CHAPTER OBJECTIVES
At the end of this chapter, the learner will be able to:
Relate the pathological changes in the vascular anatomy to the formation of arterial and venous wounds.
Differentiate between arterial and venous wounds.
Perform a vascular screening and interpret noninvasive vascular studies for arterial and venous disorders.
Use the information obtained from vascular studies to develop a plan of care for arterial wounds (before and after surgery) and venous wounds.
Determine when and if surgical intervention is needed for patients with arterial and venous wounds.
Select the appropriate compression therapy for patients with lower extremity vascular wounds based upon vascular studies.
The vascular system is an intricate system of arteries, veins, and lymphatic vessels designed to transport the blood from the heart to the core and peripheral tissue, providing tissue with the oxygen and nutrients necessary to sustain life, and from the same tissue back to the heart and lungs for recirculation (FIGURE 4-1). An interruption to blood flow in any one or more of the vessels can cause significant and critical pathologies that result in integumentary changes, wounds, or impaired healing. If the pathology is in the arterial system, the wound is termed ischemic; if it is in the venous system, it is termed venous. Both types have very defining characteristics and predictable vascular study results that are used to determine the optimal plan of care for the individual patient. This chapter focuses on the pathophysiology, prevention, and treatment of arterial and venous wounds; lymphatic disorders are discussed in Chapter 5, Lymphedema.
FIGURE 4-1
Anatomy of the arterial and venous circulatory systems The circulatory system consists of the cardiac, arterial, venous, and lymphatic systems. The arterial system is further delineated into the macrocirculation (arteries large enough to be named) and microcirculation (capillaries and arterioles too small to be named). The lymphatic system is illustrated in Chapter 5.
Vascular diseases such as peripheral artery disease (PAD) and chronic venous insufficiency (CVI) cause the majority of lower extremity wounds; the majority of arterial wounds are caused by PAD. The clinical spectrum of PAD ranges from asymptomatic disease to mild claudication, to tissue loss or gangrene of the foot or lower extremity. When patients with PAD have an ulcer or gangrene of the lower extremity, it is termed critical limb ischemia (CLI). The major cause of CLI is a reduction in distal tissue perfusion below the resting metabolic requirements usually associated with atherosclerosis; however, other conditions may cause wounds that appear to be arterial or ischemic (TABLE 4-1). Diabetes mellitus (DM) is one of the most serious and prevalent of these disorders. The combination of DM and PAD may lead to foot ulceration or gangrene, which may result in amputation. The overall risk of amputation is 15 times higher for patients with DM than in those without diabetes. The reason for the increased amputation rate is related to the complex pathophysiology of neuropathy and ischemia in the diabetic foot.1
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The presence of any lower extremity wound requires an evaluation of vascular status since it will determine the ability of the wound or surgical incision to heal. Healing of a foot wound may take months despite undergoing revascularization procedures. The presence of CLI in a patient is significant not only for potential limb loss; it is also an independent risk factor for cardiovascular morbidity and mortality. The goal of taking care of these patients is to assure that the maximum amount of arterial perfusion is present to help in the healing of these wounds. There is a high rate of recidivism and subsequent amputation when the treatment of the vascular insufficiency is not performed in a timely manner.
Between 2000 and 2010, the number of people with PAD has increased by nearly 25%. An estimated 202 million cases of PAD currently exist worldwide. Of these, 20–40 million cases will likely have intermittent claudication and 100 million will have atypical lower extremity symptoms. Forty-five million of the 202 million people with PAD will die from coronary or cerebrovascular disease during a 10-year period.2
Overall, the rates for PAD are similar for men and women.3 The prevalence of PAD rises with age, increasing to over 20% in individuals over 80 years old.4 Regardless of symptoms, PAD can significantly impact a patient’s quality of life, as even patients with asymptomatic PAD demonstrate impaired lower extremity function, greater mobility loss, and quicker functional decline than people without PAD.2 The true incidence of CLI is unknown; however, some studies have estimated around 500,000 to 1 million new cases occur each year.5 A similar incidence of 400 per 1 million population per year was found in a national survey of the Vascular Surgical Society of Great Britain and Ireland.6 The majority of individuals who have CLI with ulceration or gangrene also suffer from DM. It is estimated that up to 70% of all lower extremity amputations are diabetes related and the majority of those patients present with a foot ulcer that develops into an infected limb or gangrene.7,8 Almost 50% of those patients who undergo amputation for CLI will require amputation of the opposite limb within 5 years.
The economic impact involved in the care of patients with vascular wounds is staggering. The annual cost in treating lower extremity ulcers is around $25 million and the individual cost for treating a foot ulcer can be as high as $28,000.9 In England, the cost of care for an individual with a leg ulcer was around $130,000 annually.10 Included in the estimates are physician visits, hospital admissions for wound debridement or surgical revascularization, rehabilitation, and wound care supplies.
