Peripheral Arterial Occlusive Disease

Chapter 63 Peripheral Arterial Occlusive Disease




The specialty of vascular surgery has matured dramatically over the past decade. With the advent of new devices and techniques and the expansion of catheter and guidewire skills, the management of almost all vascular pathologic processes has been undergoing a process of reevaluation. Surgeons have traditionally been called on to make diagnoses and manage patients with emergent, urgent, and elective vascular surgical conditions. Although other medical disciplines are participating in this process to a greater degree, the surgeon with advanced open skills and complete facility with endovascular techniques is ideally suited to manage these patients. As our population ages and the prevalence of vascular disease increases, along with the growing awareness of potential therapeutic benefits by an educated populace, it is incumbent on the vascular specialist to be facile with a widening set of tools and techniques—medical, surgical, and endovascular—to meet the needs of our patients.


This chapter will cover epidemiology, basic science, diagnostic workup, and medical treatment of peripheral vascular disease. Treatments of acute and chronic limb ischemia, open and endovascular, will be discussed. Management of the diabetic foot, with an emphasis on amputations, is included. Less common causes of limb ischemia are presented for completion. The rapidly changing treatment paradigm of carotid stenosis is discussed, as well as that of renovascular hypertension. Management of peripheral and splanchnic aneurysms will be reviewed. Finally, arteriovenous (AV) access for the patient with end-stage renal disease (ESRD) is presented in detail because this remains an important component of contemporary general and vascular surgical practice.



Epidemiology


Peripheral artery occlusive disease (PAOD), commonly referred to as peripheral arterial disease (PAD) or peripheral vascular disease (PVD), refers to the obstruction or deterioration of arteries other than those supplying the heart and within the brain. There are a number of pathologic processes that manifest their effects on the arterial circulation.


The common denominator among these processes is the impairment of circulation and resultant ischemia to the end organ involved. Highly prevalent in our society, arterial occlusive disease, in its myriad iterations, constitutes the leading overall cause of death. In addition to death from myocardial infarction or stroke, significant disability and loss of function from PAD result in an enormous cost in impaired quality of life for our aging population and a direct financial cost to our health care system.


The incidence of symptomatic PAD increases with age, from approximately 0.3%/year for men aged 40 to 55 years to approximately 1%/year for men older than 75 years. In the United States, PAD affects 12% to 20% of Americans aged 65 years and older.


PAD is more prevalent in nonwhite populations, and this is not completely explained by an increased incidence of comorbid diseases.1 An ankle-brachial index (ABI) less than 0.90 is almost twice as common in non-Hispanic blacks than whites. Risk is increased in smokers and in patients with hypertension (HTN), dyslipidemia, hypercoagulable states, renal insufficiency, and diabetes mellitus (DM) (Fig. 63-1). The prevalence of PAD is strikingly higher in a younger diabetic population, affecting one in three diabetics older than 50 years. Diagnosis is critical, because people with PAD have a risk of heart attack or stroke four to five times higher than the age-matched population (Fig. 63-2). The risk of PAD also increases in individuals who older than 50 years, male, obese, or with a family history of vascular disease, heart attack, or stroke. Other risk factors that are being studied include levels of various inflammatory mediators, such as C-reactive protein and homocysteine.





Basic Science of Vascular Disease




Atherosclerosis


Atherosclerosis is the most common pathology associated with PAD. There are a number of terms used to describe this process that are similar and yet distinct in spelling and meaning, and are often confused. The principle root, athera, is from the Greek word meaning gruel; an atheroma can be translated literally as a lump of gruel. Atherosclerosis is a hardening of an artery specifically caused by an atheromatous plaque. The term atherogenic is used for substances or processes that cause atherosclerosis. Arteriosclerosis is a general term describing any hardening (and loss of elasticity) of medium or large arteries (from the Greek arteria, meaning artery, and sclerosis, meaning hardening); arteriolosclerosis is any hardening (and loss of elasticity) of arterioles (small arteries).


