With the increase in life expectancy that has occurred since the early twentieth century, greater numbers of older adults are suffering from atherosclerosis and vascular-related diseases.
Atherosclerosis is a generalized disorder of the arterial tree, manifested by plaque formation along the inner surface of arteries. The formation of plaque involves a dynamic process of biologically active endothelial cells (cells lining the inner surface of arteries) interacting with various hemodynamic, mechanical, metabolic, and chemical forces and substances. Normally, endothelial cells serve to maintain the integrity of the arterial wall, adapting to stress and injury by increasing wall thickness or altering the diameter to the lumen (channel cavity) of the vessel, increasing (vasodilatation) or decreasing (vasoconstriction) its size.
In atherosclerosis, the usual endothelial response to stress and injury becomes maladaptive. Dead cells, tissue debris, cholesterol, calcium, and other products are deposited beneath a layer of over-exuberant healing (hyperproliferative) endothelial cells to form a plaque. As the plaque continues to mature, its core becomes necrotic and a fibrous cap forms over the surface. Over several years, this narrowing ultimately reduces blood flow to the heart and the extremities to the point where it becomes insufficient to meet its aerobic and metabolic demands. In some cases, the fibrous cap that forms on top of the plaque can rupture, thus exposing the previously contained debris to the coagulation factors of the bloodstream, leading to an acute thrombosis (blood clot) that may completely occlude the vessel lumen, often with catastrophic consequences.
Large-vessel atherosclerosis. Large-vessel atherosclerosis refers to disease in the aorta and its major branches above the level of the chest. Some arterial thickening and changes in the size of arterial walls appear to be, in part, due to the aging process. While there does not appear to be any one single identifiable etiologic cause, several risk factors have been associated with the genesis of atherosclerosis. Nonmodifiable factors include gender, age, and genetics. Males are more prone than females. Incidence increases with age, reaching approximately 10 percent in adults over the age of seventy. There also appears to be an increased incidence of significant atherosclerosis in those having a first degree relative who has experienced atherosclerosis. Additionally, people with a family history of atherosclerosis, high blood pressure, or heart disease are at greater risk than the rest of the population.
Modifiable risk factors include smoking, hyperlipidemia, hypertension, and diabetes. The disease appears to be exacerbated in those who have a sedentary lifestyle, who are obese, and who have high levels of emotional stress. Elderly persons carry the additional complication of being prone to multi-system disease (disease that affects more than one organ).
The lower legs and feet, being farthest ‘‘down the pipe’’ of the arterial circulation, are often the first areas of the body to show the effects of this disease. Alternatively, other patients may manifest their initial symptoms as a transient ischemic attack (TIA, or mini-stroke) or significant permanent stroke from plaque formation in the carotid arteries in the neck. This arterial disease can occur anywhere along the vascular tree, but occurs more commonly at branch points, where blood vessels bifurcate.
Symptoms vary, depending on the degree of restriction of blood flow caused by the atherosclerotic stenosis (narrowing of the vessel lumen). Initially, patients may experience intermittent claudication which is an exercise-induced, crampy, heavy feeling in the muscles of the calf, and thigh, or disease in the arterial tree. With disease progression, ischemic symptomology is elicited with less and less activity, eventually occurring at rest. Patients may also experience cyanosis (a blue or pale discoloration) and decreased sensation or parathesias (a pins and needles feeling) in toes or feet. Additionally, patients with this disease may experience decreased hair growth; nail bed changes (onycogryphosis, or the thickening of the toenails); persistent, nonhealing ulcers or infections, and gangrenous (dead tissue) changes in the lower extremities. This is referred to as critical ischemia and occurs in about twenty percent of patients with large-vessel atherosclerosis.