The prevalence of PAD with intermittent claudication among males and females is between a ratio of 1:1 and 2:1. This ratio increases when an ulcer or gangrene is present to at least 3:1. The prevalence of CLI increases substantially as the population ages.11
The natural progression of CLI is limited since published studies include performance of some revascularization procedure. However, there are some patients for whom an operation is prohibitive due to multiple comorbidities or limited life expectancy. A recent study by Marston et al. followed a cohort of patients with CLI who presented with uncomplicated limb ulcers.12 Revascularization was not performed due to medical comorbidities or anatomic considerations that did not allow surgical intervention. A total of 142 patients were followed for 1 year with the primary endpoint being major limb amputation. During the study, the wounds were treated with a specific protocol that emphasized pressure redistribution, debridement, infection control, and moist wound healing. The limb loss or amputation rate for these patients was 19% at 6 months and 28% at 12 months. Interestingly, complete wound closure was achievable in 25% at 6 months and 52% at 12 months. The only significant factor that affected wound closure was the initial size of the wound.
Arterial insufficiency not only causes wounds, it also portends negatively on the patient lifespan. The most common cause of death in patients with severe PAD or CLI is coronary artery disease. Depending upon the severity of the CLI, patients with resting pain have more than 70% mortality rate at 5 years. Even though this patient population may have a high mortality rate and are often treated in a palliative manner, conservative care can help alleviate pain and/or heal wounds.
The most common causes of PAD are arteriosclerosis and atherosclerosis (FIGURE 4-2). Risk factors for the development of these pathologies include age, smoking, diabetes mellitus, hypertension, hypercholesterolemia, dyslipidemia, family history, and obesity. Prevention and treatment of arterial wounds depend upon adequate identification and management of these risk factors.
FIGURE 4-2
Atherosclerosis Atherosclerosis is one type of arteriosclerosis in which fatty plaques composed of low-density fatty acids erode the artery wall with resulting deposition of macrophages and white blood cells. The plaque increases in size over a period of time, causing a gradual decrease in the size of the arterial lumen and reduced blood flow to the distal tissues. The critical level is occlusion of more than 80% of the arterial lumen. In addition, particles of plaque can break away, migrate to smaller arteries or arterioles (termed thromboemboli), and also cause tissue ischemia. (Copyright Medmovie.com with all rights reserved.)
Occlusion of the arterial system can occur in either the macrocirculation (defined as those arteries large enough to be named or with a diameter more than 0.5 mm) or the microcirculation (defined as the arterioles and capillaries too small to be named or with a diameter less than 0.5 mm). Tissue ischemia that leads to lower extremity wounds tends to occur more in the presence of large vessel or mixed disease. In addition to PAD, the arterial vessels can be occluded by a thrombus or emboli (eg, after surgery or trauma).
In the early stages of PAD, the circulatory system compensates by establishing collateral circulation around the occlusions in order to maintain peripheral blood flow. The first critical phase of the disease occurs when the collateral circulation is insufficient for the metabolic needs of the affected extremity; therefore, the limited blood supply is shunted to the muscle arteries where flow resistance is low instead of to the skin where resistance is high. A wound caused by trauma (eg, a blister from poorly fitting shoes, a skin tear, or a cut from poor foot care) during this period of decreased skin perfusion will heal more slowly than normal, or will be more likely to become infected and fail to heal. The non-healing wound may be the first indication that a patient has PAD.
Because exercise increases the muscle oxygen demand, and thereby its blood volume requirements, a second critical phase occurs when activity or exercise causes relative ischemia and pain. Intermittent claudication, the term for the symptoms of muscle pain and cramping that occur with exercise, is a second indication that the patient may have PAD.
When the PAD becomes severe, the third critical phase, the patient will probably experience resting pain, gangrene, and non-healing wounds in the extremity below the occlusion. During this phase, the patient may exhibit dependent leg syndrome, a position that allows gravity to assist blood flow to the distal extremity and thereby alleviate some of the pain. The patient frequently complains of rest pain during the night, a result of lower blood pressure and subsequent diminished flow to the lower leg and foot.
CLINICAL CONSIDERATION
Symptoms similar to PAD may be caused by lumbar spinal stenosis. A person with ischemic pain will feel relief with cessation of activity, whereas a person with spinal stenosis claudication will feel relief only with a change of position, for example, standing to sitting or sitting to lying. Determination of whether gluteal/lower extremity pain is due to spinal stenosis or due to ischemia and arterial insufficiency to the painful muscles is important for effective and appropriate medical management.
Impairment of blood flow can occur acutely (trauma or thrombosis) or chronically (atherosclerosis or arteriosclerosis). Both acute and chronic arterial insufficiency at any level (arteries, arterioles, capillaries) can lead to the formation of lower or upper extremity wounds. Reduced capillary flow (also called small vessel disease) is observed most frequently as a result of diabetes.
