Utilizing the Ankle Brachial Index in Clinical Practice

Lower extremity vascular changes have been highly correlated with claudication pain, ischemic tissue loss, and functional limitations that include poor standing balance and mobility.1,2

A thorough peripheral vascular assessment is essential in the clinical management of individuals with peripheral arterial occlusive disease (PAOD). Intermittent claudication, diminished distal lower extremity pulses and skin temperature, texture, and color changes are common indicators of PAOD.3 Tests that provide more objective and quantifiable values should be used to monitor vascular disease progression, therapeutic interventions, and for screening purposes in those individuals with asymptomatic PAOD. The ankle brachial index (ABI), when used with pulse volume recordings (PVRs), segmental systolic limb pressures (SLPs), and transcutaneous oximetry mapping (TCOM) can provide an accurate assessment of an individual's peripheral vascular status. Technique and Interpretation The ABI is a noninvasive test performed with a blood pressure cuff and a Doppler ultrasound that magnifies vascular sounds. Individuals are tested in the supine position following a 5-minute rest period. Initially, brachial systolic blood pressure is recorded by inflating the blood pressure cuff above the elbow. The Doppler probe is coupled to the skin over the brachial artery with ultrasound gel. The probe should be held at a 45-degree angle that opposes the direction of brachial artery blood flow. The cuff is slowly deflated after the brachial artery has been occluded and the pressure at which the pulse sound returns is recorded as a brachial systolic pressure. Systolic pressure is measured in each arm two times and the highest value is used in the ABI calculation. Following the brachial recording, ankle systolic pressure is recorded by inflating the cuff approximately 5 cm above the ankle's medial malleolus and listening for vascular occlusion with the Doppler probe placed over the posterior tibial or dorsalis pedis arteries (see Figure 1). The cuff is slowly deflated and the pressure at which the pulse sound reappears is recorded as an ankle systolic pressure. After two posterior tibial or dorsalis pedis measures on each side, the highest systolic value is used in the ABI calculation. The ABI is calculated by dividing ankle systolic pressure by brachial systolic pressure: ABI = ankle systolic brachial systolic Investigators4,5 report improved reliability when using multiple measurements and consistent cuff size and placement through all measures. A low normalized ABI measure fluctuation (1.7%) was reported during repeated measures in a 6-week study of 15 individuals with intermittent claudication.6 In another ABI reliability study,7 intraclass correlation coefficients (ICC) were calculated for intraobserver and interobserver variability within the same day and after a 1-week period. Fifty-four patients with various stages of PAOD were evaluated; ICCs were as follows: 0.98 (same observer/same day measures), 0.89 (same observer/measures separated by 1 week), 0.92 (different observers/same day measures), and 0.87 (different observers/measures separated by 1 week). Normally, ankle systolic pressure should be equal or slightly higher than brachial systolic pressure (see Table 1). An ABI > 1.0 to 1.2 is considered normal, while progressively low ABIs are indicative of arterial narrowing associated with PAOD.8 Recently, two research studies9,10 involved performing ABIs on sample populations with (n = 50) and without PAOD (n = 353). An average ABI of 0.68 (+ 0.12) was reported for the PAOD population, while the sampled population without PAOD had an average ABI of 1.16 (+0.13). When considering measurement error, most clinicians will use an index change of 0.15 as a significant difference either from disease progression or therapeutic intervention (ie, arterial bypass). Enzler11 reported a good clinical correlation between ABI and lower extremity vascular status. Ankle brachial indices between 0.3 and 0.9 were associated with increased claudication pain following physical activity. Individuals with ABIs < 0.5 were reported to have an increased incidence of resting ischemic pain and increased risk for ischemic tissue loss. A high correlation existed between critical limb ischemia and ABI values < 0.4 or absolute ankle systolic pressures < 50 mm Hg.12 Lower leg and foot ulcers were less likely to heal without surgical intervention if an individual presented with an ABI < 0.3.11 Integrating SLPs and PVRs with the ABI The ABI is not always reliable in individuals with PAOD who have distal lower extremity arterial calcification.8,13 High cuff pressures are required to occlude calcified vessels during ankle systolic pressure evaluation. The high cuff pressure results in an abnormally high ABI (> 1.2). A high value is not considered a reliable index because the elevated ankle systolic pressure is due to noncompressible calcified arteries. Indices above 1.2 should be checked with an individual?s full clinical presentation (ie, changes in skin temperature and integrity and presence of claudication pain) to ensure the value is a valid representation of ankle systolic pressure. To obtain a more accurate assessment