Vascular diseases leading to wounds and chronic ulcers affect more than 1% of the adult population and nearly 5% of the population over 65 years of age. The low blood circulation state that occurs in many vascular conditions like sequelae, ischemia and venous stasis, cause maladaptive changes in cell function and maintenance.
These changes include a decreased ability for cells to make use of oxidative radicals to address bacteria along with a propensity towards cellular apoptosis, or cell death. The combined effect of these changes leads to tissue breakdown and high levels of bacterial invasion, establishing chronic, nonhealing ulcers.
Though wounds associated with vascular diseases in many cases are multifactorial, they largely fall under four main categories. Over 50% of these wounds are caused by venous insufficiency. Arterial insufficiency, diabetes and a number of rare underlying disorders comprise the rest of vascular wounds. An incorrect diagnosis can result in incorrect treatment; therefore, a careful assessment and detailed understanding of the clinical picture, pathogenesis, likely causes and treatment option is essential.
Wounds of venous origin are caused by increased pressure in the venous system. This pressure results from a malfunction of the valvular system in the deep veins of the leg. Normally, the retrograde blood circulation with each contraction from the calf muscle ("the muscle pump") is prevented by a valvular system present in the deep veins. This leads to an obligatory anterograde flow as pressure builds in the veins due to this muscular contraction. In patients with venous insufficiency, preventing retrograde flow is lost, or the promotion of forward flow through contraction does not occur.
Causes ranges from congenital weakness of the valves or loss of normal valvular function, to conditions that weaken muscle contraction for example immobility or paralysis (an ailment referred to as dependency syndrome). Valvular function is often compromised after anatomical changes to the valves resulting from either venous thrombosis (post-thrombotic syndrome), a history of phlebitis in the deep veins, or from trauma (fractures, burns or crush injuries towards the limb). Furthermore, valvular dysfunction can also be more likely to occur in patients having a family history of spider veins, suggesting an inherited component.
Whatever the initiating event, valvular dysfunction leads to the pooling of blood in the capillary system, vascular congestion and resultant dilatation and congestion from the lymphatic system. Poor blood circulation can lead to ischemia due to slowed oxygen delivery, the development of capillary microthrombi and leakage of plasma and erythrocytes into surrounding tissue.
With this nonphysiologic ischemic environment, the slightest trauma puts too great a requirement on the cells in the region along with a chronic, nonhealing ulcer is established. Fibroblasts migrate to the area and lay down fibrin, resulting in the characteristic "fibrin cuff " seen in many ulcers of venous origin.
Classically, wounds are simply in the "gaiter" distribution round the lower extremities and around the medial malleoli. While not usually very painful, they are able to cause discomfort as well as moderate pain in certain patients. Trophic changes including hair thinning on shiny, indurated, scaly, erythematous skin. Deeper induration can present as panniculitis, followed by the fibrinous, exudative ulcers of venous stasis.
The traditional form of peripheral vascular disease, arterial insufficiency, is a result of the occlusion of vessels and prevention of forward blood circulation, leading to ischemia and tissue death. This typically is because of atherosclerosis of peripheral vessels and presents in the lower extremities. Embolic events and vasculititis) is also less frequent causes of arterial disease and may also occur in the upper extremities as well. Risk factors for arterial insufficiency include: diabetes, smoking, hyperlipidemia, hypertension, obesity and age.
Any artery along the course of the femoropopliteal distribution can be affected. If larger vessels such as the popliteal, peroneal or either the tibialis anterior or posterior are involved, severe tissue injury is visible. Limited injury will occur with more distal arterial involvement. Usually, ulcers in arterial disease occur in the distal regions of the feet and toes as much as the malleoli or on the shin.
Typically presenting in men ages 50 to 70, patients will report symptoms for example intermittent claudication, rest pain, pain with extremity elevation and disuse atrophy. Physical findings include asymmetric or absent distal pulses and doppler signals, temperature discrepancies between limbs, delayed capillary refill, audible bruits, skin tone changes (mottled, dusky appearance) and an ankle-brachial index (ABI) less than 0.8.
