Peripheral Arterial Perfusion: Is it Adequate for Wound Healing?

     More than 8 million Americans are affected by peripheral arterial occlusive disease (PAOD).¹ The presence of PAOD can seriously inhibit the ability of a lower extremity ulceration to heal. Many wounds will not heal unless adequate arterial perfusion is reestablished. Traditionally, revascularization was achieved by open surgical bypass,² but recent advances in percutaneous angioplasty and stenting techniques have provided new options. These innovations offer promising new treatment alternatives for those patients who were previously considered unsuitable candidates for open procedures or for those whose wounds overlie the path of standard surgical incisions.^3,4 Clinicians must be able to recognize wounds whose healing potential is compromised by PAOD so that revascularization can be undertaken before tissue loss progresses to the point that limb preservation is not an option.      

Patient Evaluation

Identification of patients with inadequate perfusion for healing is critical. Initial assessment of any wound begins with a complete history and a thorough physical examination.      History. The existence of risk factors for PAOD should alert the clinician to the possibility of an arterial insufficiency component that may adversely affect wound healing. Commonly identified risk factors include diabetes mellitus, coronary artery disease, hyperlipidemia, cigarette smoking, and hypertension.⁵      Reports of intermittent claudication should increase the clinician’s suspicion of PAOD. Claudication is reproducible leg pain that occurs when a stenotic or occlusive lesion prevents sufficient arterial blood flow from meeting the increased metabolic needs of an exercising muscle.⁶ Classically, pain or cramping occurs repeatedly in the posterior calf after walking approximately the same distance and is relieved by rest. Claudication pain may also occur in the posterior thigh, buttock, or hip, and rarely in the foot.⁷      Ischemic rest pain may occur in an advanced disease state. This is severe pain, typically localized in the dorsal aspects of the toes and distal forefoot.⁶ Ischemic rest pain is experienced most frequently at night when the extremities are elevated in bed. The pain is reduced with dependency and affected patients will often hang their leg over the side of the bed or get up to walk in an effort to relieve the pain.      Current and previous wound care regimens and the clinical response should be reviewed in detail. Reasonable regimens with increasing tissue loss should also alert the clinician that a vascular etiology should be considered. A history of revascularization with a lack of response to treatment should warrant reassessment of the revascularization for technical adequacy and the patient’s foot perfusion.      Physical examination. Physical examination findings that are indicative of PAOD include atrophic skin changes, which suggest a lack of adequate arterial perfusion. The skin covering the lower extremity and foot is thin, taut, and shiny.⁸ Thinning or actual loss of the hair over the distal third of the leg and the foot will typically occur. The skin is cool to the touch, pale, or even mottled, while toenails become thick and dystrophic.      Extremities affected by PAOD will frequently display Buerger’s sign, characterized by dependent rubor and pallor with elevation from chronic dilatation of the vascular bed.⁶ This physical sign is due to loss of vasomotor control of the microcirculation and is seen in cases of advanced ischemia.⁹ When in a dependent position, a deep, dusky red or “ruddy” flush spreads proximally from the toes over the dorsum of the foot. When the leg is elevated above 45 degrees, the foot becomes pale. This physical finding is indicative of advanced occlusive disease and inadequate perfusion for healing. It can also be seen in patients with peripheral neuropathy who have lost control of the microcirculation as a result of autonomic nerve dysfunction unrelated to ischemia.⁷ It should also not be confused with cellulitis, which is typically associated with concomitant swelling, warmth, and tenderness.