A number of causative factors have been identified for atherosclerosis. Hyperlipidemia, hypercholesterolemia, hypertension, diabetes mellitus, and exposure to infectious agents or toxins such as from cigarette smoking are all important and independent risk factors. The common mechanism is thought to be endothelial cell injury, smooth muscle cell proliferation, inflammatory reactivity, and plaque deposition.


There are several components found in atherosclerotic plaque—lipids, smooth muscle cells, connective tissue and inflammatory cells, often macrophages. Lipid accumulation is central to the process and distinguishes atheromas from other arteriopathies. In advanced plaques, calcification is seen and erosive areas or ulcerations can occur, exposing the contents of the plaque to circulating prothrombotic cells. There is an important correlation between plaque morphology and clinical sequelae. The plaque’s lipid core may become a necrotic mix of amorphous extracellular lipid, proteins, and prothrombotic factors covered by a layer of smooth muscle cells and connective tissue of variable thickness, the fibrous cap. If the thin fibrous cap ruptures and the contents of the lipid core are exposed to circulating humoral factors, the body, perceiving the ulceration as an injury, may lay down platelets and initiate clot formation. In this manner, a relatively low-grade, hemodynamically insignificant narrowing can precipitate an acute thrombosis and result in a dramatically significant ischemic event, such as a myocardial infarction.


Plaque morphology can be evaluated by ultrasound and magnetic resonance imaging. The heterogenous plaque with a thin fibrous cap or ulceration, often described as unstable or vulnerable, is more likely to be virulent in nature, with an increased risk for embolization of particulate and thrombotic potential. Ischemia, therefore, can result from a number of possible plaque behaviors, such as encroachment on the lumen (stenosis or narrowing) with hypoperfusion, stagnation, and thrombosis; rupture of the fibrous cap inducing thrombus formation in the lumen, with outright occlusion; and embolization of thrombotic debris into the downstream circulation.


Although atherosclerosis is a systemic disorder, there is an interestingly predictable pattern of distribution of atheromatous plaques throughout the arterial tree that is likely a result of consistent hemodynamic stresses associated with human anatomic design. Plaques tend to occur at bifurcations or bends associated with repetitive external stresses. Areas at which shear stress increases from disturbances in flow or turbulence, with lateralizing vectors and eddy formation, are prone to atheromatous degeneration. The infrarenal abdominal aorta, iliac bifurcations, carotid bifurcations, superficial femoral arteries as they exit at Hunter’s canal, and ostia of the coronary, renal, and mesenteric arteries, are all common sites of plaque formation. Conversely, the upper extremity arteries and common carotid, renal, and mesenteric arteries, beyond their origins, are often much less involved.



Evaluating And Treating The Patient With Peripheral Arterial Disease


Patients are typically referred to the vascular specialist to clarify a diagnosis and determine a strategy for treatment. The process involves clinical assessment, establishing the particulars of the patient’s medical history and performing a physical examination, diagnostic studies to clarify and localize the problem and potentially elucidate the functional severity of the condition, and ultimately balancing the severity of the patient’s condition with the potential risks and benefits of therapeutic intervention.




Chronic Arterial Insufficiency


The clinical presentation ranges from asymptomatic to gangrenous tissue loss. Intermittent claudication is a common presentation in the outpatient setting, and usually signifies mild to moderate vascular occlusive disease. Classically, pain occurs with activity or ambulation and is relieved with rest. Because of the frequency of superficial femoral arterial disease, the usual location of the pain is in the calf, but claudication may also involve the thighs or the buttocks because the arterial disease may be located in the aorto-iliac segment. The arterial disease is usually one level above the symptomatic muscle group. The differential diagnosis of leg pain is broad and the treatment modalities are equally disparate. Table 63-1 outlines an approach to the differential diagnosis of claudication.



