathy" 2009 5. ^ "NIHSeniorHealth:
Diabetic Retinopathy - Causes and Risk Factors". Diabetic
Retinopathy. NIHSenior Health. 2005.
http://nihseniorhealth.gov/diabeticretinopathy/causesandriskfactors/02.html.
6. ^ "Screening for Diabetic Retinopathy". Diabetic Retinopathy.
American Diabetes Association. 2002.
http://care.diabetesjournals.org/cgi/content/full/25/suppl_1/s90.
7. ^ "Report of the expert committee on the diagnosis and
classification of diabetes mellitus". Diabetes Care 26 Suppl 1:
S520. 2003. PMID 12502614.
http://care.diabetesjournals.org/cgi/pmidlookup?view=long&pmid=12502614.
8. ^ "Report of the Expert Committee on the Diagnosis and
Classification of Diabetes Mellitus". Diabetes Care 20 (7): 118397.
1997. PMID 9203460. 9. ^ Wong TY, Liew G, Tapp RJ, et al. (2008).
"Relation between fasting glucose and retinopathy for diagnosis of
diabetes: three population-based crosssectional studies". Lancet
371 (9614): 73643. doi:10.1016/S01406736(08)60343-8. PMID 18313502.
http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(08)60343-8.
10.^ Williams R, Airey M, Baxter H, Forrester J, Kennedy-Martin T,
Girach A (2004). "Epidemiology of diabetic retinopathy and macular
oedema: a systematic review". Eye 18 (10): 96383.
doi:10.1038/sj.eye.6701476. PMID 15232600. 11.^
http://journals.lww.com/jcraniofacialsurgery/Abstract/2009/03001/Role_of_Endo
genous_Angiogenesis_Inhibitors_in_Down.9.aspx 12.^ "Diabetes Ocular
complications". Chronic Complications of Diabetes. Armenian Medical
Network. 2006.
http://www.health.am/db/diabetes-ocularcomplications/.
13.^ http://www.ncbi.nlm.nih.gov/pubmed/18408491?
ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu
bmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=5&log$=relatedreviews
&logdbfrom=pubmed 14.^ PJ Kertes TM Johnson, Eds,
Evidence-Based Eye Care (C)2007 15.^ Wahren, J., Ekberg, K., &
Jrnval, H. 2007. C-peptide is a bioactive peptide. Diabetologia.
Volume 50, Number 3 16.^
http://www.eurekalert.org/pub_releases/2009-12/mg-ssp113009.php
"Study shows pine bark improves circulation, swelling and visual
acuity in early diabetic retinopathy" Dec 2009
The original text of this document was taken from the public
domain resource document "Facts About Diabetic Retinopathy", at
http://www.nei.nih.gov/health/diabetic/retinopathy.asp See the
copyright statement at http://www.nei.nih.gov/order/index.htm,
which says "Our publications are not copyrighted and may be
reproduced without permission. However, we do ask that credit be
given to the National Eye Institute, National Institutes of
Health."
[edit] See also
PERSPECTIVE
Diabetic retinopathy in pregnancyR M Best, U
ChakravarthyDiabetic retinopathy is one of the major causes of
preventable blindness in the UK and USA in those aged between 24
and 64 years.1 For a proportion of diabetic women, the first half
of this period coincides with peak fertility and childbearing
years. Diabetic eye disease may develop for the first time during
pregnancy, and visual loss at this stage has serious implications
for both the patient and her family. In the past, the prognosis for
pregnancy in diabetic women with microvascular disease was so poor
that many physicians advised avoidance or termination of pregnancy.
2 With the recognition that the level of glycaemia during pregnancy
is directly related to the incidence of congenital malformations,
the emphasis on the management of diabetic pregnancy has been one
of meticulous control of blood sugar and this has undoubtedly
resulted in lower rates of fetal malformations. However, intensive
control of glycaemia may carry risks to diabetic mothers
particularly to those with established microvascular diseases such
as retinopathy and nephropathy. Studies on the influence of
pregnancy on the natural history of diabetic retinopathy have shown
that deterioration is frequently observed. 3 4 Until recently there
has been controversy as to whether the progression of retinopathy
which occurs in such women is due to the natural tendency of
diabetic retinopathy to worsen or to unique factors operative
during pregnancy. Several major studies have gone some way towards
explaining the mechanisms underlying
progression of retinopathy during pregnancy. Klein et al
performed a prospective study on a large series of individuals,
comprising 171 pregnant and 298 non-pregnant insulin dependent
diabetic women. 5 The level of diabetic retinopathy in the first
trimester was assessed using standard retinal photographs and
compared with postpartum photographs. After adjusting for duration
of diabetes, glycaemic control, and blood pressure current
pregnancy was found to be a major risk factor for the progression
of retinopathy. 5 Similarly, Moloney and Drury, also using retinal
photography as a means of assessing retinopathy, found that current
pregnancy in 53 pregnant diabetic women was associated both with an
increased prevalence (from 62% to 77%) and severity of retinopathy
whereas in the control group of 39 non-pregnant diabetic women the
prevalence of retinopathy remained unchanged at 46% throughout the
study period.3 That retinopathy worsens during pregnancy is now
undisputed, although the mechanism by which progression occurs is
not entirely clear. Risk factors for the progression of retinopathy
in pregnancyMETABOLIC CONTROL
An elegant study by Phelps et al 6 monitored changes in diabetic
retinopathy status during pregnancy and correlated these findings
with blood sugar measurements made at corresponding time points.
