The diabetic patient is susceptible to series of complications that cause morbidity and premature mortality. While some patients never develop these problems and in others they begin early, on average, symptoms develop 15 to 20 years after appearance of overt hyperglycaemia. Rare patients have complications at the time of diagnosis. A given patient may experience several complications simultaneously, or a single problem may dominate (Unger and Foster, 1997).
Diabetic complications are dependent upon long term management of blood glucose levels. Poorly controlled blood glucose results in destruction of smallest of blood vessels
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in the body called microvasculature. These small vessels supply blood and nutrition to many of the organs of the body.
Most blood vessels have a central layer of muscle that can respond to pressure changes.
As a result, blood vessel is elastic in nature and able to adapt to change, such as exercise or transient high blood pressure. The increased load of carrying a more viscous fluid (blood laden with heavy sugar water) forces musculature of the vessel to be „on the job‟
at all times, and over time forces vessel to be less able to respond to change. The result is that the vessel hardens (arteriosclerosis) and is less able to carry blood. The nutrients needed to heal the skin and soft tissues are now denied to the organ, making normal daily function particularly troublesome.
The organs most affected by micro vascular changes of DM are the eye (retinopathy), the kidney (nephropathy) and the peripheral nervous system (peripheral neuropathy) of especially the leg and foot (Mueller, 1996).
2.9.2.1. Diabetic retinopathy
Within the eyes, diabetes can affect retina leading to visual impairment or even blindness.
Retinopathic lesions are divided into two large categories: simple (background) and proliferative (Aiello, 1994).
The frequency of diabetic retinopathy appears to vary with age of onset as well as duration of the disease. Approximately 85% of patients eventually develop the complication, but some never develop lesions even after 30 years of disease. Retinopathy appears to develop earlier in older patients, but proliferative retinopathy is less common.
Some 10–18% of patients with simple retinopathy progress to proliferative disease in a 10 year period. About half of patients with proliferative disease progress to blindness within 5 years. Proliferative retinopathy appears to be more common in insulin–treated patients than in those, not treated with insulin (Beisswenger, 1994).
2.9.2.2. Diabetic nephropathy
Renal disease is a leading cause of death and disability in diabetes. Approximately 35%
of patients with Type 1 diabetes develop this complication. The prevalence in Type 2 diabetes varies from 15 to 60% depending on ethnic background. Pima Indians have the highest rates, while Europeans have the lowest. Nephropathy, like other complications, is probably influenced by genetic background of patient. Some families with multiple
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diabetic members rarely have renal disease, while in others; more than 80% of persons at risk have nephropathy (Unger and Foster, 1997). Diabetic nephropathy involves two distinct pathologic patterns, which may or may not coexist: diffuse and nodular. The former, which is more common, consists of widening of glomerular basement membrane together with generalized mesangial thickening. In the nodular form, large accumulations of periodic acid–schiff–positive material are deposited at periphery of the glomerular tufts, the Kimmelstein–Wilson lesion. In addition, there may be hyalinization of afferent and efferent arterioles, “drops” in Bowman‟s capsule, fibrin caps, and occlusion of glomeruli. Deposition of albumin and other proteins occurs in both glomeruli and tubules.
The most specific lesions of diabetic glomerulosclerosis are hyalinization of afferent glomerular arterioles and the Kimmelstein–Wilson nodules (Sequist, 1989).
Diabetic nephropathy may be functionally silent for long periods (10–15 years). At onset, kidneys are usually enlarged and show “super–function” (i.e. glomerular filtration rates may be 40% above normal). The next stage is appearance of microproteinuria (microalbuminuria), excretion of albumin in the range of 30 to 300 mg/d. Normal persons excrete less than 30 mg/d (Krolewski, 1995). Microalbuminuria is not detected by reagent sticks for urinary protein, which generally become positive only when proteinuria is greater than 550 mg/d, a degree of leakage termed macroproteinuria. Once macroproteinuric phase begins, there is a steady decline in renal function, with glomerular filtration rate falling, an average 1 ml/min per month. Ordinarily, azotaemia begins about 12 years after diagnosis of diabetes. The nephrotic syndrome may occur prior to azotaemia. Progression of renal disease is accelerated by hypertension.
Meticulous control of diabetes can reverse microalbuminuria in some patients, and progression of diabetic nephropathy may be slowed. Also, hypertension must be treated whenever present (Viberti, 1992).
2.9.2.3. Diabetic neuropathy
This may affect every part of the nervous system, with possible exception of the brain.
While rarely a direct cause of death, neuropathy is a major cause of morbidity. Several distinct syndromes are recognized, and more than one type may be present in the same patient (Partanen, 1995). Diabetic neuropathy is divided into autonomic and peripheral neuropathy.
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2.9.2.3.1. Autonomic neuropathy: This may present in a variety of ways:
(a) Gastrointestinal tract is a prime target, and there may be oesophageal dysfunction with difficulty in swallowing, delayed gastric emptying, constipation, or diarrhoea. The latter symptom is often nocturnal.
(b) Orthostatic hypotension and (c) Frank syncope may occur.
Cardio–respiratory arrest and sudden death, thought to be due solely to autonomic neuropathy, have been reported. Bladder dysfunction or paralysis is particularly distressing and often leads to the necessity of chronic catheter drainage. Impotence and retrograde ejaculation are additional manifestations in men. Erectile dysfunction is associated with a failure of nitric oxide generation in penile vasculature. Deficiency of vasoactive intestinal polypeptide (VIP) may also be involved (Unger and Foster, 1997).
2.9.2.3.2. Peripheral neuropathy (peripheral neuritis): This is a disease process that affects the sensory, reflex, motor and vasomotor (pertaining to the blood vessel) responses of peripheral nerves. Some forms of neuropathy affect the motor function of the nerve while others are selective for sensory function. This disease can further be divided into subgroups that define the extent or distribution of disease;
Mononeuropathy – affecting one of the peripheral nerves.
Multiple neuropathy – two or more nerves being affected in more than one area.
Polyneuropathy – multiple nerves affected at the same time (Melton and Dyck, 1987).
Diabetic peripheral neuropathy is a complication that can be expected in 60–70%
of all cases of DM. Many cases of diabetic peripheral neuropathy may remain sub–clinical but will show signs of change on nerve conduction testing (EMG–
electromyelogram) (Brown and Asbury, 1984).
The symptoms of diabetic neuropathy are described as a „stocking and glove‟
distribution. This implies that symptoms affect the foot, leg and hand. The symptoms are also described as a burning sensation and electrical shock sensation that becomes worse at night or when the patient is not on his/her feet (Apelqvist et al., 1990).