Tuesday, October 23, 2007

Diabetic Retinopathy - Treatment & Prevention


Diabetic retinopathy is treated in many ways depending on the stage of the disease and the specific problem that requires attention. The retinal surgeon relies on several tests to monitor the progression of the disease and to make decisions for the appropriate treatment. These include: fluorescein angiography, retinal photography, and ultrasound imaging of the eye.
The abnormal growth of tiny blood vessels and the associated complication of bleeding is one of the most common problems treated by vitreo-retinal surgeons. Laser surgery called pan retinal photocoagulation (PRP) is usually the treatment of choice for this problem.
With PRP, the surgeon uses laser to destroy oxygen-deprived retinal tissue outside of the patient’s central vision. While this creates blind spots in the peripheral vision, PRP prevents the continued growth of the fragile vessels and seals the leaking ones. The goal of the treatment is to arrest the progression of the disease.
Vitrectomy is another surgery commonly needed for diabetic patients who suffer a vitreous hemorrhage (bleeding in the gel-like substance that fills the center of the eye). During a vitrectomy, the retina surgeon carefully removes blood and vitreous from the eye, and replaces it with clear salt solution (saline). At the same time, the surgeon may also gently cut strands of vitreous attached to the retina that create traction and could lead to retinal detachment or tears.
Patients with diabetes are at greater risk of developing retinal tears and detachment. Tears are often sealed with laser surgery. Retinal detachment requires surgical treatment to reattach the retina to the back of the eye. The prognosis for visual recovery is dependent on the severity of the detachment.

Researchers have found that diabetic patients who are able to maintain appropriate blood sugar levels have fewer eye problems than those with poor control. Diet and exercise play important roles in the overall health of those with diabetes.
Diabetics can also greatly reduce the possibilities of eye complications by scheduling routine examinations with an ophthalmologist. Many problems can be treated with much greater success when caught early.

Diabetic Retinopathy - Signs & Symptoms, Detection & Diagnosis

Signs and Symptoms

The affect of diabetic retinopathy on vision varies widely, depending on the stage of the disease. Some common symptoms of diabetic retinopathy are listed below, however, diabetes may cause other eye symptoms.

* Blurred vision (this is often linked to blood sugar levels
* Floaters and flashes
* Sudden loss of vision

Detection and Diagnosis

Diabetic patients require routine eye examinations so related eye problems can be detected and treated as early as possible. Most diabetic patients are frequently examined by an internist or endocrinologist who in turn work closely with the ophthalmologist.
The diagnosis of diabetic retinopathy is made following a detailed examination of the retina with an ophthalmoscope. Most patients with diabetic retinopathy are referred to vitreo-retinal surgeons who specialize in treating this disease.

Diabetic Retinopathy- Overview


Diabetes is a disease that occurs when the pancreas does not secrete enough insulin or the body is unable to process it properly. Insulin is the hormone that regulates the level of sugar (glucose) in the blood. Diabetes can affect children and adults.

How does diabetes affect the retina?

Patients with diabetes are more likely to develop eye problems such as cataracts and glaucoma, but the disease’s affect on the retina is the main threat to vision. Most patients develop diabetic changes in the retina after approximately 20 years. The effect of diabetes on the eye is called diabetic retinopathy.
Over time, diabetes affects the circulatory system of the retina. The earliest phase of the disease is known as background diabetic retinopathy. In this phase, the arteries in the retina become weakened and leak, forming small, dot-like hemorrhages. These leaking vessels often lead to swelling or edema in the retina and decreased vision.
The next stage is known as proliferative diabetic retinopathy. In this stage, circulation problems cause areas of the retina to become oxygen-deprived or ischemic. New, fragile, vessels develop as the circulatory system attempts to maintain adequate oxygen levels within the retina. This is called neovascularization. Unfortunately, these delicate vessels hemorrhage easily. Blood may leak into the retina and vitreous, causing spots or floaters, along with decreased vision.
In the later phases of the disease, continued abnormal vessel growth and scar tissue may cause serious problems such as retinal detachment and glaucoma.

Friday, October 12, 2007

Diabetes ABC’s

An important concept that has is used by organizations is to “Manage the ABCs of Diabetes.”