Embolic phenomena are seen in patients with risk factors for example atrial fibrillation, atrial or ventricular thrombus (either left-sided, or right-sided having a patent foramen ovale), valvular vegetation, recent surgery or angiography, or more proximal vascular disease. Other causes include amniotic fluid, fat or bile emboli and intra-arterial injections of air or medication; however, these are much less common than emboli from a cardiac source or perhaps a more proximal plaque in the extremity.
Embolic events and in situ thrombosis should be considered in hypercoagulable states such as in patients with a known or suspected malignancy or disorders of the coagulation system (e.g., lupus, protein c/s or antithrombin deficiencies). Embolic occlusion presents with acute and often painful distal symptomatology. When smaller vessels may take a hit, it's not uncommon to see distal finger or toe color changes and necrosis in the setting of palpable pulses. Finally, any patient that has a distal arterial embolism should undergo an echocardiogram to evaluate the heart and should be ruled out to have an aneurysm (aortic, iliac or popliteal) as the causes of the embolus.
Though not really a disease of the vascular system primarily, it is important to have an understanding of the role of diabetes in the lower extremity wound. At least 15% of diabetics will build up a chronic, nonhealing wound during their lifetime, and approximately 40% of those will have a part of peripheral vascular disease like a contributing factor. Furthermore, diabetic patients are in risk of arteriosclerosis of peripheral vessels at a younger age.
Many diabetic ulcers derive from peripheral neuropathies resulting in pressure ulcers. Once the usual sensory signaling that control distribution of weight and pressure across a large surface of the skin is lost, micro-ischemic environments occur in the sights of prolonged pressure, leading to tissue death and bacterial invasion. Furthermore, it's been shown that there is impairment to neovascularization, prolonged inflammation and decreased wound repair in diabetic wounds. Combining these pathophysiologic changes with the tendency towards arterial occlusive disease in diabetics, a wound with multiple allies may appear.
A subset of patients will show with a picture that doesn't fit one from the classic causes for vascular wounds or will describe a history that suggests one of the rare causes for wounds of vascular origin. Because of the fact that the vasculitides comprise a broad group of different diseases, no one disease process explains the most popular final pathway of vessel wall inflammation. Immune complex disease, antibody-dependent cellular cytotoxicity (ADCC), endothelial activation and coagulopathy happen to be invoked in types of inflammatory disease from the vasculature.
The vasospastic condition known as Raynaud's disease classically presents in a young woman after contact with cold or after cigarette use. The patient reports paresthesias, along with a typical triphasic pattern of color change is seen in the affected acral body part, progressing from blue to white to red.
The disorder is considered to derive from increased serotonin release or an imbalance in vasoactive prostaglandins, and it is known as Raynaud's phenomenon when related to one of a number of underlying diseases, including lupus erythematosus, scleroderma or drug use. Treatment involves avoidance of the instigating stimuli, using vasodilators such as calcium-channel blockers or serotonin antagonists and surgical debridement associated with a necrotic tissue.
Inflammatory vasculititis for example thromboangiitis obliterans (Buerger's disease) or Wegener's disease often present in younger patients. These conditions are seen as a how big the vessels involved (large, medium or small vessel disease) and cause distinct cutaneous findings. Small-vessel vasculitis often presents with urticarial-like lesions and palpable purpura, while medium- and large-vessel vasculitis commonly results in livedo reticularis, purpura, necrosis and ulceration. End-stage renal disease can lead to a phenomenon referred to as calciphylaxis syndrome.
The findings of hyperparathyroidism, hypocalcemia, hyperphosphatemia, hypertriglyceridemia and hypomagnesemia make in the metabolic derangement of the disorder. Patients develop cutaneous calcium deposition typically in a trunk and limb girdle distribution, and continue to possess painful full-thickness necrosis in these areas. Treatment involves correction from the metabolic changes and debridement and skin grafting once disease progression continues to be controlled.
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