These findings were further supported and extended by the Diabetes
in Early Pregnancy Study (DIEP), 7 a prospective cohort study on
140 pregnant diabetic women who were followed from early pregnancy
to delivery using retinal photography. It was clearly shown that
those women with the greatest reduction in glycosylated haemoglobin
(HbA1c) over the first 14 weeks of pregnancy were at an increased
risk of progression of retinopathy. 7 Patients in whom retinopathy
was most likely to progress had both the poorest control at
baseline and the largest improvement during early pregnancy.
However, it was impossible to separate these two risk factors as
virtually all patients had improved metabolic control during early
pregnancy.DURATION OF DIABETES
Another risk factor which has been shown to adversely influence
progression of retinopathy is the duration of diabetes before
pregnancy. 8 Dibble et al followed 55 insulin dependent diabetic
women through their pregnancies and found a positive correlation
between duration of diabetes and progression of retinopathy. 8
However, the results of the more recent and larger DIEP study
suggest that duration of diabetes is probably not as important a
risk factor for any change in retinopathy as baseline severity of
retinopathy. Retinopathy was noticed to progress by two or more
steps in 55% of patients with less than 15 years of disease and 50%
of those with more than 15 years of disease and these differences
were not significant. 7 But, when the rate of development of
retinopathy was compared in patients stratified by duration of
diabetes, retinopathy progressed to proliferative levels in 39% of
patients with more than 15 years of diabetes as opposed to 18% of
patients with a disease duration of less than 15 years.7 These
findings indicate that duration of diabetes, which is strongly
correlated with level of baseline retinopathy, may be a significant
factor in the development of more severe changethat is,
proliferative
retinopathy in pregnancy.BASELINE SEVERITY OF RETINOPATHY
It has been shown that risk of visual loss is low in those with
no pre-existing retinopathy. Approximately 12% of women with no
retinopathy at the start of pregnancy will develop minor background
retinopathy consisting of a few microaneurysms but regression in
the postpartum period is the norm.9 Using fluorescein angiography
Soubrane et al showed that in women with mild background diabetic
retinopathy the number of retinal microaneurysms increased
progressively during pregnancy but underwent substantial regression
postpartum though not quite returning to preconception levels.10 On
the other hand when pre-existing retinopathy is more severe,
proliferative changes can develop in a significant number of cases.
Thus in the DIEP study, 29% of patients whose fundal appearance was
classified as showing moderate retinopathy at baseline went on to
develop proliferative changes during pregnancy. This was in
contrast with those women who had minimal retinopathy at baseline
where only 6.3% progressed to the proliferative category. 7 These
findingsBritish Journal of Ophthalmology 1997;81:249251 249
indicate that severity of existing diabetic retinopathy
profoundly influences the level of progression.RETINAL BLOOD
FLOW
Pregnancy is associated with major changes in the systemic
vasculature. There is an augmentation in cardiac output and plasma
volume and a decrease in peripheral resistance, all of which cause
increased blood flow. Chen et al, using laser Doppler velocimetry
to measure retinal blood flow, demonstrated the lack of change of
retinal blood flow in normal pregnancy, thus confirming the
efficacy of the autoregulatory processes in the retinal
vasculature. 11 In diabetic patients who showed progression of
retinopathy in pregnancy, an increase in blood flow was documented
in the first trimester. By contrast, women with diabetes whose
retinal blood flow remained unchanged developed no retinopathy. 11
They therefore suggested that the hyperdynamic circulatory state of
early pregnancy is accompanied by compensatory mechanisms both in
normal women and in those diabetes sufferers who retain
autoregulatory control of retinal blood flow. In some diabetic
women, however, these autoregulatory mechanisms are flawed
resulting in an increase in blood flow. Such a hyperdynamic
circulatory state could potentially inflict additional shear stress
and cause endothelial damage particularly at the capillary level.12
However, local hypoxia associated with worsening retinopathy could
account for the compensatory increase in blood flow which may
merely represent an epiphenomenon rather than failure of
autoregulation in pregnancy.HYPERTENSION
Hypertension is a known risk factor for the progression of
retinopathy and is additionally hazardous during pregnancy. 5 13
Rosenn et al followed 154 insulin dependent diabetic women
throughout their pregnancies of whom approximately a third had
either chronic hypertension or pregnancy induced hypertension or
both. Fifty five per cent of those with a hypertensive disorder
developed progression of retinopathy as opposed to 25% of those
that did not.13 Pharmacological treatment of hypertension in
pregnancy is most suitable for early onset, severe disease when an
attempt to delay delivery is indicated and methyldopa,
blockers, and vasodilators have been used with some success.14 A
recent report has indicated that treatment of women with diabetes
with the angiotensin converting enzyme (ACE) inhibitor captopril
for 6 months before the onset of pregnancy reduces proteinuria,
improves renal function, and is associated with favourable maternal
and fetal outcome. 15 In at least one major study all patients with
severe proliferative retinopathy also had proteinuria indicating a
generalised vasculopathy. 6 Thus, it is not inconceivable that
functional improvement in one circulatory bed might be mirrored in
others. However, the use of ACE inhibitors during pregnancy is not
recommended as they are extremely fetotoxic resulting in
hypotension, renal tubular dysplasia, anuriaoligohydramnios, growth
restriction, and death of the fetus.16 Nevertheless, clinical
studies of ACE inhibitors in diabetic retinopathy carried out
before the onset of pregnancy might well be worthwhile. Fundus
changes in diabetic retinopathy in pregnancy Cotton wool spots
develop in a proportion of patients with background retinopathy as
pregnancy advances and have been seen to be associated with low
fasting blood sugar. 3 As hypoglycaemia often occurs in the wake of
