ndicated for patients who are limited by their pain or treatment of some arterial occlusive disease and is an invasive procedure. Other adjunctive interventional techniques to treat the iliac, femoral, popliteal, and tibial arteries include the use of lasers, cutting balloons, atherectomy devices, and thermal devices.
Surgical management can be performed for debilitating peripheral vascular disease. This include arterial bypass to surgically revascularize. Surgery can be done when a patient has disabling claudication and/or limb-threatening ischemia due to blocked arteries in the lower extremities. Other bypasses include aortoiliac bypass, aortobifemoral bypass, iliac endarterectomy, or iliofemoral bypass, axillofemoral bypass, and femoropopliteal bypass. Amputation may be required for uncontrolled infection, uncontrolled pain, extensive tissue loss, and in cases where revascularization cannot be accomplished.
Hyperbaric oxygen therapy is also used an as adjuvant therapy in wound care. It involves intermittent treatment of the entire body with 100% oxygen at 20 times greater than normal atmospheric pressures. It reduces amount of hypoxic leukocyte dysfunction occurring within an area of hypoxia and infection. It provides oxygenation to otherwise ischemia areas and arterial blockage by stimulating growth of new blood vessels.
(Osborn, 2014 p.1070, 1912)
Patient is on 81mg of aspirin and Plavix for antithrombotic effects. Patient had a femoropopliteal bypass done on 2/18 in an attempt to revascularize to his L foot. However, the doctors recommended amputation of the 2nd and 3rd toe because of extensive tissue loss and revascularization cannot be accomplished. The patient is also receiving hyperbaric oxygen therapy for wound healing in addition to controlling his blood glucose levels.
DM type II
Type 2 Diabetes is a heterogeneous group of disorders characterized by decreased liver, muscle, and adipose tissue sensitivity to insulin and a defect in insulin secretion from the pancreatic beta cells. Type 2 Diabetes results from decreased insulin production by the pancreas and increased insulin resistance, which is characterized by an inability to use insulin effectively.
In the first stage, genetic factors probably influence both insulin sensitivity and insulin secretion. There is an initial period of hyperinsulinemia in which the pancreatic beta cells are able to overcome insulin resistance. In the second stage, insulin resistance continues to increase, and this compensatory hyperinsulinemia becomes insufficient to maintain normal glucose homeostasis. Under conditions of insulin resistance, visceral adipose tissue is very sensitive to the effects of catecholamines, and insulin resistance is associated with enhanced lipolysis. This leads to increased fatty acid production and mobilization, exacerbating resistance in liver and muscle tissue. In addition, impairments in insulin-mediated glucose transport into skeletal muscle, the major target for glucose disposal, becomes impaired. Also in this stage, physiologic stress states that increase the production of hormones such as catecholamine, cortisol, growth hormone, and glucagon will cause hyperglycemia.
In the third stage, there is further increase in insulin resistance. The restraining effects of insulin on hepatic glucose production become impaired, and plasma glucose levels increase. Fasting and postprandial hyperglycemia result from increased insulin resistance, unrestrained hepatic glucose production and glucose toxicity.