Obstruction of arterial flow can also be classified as anatomic or functional. Anatomic causes of obstruction include thromboemboli and vasculitis (FIGURES 4-3A–D and 4-4). Functional impairment occurs in conditions such as Raynaud’s phenomenon in which abnormal vasomotor function leads to reversible obstruction (FIGURE 4-5). In severe cases this may result in ulceration. Other potential causes of impaired arterial flow include upper extremity arteriovenous fistulas and aneurysms (FIGURES 4-6A and 4-6B).
CLINICAL CONSIDERATION
A wound that has the characteristics of arterial insufficiency on the foot of a young person is a red flag that the etiology is probably not arteriosclerosis. Other atypical disorders (eg, Buerger’s disease) need to be considered.
FIGURE 4-3
A, B, C. Arterial wounds due to thromboemboli Arterial wounds that are caused by thromboemboli begin as dusky discoloration (as noted in the third toe of A and the foot of B and C) and progress to dry or wet gangrene (as noted in the fourth and fifth toes of A). If the tissue reperfuses as the medical condition improves, milder cases can resolve and healing can progress almost like a bruise healing. The tissue necrosis may become well-defined by a process termed demarcation (as noted in the second toe of D). Debridement is usually deferred until demarcation is completed unless there are signs of clinical infection; protective measures are recommended to prevent further tissue loss. Keeping the extremity warm facilitates vasodilation, which can help maximize perfusion. D. Arterial wound due to trauma Trauma from multiple causes, including surgery, can result in clotting and thrombi that occlude vessels of any size. Distal tissue will become necrotic unless flow is restored emergently.
FIGURE 4-4
Ischemic wound due to vasculitis Vasculitis, an inflammation of the vessels that results in edema and occlusion, most often occurs in patients who have autoimmune disorders (eg, systemic lupus erythematosus, rheumatoid arthritis, untreated hepatitis). The wounds are exquisitely painful, do not become necrotic like other arterial wounds, and may occur on any part of the body. (See Chapter 8, Atypical Wounds.)
FIGURE 4-5
Raynaud’s phenomenon Raynaud’s syndrome is caused by vasospasm of the small arteries and arterioles resulting in ischemic changes such as skin color, numbness, and cold sensations. The attacks can be triggered by cold exposure or emotional distress. Symptoms are bilateral, begin distal and progress proximally, and in severe chronic cases can result in ulceration or gangrene.
Non-atherosclerotic or vasculitic disorders need to be considered in the patients who present with signs of tissue ischemia in the presence of normal pulses or diminished pulses. For example, thromboangiitis obliterans, also known as Buerger’s disease, is a macrovascular disorder. Common in men who are heavy smokers, the pathology is an immune and inflammatory disease of the peripheral arteries accompanied by vasospasm and thrombi in the arterial segments to the feet and/or hands. Occlusion of the arteries causes tissue ischemia with resulting thin, shiny skin and thickened malformed nails. Other symptoms include pain, tenderness, erythema caused by dilated capillaries, thin, shiny skin, and cyanosis caused by deoxygenated blood cells in the interstitium. If the disease exacerbates, the patient is at risk for gangrene or ulceration. Successful treatment must include cessation of smoking (FIGURES 4-7 and 4-8).13 Chapter 8, Atypical Wounds, includes further discussion of ischemic wounds due to unusual pathologies.
The initial assessment of any wound begins with a thorough history and physical examination, a process necessary to establish a diagnosis of wound etiology. The history includes screening for risk factors of atherosclerosis—especially smoking, diabetes, hyperlipidemia, and hypertension. Patients who have these risk factors need aggressive education and treatment to modify these factors and to encourage lifestyle changes. A thorough vascular medical history of coronary artery disease (angina pectoris or myocardial infarction) and carotid disease (transient ischemic attacks or ischemic stroke) increases the likelihood of PAD because atherosclerosis is a systemic disease and not just localized to a specific part of the body. Assessment of ambulation tolerance (by both patient report and treadmill testing) may uncover mild chronic limb ischemia with intermittent claudication. Other comorbidities, medications, and surgical history are obtained to determine any other contributing factors that may inhibit wound healing.
A thorough wound assessment and information about how the wound began are important in determining the etiology. Refer to Chapter 3, Examination and Evaluation of the Patient with a Wound, for more details on obtaining a subjective history.
The location, size, and depth of the wound are defining characteristics of ischemic wounds, which tend to be small and round with smooth, well-demarcated borders. The wound base is typically pale (lack of arterial inflow), lacks granulation tissue, and may be shallow or deep (FIGURE 4-9). Wet or dry necrotic tissue may be present; wet gangrene is significant for active infection and must be urgently debrided (FIGURES 4-10 and 4-11). Arterial wounds tend to occur at the distal digits, although wounds that occur on other parts of the foot (eg, the malleoli) from pressure may not heal due to arterial insufficiency (FIGURE 4-12). Because of the ischemia, arterial wounds are painful and often accompanied by complaints of pain when the feet are elevated, especially at night. Pain that is reduced with leg dependence is indicative of rest pain and is termed dependent leg syndrome.