institution of rapid metabolic control,6 it has been suggested that
low plasma glucose may be responsible for the retinal hypoxia and
damage.3 These morphological alterations are not dissimilar to
those observed in non-gravid diabetic individuals who may
experience transient worsening of retinopathy when subjected to
strict glycaemic control in whom the major changes are cotton wool
spots and intraretinal microvascular abnormalities.17 However,
Phelps et al 6 have reported that the components of retinopathy
which increased most commonly in pregnancy were haemorrhages and
microaneurysms, suggesting that there may be differences in
pathophysiological aetiology between gravid and non-gravid
subjects. Effect of diabetic retinopathy on pregnancy Increasing
severity of diabetic retinopathy has been shown to adversely affect
outcome in pregnancy. Price et al retrospectively reviewed 23
pregnancies in insulin dependent diabetics who had had serial
retinal examinations during pregnancy. 18 They noted that 30% of
patients who had no observable retinopathy and 70% of patients with
background retinopathy at the inception of pregnancy developed
obstetric complications. It was noteworthy that all of those with
proliferative retinopathy at the start of pregnancy developed
pregnancy induced hypertension or other obstetric complications.18
In another study the impact of diabetic retinopathy on pregnancy
was examined in 179 women with diabetes.19 The pregnancies in 43%
of the women with proliferative retinopathy had an unfavourable
outcome compared with 13% of those with nonproliferative or no
retinopathy and, overall, a fifth of the pregnancies resulted in
fetuses with severe congenital malformations and/or fetal death. 19
Thus, severity of retinopathy at baseline was strongly predictive
of an adverse outcome in these patients. Long term consequences of
pregnancy on diabetic retinopathy In an attempt to determine
whether pregnancy had an
unfavourable effect on retinopathy in the long term Klein and
Klein investigated the severity of retinopathy in two groups of
diabetic women, one of which had experienced pregnancy and the
other had never been pregnant. 20 No difference was observed in
severity of retinopathy between the groups suggesting the absence
of any deleterious effects attributable to pregnancy. 20 These
findings have been supported by other studies which have shown no
long term detrimental effects due to pregnancy in other organs such
as the kidney or peripheral nervous system. 21 22 Conversely,
retinopathy of less overall severity in parous women has been
reported,21 and the rigorous and intensive control of diabetes
instituted during pregnancy in these women has been cited as having
a possible protective effect in the long term. Management of
diabetic retinopathy in pregnancy Before the advent of laser
photocoagulation, proliferative retinopathy was a contraindication
to pregnancy because of the substantial risk of severe visual loss,
so that women with diabetes who became pregnant were advised to
consider termination.2 With the use of laser photocoagulation and
the establishment and recognition of high risk characteristics23
the likelihood of visual loss has been reduced. Progression of
proliferative retinopathy may depend upon whether or not laser
photocoagulation has been carried out before pregnancy. One study
of patients with proliferative retinopathy detected in early
pregnancy and subsequently treated by laser showed that 58%
experienced significant progression and visual loss.9 On the other
hand only 26% of patients in whom retinopathy was diagnosed and
treated before onset of pregnancy showed progression of retinopathy
during an ensuing gestation250 Best, Chakravarthy
period.9 The indications for treatment and the response to laser
photocoagulation are exactly the same as for other diabetes
sufferers.24 Nevertheless, some studies have found that vascular
proliferation is reversible and postpartum regression is common,25
and currently therefore most ophthalmologists would perform a
restricted or limited photocoagulation procedure. However, there
are a group of women in whom retinopathy is aggressive, responds
poorly to photocoagulation, and continues to progress postpartum.
26 Thus, it is important that proliferative retinopathy is detected
and treated preferably before the onset of pregnancy. Those who
develop proliferative retinopathy during pregnancy should have
prompt laser photocoagulation treatment sufficient to induce
regression. Sinclair et al 27 have identified a group of insulin
dependent diabetics who developed macular oedema in pregnancy and
who also typically developed proteinuria and mild hypertension
concomitantly. Laser photocoagulation may be required to treat
macular changes but this in itself can exacerbate the oedema
particularly in those with a compromised macular capillary
circulation. Alternative therapies for this condition include salt
restriction diets and diuretics which have been used with limited
success. 28 When macular oedema occurs it is thought to be due to
an ischaemic capillaropathy and may be accompanied by proliferative
retinopathy. In some cases macular oedema regresses postpartum but
in others it may persist and cause long term visual loss.27
Generally, the diagnosis of sight
threatening retinopathy is made on ophthalmoscopic appearances.
However, fluorescein angiography is a more sensitive tool to assess
the extent of capillary non-perfusion and early neovascularisation
and may be of value in the management of pregnant diabetics
particularly since there is no evidence that it has any detrimental
effect on the developing fetus.29 Despite the tendency for
retinopathy to worsen after the institution of strict glycaemic
control, there is an overall strong beneficial effect of near
normoglycaemia which includes a reduction of retinopathy by 50% at
2 years of follow up.30 31 It is also recognised that normalisation
of blood sugar during pregnancy is the most important factor for
the successful outcome of pregnancy in diabetes, 32 33 as a high
rate of preterm deliveries (39%) and frequent occurrence of
intrauterine growth retardation (9%) characterise the fetal outcome
in women with uncontrolled diabetes.34 It is therefore recommended
that diabetic women who are contemplating pregnancy and who are
suboptimally controlled (glycosylated haemoglobin > 6 SD above
the control mean) should be targeted for the institution of strict
glycaemic control.7 Ideally, young women with diabetes should be
seen for counselling and management before the onset of pregnancy.