Patients who are limited in ambulation because of arthritis, severe lung disease, or heart failure, or who are diabetic with neuropathy, may not experience leg pain and may present initially with advanced disease. Worsening perfusion leads to critical limb ischemia (CLI), which may be manifested by rest pain. This is described as pain that occurs at rest; it may wake the patient from sleep. CLI patients present also with tissue loss with ulceration or nonhealing wounds of the foot. This usually in the dorsum of the foot, relieved with dangling the leg over the edge of the bed. Patient may also have tissue loss with ulcerations or nonhealing wounds of the foot (Table 63-2).



Initial evaluation must include a detailed medical history of comorbid conditions. In addition to coronary artery disease (CAD), carotid artery stenosis (CAS), and prior stroke, risk factors for atherosclerosis (e.g., diabetes, hypertension, dyslipidemia, tobacco abuse, hyperhomocysteinemia) should be queried and their level of optimization understood. Because medical management is a cornerstone of vascular therapy, a review of the patient’s medications is imperative, with attention to the potential need for antiplatelet agents, beta blockers, angiotensin-converting enzyme (ACE) inhibitors, and statins as a matter of course. Previous exposure to heparin, protamine, and NPH insulin (neutral protamine Hagedorn)2 should be noted. Allergies to contrast agents or iodine should be documented.


The surgical history and physical examination include details of surgical incisions as indicative of prior surgical intervention. Many patients will have undergone coronary artery bypass grafting; the presence of a left internal mammary–left anterior descending coronary graft and previous great saphenous vein harvest can change the surgical plan for peripheral revascularization. Frequent or recent coronary catheterization (or peripheral angiograms) can suggest challenging groin access with significant scar tissue. Procedure reports should be reviewed for details of access closure or incidental findings of peripheral artery stenoses. Previous surgery, whether neck, abdominal, spine, joint, or vascular operations, can affect decision making and efforts to gain the details of these are important. A family history of a first-degree relative with abdominal aortic aneurysm, stroke, or early myocardial infarction should be sought.


A vascular review of symptoms documents the presence or absence of transient ischemic attack or stroke, such as unilateral weakness or sensory deficit, difficulty with speech or swallowing, word-finding difficulties or memory changes, dizziness, drop attacks, blurry vision, arm fatigue, weight loss or pain after eating, renal insufficiency or poorly controlled hypertension, impotence, claudication, rest pain, or tissue loss. As for all patients, a detailed understanding of the patient’s functional status helps delineate goals of therapy and perioperative risk. Patients who are limited in their activities of daily living by their vascular disease or other comorbidities cannot provide an accurate picture of their cardiac function and will likely require further cardiac workup. History of tobacco abuse must be documented, as well as all clinical efforts for encouraging smoking cessation.


The physical examination begins with vital signs, which often reveals hypertension and tachycardia. Blood pressure in both arms should be documented. The presence or absence of carotid bruits, cardiac murmurs, abdominal, flank, or groin bruits should be noted. The abdomen should be palpated for the aortic pulsation. Incision scars should be noted. Bilateral carotid, radial, ulnar, femoral, popliteal, dorsalis pedis (DP), and posterior tibial (PT) pulses should be palpated and characterized. If pulses are not palpable, a continuous wave Doppler can be used to check for signals. Common physical findings of PAD include hair loss and dry shiny skin with nail hypertrophy. In CLI, the classic findings of dependent rubor and pallor with elevation of the limb can be observed. In cases of severe rest pain, patients may have peripheral edema because they are unable to take their legs from the dependent position without pain. The feet should be meticulously inspected for wounds and signs of skin breakdown. A neurologic examination documenting equivalent strength and sensation in the limbs and cranial nerves should be performed.


Routine laboratory work should include a complete blood count, chemistry (to evaluate renal function and glucose), and a lipid panel. An albumin level can be helpful in delineating the adequacy of a patient’s nutritional status, if this is in question. The hemoglobin A1c (HbA1c) level indicates the patient’s level of glycemic control over the previous 120 days.


A baseline electrocardiogram should be obtained. Any previous cardiac testing, including echocardiography, stress echocardiography, dobutamine-adenosine sestamibi scan, and coronary catheterization, should be reviewed and documented.