FIGURE 4-12
Non-healing pressure ulcer secondary to arterial insufficiency Wounds of other etiologies (eg, trauma, pressure, or venous insufficiency) that fail to heal may be one of the first signs that a person has PAD. If the edges stay adhered with no signs of infection, debridement is deferred or not recommended until perfusion is restored and signs of angiogenesis are visible at the edges. Loose detached edges, as seen in this heel pressure ulcer, may be removed to increase the oxygen perfusion of the periwound skin and decrease the risk of infection.
Clinical signs of infection such as malodor, exudate, and erythema are noted in order to initiate appropriate antibiotic treatment and proper debridement. The presence of any exudate should also be characterized by the amount and color (refer to Chapter 3). If the wound can be probed to bone, there is a high probability of osteomyelitis (FIGURE 4-13).
Other observations indicative of PAD include hair loss, muscle atrophy, atrophy of subcutaneous tissues and skin and appendages, dry, fissured skin, discoloration, and dependent hyperemia (FIGURE 4-14).
Wound classification systems exist to stratify the severity of the ulceration and are based on the size, location, amount of tissue loss, presence of infection, and the status of the arterial blood flow. The following three classification systems are specific to diabetic foot wounds: Wagner grading; the University of Texas (UT) classification; and PEDIS or Perfusion, Extent, Depth, Infection, Sensation, which was developed by the International Consensus on the Diabetic Foot (TABLE 4-2).7 A fourth classification system exists for the lower extremity threatened limb and stratifies patients based on wound, ischemia, and foot infection (WIfI) (FIGURE 4-15).14
FIGURE 4-15
The WIfI Lower Extremity Threatened Limb Classification The Society for Vascular Surgery developed the WIFI classification system to “permit more meaningful analysis of outcomes for various forms of therapy” in patients who have critical limb ischemia.14 The system takes into consideration the extent of the wound, the degree of perfusion, and the presence of infection (Compliments of Dr. David G. Armstrong. Used with permission.)
System | Classification | System | Classification |
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The initial step of any vascular examination is palpation of pulses in the involved extremity that are compared with pulses of the contralateral limb in order to help determine the extent of diminished flow. The palpation of peripheral pulses is affected by the skill of the examiner and the room temperature. Patience is sometimes needed to feel the pedal pulses and the examiner may be misled by “feeling” one’s own pulse, especially when using the forefinger which has a strong digital pulse. Strength and interpretation of pulses have two different commonly used grades, thus consistency among team members is needed for accurate communication (TABLE 4-3).
CLINICAL CONSIDERATION
Suggestions for palpating pulses include the following:
Test in a warm room that optimizes arterial dilation, not constriction.
Position the patient in supine with access from both sides of the bed.
Avoid the use of the thumb, which has less discriminating sensation.
Palpate pulses on the contralateral side for an indication of anatomical location.
Encourage the patient to relax so as not to be confused by moving tendons, etc.15
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The character of the pulse refers to the upstroke, downstroke, and presence of thrills. In stiffened vessels or in vessels with high outflow resistance, the upstroke or radial expansion of the vessel may be slowed. In the presence of low outflow resistance, such as proximal to a traumatic arteriovenous fistula, downstroke may be significantly reduced. The absence of pulses suggests a proximal critical stenosis or occlusion. After palpation of the pulses, auscultation of the pulses by the examiner permits the detection of bruits, frequently an indicator of an upstream or nearby stenotic lesion. The pulse examination, when correlated with clinical symptoms, helps identify the site and severity of arterial occlusive lesions and indicates when further vascular testing is necessary.
CASE STUDY
Mr. LH is a 74-year-old male admitted to acute care with a non-healing wound on the right lateral heel of more than 6 months duration (FIGURE 4-16). Medical history includes type 2 diabetes, end-stage renal disease requiring hemodialysis three times a week, and hypertension. He has been admitted for further vascular studies, pain management, and possible revascularization of the lower extremity. A popliteal artery angioplasty and stent failed to establish blood flow sufficient for healing to occur.
Daily medications include the following:
Aspirin 81 mg daily
Clopidogrel (Plavix) 75 mg daily
Furosemide 40 mg daily
Isoniazid 300 mg daily
Sevelamer (Renvela) 800 mg daily
Sitagliptin (Januvia) 25 mg
Fish oil
Vitamin B6
Vital signs: normal for age
Laboratory values include the following:
Hematocrit—31.3%
Hemoglobin—10.4 g/dL
Platelets—140,000/mm3
Albumin—3.8 g/dL
HbA1C—8.7
INR—1
Prothrombin time (PT)—13.3 seconds
Partial thromboplastin time (PTT)—30.4
BUN—50 mg/dL
Creatinine—8.33 mg/dL
When you enter the room, the patient is sitting in bed with the right leg dangling over the side.