of a patient?s vascular status, lower extremity SLPs need to be evaluated in conjunction with the ABI. In particular, systolic toe pressures provide a more accurate assessment of distal lower extremity perfusion since the calcification observed in advanced cases of diabetes does not appear to extend into the toes.14 An absolute toe systolic pressure is normally 60% to 90% of the brachial systolic pressure, and a toe pressure < 30 mm Hg indicates that an individual with ischemic tissue loss will require some form of surgical revascularization for healing.15,16 In addition to systolic toe and ankle pressure, a segmental evaluation includes systolic pressure of the: 1) proximal femoral artery (proximal thigh), 2) distal femoral artery (distal thigh), and 3) distal popliteal/proximal tibial and peroneal arteries (below knee). A properly fitting blood pressure cuff is positioned over each site and the Doppler probe is placed over the posterior tibial or dorsalis pedis artery to determine the return of the arterial pulse following a single segmental compression (see Figure 2). Each area is evaluated individually as the cuff is slowly deflated following inflation beyond systolic pressure. Arterial pulse return is noted during cuff deflation and recorded as the systolic pressure for that segment. As the test progresses down the leg, a pressure drop > 20 mm Hg between adjacent segments (upper thigh to lower thigh, lower thigh to below knee, and below knee to above ankle) is indicative of a significant vascular lesion.17,18 In addition to comparing pressures vertically between segments, a horizontal comparison to corresponding segments on the contralateral leg should not differ by > 20 mm Hg (see Table 2).18 Pulse volume recordings are also indicated when performing noninvasive vascular tests. The device required for PVRs is a pneumoplethysmograph that can sense very small changes in air pressure. These changes are detected from a pressure-sensitive cuff that is inflated to create compression (usually between 40 to 60 mm Hg) over the soft tissue that covers the arterial vessel to be evaluated. Slight arterial vessel volume increase during the cardiac cycle?s systole phase is detected by the cuff?s pressure transducers and converted to a recording that resembles an arterial pressure wave tracing. A normal pulse volume tracing has a brisk upstroke and second elevation or notch as the wave returns to baseline (see Table 3). In individuals with occlusive disease, the waveform is more rounded and flattened.19 Detection of abnormal waves need to be studied along with ABI and SLP results. When surgical intervention is being considered, more detailed anatomic information needs to be obtained with diagnostic imagery tests such as arteriograms or magnetic resonance angiography.19,20 Although the focus of this article is the ABI, it must be stressed that the ABI needs to be integrated with the other noninvasive and diagnostic imagery vascular tests to provide the most accurate assessment of an individual's peripheral vascular status. Clinical Applications Lower extremity ankle systolic pressures and corresponding ABIs have been used to evaluate individuals with vascular disease.21-28 Ankle brachial index measures, along with vibratory and cutaneous sensory testing, provide a simple and reliable method to evaluate pathological changes associated with the diabetic foot.23 Investigators reported a reduction in misdiagnosis (underestimation of PAOD) when using ABIs in conjunction with distal lower extremity pulse palpation.24 Early stage PAOD in which symptoms are not yet present has been detected with vascular assessments that include the ABI.25 An index below 0.9 was highly correlated with PAOD presence as determined by duplex scans in individuals that did not demonstrate claudication pain or diminished pulses. Investigators concluded that the ABI is a simple adjunct to other diagnostic tests to identify individuals with asymptomatic PAOD.26 The ABI was a better predictor of future lower extremity amputation than claudication history or pulse palpation in individuals with PAOD.27 A high correlation is reported between low ABIs and coronary atherosclerosis and cardiovascular events in individuals with coronary artery disease (CAD).28 Coronary and peripheral atherosclerosis severity were highly correlated to ABI values, as investigators observed an increased CAD risk in those individuals with low ABIs.22 Further research is required to evaluate ABI use as a screening tool to assess CAD risk in older individuals. The effects of surgical revascularization have been studied with ABIs.29-32 Individuals displaying an ABI below 0.5 or a decreased ABI ( > 0.15) during follow up studies were more likely to require surgical intervention to prevent wounds and other risks associated with PAOD.29 Individuals with an ABI > 0.7 were given a better prognosis with less need for surgical intervention.30 Presurgical ABIs closer to 0.5 had an improved prognosis for successful bypass when compared to individuals with ABIs below 0.4.31 Harris et al31 and Stein et al32 report a 0.24 and 0.35 increase in ABI, respectively, following arterial bypass for individuals with claudication. An improved ABI was associated with enhanced arterial patency rates and