The most common cause of an arterial aneurysm is atherosclerotic degeneration of the arterial wall. The pathogenesis is a multifactorial process, involving atherosclerosis along with genetic predisposition, aging, inflammation, and localized activation of proteolytic enzymes (Sawabe, 2010). A true aneurysm is a dilation of all layers of the artery wall. A dissecting aneurysm results from a tear in the artery wall, allowing blood to dissect between the layers of the vessel wall. A false aneurysm, or pseudoaneurysm, is not an aneurysm but a disruption through all the layers of a vessel wall with the escaping blood being contained by the perivascular tissues. False aneurysms may result from trauma, infection, or disruption of an arterial suture line after surgery. True aneurysms are most frequently found in the abdominal aorta but are also found in the thoracic aorta and iliac, femoral, and popliteal arteries. More men than women are affected, and aneurysmal disease tends to be a disease of older adults. As early as 1977, a familial tendency was observed that subsequent research verified; as many as 18% of patients with abdominal aortic aneurysms have a first-degree relative with a similar diagnosis (Sawabe, 2010).

Abdominal aortic aneurysms (AAAs), which account for most aneurysms, occur primarily between the renal arteries and the aortic bifurcation (Little, 2013). An aneurysm involves intimal damage of the aorta and weakening of the tunica media (Sawabe, 2010) or elastic portion (collagen and elastin defects) of the arterial wall. Gradually the vessel wall in the damaged area expands and atheroma develops within the aneurysm sac (Figure 24-3). An AAA has minimal symptoms and is generally discovered on routine history and physical examination. In men, the diameter of the infrarenal aorta normally measures between 14 and 24 mm and in women it measures between 12 and 21 mm. An AAA is diagnosed if the diameter is 3 cm or larger for men or 2.6 cm or larger for females. Mortality is low with elective repair of the aneurysm. Dissection and rupture of the aneurysm (aortic dissection) dramatically increase operative mortality because of the abrupt and massive hemorrhagic shock that accompanies the rupture (Research Highlight). Aortic dissection is believed to arise from a sudden tear in the aortic intima, opening the way for blood to enter the aortic wall.

Arterial insufficiency may result from an acute occlusion, as in embolic disease, or from the rupture of an unstable atherosclerotic plaque, causing acute thrombosis of the vessel. Emboli usually arise from the heart as a result of atrial fibrillation but may occasionally result from a myocardial infarction (MI), where a clot forms on the endocardium (the lining of the heart) in an area of muscle damage. Atherosclerotic plaque can also break loose from other areas and result in an acute arterial blockage. Patients with acute arterial occlusion usually present with the onset of the six P’s: sudden severe pain, pulselessness, paresthesia, paralysis, pallor, and poikilothermia (coolness) of an extremity (Little, 2013). Heparin is the mainstay to prevent the enlargement of emboli while allowing time for collateral blood flow to develop. However, in the threatened limb there are basically two options: surgical removal of the clot (embolectomy) or chemical removal of the clot with the use of a thrombolytic medication. If the limb reaches the point where the muscle is rigid, the limb is not salvageable and amputation is a lifesaving procedure.

Chronic arterial insufficiency occurs because of the deposition of calcium and cholesterol within the wall of the artery. Arteriosclerosis is a natural part of the aging process and occurs when the walls of the arterial vasculature undergo changes such as increased thickness and hardening, reducing the elasticity of the arteries. The decrease in elasticity should not be confused with atherosclerosis obliterans, which is a pathologic process that affects the intimal layer of the artery with the buildup of a fibrous plaque of lipids that can calcify and necrose. Atherosclerosis is the most common cause of PAD, the probable mechanism being initial damage to the intima and subsequent activation and aggregation of the body’s platelets. Inflammation follows, with the deposition of lipoproteins forming an atheroma. Calcification of this lesion leads to the development of an atherosclerotic plaque, resulting in inadequate muscle perfusion and ischemia (Zeller et al, 2009). The process is a gradual one, and a localized lesion usually indicates systemic disease. The body develops a network of collateral vessels as an adaptive mechanism to supply the tissues with oxygenated blood. Many theories have been postulated to explain the process of atherogenesis. The inflammatory process of intimal injury, as just described, seems to be the current and most widely accepted hypothesis. Box 24-1 presents risk factors for atherosclerosis. A large number of vascular surgical procedures revolve around the results of chronic arterial insufficiency.

Cerebrovascular accident (CVA or stroke) is a leading cause of death in the United States and most industrialized countries. In the United States, approximately 795,000 people experience a new or recurrent stroke each year (Roger et al, 2012). Cerebrovascular disease may manifest itself as a transient ischemic attack (TIA) or as a major or minor stroke. A TIA is an episode of neurologic dysfunction that resolves in 24 hours. It may be caused by atheromatous debris or a thromboembolism from a carotid artery or the vertebral basilar system. Vascular lesions in the carotid artery occur primarily at the bifurcation of the common carotid artery into the internal and the external carotid arteries. The internal carotid artery supplies the brain with needed oxygenated blood. Obstruction in this arterial vessel leads to cerebrovascular insufficiency.

The right and the left carotid and vertebral arteries supply the brain (Figure 24-4). The first major branch of the internal carotid artery is the ophthalmic artery. Thromboembolic events that affect this artery may result in visual disturbances, ocular TIAs, or “amaurosis fugax” (complete or partial loss of vision). Patients often describe amaurosis fugax as a curtain over a partial field of vision, usually the top. Clinical conditions that generally indicate the need for a carotid endarterectomy (CEA) are transient cerebral ischemia, asymptomatic severe stenosis, and stable strokes. Carotid disease may recur after a CEA. Redo surgery for restenosis poses the same complication risks as the original procedure.