(A) is for A1C.
This test shows average blood sugar for the past 2 to 3 months. An A1C test can help monitor how well the treatment plan is working. The ADA recommends that an A1C test be completed twice a year.

(B) is for Blood Pressure. The American College of Physicians has made the following important recommendations.
· Blood Pressure control must be a priority if the person has hypertension and type 2 diabetes.
· Blood pressure should be checked with each visit to the doctor and the goal should be a reading of no more than 135/80.
· Thiazide diurectics or ACE inhibiorts are types of medication that the doctor might prescribe to control blood pressure.

(C) is for Cholosterol.
Colesterol numbers tell the amount of fat in the blood. HDL cholesterol helps protect the heart. LDL cholesterol can clog arteries and lead to heart disease. Triglycerides are another kind of blood fat the can affect the risk of heart attack or stroke. The American Diabetes Association recommends that cholesterol be checked at least once a year.

Diabetes Insulin Resistance of Pregnancy

One of the dominant metabolic effects of normal pregnancy is an increase in insulin resistance, probably induced by placental hormones including progesterone and placental lactogen. This leads to higher postprandial glucose concentrations that are considered to improve fetal growth; it is termed 'facilitated anabolism'. Fasting glucose concentrations decrease as a result of placental glucose transfer and in the later stages of pregnancy, there is also enhanced maternal lipolysis. This is considered to spare glucose for the fetus and is termed 'accelerated starvation'.

In genetically predisposed women, the normal insulin resistance of pregnancy may lead to the diagnosis of DM for the first time, termed 'gestational diabetes'. This may disappear within hours of giving birth depending on individual factors such as islet b-cell function and predisposing factors such as obesity. Women with pre-existing DM require higher doses of insulin during pregnancy and patients who are usually controlled using oral hypoglycemic agents are transferred to insulin at this time.

The effects of pregnancy-induced insulin resistance in women with DM lead to poorer control of blood glucose and also an increased likelihood of ketoacidosis. The hyperglycemia in early pregnancy has considerable effects on the development of the fetal pancreas. Maternal ketoacidosis leads to fetal loss.

Diabetes Complications

Diabetes can cause serious health complications including heart disease, blindness, kidney failure, and lower-extremity amputations.

Some of the complications that can arise from diabetes are:

Heart disease and stroke
· Heart disease and stroke account for about 65% of deaths in people with diabetes.
· Adults with diabetes have heart disease death rates about 2 to 4 times higher than adults without diabetes.
· The risk for stroke is 2 to 4 times higher among people with diabetes.

High blood pressure
· About 73% of adults with diabetes have blood pressure greater than or equal to 130/80 millimeters of mercury (mm Hg) or use prescription medications for hypertension.

· Diabetes is the leading cause of new cases of blindness among adults aged 20-74 years.
· Diabetic retinopathy causes 12,000 to 24,000 new cases of blindness each year.

Kidney disease
· Diabetes is the leading cause of kidney failure, accounting for 44% of new cases in 2002.
· In 2002, 44,400 people with diabetes began treatment for end-stage kidney disease in the United States and Puerto Rico.
· In 2002, 153,730 people with end-stage kidney disease due to diabetes were living on chronic dialysis or with a kidney transplant in the United States and Puerto Rico.

Nervous system disease
· About 60% to 70% of people with diabetes have mild to severe forms of nervous system damage. The results of such damage include impaired sensation or pain in the feet or hands, slowed digestion of food in the stomach, carpal tunnel syndrome, and other nerve problems.
· Almost 30% of people with diabetes aged 40 years or older have impaired sensation in the feet (i.e., at least one area that lacks feeling).
· Severe forms of diabetic nerve disease are a major contributing cause of lower-extremity amputations.

· More than 60% of nontraumatic lower-limb amputations occur in people with diabetes.
· In 2002, about 82,000 nontraumatic lower-limb amputations were performed in people with diabetes.

Dental disease
· Periodontal (gum) disease is more common in people with diabetes. Among young adults, those with diabetes have about twice the risk of those without diabetes.
· Almost one-third of people with diabetes have severe periodontal disease with loss of attachment of the gums to the teeth measuring 5 millimeters or more.