claudication relief and a postsurgical ABI decrease (> 0.15 ) indicated the need for further surgical intervention. Ankle systolic pressure and corresponding ABI have been used to monitor conservative clinical management of individuals with PAOD. The effects of exercise therapy, cigarette smoking cessation, and posture on peripheral blood flow have been studied with ABIs.33-43 Treadmill walking and cycling programs designed to reduce the risks associated with PAOD have been integrated with ABI measures. Following treadmill walking, individuals with claudication typically demonstrate a sudden and sharp fall in ankle systolic pressure that requires several minutes before a return to baseline pressure.33 Individuals with PAOD experienced a larger drop in systolic ankle pressure and a longer recovery time to baseline pressure when compared to individuals without PAOD.34 More strenuous exercise is required before a significant drop in ankle systolic pressure occurs in individuals without vascular compromise.35 These findings have led to increased use of exercise protocols in which ABIs are monitored before and after exercise. Feinberg et al34 identified an ischemic window that represents the area created by the initial exercise-induced ABI reduction and the postexercise time required for recovery to baseline. The ischemic window measures were used with the claudication time test (time required to reach claudication pain during treadmill walking) to monitor exercise therapy designed to decrease the symptoms associated with PAOD. The maximal distances walked without claudication increased and the ischemic window was reduced (based on a less severe drop in the ABI and a more rapid return to ankle baseline pressure) following a 12-week program of treadmill walking.34 These findings are consistent with the present clinical practice of graded exercise programs to improve function in individuals with PAOD. Some individuals with PAOD cannot perform or tolerate treadmill exercise protocols. A reactive hyperemia test has been used as an exercise testing alternative.36 The test is performed by femoral artery occlusion with a blood pressure cuff (beyond femoral systolic pressure) to produce a temporary reduction in blood flow. Blood pressure cuff occlusion decreases blood flow distally and results in a decreased ankle systolic pressure. Similar to treadmill walking, an initial drop in ankle systolic pressure occurs, followed by a slow return to the baseline pressure. Systolic pressure and corresponding ABIs correlated well between exercise and reactive hyperemia protocols, and both tests were able to detect mild PAOD.36 The reactive hyperemia test was determined to be an alternative to the treadmill test in cases where an individual is unable to perform or tolerate treadmill testing. Significant ABI differences related to lifestyle also have been studied in individuals without PAOD. High activity levels were associated with higher ABIs when comparing high and low activity groups in a non-PAOD population.10 The positive relationship between ABI and physical activity level in subjects free of PAOD persisted after controlling for other factors such as race, hypertension, current smoking status, and body mass index. A low ABI was correlated to each of the following PAOD risk factors: high cholesterol levels, obesity, hypertension, physical inactivity, and smoking in individuals without PAOD.10 Cigarette smoking is identified as a significant risk factor for the development of chronic PAOD. Disease progression and increased symptoms such as disabling claudication, limb-threatening ischemia, and amputation have been linked to smoking.37 The transient peripheral vascular response to nicotine during cigarette smoking was indirectly studied by comparing smoking and nonsmoking day ABIs in 10 chronic smokers.38 The smoking day ABI was lower (0.55 +/- 0.11) when compared to the nonsmoking day ABI (0.64 +/- 0.14). Brachial systolic pressures were not altered, but ankle systolic pressure dropped by an average of 12 mm Hg. Low ABIs were also associated with smoking history in a study of more than 350 individuals not diagnosed with PAOD.39 Common clinical practice encourages smoking cessation for individuals with wounds and other complications associated with poor circulation. Postural changes effect peripheral blood flow and have an impact on individuals with wounds and other complications associated with PAOD. The dependent foot position is used as a simple means of improving arterial blood flow to the foot. Higher ABIs were observed when the foot was placed in a dependent position and compared to the neutral supine position in individuals with PAOD.40 In contrast to venous wounds in which elevation is recommended, the dependent foot position is indicated for arterial wounds. Clinicians should use the ABI along with wound presentation (location, shape, surrounding tissue appearance) to assist in determining appropriate wound healing interventions that include leg position. Extreme hip and knee flexion postures alter blood flow in the lower extremity. A marked ABI decrease was observed with extreme hip and knee flexion in individuals free of PAOD.41 Hip and knee flexion are believed to create arterial kinking that alters blood flow to the lower