The initial and most important symptom of vascular disease in the aortoiliac vessels and distal arteries is intermittent claudication. The term claudication is derived from the Latin word claudicare, which means “to limp.” This is the most common symptom of lower-extremity PAD and occurs distal to the arterial obstruction while the patient is exercising. Many patients are asymptomatic and do not experience pain. When this symptom does occur, it is typically located in the working muscle, occurs with the same amount of exercise each time, and is relieved with rest. This is referred to as functional ischemia; blood flow is adequate at rest but inadequate to sustain exercise. The increased muscle demand for oxygen with exercise cannot be met distal to the arterial obstruction. Anaerobic metabolism occurs, and muscle cramping develops. Walking difficulties are often seen in the elderly patient with PAD (Patient-Centered Care). Surgery is not usually performed for claudication unless it is unusually disabling.

The second symptom—rest pain, which is located in the foot—develops as the vascular disease progresses (Oka et al, 2012). At this stage the ischemia is termed critical. Rest pain occurs without exercise and is a constant discomfort, often aggravated at night. The body is now unable to meet the oxygen needs of distal tissues even at rest. Rest pain may be somewhat relieved by analgesics or by lowering the legs off the bed. Gravity assists in increasing the tissue perfusion and oxygen supply to decrease the pain. Unless the vascular disease is corrected, nonhealing ulcers and gangrene can develop. Gangrene occurs when the arterial vessels are unable to meet the oxygen needs of distal tissues even at complete rest.

Acute venous insufficiency is caused by a clot in the deep venous system, or deep vein thrombosis (DVT). Such venous insufficiency can be a diagnosis of DVT, phlebitis, thrombophlebitis, or phlebothrombosis, which merely indicates that there is a clot, usually in the lower extremity. Virchow, a pathologist, identified the three elements that trigger venous thrombosis. Referred to as Virchow’s triad, these elements, or risk factors, are endothelial injury, venostasis, and hypercoagulability (Little, 2013). The cause of hypercoagulability is sometimes unknown but is seen in patients with tissue trauma (e.g., surgery, burns, or stroke), malignancy, sepsis, pregnancy or estrogen use, and diabetes mellitus. The patient may be asymptomatic or present with limb swelling, pain, and a skin color change. The danger lies in the potential emboli migrating to the right ventricle and proceeding to the lungs. A pulmonary embolus (PE) can be fatal. The majority of pulmonary emboli cases are caused by DVT. The majority of these originate in the lower extremities. The use of heparin and bed rest is the usual medical treatment. In cases that preclude the use of systemic heparin or in which heparin is ineffective, surgical insertion of a vena cava filter may be indicated.

The severity of these conditions is conveyed by diagnoses and sequelae (e.g., necrotizing fasciitis, gas gangrene, ascending cellulitis, and infection with systemic toxicity or metabolic instability). Because patients with diabetes mellitus may have peripheral neuropathies, they may not feel and therefore not notice any tenderness or early signs of infection. These foot infections can lead to hospitalization and eventual lower extremity amputation for patients with preexisting ulcerations; surgical management is often required for the severe infections. The experienced surgeon determines when and how to intervene. Main principles for management include stabilization of the patient; adequate debridement along with antibiotic therapy; vascular evaluation and revascularization as necessary; delayed soft tissue reconstruction; and postoperative information and intervention for medical and surgical issues. In addressing all these aspects, the surgeon optimizes the possibility for limb salvage. This overview serves as a reminder to emphasize the importance of overall adherence in managing diabetes mellitus to prevent further complications (Aragón-Sánchez et al, 2011).

These complex patients are best handled with multidisciplinary consultations to coordinate care and determine optimal timing for soft tissue reconstruction. Primary closure may not be an option and secondary healing is not necessarily reliable. The proactive surgical approach aims to salvage the diabetic limb by improving overall health and to provide a stable, mechanically sound limb that will resist further breakdown once the patient is able to walk again. Patients need ongoing support and validation to prevent complications. Hospital care focuses on dressing changes, wound care, physical therapy, limb position, and laboratory testing. Postoperative nursing care should provide instruction for follow-up and frequency of monitoring of the surgical results, ambulatory status, work and social restrictions, and bathing. Especially important for the perioperative nurse to review with the patient are identification of infection and ways of contacting the surgical team if problems arise (Aragón-Sánchez et al, 2011).

Nursing diagnoses related to the care of patients undergoing vascular surgery might include the following:

Outcomes identified for the selected nursing diagnoses could be stated as follows:

Before the patient is transported to the OR, the perioperative nurse should procure the necessary supplies and equipment for the intended surgical intervention. Because the need for intraoperative arteriography or fluoroscopy for endovascular procedures is a possibility, the patient with a vascular disorder should be positioned on an appropriate OR bed with x-ray capabilities. The perioperative nurse needs to coordinate the availability of x-ray department personnel. Appropriate contrast media, catheters, and impermeable sterile x-ray covers must be available. Radiation-protection devices, such as lead aprons and shields, should be used for the patient when possible and for surgical team members. A typical plan of care for a patient undergoing vascular surgery, using the suggested nursing diagnoses, is seen in the Sample Plan of Care below.