Complications of pregnancy
· Poorly controlled diabetes before conception and during the first trimester of pregnancy can cause major birth defects in 5% to 10% of pregnancies and spontaneous abortions in 15% to 20% of pregnancies.
· Poorly controlled diabetes during the second and third trimesters of pregnancy can result in excessively large babies, posing a risk to both mother and child.

Other complications
· Uncontrolled diabetes often leads to biochemical imbalances that can cause acute life-threatening events, such as diabetic ketoacidosis and hyperosmolar (nonketotic) coma.
· People with diabetes are more susceptible to many other illnesses and, once they acquire these illnesses, often have worse prognoses. For example, they are more likely to die with pneumonia or influenza than people who do not have diabetes.

Glucose Metabolism Physiology

Glucose is an essential fuel for the body. The amount of glucose in the bloodstream is regulated by many hormones, the most important being insulin.

Insulin has been described as the "hormone of plenty" it is released when glucose is abundant and stimulates the following:

Muscle and fat cells to remove glucose from the blood

Cells to breakdown glucose, releasing its energy in the form of ATP (via glycolysis and the citric acid cycle)

The liver and muscle to store glucose as glycogen (short-term energy reserve)

Adipose tissue to store glucose as fat (long-term energy reserve)

Cells to use glucose in protein synthesis

Glucagon is the main hormone opposing the action of insulin and is released when food is scarce.
Whereas insulin triggers the formation of glycogen (an energy-requiring process, or an anabolic effect), glucagon triggers glycogen breakdown, which releases energy (a catabolic effect). Glucagon also helps the body to switch to using resources other than glucose, such as fat and protein.

Blood glucose levels are not constant they rise and fall depending on the body's needs, regulated by hormones. This results in glucose levels normally ranging from 70 to 110 mg/dl.

The blood glucose level can rise for three reasons: diet, breakdown of glycogen, or through hepatic synthesis of glucose.

Eating produces a rise in blood glucose, the extent of which depends on a number of factors such as the amount and the type of carbohydrate eaten (i.e., the glycemic index), the rate of digestion, and the rate of absorption. Because glucose is a polar molecule, its absorption across the hydrophobic gut wall requires specialized glucose transporters (GLUTS) of which there are five types. In the gut, GLUT2 and GLUT5 are the most common.

The liver is a major producer of glucose. It releases glucose from the breakdown of glycogen and also makes glucose from intermediates of carbohydrate, protein, and fat metabolism. The liver is also a major consumer of glucose and can buffer glucose levels. It receives glucose-rich blood directly from the digestive tract via the portal vein. The liver quickly removes large amounts of glucose from the circulation so that even after a meal, the blood glucose levels rarely rise above 110 mg/dl in a non-diabetic.

The rise in blood glucose following a meal is detected by the pancreatic beta cells, which respond by releasing insulin. Insulin increases the uptake and use of glucose by tissues such as skeletal muscle and fat cells. This rise in glucose also inhibits the release of glucagon, inhibiting the production of glucose from other sources, e.g., glycogen break down.

Use Glucose - Once inside the cell, some of the glucose is used immediately via glycolysis. This is a central pathway of carbohydrate metabolism because it occurs in all cells in the body, and because all sugars can be converted into glucose and enter this pathway. During the well-fed state, the high levels of insulin and low levels of glucagon stimulate glycolysis, which releases energy and produces carbohydrate intermediates that can be used in other metabolic pathways.

Make Glycogen - Any glucose that is not used immediately is taken up by the liver and muscle where it can be converted into glycogen (glycogenesis). Insulin stimulates glycogenesis in the liver by:

Stimulating hepatic glycogen synthetase (the enzyme that catalyzes glycogen synthesis in the liver)

Inhibiting hepatic glycogen phosphorylase (the enzyme that catalyzes glycogen breakdown in the liver)

Inhibiting glucose synthesis from other sources (inhibits gluconeogenesis)

Insulin also encourages glycogen formation in muscle, but by a different method. Here it increases the number of glucose transporters (GLUT4) on the cell surface. This leads to a rapid uptake of glucose that is converted into muscle glycogen.

