Diabetes happens to be one of the very common diseases in the USA with approximately 800,000 new cases diagnosed annually. This number is expected to improve using the growing incidence of obesity in this country, particularly one of the young. Diabetes may be the seventh leading reason for death in the United States with an annual health care cost at a number of billion dollars.
For patients with diabetes, foot disease is the most common cause of hospitalization and up to one in five are expected to develop foot ulceration within their lifetime. Additionally, the relative risk of lower extremity amputation is 40 times greater in diabetics. The strongest risk factor for lower limb loss, diabetes makes up about half of all lower extremity amputations in the United States. Of diabetics undergoing amputation, 50% are required to have another amputation within five years.
The reconstructive plastic surgeon should be well versed in the pathophysiology, evaluation and treatment of the diabetic foot. Our role in treatment would be to protect the limb by optimizing wound healing and providing soft tissue coverage to exposed bone, tendon, muscle and nerve, with the goal of delaying or averting amputation.
The pathogenesis of diabetic foot ulcers is due to the combined effects of ischemia, neuropathy and infection.
Both macrovascular and microvascular circulation are impaired by diabetes. Macrovascular occlusive disease secondary to atherosclerosis is well characterized among diabetics. The relative risk of developing peripheral arterial disease is 2 to 3 times higher in diabetic versus nondiabetic patients. Additionally, diabetics are apt to have a quicker continuing development of disease from intermittent claudication to limb-threatening ischemia compared with their nondiabetic counterparts.
The cause of the accelerated atherosclerosis observed in diabetics is probably a direct result dyslipidemia, enhanced platelet adhesiveness and endothelial injury/dysfunction. The spatial pattern of large vessel disease also differs between the two groups. In the lower extremity, nondiabetics tend to have proximal disease, which affects the superficial femoral and popliteal arteries.
Diabetics are apt to have distal disease affecting the tibial and peroneal arteries, using the superficial femoral and proximal popliteal vessels spared from advanced disease. The arteries of the foot, especially the dorsalis pedis, are typically affected to a lesser degree, permitting extreme distal bypass reconstruction in select patients.
Microvascular disease involves a nonocclusive microcirculatory impairment, characteristically affecting the capillaries and arterioles of the kidneys, retina and peripheral nerves. The sequelae of this process results in the characteristic complications of nephropathy, retinopathy and neuropathy commonly seen in diabetic patients. Microcirculatory disease may also impair wound healing and increase susceptibility to wound infection.
The physiologic mechanisms underlying microcirculatory disease have not been fully elucidated. Nonenzymatic glycosylation from the capillary basement membrane, seen in diabetics, may increase vascular permeability, resulting in protein transudation and local edema. The well-characterized thickening of the capillary basement membrane is considered to impair migration of leukocytes to diseased areas.
Peripheral neuropathy, a common complication in diabetics, poses a lifetime risk approaching 60%, and it is seen in as much as 80% of patients presenting with foot disease. The condition process includes sensory, motor and autonomic neural dysfunction. The pathogenesis remains to be fully elucidated, however the mechanism is probably because of both metabolic and microvascular defects.
Diabetic neuropathy affects all nerve fibers with a predilection towards the longest and greatest fibers, leaving the nerves innervating the distal lower extremity most susceptible. Neuropathic disease characteristically affects the low legs symmetrically, with a distal to proximal progression.
Sensory nerve disease initially involves vibratory fibers, followed by pain and temperature fibers, and ultimately, all sensory nerves leading to the insensate foot. Poorly fitting shoes, small stones and particulate matter can result in undetected focal trauma, which could later become full-thickness ulceration. In addition to diminished sensibility, patients with sensory neuropathy may feel burning, tingling and hyperesthesia in impacted areas. These sensory changes, fortunately, diminish as time passes.
Motor dysfunction leads to atrophy and weakness of the intrinsic muscles from the foot, resulting in an imbalance between your flexor and extensor mechanisms, clawing of the toes and increased prominence of the metatarsal heads. The resultant claw-foot deformity creates abnormal pressure points along the plantar metatarsal heads, tips of the toes and the dorsal surface of the PIP joints. Coupled with an insensate foot, pressure points become susceptible to undetected focal trauma, skin breakdown and foot ulceration.
Autonomic neuropathy results in lack of sympathetic tone and increased arteriovenous shunting in the foot, resulting in decreased nutrient flow. Deinnervation of sweat glands results in dried-out skin, predisposing to skin cracking and local infection. In addition, loss of sympathetic innervation towards the bone can lead to increased bone blood flow, resulting in osteopenia and "bone washout."
The combination of advanced sensory, motor and autonomic dysfunction contributes to the introduction of the Charcot foot, a deformity now seen almost exclusively in diabetics. The combination of foot deformity, walking on an insensate foot, and bone resorption results in joint instability, resulting in bone and joint destruction. Breakdown from the tarsometatarsal joints and eversion of the plantar arch create the characteristic "rocker-bottom" foot. The deformity creates new pressure points on the plantar surface, be responsible for ulceration to represent a total breakdown of foot architecture.
Diabetic foot infections would be the outcome of the combined effects ischemia and neuropathy. The lesion typically starts as a neglected or unrecognized infection in the insensate foot. A rest in skin integrity, like a puncture wound, a neuropathic ulcer, an ingrown nail or perhaps a crack in the skin allows bacteria to locally disseminate. Poor tissue perfusion, diminished sensibility as well as an impaired inflammatory response lead to a rapid continuing development of what would otherwise be an area infection.
The bacterial flora present in the wound is variable. In outpatients with localized and superficial infections, at fault is generally a Gram-positive cocci such as Staphylococcus or Streptococcus. Deep ulcers and more advanced limb infections are often polymicrobial. Organisms include Gram-positive cocci, as well as Gram-negative bacilli such as Escherichia coli, Klebsiella, Enterobacter, Proteus and Pseudomonas. Anaerobic flora for example Bacteroides can also be common.
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Note: This article was sent to us by: Steven J. Miller at 02092011
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