DISCUSSION QUESTIONS
Based upon the information in Chapter 3 on evaluation of the patient with a wound, describe the patient’s wounds and foot.
Classify the patient’s wounds using the Wagner, UT, and WIfI classification systems.
What information is needed to use the PEDIS classification system for these wounds?
Using the information in Chapter 11, what are the factors that might impede this patient’s ability to heal?
If pulses are faint or not palpable, a hand-held Doppler can detect flow within the vessel; however, the presence of a signal is not an indication of normal flow (FIGURE 4-17). Even in the most severe cases of PAD and gangrene, patients may continue to have Doppler signals in the pedal arteries. The Doppler examination is usually begun distally, and is not indicated at the more proximal locations if a pulse is palpable or audible.
FIGURE 4-17
Hand-held Doppler A hand-held Doppler is used to detect blood flow if pulses are not palpable; however, a positive Doppler sound is not indicative of normal blood flow. Doppler sounds can be described as triphasic, biphasic, monophasic, or absent; or they can be described as weak or strong.
The severity of microvascular disease (eg, with patients who have diabetes or Raynaud’s phenomenon) can be estimated by counting capillary refill time (CRT). CRT is measured by pressing the end of the toe or the skin just proximal to the wound until the color disappears and by measuring the time for recovery to the original color (FIGURE 4-18). Normal CRT is less than 3 seconds; however, it is prolonged in extremities with microvascular disease and may vary greatly among patients. Thus CRT is only a screening test and an indicator that more precise vascular testing may be indicated.
FIGURE 4-18
Capillary refill time Capillary refill time is measured by pressing the skin until it blanches, releasing, and counting the seconds it takes to return to normal color. Normal capillary refill time is 2 seconds; more than 3 seconds is indicative of microcirculation or small vessel disease.
Rubor of dependency test is a screening procedure for ischemia that can be performed at bedside; thus, it is not definitive but indicative of PAD. The extremity is elevated to 30° and observed for pallor. When the foot with normal circulation is placed into a dependent position, it will become a healthy pink color in approximately 15 seconds. If the reperfusion takes 30 seconds or longer and causes a dark-red or rubor appearance, the test is positive for severe ischemic disease.16 The faster the pallor appears in the elevated position or the longer it takes for the rubor to appear in the dependent position, the more severe the PAD.
The ankle-brachial index (ABI), a ratio of the ankle systolic blood pressure to the brachial systolic blood pressure, indicates the severity of peripheral arterial disease present in the lower extremity. A 10–12 cm sphygmomanometer cuff is placed just above the ankle and inflated. A hand-held Doppler is used to measure the systolic pressure of the posterior tibial and the dorsalis pedis arteries of each leg by noting the pressure at which the pulse returns as the cuff is deflated. Then, the pressures are normalized to the higher of the brachial pressures. The equations for the ABI are as follows:
Right ABI
Left ABI
The only contraindication for performing the ABI examination is the presence of an ulcer near the ankle, since compression of the ulcer with the sphygmomanometer cuff may cause significant pain to the patient. Interpretations of ABI values are listed in TABLE 4-4. In some patients with diabetes, renal insufficiency, or other diseases that cause vascular calcification, the pedal vessels at the ankle become non-compressible. This leads to an elevation of the ankle pressure and consequently an ABI >1.30. In these patients additional non-invasive diagnostic testing is indicated to evaluate the patient for PAD. Another scenario when the ABI may be inaccurate and unreliable is for patients who have heel pressure injuries; the anterior tibial artery may be compressible when the posterior tibial artery is not compressible, making the calculated ABI a misleading indicator of adequate perfusion for wound healing.17
1.0–1.2: Normal |
0.8–1.0: Minimal peripheral arterial disease. Compression for edema control is safe to use. |
0.5–0.8: Moderate peripheral arterial disease, often accompanied by intermittent claudication. Referral to a vascular specialist is advised. Compression therapy is contraindicated if <0.6; modified compression is indicated if 0.6–0.8. |
<0.5: Severe ischemia with resting pain. Compression therapy is always contraindicated. |
<0.2: Tissue death will occur. |
1–1.3: May occur with venous hypertension. |
>1.3: Non-reliable in patients with diabetes due to calcification of the arteries. |
Toe pressures are used in patients with calcified vessels and abnormally high ABI or non-compressible vessels, typical of patients with diabetes. A pneumatic cuff, about 1.2 times the diameter of the digit, is wrapped around the proximal phalanx and a flow sensor is applied distally to the digit. Toe pressures that are greater than 50 are considered normal and those that are less than 50 are abnormal. The majority of patients with foot ulcers or wounds that are caused by PAD have a toe pressure less than 30. In non-diabetic patients, a toe pressure greater than 30 mmHg, and in diabetic patients, 55 mmHg, will usually lead to healing.18 The normal toe/brachial index, also considered a reliable indicator of lower extremity vascular status, is 0.8–0.99.19 A toe pressure <30 mmHg or a TBI ≤0.2 infers a diagnosis of severe ischemia or critical limb ischemia.20
Segmental limb pressure is measured by combining Doppler ultrasound or plethysmography with blood pressure measurements at various locations in the arms and legs. Segmental pressures are a useful adjunct to the physical examination and ABI because they can illustrate differences in blood pressure at specific sites in the extremities and identify gradients that indicate the presence of disease.