Although studies suggest that most patients recognise the value of
good blood glucose control,35 a significant proportion may be
unaware of the potential risks to vision. In summary, progression
of retinopathy in pregnancy depends on a variety of factors
including severity of retinopathy at conception, adequacy of
treatment, duration of diabetes, metabolic control before
pregnancy, and the presence of additional vascular damage such as
preexisting or concomitant hypertensive disorder. The risks of
visual loss in those with minimal retinopathy at the inception of
pregnancy are minor, and for these mothers a fundus examination
every 3 months should suffice. In those with moderate background
retinopathy, funduscopy should be performed at each obstetric visit
(which is usually every 4 to 6 weeks) and if progression is
detected the patient should be examined at 2 week intervals to
detect any high risk characteristics. If high risk characteristics
develop photocoagulation should be carried out promptly and
monitored by funduscopy. In those with severe sight threatening
retinopathy, laser photocoagulation should be performed before
pregnancy or promptly when high risk characteristics develop.R M
BEST U CHAKRAVARTHY Department of Ophthalmology, Queens University
of Belfast, Royal Victoria Hospital, Belfast BT12 6BA1 Kohner EM,
Porta M. Protocols for screening and treatment of diabetic
retinopathy in Europe. Eur J Ophthalmol 1991;1:4554. 2 White P.
Diabetes mellitus in pregnancy. Clin Perinatol 1974;1:33147. 3
Moloney JB, Drury MI. The effect of pregnancy on the natural course
of diabetic retinopathy. Am J Ophthalmol 1982;93:74556. 4 Klein R,
Klein BE, Moss SE, Davis MD, DeMets DL. The Wisconsin epidemiologic
study of diabetic retinopathy. III Prevalence and risk of diabetic
retinopathy when age at diagnosis is 30 or more years. Arch
Ophthalmol 1984;102:52732. 5 Klein BE, Moss SE, Klein R. Effect of
pregnancy on progression of diabetic retinopathy. Diabetes Care
1990;13:3440. 6 Phelps RL, Sakol P, Metzger BE, Jampol LM, Freinkel
N. Changes in diabetic retinopathy during pregnancy. Correlations
with regulation of hyperglycemia. Arch Ophthalmol 1986;104:180610.
7 Diabetes in Early Pregancy Study. Metabolic control and
progression of retinopathy. Diabetes Care 1995;18:6317. 8 Dibble
CM, Kochenour NK, Worley RJ, Tyler FH, Swartz M. Effect of
pregnancy on diabetic retinopathy. Obstet Gynecol
1982;59:699704. 9 Sunness JS. The pregnant womans eye. Surv
Ophthalmol 1988;32:21938. 10 Soubrane G, Canivet J, Coscas G.
Influence of pregnancy on the evolution of background retinopathy.
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Inte Ophthalmol 1985;8:24955. 11 Chen HC, Newsom RS, Patel V,
Cassar J, Mather H, Kohner EM. Retinal blood flow changes during
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diabetes. A physiological perspective. Diabetes 1995;44:7216. 13
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Rubin PC. Pre-eclampsiathe disease of theories. Br Med Bull
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glucose control and the evolution of diabetic retinopathy and
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Gynaecol 1984;91:117. 19 Klein BE, Klein R, Meuer SM, Moss SE,
Dalton DD. Does the severity of diabetic retinopathy predict
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BE, Klein R. Gravidity and diabetic retinopathy. Am J Epidemiol
1984;119:5649. 21 Chaturvedi N, Stephenson JM, Fuller JH. The
relationship between pregnancy and long-term maternal complications
in the EURODIAB IDDM Complications Study. Diabetic Med
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influence of pregnancy on IDDM complications. Diabetes Care
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Arch Ophthalmol 1994; 112:121728. 24 Hercules BL,Wozencroft M,
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Conway M, Baldwin J, Kohner EM, Schulenburg WE, Cassar J.
Postpartum progression of diabetic retinopathy. Diabetes Care
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Gabbe S. Macular edema and pregnancy in insulin-dependent diabetes.
Am J Ophthalmol 1984;97: 15467. 28 Cassar J, Hamilton AM, Kohner
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Arch Ophthalmol 1995;113:3651. 32 Reid M, Hadden D, Harley JMG,
Halliday HL, McClure BG. fetal malformations in diabetics with high
haemoglobin A1c in early pregnancy. BMJ 1984;289:1001. 33 Jovanovic
R, Jovanovic L. Obstetric management when normoglycemia is
maintained in iabetic pregnant women with vascular compromise. Am J
Obstet Gynecol 1984;149:61723. 34 Hopp H, Vollert W, Weitzel H,
Glockner E, Jahrig D. Diabetic retinopathy and nephropathy.
Complications during pregnancy and delivery. Geburtshilfe und
Frauenheilkunde 1995;55:2759. 35 Gibb D, Hockey S, Brown LJ, Lunt
H. Attitudes and knowledge regarding contraception and
prepregnancy. NZ Med J 1994;107:4846.
Diabetic retinopathy in pregnancy 251
Diabetes Mellitus in Pregnancy (Gestational Diabetes)
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(See also Diabetes Mellitus and Disorders of Carbohydrate
Metabolism) Pregnancy aggravates preexisting type 1
(insulin-dependent) and type 2 (non insulin-dependent) diabetes but
does not appear to exacerbate diabetic retinopathy, nephropathy, or
neuropathy. Gestational diabetes (diabetes that begins during
pregnancy) can develop in overweight, hyperinsulinemic,
insulin-resistant women or in thin, relatively insulin-deficient
women. Gestational diabetes occurs in 1 to 3% of all pregnancies,
but the rate may be much higher in certain groups (eg, Mexican
Americans, American Indians, Asians, Indians, Pacific Islanders).
