| Diabetes Mellitus  Signs and Symptoms
Diabetes mellitus is the most common endocrine disorder, and is defined as
a group of disorders that exhibit a defective or deficient insulin secretory process,
glucose underutilization, and hyperglycemia. Possible systemic signs and symptoms include
polyuria (increased frequency of urination), polydipsia (increased thirst), polyphagia
(increased appetite), glycosuria, weakness, weight loss, neuropathy, and nephropathy.
Ophthalmic signs and symptoms may include chronic conjunctival injection, changes in
corneal curvature, large fluctuations in refraction, premature cataractogenesis,
nonproliferative and proliferative retinopathy and cranial nerve III, IV or VI palsy.
Type 1 diabetes, formerly known as insulin-dependent diabetes (IDDM) is
also referred to as juvenile-onset or ketose prone DM, usually begins by age 20 and is
defined by a severe, absolute lack of insulin caused by a reduction in the beta-cell mass
of the pancreas. This may be the result of autoimmune processes and may involve genetic
susceptibility.
Type 2 diabetes, formerly known as non-insulin-dependent diabetes
(NIDDM), sometimes referred to as adult-onset DM, usually begins after age 40 as a
multifactorial disease that may involve improper insulin secretion, malfunctioning insulin
and/or insulin resistance in peripheral tissues. Approximately 10 percent of diabetic
cases are type 1 and approximately 90 percent are Type 2.
Pathophysiology
The pancreas plays a primary role in the metabolism of glucose by secreting
the hormones insulin and glucagon. The Islets of Langerhans secrete insulin and glucagon
directly into the blood. Inadequate secretion of insulin, inadequate structure or function
of insulin or its receptors results in impaired metabolism of glucose, carbohydrates,
proteins and fats, characterized by hyperglycemia and glycosuria. Hyperglycemia is the
most frequently observed sign of diabetes and is considered the etiologic source of
diabetic complications both in the body and in the eye.
Glucagon is a hormone that opposes the action of insulin. It is secreted
when blood glucose levels fall. Glucagon increases blood glucose concentration partly by
breaking down glycogen in the liver. Following a meal, glucose is absorbed into the blood.
In response to increased blood glucose levels, insulin is secreted causing rapid uptake,
storage, or use of glucose by the tissues of the body. Unused glucose is stored as
glycogen in the liver. Between meals, when blood glucose is at minimal levels, tissues
continue to require an energy source to function properly. Stored glycogen, via glucagon,
is converted to glucose by a pathway known as glycogenolysis. Gluconeogenesis is the
production of glucose in the liver from noncarbohydrate precursors such as glycogenic
amino acids.
Elevated glucose levels result in the formation of sorbitol (a sugar
alcohol) via the aldose reductase pathway. Since sorbitol cannot readily diffuse through
cell membranes, cell edema and changes in function can ensue. With respect to the eye,
this contributes to the evolution of premature cataractogenesis (nuclear sclerotic, senile
and snowflake posterior subcapsular cataracts) and sight threatening diabetic retinopathy
(compromising the pericytes that line capillary walls).
An additional complication of hyperglycemia is nonenzymatic
glycosylation. Nonenzymatic glycosylation is the binding of excess glucose to the amino
group of proteins in the tissues. As a possible result, at the level of the capillary
membranes, altered cell function may lead to the development of microaneurysms, vascular
loops, and vessel dilation, allowing blood leakage. Platelet aggregation secondary to
these changes initiates tissue hypoxia. These changes result in the system wide
accumulation of edema and in the eye, increase the potential for retinal sequelae.
Glycemic control over the course of the disease has been shown to reduce
the risk of developing debilitating organ disease and retinopathy. Blood glucose levels
are of even greater importance in diabetic pregnant women, as hyperglycemia during
pregnancy may initiate swift and severe progression of diabetic retinopathy. Other
concurrent systemic variables that may potentiate the onset of diabetic retinopathy
include hypertension, nephropathy, cardiac disease, autonomic neuropathy and ocular
findings such as elevated intraocular pressure and myopia.
Management
The easiest method of treating Type 2 diabetes is with diet control.
Dietary regulation is set by basing the caloric intake on the patient’s ideal body
weight, selecting adequate sources of protein and carbohydrate, while maintaining a
reasonable distribution of foods. When hyperglycemia persists despite dietary changes,
oral hypoglycemic agents become necessary. These agents can be prescribed in small doses,
adjusting the dosage to larger levels to achieve tighter control, as necessary.
Insulin is always required for Type 1 and is an option for recalcitrant
cases involving Type 2 diabetes. Conventional therapy involves the administration of an
intermediate-acting insulin (NPH or lente), once or twice a day, with or without small
amounts of regular insulin.
Clinical Pearls
Large changes in refraction may be the first sign of
diabetic disease. Often, myopic or hyperopic shifts are created as the lens swells,
secondary to sorbitol effects, resulting in large refractive changes, in what were
otherwise noted as "stable eyes." Cataracts (senile posterior subcapsular and
snowflake posterior subcapsular) may form as well. The cataracts may mature quickly but
have been documented to regress once the sugar levels are stabilized. Avoid prescribing
during this time period, instead educate patients as to why this may have occurred and
order appropriate tests such as fasting blood glucose. The test of choice for monitoring
diabetic control is the glycosylated hemoglobin test (HgbA1C). In most circumstances the
patient can be re-refracted in two to four weeks time, when the condition has been
stabilized. Many practitioners refract these individuals two to three times over a
six-week period to ensure accuracy and stability. If the need to see is urgent, patients
must be educated that the prescription they will be given is temporary and subject to
change. This should be carefully documented. Further prescriptions should ensure that the
patient understands the need for follow up.
When patients present with asymmetric retinopathy,
certainly consider stenosis of the internal carotid artery and ocular ischemic syndrome.
The effects of hyperinsulinemia on atherosclerosis may also alter these vessels. Prudent
care may also include consulting with the patient’s primary care physician to discuss
the need for further diagnostic testing such as carotid duplex ultrasonography.
Many diseases have been found to display findings similar
to those seen in diabetic retinopathy. In undiagnosed patients or patients known to have
diabetes with peculiar retinopathy, other considerations should include: retinal vein
occlusion, ocular ischemic syndrome, hypertensive retinopathy, idiopathic juxtafoveal
retinal telangiectasia, radiation retinopathy, sickle cell retinopathy, sarcoidosis,
syphilis, Lyme disease, cytomegalovirus, AIDS, Eales’ disease, Bechet’s disease,
Coats’ disease, hemoglobinopathies and embolization resulting from IV drug use.
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