¹⁰      The majority of lower extremity ulcers arise from ischemic, venous, neuropathic, or mixed origins. Distinguishing the etiology of the ulcer and whether or not an ischemic component exists is critical in determining an appropriate care plan for the patient. The basic physical findings associated with each etiology are summarized in Table 1.      Ischemic ulcerations tend to occur over the distal portion of the toes or forefoot, spontaneously at pressure points or as the result of minor trauma. They are typically found on the dorsum of the foot, heel, and metatarsal heads, the tips of the toes, or the bunion area.¹¹ Initially, they may have irregular edges but tend to become “punched out” in appearance with chronicity.⁶ They are usually small and round with smooth, well-demarcated edges.¹¹ The wound base may have pale granulation tissue or even be a pale gray color.⁶ The wound can be covered by white fibrinous tissue or a dry, necrotic eschar. Surrounding edema, inflammation, and drainage is usually minimal.
     When arterial blood supply falls below minimal tissue metabolic requirements, dry gangrene develops. Dry gangrene is black with a hard, dry texture and most frequently occurs at the distal aspect of toes.¹² There is often clear demarcation between viable and necrotic tissue. A distinctive smell of decomposition from the affected tissue may be present. Typical findings of a patient with advanced ischemia and tissue loss are shown in Figure 1.      Peripheral pulses are diminished or absent with PAOD. Bilateral femoral, popliteal, posterior tibial, and dorsalis pedis pulses should be palpated and assessed for symmetry and intensity.⁷ Bruits may be heard over the femoral arteries, which is suggestive of occlusive disease at or proximal to the level examined. Lower extremity edema may interfere with an accurate assessment of foot pulses. In these instances, a handheld Doppler can be used to assess the pulse quality more accurately. An experienced examiner can estimate the degree of occlusive disease by the sound characteristics of the Doppler signal; normal pulses are triphasic. As arterial perfusion is compromised, the signal becomes biphasic and finally, monophasic. Capillary refill, another noninvasive method to assess adequacy of arterial perfusion, involves compressing the pad of the patient’s great toe between the forefinger and thumb.⁶ If the color returns to the compressed area in 3 seconds or less it is considered normal. Longer refill times indicate decreased perfusion.      In contrast, venous ulcerations resulting from venous hypertension tend to occur in the “gaiter distribution” or lower third of the leg, usually above or around the malleoli.⁶ Frequently superficial and diffuse, they have irregular edges without undermining.¹¹ The wound bed appears “beefy” red, moist, and granular (Figure 2A). Wound drainage can be copious which can result in tissue maceration. It is always bordered by inflammatory skin changes and the skin in the gaiter distribution is thick and edematous with a reddish-brown hyperpigmentation.¹¹ Diffuse hyperkeratosis and soft tissue fibrosis (lipodermatosclerosis) are common findings with chronic venous disease.⁶ Pain is usually mild and improves with elevation but can be severe with open wounds. An arterial insufficiency component should be suspected if the wound bed appears pale, with minimal granulation tissue, or necrotic tissue covers all or some of the wound surface (Figure 2B).      Neuropathic ulcers are commonly located at the pressure points on the foot, including the tips of the toes and under calluses on the plantar surface of the foot.⁶ Bone deformities of the foot often exacerbate areas of pressure among patients with diabetes. Secondary to the neuropathy the wounds tend to be nontender or minimally tender. Surrounding skin changes indicating acute and chronic inflammation and callus are common.⁶ Neuropathic ulcers tend to be deep and punched out often with a deep sinus^,6 but often a good granulation base is present (Figure 3A). Neuropathic ulcers with coexisting arterial occlusive disease may appear pale with minimal granulation tissue, absent granulation tissue, or even gangrene (Figure 3B).      