Physiologic Testing and Imaging


The vascular laboratory is a powerful tool in the armamentarium of the surgeon. Noninvasive testing confirms and localizes disease, provides end points to demonstrate improvement following intervention, enables long-term follow-up of bypass grafts and percutaneous interventions, and can detect silent disease recurrence. Tests commonly performed in the laboratory include the ABI, with multisegmental pressures, waveforms, and toe-brachial index (TBI), pulse volume recording (PVR), photoplethysmyography (PPG), and arterial duplex examination. The vascular laboratory represents one of the last arenas in which a nonimaging indirect measure of physiology is still widely used as a diagnostic tool.


Regardless of plans for intervention, it is recommended that asymptomatic patients at risk for PAD and those with symptoms undergo ABI testing. This examination can be performed simply with a manual blood pressure cuff at the ankle and a continuous wave Doppler probe. With the patient in a supine position, after several minutes of rest to allow limb pressure to return to baseline, the cuff is inflated at the ankle, with the Doppler probe held at the location of the distal DP or PT signal. The systolic pressure is recorded as the pressure in the cuff when the Doppler signal returns. This process can be performed with multiple cuffs allowing for segmental pressure determination (Fig. 63-3), which is helpful in localizing the level of the obstructing lesion. The ABI for a limb is calculated using the higher of the two ankle pressures divided by the higher of the two brachial pressures (Tables 63-3 and 63-4). Patients with an ABI of 0.90 or less have a three- to sixfold increased risk of cardiovascular mortality.



Table 63-3 Clinical Correlation of Different Levels of ABI*


















ABI PRESENTATION
1.11 ± 0.10 Normal
0.59 ± 0.15 Intermittent claudication
0.26 ± 0.13 Ischemic rest pain
0.05 ± 0.08 Tissue loss

* The diagnosis of PAD is given to ABI <0.9. ABI >1.3 is interpreted as abnormal because of incompressible tibial arteries, frequently seen in diabetes and end-stage renal failure. Example: The ABI is calculated using the higher of the two ankle pressures (as indicative of limb perfusion), and the higher brachial pressure (as indicative of systemic pressure). In this example, the left and right ABI values are both 0.30.


From Moneta GL, Zaccardi MJ, Olmsted KA: Lower extremity arterial occlusive disease. In Zierler RE, editor: Strandness’s duplex scanning in vascular disorders, ed 4, Philadelphia, 2010, Lippincott Williams & Wilkins, Wolters Kluwer Health, pp 133–147.


Table 63-4 Calculation of ABI























PARAMETER RIGHT LEFT
Brachial blood pressure 150 mm Hg 100 mm Hg
Dorsalis pedis 50 mm Hg 25 mm Hg
Posterior tibia 25 mm Hg 50 mm Hg
ABI 0.30 0.30

Continuous wave Doppler analog waveforms can be obtained along with the segmental pressures. PPG uses an infrared light-emitting source and a photosensor; it is based on the principle that red light is decreased with increased blood flow in tissues to generate a pressure and waveform within the digit. The data generated from these studies should include bilateral brachial artery, high thigh, low thigh, calf, DP, PT, and toe pressures with waveforms (Fig. 63-4). A decrease in pressure of 20 to 30 mm Hg between adjacent segments is indicative of a significant lesion. The normal Doppler arterial waveform demonstrates triphasic flow with a sharp systolic upstroke, reversal of flow in early diastole from vessel compliance, and low-amplitude forward flow throughout diastole. With obstructive disease, the initial feature lost is the reversal of the flow component, leading to multiphasic (previously called biphasic) flow. Severe disease leads to blunting of the arterial waveform, with decreased amplitude and decreased slope of the upstroke. With worsening symptoms, there is increased diastolic flow, resulting in monophasic flow. A change in waveform can be interpreted, along with a change in pressure, as indicative of disease at that level. Limitations of ABI and segmental pressure determinations include mural calcification, such as seen in DM and ESRD, leading to elevated pressures that do not accurately reflect intra-arterial perfusion pressure. With a noncompressible vessel, a TBI higher than 0.70 with an absolute digit pressure higher than 50 mm Hg, with a normal waveform, is indicative of preserved flow because digit arteries are relatively resistant to the intramural calcification. The high thigh pressure cannot always distinguish among common iliac, external iliac or common femoral disease. A proximal stenosis can decrease flow to the extent that accuracy is lost when interpreting gradients downstream.