A normal variation in the pressures between limb segments is 20–30 mmHg. A difference of 30 or greater indicates significant obstruction. Similarly, variations of pressure between symmetric limb segments do not differ by more than 20 mmHg unless there is an abnormality. Although they are strong indicators, limb pressure measurements are far less sensitive and specific than duplex imaging in the accurate diagnosis of arterial disease (FIGURE 4-19).21
FIGURE 4-19
Arterial profile includes segmental pressures This study shows arterial waveforms from the femoral artery through the toes. Pressures and waveforms analyses are evaluated at each arterial segment. Triphasic arterial waveforms are identified throughout all segments except the right dorsalis pedis artery where the waveform displays a biphasic pattern. Comparison to the brachial artery pressure allows calculation of the ankle-brachial index.
Another important tool in evaluating the patient with the chronic wound is measurement of transcutaneous oxygen measurements (TcPO2), defined as skin oxygenation. The measurement of TcPO2 depends on the cutaneous blood flow, the oxyhemoglobin dissociation, and the diffusion of oxygen through the tissues; thus it reflects the metabolic state of the target tissues. The measurements are taken usually on the dorsum of the foot, antero-medial calf approximately 10 cm below the patella, and in the thigh approximately 10 cm above the patella (FIGURE 4-20). The reference site is usually on the chest in the infraclavicular area. The limb is maintained in the dependent position to help increase blood flow.
A normal TcPO2 is between 60 and 90 mmHg. A measurement greater than 30 mmHg indicates adequate perfusion for healing, whereas if the tissue surrounding an ulcer has a TcPO2 less than 20 mmHg, the wound typically will not heal. In addition, patients with a TcPO2 less than 20 mmHg will typically experience rest pain. A TcPO2 value greater than 40 mmHg is desirable to support minor amputation site healing (toe amputation or transmetatarsal amputation) (TABLE 4-5).
<20 mmHg: Unlikely for healing to occur. |
20–30 mmHg: Healing can be expected, but may be delayed. |
>30 mmHg: Proximal to the toes: wound can be debrided. |
<30 mmHg: Proximal to the toes: wound should not be debrided until revascularization is accomplished. |
>40 mmHg: Desired for healing of minor amputation site. |
60–90 mmHg: Normal. |
The exercise stress test (EST) assesses PAD in patients with borderline ABIs (0.92–1.0) and symptoms of claudication. A resting ABI is performed first, after which the patient walks on a treadmill (typically at 2 miles per hour with an incline of 10–12%) for 5 minutes or until symptoms of claudication cause the patient to cease the activity. An alternative exercise activity is performance of 50 heel raises in the standing position. The duration of exercise and the nature of the symptoms are recorded. The patient is placed in a supine position and the ankle pressure measurements are recorded every 30 seconds until (1) the BP has returned to baseline or (2) 10 minutes have elapsed. BP values after exercise are compared to pre-exercise values. Normally, there is little or no change in the ankle or brachial BPs; however, PAD sufficient to cause claudication will result in a drop in the ankle pressure of at least 25 mmHg, 25% decline of the resting ankle pressure, or a decrease in the ABI >0.15. A negative EST with the same symptoms suggests cardiorespiratory, neurologic, or musculoskeletal disease.22
Ultrasonography is one of the most important diagnostic tools for the vascular system. Many of the terms associated with ultrasound are often used interchangeably and/or incorrectly. A basic understanding of how the technology is applied will help understand when each test is needed.
The principle of ultrasound is bouncing sound waves away from a probe and back to a receiver and measuring the time for the echo or returning sound wave to return after it was emitted. Time and strength of the returned sound waves are amplified and transformed into a visual representation described as A-mode or B-mode. A-mode or “amplitude” mode represents the signal as an amplitude (FIGURE 4-21). B-mode or “brightness” mode adds a linear array of scanners that scan a plane through the body to create a 2D image with densities represented as varying degrees of “brightness.” This creates a more anatomical representation (FIGURE 4-22).
FIGURE 4-21
Ultrasound, A-mode A-mode ultrasound simply shows the amplitude of the sound waves and is rarely used for diagnostic purposes with the development of Duplex scans. (Used with permission from DeMaria AN, Blanchard DG. Echocardiography. In: Fuster V, Walsh RA, Harrington RA, eds. Hurst’s The Heart. 13th ed. New York, NY: McGraw-Hill; 2011:chap 18. Available at: http://www.accessmedicine.com/content.aspx?aID=7805593. Accessed August 23, 2018.)