Diabetes during pregnancy increases fetal and maternal morbidity
and mortality. Neonates are at risk of respiratory distress,
hypoglycemia, hypocalcemia, hyperbilirubinemia, polycythemia, and
hyperviscosity. Poor control of preexisting or gestational diabetes
during organogenesis (up to about 10 wk gestation) increases risk
of major congenital malformations and spontaneous abortion. Poor
control of diabetes later in pregnancy increases risk of fetal
macrosomia (usually defined as fetal weight > 4000 or > 4500
g at birth), preeclampsia, and spontaneous abortion. However,
gestational diabetes can result in fetal macrosomia even if plasma
glucose is kept nearly normal. Treatment
Close monitoring Tight control of plasma glucose Management of
complications
Preconception counseling and optimal control of diabetes before,
during, and after pregnancy minimize maternal and fetal risks,
including congenital malformations. Because malformations may
develop before pregnancy is diagnosed, the need for constant,
strict control of glucose levels is stressed to women who have
diabetes
and who are considering pregnancy (or who are not using
contraception). Most experts recommend that all pregnant women be
screened for gestational diabetes. A glucose tolerance test is
usually recommended, but the diagnosis can probably be made by a
fasting plasma glucose of > 126 mg/dL or a random plasma glucose
> 200 mg/dL (see Approach to the Pregnant Woman and Prenatal
Care: Laboratory testing). To minimize risks, clinicians should do
all of the following:
Involve a diabetes team (eg, physicians, nurses, nutritionists,
social workers) and a pediatrician Promptly diagnose and treat
complications of pregnancy, no matter how trivial Plan for delivery
and have an experienced pediatrician present Ensure that neonatal
intensive care is available
In regional perinatal centers, specialists in management of
diabetic complications are available. During pregnancy: Treatment
can vary, but some general management guidelines are useful (see
Table 1: Pregnancy Complicated by Disease: Management of Type 1
Diabetes Mellitus* During Pregnancy , Table 2: Pregnancy
Complicated by Disease: Management of Type 2 Diabetes Mellitus*
During Pregnancy , and Table 3: Pregnancy Complicated by Disease:
Management of Gestational Diabetes During Pregnancy ). Women with
type 1 or 2 should monitor their plasma glucose levels at home.
During pregnancy, normal fasting plasma glucose levels are about 76
mg/dL (4.2 mmol/L); treatment aims to keep fasting plasma glucose
levels at < 95 mg/dL (5.3 mmol/L) and 2-h postprandial levels at
120 mg/dL ( 6.6 mmol/L). The goals are no wide plasma glucose
fluctuations and glycosylated Hb (Hb A1c) levels kept at < 8%.
Table 1 Management of Type 1 Diabetes Mellitus* During Pregnancy
Time Frame Measures Before conception Diabetes is controlled. Risk
is lowest if Hb A1c levels are 8% at conception. Evaluation
includes
24-h urine collection (protein excretion and creatinine
clearance) to check for renal complications Ophthalmologic
examination to check for
retinal complications Prenatal ECG to check for cardiac
complications Prenatal visits begin as soon as pregnancy is
recognized. Frequency of visits is determined by degree of glycemic
control.
Diet should be individualized according to ADA guidelines and
coordinated with insulin Some Trade Names HUMULIN NOVOLIN Click for
Drug Monograph administration. Three meals and 3 snacks/day are
recommended, with emphasis on consistent timing. Women are
instructed in and should do plasma glucose self-monitoring. Women
should be cautioned about the dangers of hypoglycemia during
exercise and at night. Women and their family members should be
instructed in glucagon administration. Hb A1c level should be
checked every trimester. Fetal monitoring with the following should
be done weekly from 32 wk to delivery (or earlier if
indicated):
Nonstress tests Biophysical profiles Kick counts
Amount and type of insulin Some Trade Names HUMULIN NOVOLIN
Click for Drug Monograph should be individualized. In the am; 2/3
of total dose (60% NPH, 40% regular) is taken; in the pm; 1/3 (50%
NPH, 50% regular) is taken. During labor and delivery Vaginal
delivery at term is possible if women have documented dating
criteria and good glycemic control.
Amniocentesis is not done unless indicated for another problem
or requested by the couple. Cesarean delivery should be reserved
for obstetrical indications or fetal macrosomia (>4500 g), which
increases risk of shoulder dystocia. Delivery should occur by 38-40
wk. During delivery, a constant low-dose insulin Some Trade Names
HUMULIN NOVOLIN Click for Drug Monograph infusion is usually
preferred, and the usual sc administration of insulin Some Trade
Names HUMULIN NOVOLIN Click for Drug Monograph is stopped. If
induction is planned, the usual PM NPH insulin Some Trade Names
HUMULIN NOVOLIN Click for Drug Monograph dose is given on the day
before induction. Postpartum and continuing diabetes care should be
arranged. Postpartum insulin Some Trade Names HUMULIN NOVOLIN Click
for Drug Monograph requirements may decrease by up to 50%. *
Guidelines are only suggested; marked individual variations require
appropriate adjustments. Normal values may differ depending on
laboratory methods used. Some hospital programs recommend up to 4
insulin Some Trade Names HUMULIN NOVOLIN Click for Drug Monograph
injections daily. Continuous sc insulin Some Trade Names HUMULIN
NOVOLIN Click for Drug Monograph
infusion, which is labor-intensive, can sometimes be given in
specialized diabetic research settings. ADA = American Diabetes
Association; Hb A1c = glycosylated Hb; NPH = neutral protamine
Hagedorn. Table 2 Management of Type 2 Diabetes Mellitus* During
Pregnancy Time Frame Measures Before conception Hyperglycemia is
controlled. Risk is lowest if Hb A1c levels are 8% at conception.