Diagnosis. Diagnosis of chronic occlusion atheromatous disease consists of a thorough clinical exam, including both noninvasive and invasive testing. A Doppler ultrasound is used to determine flow patterns in the legs and ascertain the level and severity of disease. The information gathered will establish the appropriate course of treatment. If the findings indicate that surgery is required, a catheter-based dye test (angiogram) is performed to develop a ‘‘road-map’’ of the diseased arteries and determine the appropriate operative strategy.
Treatment. The initial treatment for limb ischemia should be conservative, consisting of a daily walking and biking regimen in an attempt to stimulate collateral vessel growth (vessels that naturally ‘‘bypass’’ the blockage in the artery). Often, in a diligent patient, this may be the only treatment necessary. Other medical therapy consists of agents that dilate vessels or decrease blood viscosity. However, both of these approaches may not be suitable for elderly patients due to concurrent comorbidities (i.e., osteoarthritis) and possible polypharmaceutical interactions.
The goal of surgical treatment is to reestablish flow to (revascularize) the ischemic tissue. This can be done percutaneously with angioplasty and stenting, or (more invasively) by using an alternate conduit to bypass the blockages in the diseased artery. For the a peripheral artery bypass a vein graft synthetic material (e.g., Gortex) is used, depending on the location of the stenosis. Both of these interventional concepts are also the current standard treatment of coronary arteriosclerosis. If these treatments are unsuccessful or the patient is deemed to be unsuitable for them, amputation of nonviable portions of the foot or leg is the only remaining surgical recourse. Approximately 2 to 10 percent of patients with critical ischemia will require amputation of the affected limb.
Deciding on a surgical treatment for large-vessel atherosclerosis involves an analysis of the risk/benefit ratio for each patient. In other words, is the risk of morbidity and mortality greater than the probable benefit of the surgery for the patient? The methodology of determining this ratio involves looking at epidemiological surgical outcomes and application of the data to the individual patient. It has traditionally been felt that elderly patients carry a greater risk than benefit for vascular reconstruction, and amputation has thus principally been the procedure of choice for these patients. However, many studies looking at this population have been incomplete and/or flawed, leaving the question open to debate.
Amputation carries high rates of mortality (13 to 23 percent) in elderly patients. Reasons for this high mortality is multifactorial, and contributing factors include a multi-system disease, associated comorbidity, and inadequate nutrition. Additionally, it has been shown that up to twothirds of elderly amputees (depending on the level of amputation) are unable to be adequately rehabilitated, resulting in further functional disabilities. Anesthetic techniques that avoid a general anesthetic and increased use of invasive and noninvasive surgical techniques have substantially decreased morbidity and mortality in elderly patients following vascular procedures. Additionally, octogenarians with critical ischemia have an average life expectancy of four years. For these reasons, utilization of more aggressive interventions appear warranted.
The incidence of abdominal aortic aneurysm (AAA) tripled in the United States between 1970 and 2000, accounting for more than 15,000 deaths per year in 2000. A ruptured AAA is the tenth leading cause of death among those over fifty-five. The incidence of AAA in men over the age of eighty is 6.0 percent, and in women over the age of ninety it is 4.5 percent.
An aneurysm is a dilatation of the arterial vessel to between one-and-a-half and two times its normal diameter. These abnormal vessels can be subsequently divided into two broad categories: true and false aneurysms. A true aneurysm is one that involves a weakness of all three layers of the vessel wall (the intima, media, and adventitia). These are likely to be congenital malformations (e.g., Marfan’s syndrome or some other connective tissue abnormality) or, more commonly, an acquired weakness (e.g., atherosclerosis) of the blood vessel. Conversely, a false aneurysm is one that involves only part of the arterial wall. Examples of these are usually seen following a traumatic injury to the vessel, at sites of previous vascular surgery, anastomosis (surgical opening between blood vessels), and arterial puncture sites for diagnostic catheterization.
Aneurysms, like atherosclerosis, can occur anywhere in the arterial tree, but they most commonly involve the aorta. The aorta is the large artery that conducts the oxygenated blood from the heart to the rest of the body. The normal diameter of the abdominal aorta is between 1.8 and 2.5 centimeters (cm). When the aorta becomes larger, 3.5 or 4 cm, it is deemed aneurysmal.