FIGURE 4-22
Ultrasound, B-mode B-mode ultrasound is the reflected sound waves plotted on an oscilloscope to create a two-dimensional image of the anatomical structure. Figure A is the external iliac artery without color (the artery is the dark area in the middle of the image), and figure B is the right common femoral artery with color added to show direction of flow. Red is typically flow away from the heart and blue is flow toward the heart. A mosaic of color is interpreted as a stenosis, a point at which flow is scattered in both directions.
Doppler ultrasound builds on this by combining the Doppler effect with the ultrasound (FIGURE 4-23). Doppler effect is a change in the frequency of a detected wave when the source or the detector is moving, and can measure flow, or in arterial studies, specifically blood flow from the heart to the peripheral extremities. Differences in flow can be represented as changes in color flow Doppler. Additionally, Doppler ultrasound can be continuous or pulsed waves. Pulsed wave Doppler has the advantage of detecting velocities in a small area very accurately, whereas continuous wave can measure higher velocity flows over a larger area. Finally, the term duplex ultrasound refers to a simultaneous presentation of Doppler (usually pulsed wave) and 2D or B-mode imaging (FIGURE 4-24).
FIGURE 4-23
Doppler with color flow imaging The Doppler effect is used to measure the velocity of blood flow in a vessel and is based upon the principle that flow toward the receiver creates shorter waves than flow away from the receiver. The velocity of flow in the vessel (in this case a vein) is shown on the bottom of the screen in the color flow imaging.
FIGURE 4-24
Arterial duplex with color flow imaging Arterial duplex scan of the common femoral artery. The flow pattern is laminar in nature (as identified by the homogeneous color of the moving blood through the vessel imaged). The waveform is a triphasic waveform with a peak systolic velocity of 110.9 cm/sec. Signs of a stenotic lesions would show a more mosaic flow color and higher velocities (over 250 cm/sec).
Duplex ultrasound imaging provides both anatomic and hemodynamic blood flow assessment in a non-invasive manner. Duplex ultrasound can provide spectral analysis, which shows the complete spectrum of frequencies (that is, blood flow velocities) found in the arterial waveform during a single cardiac cycle.
The normal (“triphasic”) waveform is made up of three components that correspond to different phases of arterial flow: rapid antegrade flow reaching a peak during systole, transient reversal of flow during early diastole, and slow antegrade flow during late diastole. Lesions are identified by a change in waveform from triphasic to monophasic, or an increase in peak systolic velocity (PSV) followed by a drop in velocity (FIGURE 4-25A, B). Certain ratios of the PSV within an area of stenosis to the PSV of the proximal normal segment correlate with the degree of stenosis.
Accurate evaluation of the arterial blood supply is paramount for successful revascularization of the ischemic extremity for patients with or without diabetes. Arterial imaging is challenging for patients with ischemic complications because they frequently have underlying renal insufficiency, a condition that limits the amount of iodinated contrast that can be injected.
Computerized tomographic arteriography (CTA) involves injection of contrast medium into an upper extremity vein followed by CT scan of the diseased arteries. CTA is a safe, non-invasive procedure that provides high-quality imaging of the arteries; however, significant arterial calcification can impede the transit of contrast in the distal segments of the extremity, in which case more images and higher radiation doses are required. In addition, CTA is only a diagnostic tool and not sufficient for pre-surgical evaluation.
Magnetic resonance angiography (MRA) can be performed with a contrast agent injected intravenously, termed flow dependent, because the presence of the contrast in the diseased arteries depends upon the blood flow getting to that area. The MRA can also be done without contrast, termed flow independent. MRA images are not obscured by arterial calcification; however, the disadvantages are motion artifact, long acquisition times, anxiety in patients who are claustrophobic, and possible nephrogenic systemic fibrosis in the patient with renal insufficiency.
For patients who require revascularization, arteriography using digital subtraction techniques is preferred to determine appropriateness for endovascular revascularization versus surgical bypass (FIGURES 4-26 and 4-27).
Angiography (or arteriography when referring specifically to the arterial system) is radiographic imaging of a contrast-filled blood vessel (FIGURE 4-28). Despite advances in the quality and availability of the previously described modalities, arteriography remains the gold standard for pre-surgical evaluation of the diseased arteries. There are clinical scenarios in which angiography is not the first choice because of its invasiveness; however, the explosion of endovascular therapy of vascular disease has strengthened angiography as a preferred method because of its sensitivity and ability to be easily combined with endovascular treatment.
FIGURE 4-28
Arteriogram of lower extremity vessels Arteriogram of the aortoiliac segment of the arterial circulation. Extensive disease is seen in the left distal common iliac and the external iliac is occluded. The vessel seen traversing through the pelvis is the internal iliac artery, which is the main collateral vessel for the occluded external iliac artery on the left.