Make Fat - When glycogen stores are fully replenished, excess glucose is converted into fat in a process called lipogenesis. Glucose is converted into fatty acids that are stored as triglycerides (three fatty acid molecules attached to one glycerol molecule) for storage. Insulin promotes lipogenesis by:

Increasing the number of glucose transporters (GLUT4) expressed on the surface of the fat cell, causing a rapid uptake of glucose
Increasing lipoprotein lipase activity, which frees up more fatty acids for triglyceride synthesis

In addition to promoting fat synthesis, insulin also inhibits fat breakdown by inhibiting hormone-sensitive lipase (an enzyme that breaks down fat stores). As a result, there are lower levels of fatty acids in the blood stream.

Insulin also has an anabolic effect on protein metabolism. It stimulates the entry of amino acids into cells and stimulates protein production from amino acids.

Fasting is defined as more than eight hours without food. The resulting fall in blood sugar levels inhibits insulin secretion and stimulates glucagon release. Glucagon opposes many actions of insulin. Most importantly, glucagon raises blood sugar levels by stimulating the mobilization of glycogen stores in the liver, providing a rapid burst of glucose. In 10 18 hours, the glycogen stores are depleted, and if fasting continues, glucagon continues to stimulate glucose production by favoring the hepatic uptake of amino acids, the carbon skeletons of which are used to make glucose.

In addition to low blood glucose levels, many other stimuli stimulate glucagon release including eating a protein-rich meal (the presence of amino acids in the stomach stimulates the release of both insulin and glucagon, glucagon prevents hypoglycemia that could result from unopposed insulin) and stress (the body anticipates an increased glucose demand in times of stress).

The metabolic state of starvation is more commonly found in people trying to lose weight rapidly or in those who are too unwell to eat. After a couple of days without food, the liver will have exhausted its stores of glycogen but continues to make glucose from protein (amino acids) and fat (glycerol).

The metabolism of fatty acids (from adipose tissue) is a major source of energy for organs such as the liver. Fatty acids are broken down to acetyl-CoA, which is channeled into the citric acid cycle and generates ATP. As starvation continues, the levels of acetyl-CoA increase until the oxidative capacity of the citric acid cycle is exceeded. The liver processes these excess fatty acids into ketone bodies (3-hydroxybutyrate) to be used by many tissues as an energy source.

The most important organ that relies on ketone production is the brain because it is unable to metabolize fatty acids. During the first few days of starvation, the brain uses glucose as a fuel. If starvation continues for more than two weeks, the level of circulating ketone bodies is high enough to be used by the brain.

This slows down the need for glucose production from amino acid skeletons, thus slowing down the loss of essential proteins.

Diabetes is often referred to as "starvation in the midst of plenty" because the intracellular levels of glucose are low, although the extracellular levels may be extremely high.

As in starvation, type 1 diabetics use non-glucose sources of energy, such as fatty acids and ketone bodies, in their peripheral tissues. But in contrast to the starvation state, the production of ketone bodies can spiral out of control. Because the ketones are weak acids, they acidify the blood. The result is the metabolic state of diabetic ketoacidosis. Hyperglycemia and ketoacidosis are the hallmark of type 1 diabetes.

Hypertriglyceridemia is also seen in diabetic ketoacidosis . The liver combines triglycerol with protein to form very low density lipoprotein (VLDL). It then releases VLDL into the blood. In diabetics, the enzyme that normally degrades lipoproteins (lipoprotein lipase) is inhibited by the low level of insulin and the high level of glucagon. As a result, the levels of VLDL and chylomicrons (made from lipid from the diet) are high in diabetic ketoacidosis .

Thursday, October 11, 2007


Diabetes is a disturbance of the metabolism of sugar by the body. This results in a build-up of sugar in the blood and a lack of sugar inside the body’s cells, which need it to function properly. Large amounts of sugar are lost in the urine. It is caused by a lack of insulin or an insensitivity of cells to the effect of insulin.

Most young diabetics require insulin, which has to be injected under the skin. Older patients may be treated by oral medications or, if mild, by a special low-sugar diet. It is very important to make sure that the blood sugar level is kept within normal limits. Tight control of the blood sugar will influence the development of complications later in the disease. Most diabetics monitor their own blood sugar by using a glucometer or by dipstick urine testing for sugar.

The high blood sugar levels damage small blood vessels and, in time, this may lead to damage to eyes, kidneys, heart, nervous system and general circulation.

The longer the diabetes is present, the more likely are complications to develop. This is true for all diabetics; irrespective of how the disease is being treated i.e. insulin, oral medication or diet.