Weight loss is encouraged if BMI is >27 kg/m2. The diet should
be low in fat, relatively high in complex carbohydrates, and high
in fiber. Prenatal Exercise is encouraged. For overweight women,
diet and caloric intake are individualized and monitored to avoid
weight gain of >9 kg; daytime snacks are discouraged. Moderate
walking after meals is recommended. Women are instructed in and
should do plasma glucose self-monitoring. The 2-h postbreakfast
plasma glucose level is checked weekly at clinic visits. Hb A1c
level should be checked every trimester. Fetal monitoring with the
following should be done weekly from 32 wk to delivery (or earlier
if indicated):
Nonstress tests Biophysical profiles Kick counts
Amount and type of insulin Some Trade Names HUMULIN NOVOLIN
Click for Drug Monograph is individualized. For obese women,
regular insulin Some Trade Names HUMULIN NOVOLIN
Click for Drug Monograph is taken before each meal. For women
who are not obese, 2 /3 of total dose (60% NPH, 40% regular) is
taken in the am; 1/3 (50% NPH, 50% regular) is taken in the pm.
During labor and Management is the same as for type 1 (see Table 1:
delivery Pregnancy Complicated by Disease: Management of Type 1
Diabetes Mellitus* During Pregnancy ). * Guidelines are only
suggested; marked individual variations require appropriate
adjustments. Normal values may differ depending on laboratory
methods used. BMI = body mass index; Hb A1c = glycosylated Hb; NPH
= neutral protamine Hagedorn. Table 3 Management of Gestational
Diabetes During Pregnancy Time Frame Measures Before conception
Women who have had gestational diabetes in previous pregnancies
should try to reach a normal weight and engage in modest exercise.
The diet should be low in fat, relatively high in complex
carbohydrates, and high in fiber. Fasting plasma glucose and Hb A1c
levels should be checked. Diet and caloric intake are
individualized and monitored to prevent weight gain of >9 kg.
Obese women are discouraged from daytime snacks. Moderate exercise
after meals is recommended. Fetal monitoring with the following
should be done weekly from 32 wk to delivery (or earlier if
indicated):
Prenatal
Nonstress tests Biophysical profiles Kick counts
Insulin Some Trade Names HUMULIN NOVOLIN Click for Drug
Monograph therapy is reserved for persistent hyperglycemia (fasting
plasma glucose >95 mg/dL or 2-h postprandial plasma glucose
>120 mg/dL) despite a trial of dietary therapy
for 2 wk. The amount and type of insulin Some Trade Names
HUMULIN NOVOLIN Click for Drug Monograph should be individualized.
For obese women, regular insulin Some Trade Names HUMULIN NOVOLIN
Click for Drug Monograph is taken before each meal. For women who
are not obese, 2/3 of total dose (60% NPH, 40% regular) is taken in
the am; 1/3 (50% NPH, 50% regular) is taken in the pm. During labor
and delivery Vaginal delivery at term is possible if women have a
well-documented delivery date and good diabetic control.
Amniocentesis may not be required. Cesarean delivery should be
reserved for obstetric indications or fetal macrosomia (>4500
g), which increases risk of shoulder dystocia. Delivery should
occur by 38-40 wk. Hb A1c = glycosylated Hb; NPH = neutral
protamine Hagedorn. Insulin is the traditional drug of choice
because it cannot cross the placenta and provides more predictable
glucose control; it is used for types 1 and 2 diabetes and for some
women with gestational diabetes. Human insulin is used if possible
because it minimizes antibody formation. Insulin antibodies cross
the placenta, but their effect on the fetus is unknown. In some
women with long-standing type 1 diabetes, hypoglycemia does not
trigger the normal release of counterregulatory hormones
(catecholamines, glucagon, cortisol, and growth hormone); thus, too
much insulin can trigger hypoglycemic coma without premonitory
symptoms. All pregnant women with type 1 should have glucagon kits
and be instructed (as should family members) in giving glucagon if
severe hypoglycemia (indicated by unconsciousness, confusion, or
plasma glucose levels < 40 mg/dL [< 2.2 mmol/L]) occurs. Oral
hypoglycemic drugs (eg, glyburide Some Trade Names DIABETA GLYNASE
MICRONASE
Click for Drug Monograph ) are being increasingly used to manage
diabetes in pregnant women because of the ease of administration
(pills compared to injections), low cost, and single daily dosing.