leg and foot. Flexed postures are expected to create more severe blood flow reduction in vessels that are already compromised by PAOD. Hip and knee flexion are commonly discouraged following arterial bypass surgery to prevent arterial kinking. Such precautions are also appropriate to prevent further arterial occlusion in individuals with PAOD who have not had surgical intervention. The ABI has been used to investigate other nonsurgical interventions designed to alter peripheral blood flow. For example, toe temperature and ABI were evaluated during thermal biofeedback in an individual with type 2 diabetes.42 An increased toe temperature was observed during large toe thermal biofeedback sessions. Improvements were reported in ABI, walking distance and speed, and stair climbing ability. Further controlled studies are recommended to evaluate thermal biofeedback as a treatment adjunct to improve lower extremity circulation. Wound Care Considerations/TCOM Individuals with wounds should have their vascular status monitored with more advanced diagnostic imagery tests such as arteriograms or magnetic resonance angiography when considering surgical intervention.19,20,43 Arteriograms provide an X-ray image of the involved vessels following the injection of a radiopaque dye; magnetic resonance angiography utilizes magnetic fields, radiofrequency signals and a nontoxic dye to generate three-dimensional images of the vessels being investigated. Such tests provide a more precise identification and localization of vascular lesions when compared with the noninvasive tests. Transcutaneous oxymetry mapping, a nonimagery and noninvasive test, is being used more frequently for evaluation of limb revascularization following surgical bypass and for wound healing potential in individuals with PAOD.44 Transcutaneous oxymetry mapping measures the transcutaneous partial pressure of oxygen (TcPO2) in the periwound area and provides the evaluator information related to oxygen supply and delivery to the underlying microvascular circulation. A special surface probe that warms the skin from 41oC to 45oC to promote cutaneous perfusion can be placed just proximal to the wound. If infection and associated inflammation and edema are present, the TcPO2 measures are not considered reliable and should not be performed until the infection resolves.45 Tissues with a TcPO2 measure less than 35 to 40 mm Hg are considered hypoxic and will require further vascular testing (see Table 4). Benscotter et al46 report a TcPO2 value of 33 mm Hg as a minimum requirement for tissue healing. Other researchers47 claim that healing can still occur when TcPO2 is at least 10 mm Hg. Further TCOM technique and instrument standardization should continue to add to the interpretation of TcPO2 values when evaluating wound healing potential and peripheral vascular status. Noninvasive tests as well as pulse palpation and skin inspection are indicated for screening individuals at risk for arterial wounds. Individuals with advanced PAOD should not use compression therapy indicated for venous stasis wounds because the external pressure may create further occlusion. An ABI of 0.8 or below, a significant systolic pressure drop between adjacent lower limb segments, or a flattened arterial pressure wave can all be used to help screen those individuals in which compression therapy is either contraindicated or modified with low pressure.48 All noninvasive tests that reveal significant PAOD need to be followed up with more detailed diagnostic imagery tests. Early PAOD detection with the noninvasive vascular tests may be valuable for preventive purposes. Disease progression and therapeutic intervention can be evaluated at any time with minimal inconvenience and financial hardship to patients. Early interventions designed to lower cholesterol and blood pressure, prevent obesity, and encourage smoking cessation and increased physical activity can be instituted to minimize the risks associated with PAOD. Wound prevention can be practiced as individuals with impaired lower extremity arterial perfusion are identified and educated in foot and skin care. In addition, pressure relief with proper footwear can be prescribed as a preventive measure. Summary The ABI is a relatively simple, inexpensive, and noninvasive test that can be used as part of a complete peripheral vascular assessment that should include PVRs, SLPs, and TCOM. Small, hand-held, and stethoscope-attached Dopplers make it possible to perform ABI assessment in both the clinical and home care setting. Technique standardization and multiple measures help improve measurement reliability. Maintaining consistent blood pressure cuff size, position, and orientation during ankle/brachial systolic measures improve measurement reliability. Investigators should practice the technique on individuals of all ages to gain experience that further contributes to measurement reliability. Individuals with arterial calcification due to chronic diseases such as diabetes have artificially high ABIs. Systolic toe pressures, TCOM, and PVRs are additional tests indicated for a more reliable evaluation of individuals with arterial calcification. More precise diagnostic imagery testing is indicated when noninvasive testing reveals poor arterial perfusion.