If control of blood sugar levels is good from the time of diagnosis, then the risk of developing complication is significantly reduced.

During pregnancy, the complications tend to worsen, as can happen if high blood pressure, high cholesterol or other general illnesses develop in the diabetic.

Vision is often transiently blurred during periods of poor control, illness or when treatment is begun. This blurring usually settles when the diabetes is controlled.

Vision can be threatened or lost by cataract (clouding of the lens), glaucoma (raised pressure in the eyeball) and retinopathy (damage to the essential membrane or ‘seeing’ layer at the back of the eye.

Clouding of the lens tens to occur at an earlier age in diabetics when compared to the non-diabetic population. It causes blurring of vision, glare in sunlight or difficulties with bright lights at night. The lens clouding is usually worse in poorly controlled diabetes mellitus.

Diabetics have a higher rate of developing glaucoma than non-diabetics. There are no symptoms of the raised pressure in the eye and it can only be detected by special pressure measuring test by the Ophthalmologist (eye doctor) or Optometrist (Optician). This test is carried out routinely during an eye test in most adults. Glaucoma can lead to blindness if undetected or untreated.
The duration of the diabetes and the level of control of the disease are the most important factors, which determine the amount of damage that occurs to the retina. (‘Seeing’ membrane at the back of the eye). Retinopathy (damage to the retina) is the commonest cause of blindness in diabetics and is often preventable and treatable. However, there are often no symptoms and the retinopathy can only be detected by specific examination of the back of the eyes

Often there are no symptoms at all, even in the presence of serious, sight-threatening diabetic eye disease. It is very important to have an eye examination carried out regularly so that problems can be detected and treated as early as possible. This will protect vision in the majority of diabetics with a retinopathy, which can threaten vision significantly. The earlier the treatment is carried out, the better the outcome in most patients.

“Cobwebs” or “floaters” or “clouds” are serious symptoms in any diabetic and the Ophthalmologist must carry out an immediate eye examination.

Clouding of vision or glare may indicate that a cataract has developed. This is usually successfully treated by the surgical removal of the cloudy lens and replacing it with a plastic lens.

Glaucoma does not cause any symptoms, except in very advanced disease when tunnel vision has developed. The damage caused by glaucoma is irreversible, so prevention of this damage development is possible by early diagnosis and treatment to control the disease. The risk of developing glaucoma is significantly higher if there is a family history of the disease.


When the lens has become cloudy and causes poor vision, it can be removed by an operation and replaced with a plastic lens.

Drops have to be instilled in to the eye regularly and on a long-term basis. Essential tests to check that the glaucoma is controlled have to be carried out regularly by the Ophthalmologist. Regular clinic appointments must be kept to make sure that the treatment is working.

Regular eye examinations will detect any disease affecting the eyes of diabetics. Since there are no symptoms in most cases, this examination is essential ton prevent serious damage to the sight. If this damage is not detected early, then sight will be lost and in severe cases, it will lead to blindness.

Laser treatment carried out as early as possible will prevent sight loss in the majority of patients. Te eye doctor will determine those patients who need to have this treatment and since it is usually painless, it is carried out in the out patients using a special laser machine and contact lens. This lens is removed after the laser treatment.

If planning a pregnancy, all female diabetics should have a special eye examination beforehand and will have regular check-ups during the pregnancy. Often, if eye disease is present before pregnancy, it is best treated before conception as pregnancy can make the eye disease worse. Laser treatment can be safely carried out during the pregnancy if deemed necessary.

Good control of blood sugars is critical in preventing and slowing down the progression of the damage to the retina caused by diabetes.

1. Always aim to keep the diabetes under tight control
2. Ensure that any high blood pressure or high blood cholesterol or fat levels are treated and monitored
3. Attend for regular diabetic check-ups with the doctor.
4. Keep an accurate record of appointments and blood sugar levels
5. Regularly check the vision in each eye separately (e.g. by reading the newspaper).
6. Make sure that an eye examination is carried out regularly. If an appointment is missed, seek another immediately.
7. Report any change in vision immediately.
8. If planning a pregnancy, have an eye examination by an Ophthalmologist before conception.
9. Remember – there are often NO symptoms, even when serious eye disease is present