Several studies have demonstrated that glyburide Some Trade Names
DIABETA GLYNASE MICRONASE Click for Drug Monograph is safe during
pregnancy and that it provides control equivalent to that of
insulin for women with gestational diabetes. For women with type II
diabetes before pregnancy, data for oral drugs are scant; insulin
is most often preferred. Oral hypoglycemics taken during pregnancy
may be continued postpartum during breastfeeding, but the infant
should be closely monitored for signs of hypoglycemia. Management
of complications: Although diabetic retinopathy, nephropathy, and
mild neuropathy do not contraindicate pregnancy, they require
preconception counseling and close management before and during
pregnancy. Retinopathy requires that an ophthalmologic examination
be done every trimester. If proliferative retinopathy is noted at
the first prenatal visit, photocoagulation should be used as soon
as possible to prevent progressive deterioration. Nephropathy,
particularly in women with renal transplants, predisposes to
pregnancy-induced hypertension. Risk of preterm delivery is higher
if maternal renal function is impaired or if transplantation was
recent. Prognosis is best if delivery occurs 2 yr after
transplantation. Congenital malformations of major organs are
predicted by elevated Hb A1c levels at conception and during the
first 8 wk of pregnancy. If the level is 8.5% during the 1st
trimester, risk of congenital malformations is significantly
increased, and targeted ultrasonography and fetal echocardiography
are done during the 2nd trimester to check for malformations. If
women with type 2 diabetes take oral hypoglycemic drugs during the
1st trimester, fetal risk of congenital malformations is unknown
(see Table 2: High-Risk Pregnancy: Drugs With Adverse Effects
During Pregnancy ). Labor and delivery: Certain precautions are
required to ensure an optimal outcome. Timing of delivery depends
on fetal well-being. Women are told to count fetal movements during
a 60-min period daily (fetal kick count) and to report any sudden
decreases to the obstetrician immediately. Nonstress testing (see
Normal Pregnancy, Labor, and Delivery: Fetal Monitoring) is begun
at 32 wk and, if
results are nonreassuring, is followed by a biophysical profile
(measurement of amniotic fluid and fetal muscle tone, movement, and
breathing pattern). These tests and similar noninvasive prenatal
fetal monitoring tests (called antenatal testing) are initiated
earlier if women have severe hypertension or a renal disorder or if
fetal growth restriction is suspected. Amniocentesis to assess
fetal lung maturity is often necessary in women with the
following:
Obstetric complications in past pregnancies Elective delivery
before 39 wk Inadequate prenatal care Uncertain delivery date Poor
glucose control
Type of delivery is usually spontaneous vaginal delivery at
term. If labor does not begin spontaneously by 38 to 40 wk,
induction is necessary because of the increasing risk of stillbirth
and shoulder dystocia. Dysfunctional labor, fetopelvic
disproportion, or risk of shoulder dystocia may make cesarean
delivery necessary. Plasma glucose levels are best controlled
during labor and delivery by a continuous low-dose insulin Some
Trade Names HUMULIN NOVOLIN Click for Drug Monograph infusion. If
induction is planned, women eat their usual diet the day before and
take their usual insulin Some Trade Names HUMULIN NOVOLIN Click for
Drug Monograph dose. On the morning of labor induction, breakfast
and insulin Some Trade Names HUMULIN NOVOLIN Click for Drug
Monograph are withheld, baseline fasting plasma glucose is
measured, and an IV infusion of 5% dextrose in 0.45% saline
solution is started at 125 mL/h, using an infusion pump. Initial
insulin Some Trade Names HUMULIN NOVOLIN Click for Drug Monograph
infusion rate is determined by capillary glucose level. Insulin
Some Trade Names HUMULIN NOVOLIN Click for Drug Monograph dose is
determined as followed:
Initially: 0 units for a capillary level of < 80 mg/dL (<
4.4 mmol/L) or 0.5 units/h for a level of 80 to 100 mg/dL (4.4 to
5.5 mmol/L) Thereafter: Increased by 0.5 units/h for each 40-mg/dL
(2.2-mmol/L) increase in glucose level over 100 mg/dL up to 2.5
units/h for levels > 220 mg/dL (> 12.2 mmol/L) Every hour
during labor: Measurement of glucose level at bedside and
adjustment of dose to keep the level at 70 to 120 mg/dL (3.8 to 6.6
mmol/L) If the glucose level is significantly elevated: Possibly
additional bolus doses
For spontaneous labor, the procedure is the same, except that if
intermediateacting insulin Some Trade Names HUMULIN NOVOLIN Click
for Drug Monograph was taken in the previous 12 h, the insulin Some
Trade Names HUMULIN NOVOLIN Click for Drug Monograph dose is
decreased. For women who have fever, infection, or other
complications and for obese women who have type 2 and have required
> 100 units of insulin Some Trade Names HUMULIN NOVOLIN Click
for Drug Monograph /day before pregnancy, the insulin Some Trade
Names HUMULIN NOVOLIN Click for Drug Monograph dose is increased.
Postpartum: After delivery, loss of the placenta, which synthesizes
large amounts of insulin Some Trade Names HUMULIN NOVOLIN Click for
Drug Monograph antagonist hormones throughout pregnancy, decreases
the insulin requirement immediately. Thus, women with gestational
diabetes and many of those with type 2 require no insulin Some
Trade Names HUMULIN NOVOLIN Click for Drug Monograph postpartum.
For women with type 1, insulin requirements decrease
dramatically
but then gradually increase after about 72 h. During the first 6
wk postpartum, the goal is tight glucose control. Glucose levels
are checked before meals and at bedtime. Breastfeeding is not
contraindicated but may result in hypoglycemia if oral
hypoglycemics are taken. Women who have had gestational diabetes
should have a 2-h oral glucose tolerance test with 75 g of glucose
at 6 to 12 wk postpartum to determine whether diabetes has
resolved. Last full review/revision December 2008 by Sean C.
Blackwell, MD Content last modified December 2008
Progression of retinopathy during pregnancy in type 1 diabetes
mellitus.Rahman W, Rahman FZ, Yassin S, Al-Suleiman SA, Rahman J.