Arteriography is performed in a procedure room with a fixed, mounted fluoroscopic unit or in an operating room with a mobile X-ray unit that has its own generator, c-arm, and image intensifier or panel detector. The contrast agent is injected manually or via a power injector into the target vessel. One emerging technique is CO2 arteriography, in which CO2 gas is injected to transiently displace blood in the vessel and thereby create an image. CO2 as a contrast agent is preferable in circumstances where systemic or renal toxicity from iodinated contrast is contraindicated or risky for the patient.
Digital subtraction refers to enhancement of the imaging prior to interpretation. The fluoroscopic image is processed, digitized, and amplified to create a more accurate anatomic picture. Arteriography is done through single-injection with staged or stepped technique (the contrast is injected and images are taken either at various points along the extremity to follow the contrast load or via a rotational method). This technique can create a 3D image of the contrast outline using a detector that rotates between two points as the contrast is injected.
The limitations of arteriography are operator dependence, contrast and radiation exposure, and the inability of the image to effectively characterize the surrounding anatomy or vessel wall.
Prevention of arterial wounds is predicated on identifying risk factors and reducing their impact on the integrity of both macro- and microcirculation. Important strategies include the following:
Instruct and encourage the patient who smokes to stop by participation in smoking cessation programs.
Educate the patient about blood glucose controls to minimize the risk of PAD.
Educate the patient on the need to control hypertension, hyperlipidemia, and hypercholesterolemia through diet and medication.
Encourage the patient to initiate supervised exercise therapy to develop collateral circulation in the lower extremity, especially in the case of intermittent claudication.23–26 Exercise tolerance is established by walking on a treadmill until onset of moderate pain and by noting the speed, grade, and time. During treatment, the patient performs the cycle of walking and resting for 30–60 minutes, 3–5 times a week for 6 months. As endurance improves, the speed increases, the grade increases, and the rest time decreases. The goal is not to increase the treatment time, but to increase the activity level, especially the incline grade, within the treatment period.27 Supervised exercise therapy has been shown to increase walking distance, improve endothelial and mitochondrial function, muscle strength, and endurance, as well as improve overall cardiovascular fitness and quality of life.24,28
All patients who have any of the risk factors for atherosclerosis should be medically optimized.28 Control of hypertension is measured with a goal of systolic pressures less than 140 mmHg and diastolic pressures less than 90 mmHg (for the non-diabetic and non-renal failure patient). Antiplatelet therapy (eg, aspirin or clopidogrel) has been shown to reduce myocardial infarction, stroke, or death in patients with symptomatic lower extremity ischemia. Cholesterol is controlled using statin medications with a goal of less than 100 mg/dL in all patients with PAD. Smoking cessation is critical in halting the progression of atherosclerosis and in reducing bypass graft failure after revascularization.
Wound care before a patient has revascularization is based on protection of the wounded tissue and at-risk areas (eg, heels and malleoli). Suggested strategies include the following, with the understanding that care is based on the individual patient’s presentation, pain, and wound location:
Debridement of an arterial wound without adequate perfusion for wound healing will make the wound larger. Therefore, intact eschar is not debrided. Infected tissue, termed wet gangrene, is debrided either with sharp or surgical techniques.
The skin and necrotic tissue are kept dry and protected with sterile gauze, lambswool, or cotton between the toes. Swabbing the wound margins with alcohol or iodine solution helps minimize the risk of infection. Dry silver dressings may also be used to prevent maceration and infection while waiting for revascularization and reperfusion (FIGURE 4-29).
The heels are protected from pressure by placing a pillow under the calf and thigh or by using an off-loading boot (FIGURE 4-30).
A foot cradle on the bed helps to keep the weight of bed linens off affected distal digits.
Post-op shoes help protect the toes from extra pressure, and assistive devices can help further off-load the involved foot.
In severe cases, the patient is advised to avoid exercise, or limit exercise to functional tasks, in order to decrease the oxygen consumption of surrounding muscles and optimize perfusion to the ischemic areas.
Elevating the head of the bed 5–7° allows gravity to assist in increasing the blood flow to the foot. Discourage limb elevation that may further reduce blood flow to the distal extremity.
Keeping the affected extremity warm helps prevent further vasoconstriction due to cold exposure. Hot soaks, hot water bottles, or heating pads are discouraged because the diabetic foot is often insensate and cannot feel burning sensations. Also, because of autonomic neuropathy, the vessels cannot vasodilate to dissipate the heat, resulting in the accumulation of heat in the tissue and subsequent blistering, ulceration, or infection.
Adjunctive therapies may be indicated for increased microcirculation (eg, electrical stimulation, low-frequency noncontact ultrasound, growth factors, and bioengineered tissue).29
Cellular and tissue-based products or biological dressings are NOT appropriate for use at this time because the wound environment is not yet optimized.