Tuesday, September 20, 2011
Feet and diabetic neuropathy
Diabetic neuropathy (peripheral neuropathy) is nerve damage caused by diabetes millitus. Diabetes is one of the most common causes of damage to nerves that supply feeling and movement in the arms and legs. It can also affect the nerves that regulate unconscious vital functions such as heart rate and digestion. Neuropathies affect up to 50% of patients with type 1 and type 2 diabetes mellitus. In the former, distal polyneuropathy typically becomes symptomatic after many years of chronic prolonged hyperglycemia. Conversely, patients with type 2 diabetes mellitus may present with distal polyneuropathy after only a few years of known poor glycemic control; sometimes, these patients already have neuropathy at the time of diagnosis. Diabetic neuropathy manifests with a wide variety of sensory, motor, and autonomic symptoms. Nerve fibres of different size mediate different types of sensation. The smaller fibres are affected first in diabetes and with continued exposure to hyperglycemia, the larger fibres become affected. Nerves are measured in micrometers (mu), and the smallest sensory nerves are C (IV) and A-delta (III) these are responsible for thermal/burning pain (0.2-1.5 mu) and sharp pain (1-5 mu) repectively. The A-alpha (I) and A- beta (II) are responsible for propioception (13 -20 mu), vibration and pressure (6 -12 mu) respectively. The primary symptoms of neuropathy can be highly unpleasant but the secondary complications (falls, foot ulcers, cardiac arrhythmias, and ileus) are even more serious. It is still unclear what factors lead to the development of diabetic neuropathy, and multiple hypotheses have been advanced. Hyperglycemia causes increased levels of intracellular glucose in nerves, leading to saturation of the normal glycolytic pathway. Extra glucose is shunted into the polyol pathway and converted to sorbitol and fructose by the enzymes aldose reductase and sorbitol dehydrogenase. Accumulation of sorbitol and fructose lead to reduced nerve myoinositol, decreased membrane Na+/K+ -ATPase activity, impaired axonal transport, and structural breakdown of nerves, causing abnormal action potential propagation. The nonenzymatic reaction of excess glucose with proteins, nucleotides, and lipids results in advanced glycation end products (ACE) that may have a role in disrupting neuronal integrity and repair mechanisms through interference with nerve cell metabolism and axonal transport. Development of symptoms depends on many factors, such as total hyperglycemic exposure and other risk factors such as elevated lipids, blood pressure, smoking, increased height, and high exposure to other potentially neurotoxic agents such as ethanol. Genetic factors may also play a role. Tight and stable glycemic control is probably the most important factor for slowing the progression of neuropathy.
Males with type 2 diabetes may develop diabetic polyneuropathy earlier than female patients. Although it can occur at any age but is more common with increasing age and severity and duration of diabetes. Patients with untreated or inadequately treated diabetes have higher morbidity than patients with tightly controlled diabetes. Repetitive trauma to affected areas may cause skin breakdown, progressive ulceration, and infection. Once neuropathy is present the symptoms persist indefinitely, but most people with diabetic neuropathy are able to lead active, fulfilling lives. Keeping blood sugar under good control may stop neuropathy from worsening.
Sensory neuropathy usually is insidious in onset and shows a stocking-and-glove distribution in the distal extremities. Sensory symptoms may be negative or positive, diffuse or focal. Negative sensory symptoms include feelings of numbness or deadness, which patients may describe as being akin to wearing gloves or socks. Loss of balance, especially with the eyes closed, and painless injuries due to loss of sensation are common. Positive symptoms may be described as burning, prickling pain, tingling, electric shock–like feelings, aching, tightness, or hypersensitivity to touch.
Motor problems may include distal, proximal, or more focal weakness.
In the upper extremities, distal motor symptoms may include impaired fine hand coordination and difficulty with tasks such as opening jars or turning keys. Foot slapping and toe scuffing or frequent tripping may be early symptoms of foot weakness. Symptoms of proximal limb weakness include difficulty climbing up and down stairs, difficulty getting up from a seated or supine position, falls due to the knees giving way, and difficulty raising the arms above the shoulders.
In the most common presentation of diabetic neuropathy with symmetrical sensorimotor symptoms, minor weakness of the toes and feet may be seen.
Autonomic neuropathy may involve the cardiovascular, gastrointestinal, and genitourinary systems and the sweat glands. People with generalized autonomic neuropathies may report ataxia, gait instability, or near syncope/syncope. In addition, autonomic neuropathies have further symptoms that relate to the anatomic site of nerve damage i.e. gastrointestinal, cardiovascular, bladder, or sudomotor.
American Diabetes Association