The principle factor for acquired aneurysm formation appears to be atherosclerosis. It is not clear what causes the arterial wall to become weakened in some people, while others develop occlusive disease. There has been some suggestion that people who develop aneurysms may have a less elastic media (the middle layer of the artery), and subsequently weaker blood vessel walls. The risk factors for aneurysm development are the same as for large-vessel atherosclerosis (see above). Additionally, sites of aneurysm formation mirror sites of aortic occlusive disease—below the level of the kidneys and major branch sites.
Complication of aneurysms include the following:
- Pain. Most AAAs are asymptomatic. A patient with an inflammatory aneurysm may have complaints of chronic back or flank pain, while a ruptured AAA usually presents as a sudden onset of severe, deep, abdominal, flank, or back pain.
- Thrombosis/embolization. The dilated portion of the vessel displays turbulent blood flow patterns that predispose these areas to blood-clot formation. Portions of the blood clot may break off and migrate (embolize) and occlude an artery downstream, or the blood clot may block off the entire lumen of the aorta, producing an acute arterial occlusion.
- Compression. As the aneurysm enlarges, it may encroach on other structures, such as the esophagus or ureters from the kidneys.
- Fistual Formation. An aneurysm can also erode into other structures and form an abnormal connection. An example is an aortoenteric fistula, in which the aorta erodes into the duodenum or some other portion of the small bowel. These patients present with catastrophic upper gastro-intestinal tract bleeding.
- Rupture. The most worrisome and devastating complication (see below).
Eighty percent of all aneurysms grow in diameter as time progresses. On average, an AAA grows about 0.2 cm in diameter per year. As the aneurysm gets larger, more tension is placed on the vessel wall and there is a greater risk of rupture. Other risk factors for rupture are: greater than 0.5 cm increase in diameter per year; an inflammatory AAA (a special type of aneurysm that involves an aggressive inflammatory process of the retro-peritoneum), elevated diastolic blood pressure, chronic obstructive pulmonary disease, and larger initial size. Aneurysms smaller than 4 cm rarely rupture. Risk of rupture for aneurysms measuring 5 to 6 cm in diameter is 10 to 12 percent per year, giving cumulative risk of 60 percent over five years. An 8 cm aneurysm has a risk of rupture of nearly 80 percent over two years.
Fifty to ninety percent of patients with a ruptured AAA do not survive the trip to the hospital. Of those that do make it to the hospital in time for an urgent procedure, only 50 percent survive to be discharged. The most common complications following repair of a ruptured AAA are cardiac complications, respiratory failure, and renal failure.
Diagnosis. A physical examination is relatively unreliable, unless the patient is thin and the aneurysm is quite large. Most commonly, the AAA is found incidentally on an abdominal ultrasound done for other reasons. Abdominal ultrasound is accurate in diagnosing and determining the size of AAA, is relatively quick and painless, and does not expose the patient to X-ray radiation. Additionally, it can be used for serial examination to monitor changes in size. Computerized tomography (CT scan) with intra-arterial contrast is still the ‘‘gold-standard,’’ however with diagnosis sensitivity of nearly 100 percent. A CT scan has an advantage over ultrasound in assessing an AAA rupture or leak. The disadvantages of a CT scan are that it is relatively time-consuming and requires exposure to contrast material and X-ray radiation.
Treatment. The goal of treatment is to prevent rupture and other complications, and to restore arterial continuity. Medical therapy has been largely unsuccessful in preventing progressive AAA dilatation. As such, surgery has been the mainstay of therapy. As with large-vessel atheromatous disease, the decision to treat an aneurysm must weigh the risks of surgery against the risk of complication of the disease process itself. The mortality and morbidity of an open, elective AAA repair is 4 to 10 percent, depending on size, characteristics, and comorbidities of the individual patient. Complications of surgery include myocardial infarction (in a nonrevascularized patient), renal failure, and colonic ischemia. These complications are greater in high-risk patients and elderly patients, again secondary to comorbidities.