Symptomatic patients with palpable distal pulses or a normal resting ABI should undergo exercise testing with measurement of the postexercise ABI. The decrease in peripheral vascular resistance that occurs with exercise-induced vasodilation will increase the drop in pressure seen across a stenotic lesion. Patients undergo resting ABI testing, followed by treadmill exercise until symptoms occur; repeat ABI testing may then reveal a decrease in ankle pressure of 20 mm Hg or a decrease in the ABI of 0.20. These changes, or a failure of the ABI to return to preexercise baseline within 3 minutes, are interpreted as a positive result.


Arterial duplex ultrasonography provides B mode (gray scale) imaging, pulsed Doppler spectral waveforms, and color flow data for analysis and, in experienced hands, can provide sensitive and specific information about the abdominal aorta and visceral, renal, iliac, and distal limb vessels. Peak systolic velocities (PSVs) and end-diastolic velocities are recorded. Waveforms are generated and analyzed. Color flow is useful for demonstrating patent vessels in very low-flow states and for distinguishing antegrade from retrograde flow. As in continuous flow Doppler analysis, a change in waveform from triphasic to monophasic, or an increase in PSV followed by a drop in velocity, indicates a hemodynamically significant lesion. A ratio of the PSV within the stenosis to the PSV of the proximal normal segment of 2.0 or more correlates with a stenosis of 50% or more. Visualization of intra-abdominal segments requires the patient to be fasting prior to the examination to eliminate bowel gas; studies can be limited by body habitus. Severe calcification of the distal vessels can impede imaging of flow (Figs. 63-5 and 63-6).





Imaging Studies


When intervention is planned, further imaging to delineate the location and nature of disease is needed. The gold standard for these purposes has been angiography. Because of the invasive nature of this test, with attendant risks of complications, imaging was previously reserved as a preoperative study for patients determined to be operative candidates because of the severity of their disease and their suitability for surgery. This algorithm has changed somewhat in contemporary practice. Most angiography is therapeutic rather than diagnostic, with lesions that are deemed amenable for endovascular intervention addressed in the same setting as the initial angiogram. Alternatively, computed tomography angiography (CTA) or magnetic resonance angiography (MRA) may enable the acquisition of the same vascular roadmap prior to a planned intervention.



Angiography


Access is usually via the contralateral common femoral or left brachial artery. A complete diagnostic study is performed in four steps: (1) abdominal aortography, with a multiside hole catheter placed at the level of the diaphragm, imaging the abdominal aorta, celiac artery, superior mesenteric artery (SMA), inferior mesenteric artery (IMA), and aortic bifurcation; (2) pelvic angiography with a multiside hole catheter at the aortic bifurcation, imaging the bilateral common iliac, hypogastric, and external iliac arteries, common femoral arteries, and proximal superficial femoral (SFA) and profunda femoris artery (Fig. 63-7). (3) The contralateral common femoral artery is then selected using an end-hole catheter, and images of the contralateral SFA, profunda, popliteal, tibial, and pedal vessels are obtained in one to three low-bolus runs. (4) The access sheath is then pulled back to the level of the distal ipsilateral external iliac artery to image the ipsilateral limb. Trans-stenotic pressure gradients and multiplanar images can clarify the significance of an ambiguous lesion. Complete assessment of the aortic and iliac inflow and bilateral lower extremities requires 75 to 100 mL of contrast.