Objective Assessment of Perfusion

The ankle brachial index (ABI) is a simple, noninvasive test that is helpful in determining the presence of PAOD.⁷ The ABI should be administered after at least 10 minutes of rest with the patient supine and the patient’s feet at the same level as the heart. A handheld Doppler probe is used to detect the arterial signal. The blood pressure cuff is placed just proximal to the ankle to obtain ankle pressures and just proximal to the antecubital crease for the brachial pressure. The ABI calculated for each side is the ratio of the highest systolic blood pressure at the ankle (posterior tibial or dorsalis pedis arteries) divided by the highest brachial systolic blood pressure. An ABI of 1 to 1.2 is considered normal since the pressure in the leg should be equivalent or slightly higher than the pressure in the arm.¹³ For screening purposes for occult PAOD, an ABI as low as 0.9 is considered normal.¹⁴ As the index decreases the degree of arterial occlusive disease increases (Table 2). For a foot ulcer to heal, the ankle systolic pressure should be > 60 mmHg, and in patients with diabetes > 90 mmHg.¹³ An ABI < 0.5 in the presence of a foot ulcer suggests the wound is unlikely to heal unless perfusion is improved by an arterial vascular intervention.¹³ A potential source of error with the ABI is that calcified vessels will not compress normally and can result in a falsely elevated systolic pressure. Any ABI > 1.3 should be suspect.¹³ An ABI difference from one study to the next that is > 0.15 is considered a significant change.¹³      Further assessment can be obtained in the vascular laboratory if the physical examination findings and ABI suggest PAOD. The two study types used are physiologic testing (segmental limb pressures and waveform analysis) and color duplex ultrasonography.      Physiologic testing involves waveform analysis (Doppler or pulse volume recording), segmental limb pressures, which include the ABI as well as digital absolute pressures and calculation of the toe-brachial index (TBI). This study is a screening test that can further define the level and extent of occlusive disease, as well as determine the adequacy of arterial perfusion to effect healing.¹³ Briefly, the study is performed by placing pressure cuffs bilaterally on the arms, thighs, below-the-knee, and just above the ankle.¹³ The patient must be in the supine position and have been at rest for at least 10 minutes. Using continuous wave Doppler, an arterial signal is found distal to the cuff (most commonly the dorsal pedis or the posterior tibial arterial signal), and the cuff is inflated until the signal is no longer heard. The cuff is then deflated and when the arterial signal returns, the systolic pressure is recorded. This procedure is done systematically for each cuff. Both dorsalis pedis and posterior tibial pressures are recorded for the ankle pressure. A significant pressure gradient (> 20 mmHg) between adjacent segments suggests occlusive disease in the intervening segment.¹³      They are used in conjunction with waveform analysis because segmental limb pressures are often falsely elevated due to medial calcification of the arteries.¹³ The type of waveform analysis used most commonly is the pulse volume recording (PVR) because it is less labor-intensive and operator-dependent. In general, the pneumatic cuff is inflated to a preset level and the volume shift that occurs over a cardiac cycle in that limb segment is transmitted and recorded as a waveform. The character of the waveform suggests adequacy of perfusion and helps substantiate whether the segmental pressures obtained are accurate or falsely elevated secondary to medial calcification.      Since digital pressures are generally not affected by medial calcification, they are diagnostically useful when ankle pressures are elevated because of noncompressible vessels.¹³ They can also be used to detect PAOD within the foot and thus provide helpful information as to perfusion of the forefoot and toes. A pneumatic cuff is placed on the toe. A photoelectrode is then placed on the end of the toe and the cuff is inflated until the waveform disappears. When the waveform returns after cuff deflation, the systolic pressure is recorded. In general, a normal digit pressure is 80% to 90% of the brachial pressure or 0.8 to 0.9.¹³ Regarding ABI, the toe-brachial index (TBI) is inversely related to the degree of arterial obstruction (Table 2). Representative ankle and digital waveforms and corresponding pressures and indices are shown in Figures 4A and 4B.      A different method of assessment is color duplex ultrasound, which provides more specific information in terms of level of occlusive disease whether there is stenosis or long segment occlusion. Still ABIs and digital pressures should be obtained as these two measures provide better measures of wound healing at the level of the foot.
Transcutaneous oxygen measurements (TcPO₂) are another noninvasive measurement, which is performed to assess arterial perfusion and healing potential. A special electrode is attached to the skin that detects the diffusion of oxygen through the surface of the skin. TcPO₂ measurements < 40 mmHg have been associated with impaired healing, while those < 20 mmHg indicate an inability to heal an open wound without revascularization (Table 3).      

Conclusion

A patient with a foot ulcer who has a significant element of arterial insufficiency enough to delay or prevent healing should be referred to a vascular specialist for further evaluation. Unless overwhelming infection is present, wound debridement should be deferred until adequate arterial perfusion has been restored.¹⁵ By removing necrotic tissue an even larger wound will be created, one that will also be unable to heal. Arterial ulcers and dry gangrenous tissue should be kept dry. Dressings that promote moist wound healing tend to promote bacterial growth and potentially expose the wound and surrounding tissue to infection.¹⁵ Furthermore, compression therapy, the mainstay of treatment for venous stasis ulcerations, should be used with caution in ulcerations with underlying occlusive disease. Those with an ABI ≥ 0.8 can and should be treated with compression up to 35 mmHg–40 mmHg.¹⁶ Reduced compression of 17 mmHg–25 mmHg can safely be used in those patients with an ABI < 0.8 but > 0.5. Compression should not be used in those with an ABI < 0.5.      It is important that clinicians are able to accurately identify those ulcerations that are not likely to heal without revascularization. Therefore, prompt referral to a vascular specialist can be made hopefully to promote limb preservation.