For an abdominal aortic aneurysm less than 4 cm the risk of rupture is nearly zero. In general, the accepted sized of an AAA that necessitates surgery is 5 cm or greater. Various surgical and epidemiological studies have determined thus that the risk/benefit ratio favors operative treatment at this size. The traditional open repair of an AAA involves a large incision in the abdomen to gain direct access to the aorta. The aneurysmal segment is then replaced by a synthetic graft (usually Gortex or Dacron) to re-establish continuity to the ‘‘normal’’ artery above and below the weakened segment (in actuality, the artery above and below is rarely entirely normal; however, the goal is to achieve continuity to a normal caliber segment). More recently, a less invasive technique of endovascular stenting is being used.
An endovascular stenting procedure is usually done in concert with both a radiologist and a vascular surgeon. Instead of the large abdominal incision, a smaller incision is made in the groin to get access to the femoral artery (the main blood vessel in the leg). A catheter is then fed in a retrograde fashion into the abdominal aorta to deploy a synthetic graft/stent in the aneurysmal area. This procedure, in essence, achieves the same goal as the open procedure by excluding the weakened dilated arterial wall and establishing arterial continuity with two relatively normal segments. Most studies on patients who have undergone this procedure report a mortality rate of less than 1.2 percent for elective procedures.
Medical treatment for a rupture has a success rate of zero percent. The only hope of survival is operative treatment. However, as stated above, the thirty-day perioperative mortality rate is extraordinarily high (nearly 50 percent).
AAA repair in elderly patients. Like large vessel atheromatous disease of the aorta, older adults with an AAA have traditionally been deemed to be high-risk patients. As such, they have often gone untreated, and thus have a great risk of rupture. As previously discussed, the survival rate in this setting is dismal. It has now been shown that elective, direct AAA resection/repair carries equivalent mortality in octogenarians as in younger counterparts. With regards to the endovascular technique in suitable patients age seventy and older, the operative mortality rate is 1 percent. This outcome is far preferred to those found in the setting of a rupture repair.
Surgical decision-making for the octogenarian with a ruptured AAA is perhaps less clear. Johnston et al. have examined the preoperative, intraoperative, and postoperative risk factors associated with poor outcomes following ruptured AAA repair. In their analysis of 147 patients, they were unable to find a combination of preoperative risk factors or comorbidities that provided little or no chance of survival. Specifically, a ruptured AAA in a patient age seventy-five or older carries a survival rate of approximately 10 percent at six years post-repair. While this rate of death is still extraordinarily high (as compared to the elective group) it is still greater than zero. As such, the decision to treat the elderly with a ruptured AAA should be made on an individual basis, with the appropriate discussion held with the patient and his or her family.
Veins (vessels that carry de-oxygenated blood) from most areas of the body contain oneway flap valves that are designed to assist in the unidirectional flow of blood towards the heart. When one or more of these valves becomes incompetent (‘‘leaky’’), some blood is able to flow retrograde (away from the heart) and tends to overfill and distend branches of superficial veins under the skin. Over a period of time, this additional pressure causes the veins to stretch and bulge. These often unsightly blue and twisted vessel are called varicose veins. They can cause the skin to itch (pruritis); the legs to swell; and the feet to be uncomfortable with a throbbing, heavy sensation. Approximately 10 to 20 percent of adults suffer from varicose veins, with a preponderance of women affected (nearly 70 percent of all patients with varicosities).
Varicose veins are most commonly experienced in the back of the calf or on the inside of the leg between the groin and the ankle, but they may occur in almost any part of the body. Varices can cause enlargement of veins around the anus (hemorrhoids), the esophagus (esophageal varices) and the testicle (varicocele).