Risks of diagnostic angiography and all endovascular procedures include groin hematoma, retroperitoneal bleeding, pseudoaneurysm, and arterial dissection. Even a small amount of bleeding after brachial artery access can cause symptomatic brachial sheath hematoma and neural compromise requiring exploration and evacuation. These risks are reduced by the routine use of ultrasound-guided access and micropuncture techniques.


The risk of contrast nephropathy is limited by prudent use of contrast, selective catheterization, which decreases the volume of the contrast bolus required to opacify the vessels, and use of lower ionic load or iso-osmolar contrast agents. Patients are counseled to increase oral hydration in preparation for and following arteriography. Metformin and ACE inhibitors, as well as diuretics, are held prior to the procedure and for 48 hours postprocedure. There is some evidence for preoperative medication with acetylcysteine, 1200 mg PO twice daily, before and after arteriography, as well as IV fluid hydration using half-normal saline with 1.5 ampules of sodium bicarbonate or DSW with three ampules of sodium bicarbonate. Patients with a history of contrast allergy should be premedicated according to institutional guidelines with steroids and histamine blockers (e.g., diphenhydramine).


Risk of radiation exposure for diagnostic procedures is limited but, with the growing complexity of endovascular interventions, cumulative exposure is a potential concern for the patient and for the physician exposed during the therapeutic procedure. Monitoring is essential and routine.



Computed Tomography Angiography

The widespread use of multidetector row CT scanners has improved the speed, volume coverage, and slice thickness of images so that a single contrast bolus can be imaged as it passes through the arterial system. One advantage of CTA (Fig 63-8A) is the depiction of the entire vessel, with the ability to appreciate thrombus and calcification; arteriography typically characterizes only the lumen of the artery. Thin slices of 0.625 mm allows for three-dimensional reconstructions and multiplanar reformatting that is not routinely achieved with conventional arteriography. CTA disadvantages are similar to those of arteriography, with the potential for complications from the use of iodinated contrast agents and significant accumulation of radiation exposure.




Magnetic Resonance Angiography

Advocates of contrast-enhanced MRA with gadolinium (see Fig. 63-8B) report a high sensitivity and specificity of this modality for demonstrating the degree of stenosis and lesion length, and even superiority in identifying distal target vessels when compared with conventional arteriography.3 Disadvantages of MRA technology include the need for patient cooperation, patient discomfort, longer studies, expense, contraindications with certain metallic implants, and renal toxicity reported with use of the contrast agent, Gadolinium. Its use is contraindicated in renal disease because of the risk of nephrogenic systemic fibrosis. This is a rare complication associated with the administration of gadolinium-based agents to patients with renal failure or renal insufficiency having a glomerular filtration rate 30 mL/min or lower.4 Patients develop fibrosed nodules of the skin, eyes, and joints. Severe contracture limiting movement or involvement of the heart, liver, and lungs has been described.





Treatment



Medical Treatment


Despite the aging of our population and increasing numbers of people afflicted by atherosclerotic arterial disease, morbidity from myocardial infarction and stroke is decreasing. This is likely secondary to advances in medical management and increasing awareness by affected individuals about the availability of medications that can limit the progression of the disease process. The American Heart Association (AHA) has published guidelines for risk modification that have grown increasingly aggressive in efforts to treat this important public health concern. In contemporary surgical practice, lipid modification, antiplatelet and antihypertensive control, and smoking cessation strategies are all becoming standard management issues for the patient with vascular disease. Table 63-5 summarizes the AHA guidelines for risk factor modification.