University Hospitals of Leicester, Leicester, UK. PURPOSE: The
incidence and risk factors for progression of retinopathy during
pregnancy in women with type 1 diabetes mellitus were
retrospectively evaluated. METHODS: Fifty-four insulin-dependent
diabetic patients at a teaching hospital in Saudi Arabia were
followed throughout the pregnancy/puerperium with serial ophthalmic
examination. Dilated fundus examination was performed in each
trimester and puerperium. RESULTS: Progression of diabetic
retinopathy in the study occurred in 13/54 (24%) patients--2/22
(9.1%) patients had no diabetic retinopathy initially, 4/20 (20%)
had non-proliferative diabetic retinopathy (NPDR) and 7/12 (58.3%)
had proliferative diabetic retinopathy (PDR). Of the eight patients
with PDR who had no laser treatment before pregnancy, six (75%)
showed progression but only one of the four patients who had PDR
and laser treatment prior to pregnancy experienced progression of
retinopathy. Eight patients in total received panretinal
photocoagulation to arrest the progression of retinal disease
during pregnancy and only one of them had laser treatment prior to
pregnancy. CONCLUSION: Laser photocoagulation for severe NPDR or
early PDR prior to pregnancy may protect against rapid progression
of PDR. Visual impairment resulting from progression of PDR can be
prevented by aggressive laser treatment during pregnancy. Duration
of diabetes>15 years, poor glycaemic control and hypertension
are high-risk factors in the progression of diabetic retinopathy in
pregnancy. PMID: 17430509 [PubMed - indexed for MEDLINE]
MeSH Termshttp://www.pakmedinet.com/4704
Chapter 36
Pregnancy in Preexisting DiabetesThomas A. Buchanan,
M.D.SUMMARY
D
ata from birth certificates in the United
States indicate that maternal diabetes complicates 2%-3% of all
pregnancies, but these data may underestimate the true prevalence
of maternal diabetes in pregnancy. Two major forms of maternal
diabetes may occur during pregnancy: preexisting or
"pregestational" diabetes, and gestational-onset or gestational
diabetes mellitus (GDM). Only the former is known prior to
pregnancy, and this form constitutes ~10% of cases of maternal
diabetes. Thus, prevalence rates for pregestational diabetes appear
to be in the range of 0.1%-0.3% of all pregnancies. These
pregnancies are at risk for both maternal and fetal complications.
Fetal complications of maternal diabetes can be divided into two
major categories. Complications that arise from the effects of
maternal diabetes on early fetal development (i.e., in the first
trimester) include spontaneous abortions and major congenital
malformations. In the absence of special preconceptional diabetes
management, spontaneous abortions occur in 7%-17% of diabetic
pregnancies and major malformations occur in 7%-13%. Rates of both
complications are highest in women with the most marked
hyperglycemia during the first trimester, and the rates of
malformations appear to be decreasing in countries and medical
centers where standards of diabetes care result in improved
maternal blood glucose control prior to and during early pregnancy.
The most prominent
fetal complications that can arise during the second and third
trimesters are stillbirth and macrosomia (an excessively large
infant). Stillbirths are now uncommon in diabetic pregnancies;
congenital malformations and complications of maternal hypertensive
disorders account for most of the 1.5- to 2-fold increase in
perinatal mortality compared with nondiabetic pregnancies.
Macrosomia appears to be the most frequent fetal complication,
affecting 10%33% of infants, depending on the definition used for
macrosomia. Macrosomia increases the risk of birth trauma and has
been associated with a long-term risk of obesity in offspring.
Maternal risks in diabetic pregnancies are greatest in the presence
of preexisting microvascular disease (retinopathy and nephropathy).
Diabetic retinopathy is present in 15%-66% of women early in
pregnancy, and the retinopathy frequently worsens during gestation,
especially when severe background or proliferative changes are
present early on. Laser photocoagulation therapy prior to pregnancy
can reduce the risk that proliferative retinopathy will worsen
during gestation. Overt diabetic nephropathy is present before
pregnancy in 5%-10% of patients; of these, two-thirds manifest
hypertensive disorders during gestation. The hypertensive disorders
precede pregnancy in approximately half of the cases and develop
during pregnancy in the other half. Overt diabetic nephropathy in
mothers increases the prevalence of intrauterine growth retardation
and prematurity in infants; fetal morbidity and mortality increase
as well. The long-term impact of pregnancy on diabetic retinopathy
and nephropathy in mothers is not known.
719
There is no national surveillance program for diabetes during
pregnancy in the United States. As a result, it is not possible to
determine true national prevalence rates for diabetes during
pregnancy or for the various maternal and fetal complications that
can occur when diabetes and pregnancy coexist. Data to help
estimate prevalence rates for diabetes and its complications during
pregnancy come from several sources. Since 1989, birth certificates
in most states and the District of Columbia have included
information on a variety of maternal and infant risk factors,
including diabetes1. The birth certificate data provide the first
national estimates of the prevalence of diabetes during pregnancy.
However, the certificates do not distinguish between the focus of
this chapter, diabetes that existed prior to
pregnancypregestational diabetes, including insulin-dependent
diabetes mellitus (IDDM) and non-insulin-dependent diabetes
mellitus (NIDDM)
and diabetes that is first detected during pregnancy (GDM,
discussed in Chapter 35). Birth certificate data may also suffer
from inaccurate reporting of maternal and fetal complications
(e.g., only 65% of maternal diabetes was recorded on birth
certificates surveyed in Tennessee in 1989)2. Other data sources
include regional or statewide data derived from a combination of
birth certificate and hospital record information and published
reports from individual medical centers. The former source may be
the most complete for a specific region, although t