The legs consist of two systems of veins. The first are the deep veins, which carry about 90 percent of the blood. The others are surface veins that are visible just underneath the skin and are less well supported. At all of these sites there is a major junction at which superficial veins (those subject to varicose veins) flow into the important deep veins of the leg, with a oneway valve to control flow at the junction.
Normally, blood is pumped upwards through the leg into the abdomen and back to the heart, and the valves in the veins prevent the blood from flowing back down the leg. Sometimes, however, these valves become defective, resulting in the pooling of blood and the back-flow of blood down the leg and causing the formation of superficial veins that become swollen and distorted.
Causes: nonmodifiable. Causes and risk factors for varicose veins include:
- Age. Incidence increases with age, and may approach 50 percent of people older than fifty years of age.
- Sex. Women are affected more often than men, and the increased weight of the uterus during pregnancy may compress the iliac veins and cause an increased backpressure in the veins leading to varicosity.
- Heredity. There is a strong familial predisposition, and this may be the most important risk of all.
- Surgery. Any surgery performed near the hips can make vein problems more likely.
- Congestive heart failure. CHF and thrombus obstruction can also promote the development of varicose veins.
- Arterial-venous fistula. This is an abnormal connection between the arterial and venous system.
Modifiable causes and risk factors include:
- Posture. Standing erect can increase the pressure in the veins several-fold (compared to lying down). It is unlikely that standing actually causes varicose veins, however, people who spend a great deal of time on their feet are certainly more likely to notice, and experience discomfort from, their veins.
- Obesity. Being overweight can increase intra-abdominal pressure, impeding blood flow in the veins or decreasing the support of the veins themselves.
- Pregnancy. The extra weight of the fetus/ uterus can increase intra-abdominal pressure, impeding the return of blood flow from the leg. Additionally, hormonal changes that occur during pregnancy may contribute to weakened support of the superficial venous system.
- Thrombophlebitis. Past history of inflammation of a vein before a blood clot forms can damage or destroy the valves in the venous system, rendering them incompetent.
Diagnosis. For successful operative treatment, a detailed understanding of the abnormal varicose veins is required. For most primary (previously unoperated) cases, a clinical examination by an experienced surgeon will establish the cause (and therefore the treatment) of the varicose veins. Most surgeons would supplement the clinical examination by using a handheld ultrasound probe or an outpatient duplex scan, both of which provide a rapid and extremely useful method of identifying sites of faulty venous valves.
A duplex scan is a more elaborate ultrasound scanner, capable of producing both the visual image and information on the direction of blood flow within the venous system. This scan produces a more detailed ‘‘roadmap’’ of superficial and deep veins in the leg and aids in the planning of more complex varicose vein surgery. A venogram (an X-ray of the vein) has traditionally been used in the diagnosis of venous system abnormalities. This test requires the injection of a radio-opaque contrast into the venous system of the leg, with subsequent images captured using standard X-ray technology. While this test can provide detailed pictures of anatomy, the dye used can be harmful to veins in and of itself, and as such is reserved for only select cases that can’t be imaged adequately with a Duplex scan. As stated above, it is paramount to have a complete understanding of the anatomy to ensure a successful operation.
Treatment. Varicose veins, particularly minor ones, may not require any treatment. However, it does appear that varicose veins are a progressive disease, and there are some surgeons who advocate for early intervention. As with all surgical procedures, it is important to understand the rationale for invasive treatments and to balance the expected benefits against the obvious disadvantages of having a surgical operation (e.g., inconvenience, post-operative pain, time off work, potential anesthetic and surgical complications).
Surgical treatment of varicose veins may be appropriate for a number of reasons including symptoms such as aching, throbbing or tenderness of the veins; medical complications such as eczema around the ankle (with or without actual skin ulceration) and thrombophlebitis (clotting and acute tender inflammation of the varicose veins); and also for cosmetic reasons—they become ‘‘unsightly’’ for the patient.