Risk factors contributing to PAD are the same as those for atherosclerosis:







Revascularization: Surgical Treatment



Intermittent Claudication


Patients with intermittent claudication (IC) are treated by risk factor modification to decrease their risk of myocardial infarction (MI) and cerebral vascular accident (CVA). A trial of cilostazol and supervised exercise is recommended; these therapies, combined with risk factor modification (particularly smoking cessation), have been shown to improve walking distance. Patients are reassured that they are at limited risk of limb loss, approximately 2% to 3% at 5 years. Although significant disability may occur as a result of IC, symptoms remain stable because of the development of collateral flow, or perhaps alterations in gait that favor nonischemic muscle groups.7 However, 25% of IC patients will see deterioration in their clinical course, usually during the first year after diagnosis; the best predictor of this decline is the initial ABI. Patients with an initial ABI of less than 0.50 have a hazard ratio of more than 2 compared with patients with an ABI higher than 0.50. IC patients with an initial ankle pressure of 40 to 60 mm Hg have an annual limb loss rate of 8.5%.


Patients who present initially with low ankle pressures or absent femoral pulses, or patients who return with unabated, severe, lifestyle-limiting symptoms that have not adequately responded to nonoperative measures, are considered for intervention (Fig. 63-10).





Diabetic Foot


PVD is common among patients with diabetes (Fig. 63-12). IC is twice as common among diabetic patients than among nondiabetic patients. An increase in HgbA1C by 1% can result in more than a 25% risk of PAD. Major amputation rates are five to ten times higher in diabetics than nondiabetics. Because of these causal relations, the American Diabetes Association recommends ABI screening every 5 years in patients with diabetes.8



The care of diabetic patients should start with preventive measures, and it is important to avoid infections in patients with insensate feet because of neuropathy. These patients need to wear properly fitted shoes at all times for protection. Orthotic inserts should be used to distribute weight evenly to avoid pressure on the metatarsal heads of the foot.


Diabetic patients may be unaware of the presence of infections or ulcerative lesions because of peripheral neuropathy and a decreased ability to sense pain. In this population, infections can progress rapidly, with significant tissue damage from a combination of delayed presentation and compromised immune function.


On presentation, a careful physical examination is important to plan for appropriate treatment. The overlying cellulitis is assessed, and any possible underlying abscess is examined by palpation for crepitus or detection of drainage of purulent fluid. Cellulitis should not be confused with dependent rubor caused by severe ischemia in patients with PAD. The presence of an abscess requires immediate drainage prior to revascularization.


The status of arterial circulation is documented. The presence or absence of lower extremity pulses in the common femoral, popliteal, and pedal arteries is examined. The pulses may be difficult to palpate because of swelling from foot infection; noninvasive arterial ultrasound can be useful in assessing the extent of arterial disease.


Insulin-dependent diabetic patients may have calcified walls of the medium and small arteries that can falsely elevate the segmental pressures of the leg. In this situation, digital pressures of the toes can be accurately measured and a pressure higher than 30 mm Hg is predictive of healing after local amputation and debridement.


Plain x-rays with multiple views of the foot can assist in assessing the extent of foot infection. Gas in soft tissue signifies deep tissue infection and the need for urgent surgical débridement. Advanced osteomyelitis can be detected; however, plain films may not show early bone infection. Magnetic resonance imaging (MRI) of the foot is a sensitive imaging modality for detecting soft tissue infection and early osteomyelitis.


Routine laboratory work is sent and evaluated for subtle signs of sepsis. Sudden worsening of glycemic control or a rise in creatinine level is seen frequently, often without leukocytosis.


In infections with only cellulitis and no underlying soft tissue involvement, patients are treated with IV antibiotic therapy. If the cellulitis does not resolve in several days, there may not be adequate antibiotic coverage and the presence of deep tissue infection is considered. The choice of the antibiotics used and the foot need to be reevaluated; reimaging the foot may be necessary.


The cause of persistent cellulitis and nonhealing infection is usually underlying deep infection or osteomyelitis. Other patients may present with gangrene, open joint or exposed bone, or abscess. In these patients, surgical débridement is required in addition to antibiotic therapy. Small open wounds can be treated with simple débridement, but often there is deep tissue involvement that is not visible on the surface. To remove all nonviable tissue and wide drainage, amputation may be required. If there is extensive infection of the foot with gas, calf pain, or systemic sepsis, the patient may require amputation as an initial therapy. After surgical débridement, patients are treated with aggressive wound care using dressing changes and continued, broad-spectrum antibiotic therapy until intraoperative culture sensitivities are finalized and allow for the use of targeted antimicrobials. Wounds are evaluated closely for persistent infection that may require additional surgical intervention. In patients with adequate arterial circulation, the wound can be closed secondarily after resolution of the infection.


All patients with evidence of concomitant arterial occlusive disease are considered for lower extremity revascularization with open bypass surgery or endovascular stenting or angioplasty to optimize wound healing and limb salvage.



Lower Extremity Amputations


Amputation, unfortunately, in the minds of most surgeons and their patients, represents a failure of therapy or care. Consent for this operation, regardless of the level, is usually imbued with an emotional gravity that few other, even more complex, dangerous, life-altering procedures carry. Not infrequently, amputations in the vascular patient are prone to breakdown and the need for revision is common, thereby prolonging the patient’s time in the hospital, lengthening the recovery process, decreasing the chances of functional recovery, and contributing to a high rate of depression. It is therefore incumbent on the surgeon to ensure that all steps are taken to minimize the risks of local and systemic complications.9


The perioperative mortality rate for below-knee amputation (BKA ) is 5% to 10% and that of above-knee amputation (AKA) even higher, 10% to 15%, testifying to the limited reserves of patient facing these procedures.10 Wound healing in BKA is poor; almost one third of patients require débridement or healing by secondary intention or conversion to AKA (Fig. 63-13). Despite optimistic preoperative counseling, functional recovery with ambulation is poor for AKA patients.11



The determination of the appropriate level for amputation has been studied extensively (Table 63-6). In an effort to preserve limb length and decrease the metabolic demands of ambulation, toe and transmetatarsal amputations (TMAs) are usually attempted. Aside from clinical judgment, segmental arterial pressures, Doppler waveforms, and toe pressures have been studied. Diabetes, combined with a toe pressure of lower than 30 mm Hg, has been correlated with failure of healing minor amputations. Transcutaneous O2 pressure (TcPO2) measurement, easily obtained via a small sensor placed on the skin in the area of proposed amputation, has an accuracy of higher than 87% for predicting wound healing. A reading higher than 40 mm Hg is associated with successful healing, whereas TcPO2 less than 20 mm Hg is associated with failure. Absolute ankle pressure higher than 60 mm Hg has been shown to predict the healing of BKAs with an accuracy of 50% to 90%.12




Ray Amputation


For ray amputation, a tennis racquet incision around the base of the affected toe is made. For first toe amputations, the handle of the racquet is oriented along the medial aspect of the metatarsal head; for the fifth toe, it is oriented laterally. For toes 2 to 4, the incision is along the dorsal midline (Fig. 63-14). Neighboring digital vessels are carefully preserved as the soft tissues are divided. The extensor tendons are divided under tension and permitted to retract. The bone is divided proximal to the metatarsal head. If sesamoid bones are encountered, these are removed. Plantar soft tissue is divided; flexor tendons are similarly allowed to retract after being divided under tension. Soft tissue is closed over the metatarsal head with absorbable sutures. Minimal handling of the skin prevents ischemic trauma. The skin is approximated without tension or left open for closure by secondary intention.



The great toe and first metatarsal bone are important for normal gait because weight is transferred from the posterolateral foot during heel strike toward the medial toes, and the transfer of weight forward occurs principally through force transmitted during push off through the first metatarsal and great toe. Because of the significant rate of repeat ulceration and need for revision in up to 60% of patients requiring a great toe ray amputation, some have advocated proceeding directly to TMA in these patients.


Partial TMA can be performed when two digits are involved and the foot is deemed salvageable. However, multiple ray amputations will narrow the foot, resulting in instability and change in gait that may lead to repeat ulceration, wound breakdown, and the need for revision.


Aug 1, 2016 | Posted by in CARDIAC SURGERY | Comments Off on Peripheral Arterial Occlusive Disease
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