Properly fitted elastic stockings may be a useful short- or long-term method of alleviating the majority of symptoms or avoiding complications if either patient or surgeon is keen to avoid surgery. Varicose veins operations take the following forms:
- Sclerotherapy. This involves the injection of a chemical that intentionally causes the affected vein to thrombose and scar, thereby obliterating the lumen of the vessel. This therapy generally produces the best results for smaller varicosities.
- Multiple ligation and local excision. The veins are identified preoperatively with a handheld ultrasound or Duplex scan, and the overlying skin is marked with ink. Using these landmarks, the abnormal veins are removed through several small stab incisions. The operation is often largely cosmetic due to the size of veins that can be avulsed (pulled out) through these tiny incisions.
- Vein stripping. This technique is utilized for the long, straight segments of varicose, superficial veins. This stripping is usually carried out in conjunction with an exploration through a 3 to 4 cm incision in the groin and/ or behind the knee. This results in a more satisfactory result when removal of superficial veins in the thigh can ensure more thorough disconnection of varicose veins lower in the calf and reduce the risk of future recurrence. Additionally, the underlying vein and its connection with the deep veins of the leg are identified. All associated superficial branches are carefully cut and tied, and the superficial vein itself is tied and divided at its junction with the deep vein. This part of the operation is essential, as it corrects the principle underlying pathology of the varicose veins.
A frequent concern is the potential side effects of tying and removing veins from the leg. Varicose vein surgery is limited to the superficial venous systems, collecting blood principally from the skin, and, as such, contributes little overall drainage from the leg. Approximately 90 percent of venous blood in the leg is contained in the deep veins within the leg. Additionally, there is a complex interconnected network of both superficial and deep veins with inherent redundancy, so that blood can travel via alternate routes out of the leg after varicose veins are tied or removed.
Complications of the operation. While the majority of operations carried out for varicose veins are routine, and serious complications are uncommon, no surgical procedure is completely free of risk. Additionally, the concurrence of increased comorbidities in elderly patients increases the possibility of complications. This should be borne in mind when considering the pros and cons of surgical treatment for varicose veins. Complications include the following:
- Anesthetic complications. Varicose vein surgery is increasingly performed with the usage of local or regional anesthetic, obviating the need for a general anesthetic. However, cardiac and respiratory complications can still occur, and are certainly more common in the elderly and in those with preexisting problems. Abnormal reactions or allergies to anesthetic drugs are uncommon and largely unpredictable.
- Bleeding. This is one of the more common complications encountered, since the operation deals directly with blood vessels. Significant hemorrhage requiring a blood transfusion is uncommon, but can occur if a major vein is injured or if the patient is on anticoagulant medications (i.e., blood thinners or an antiplatelet agent).
- Wound infection. Infection can occur following any surgical procedure, but is more common after long procedures, in obese patients, in the presence of contaminated ulcers, or in patients with a depressed immune system.
- Damage to surrounding anatomical structures. While this is uncommon, there is small risk of damage to the main arteries, veins, and even major nerves of the leg in explorations at the groin and behind the knee. Injury to small, sensory nerve branches in the skin is extremely common and largely unavoidable when veins are stripped or avulsed. This can result in small patches of numbness, burning, or altered skin sensation close to surgical scars or where varicose veins have been avulsed in the calf.
- Deep vein thrombosis (DVT). Blood clot formation (a DVT) is also an uncommon but serious complication or varicose vein surgery. Clinically significant DVTs occur in the deep venous system, which may be injured or inflamed during varicose vein surgery. A potentially lethal consequence is detachment of a blood clot that then migrates (embolizes) to the heart and lungs (pulmonary embolus). A major pulmonary embolus can result in sudden cardiac arrest and death.
See also Cholesterol; Heart Disease; High Blood Pressure; Revascularization, Bypass Surgery, and Angioplasty; Smoking; Surgery in Elderly People.
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