1. Dormandy J, Ludger H, Vig S. The natural history of claudication: risk to life and limb. Semin Vasc Surg. 1999;12:123-37.

2. McDermott MM, Criqui MH, Liu K, et al. Lower ankle brachial index and association with leg functioning in peripheral arterial disease. J Vasc Surg. 2000;32(6):1164-1171.

3. Rice KL. Peripheral arterial occlusive disease. Nursing. 1998;28:33-38.

4. Wertheim D, Trenary K, Williams R, et al. Ankle systolic pressure and cuff application. Lancet. 1996;29:1845-1846.

5. Stoffers HE, Kester AD, Kaiser V, et al. The diagnostic value of the measurement of the ankle-brachial systolic pressure in primary health care. J Clin Epidemiol. 1996;49:1401-1405.

6. Johnston KW, Hosang MY, Andrews DF. Reproducibility of noninvasive vascular laboratory measurements of the peripheral circulation. J Vasc Surg. 1987;6:147-151.

7. De Graaff JC, Ubbink DT, Legemate DA, et al. Interobserver and intraobserver reproducibility of peripheral blood and oxygen pressure measurements on the assessment of lower extremity arterial disease. J Vasc Surg. 2001;33:1033-1040.

8. Goss DE, de Trafford J, Roberts VC, et al. Raised ankle brachial pressure index in insulin-treated diabetic patients. Diabet Med. 1989;6:576-578.

9. Gardner AW, Montgomery PS. Comparison of three blood pressure methods used for determining ankle/brachial index in patients with intermittent claudication. Angiology. 1998;49:723-728.

10. Gardner AW, Sieminski DJ, Montgomery PS. Physical activity is related to ankle/brachial index in subjects without peripheral arterial occlusive disease. Angiology. 1997;48:883-891.

11. Enzler M, Zund G, Schimmer R, et al. Indications for technique and interpretation of arterial Doppler sonography from the vascular surgeon?s viewpoint. Schweiz Rundsch Med Prax. 1992;81:1074-1077.

12. Santilli JD, Santilli SM. Chronic critical limb ischemia: diagnosis, treatment and prognosis. Am Fam Physician. 1999;59:1899-1908.

13. Newman AB, Siscovick DS, Manolio TA, et al. Ankle arm index as a marker of atherosclerosis in the cardiovascular health study. Circulation. 1993;88:837-845.

14. Ramsey SE, Manke DA, Summer DS. Toe blood pressure: a valuable adjunct to ankle pressure measurement for assessing peripheral arterial disease. J Cardiovasc Surg. 1983;24:43-48.

15. Brothers TE, Esteban R, Robison, Elliott BM. Symptoms of chronic arterial insufficiency correlate with absolute ankle pressure better than with ankle brachial index. Minerva Cardioangiol. 2000;48:103-109.

16. Carter SA, Tate RB. Value of toe pulse waves in addition to systolic pressures in the assessment of the severity of peripheral arterial disease and critical limb ischemia. J Vasc Surg. 1996;24:258-265.

17. Zierler RE, Strandness DE. Nonimaging physiological tests for assessment of extremity arterial disease. In: Zwiebel WJ, ed. Introduction to Vascular Ultrasonography. Orlando, Fla: Sanders; 1992.

18. Carter SA. Role of pressure measurements. In: Bernstein EF, ed. Vascular Diagnosis. St. Louis, Mo: Mosby, 1993; 486-507.

19. Carpenter JP. Noninvasive assessment of peripheral vascular disease. Adv Skin Wound Care. 2000; 84-85.

20. Wilde WL. Femoral arteriography in outpatients. Am J Surg. 1975;129:606-607.

21. Leng GC, Fowkes FG, Lee AJ, et al. Use of ankle brachial index to predict cardiovascular events and death: a cohort study. BMJ. 1996; 313:1440-1444.

22. Abbott RD, Petrovitch H, Rodriquez BI, et al. Ankle brachial blood pressure in men >70 years of age and the risk of coronary heart disease. Am J Cardiol. 2000;86:280-284.

23. Shin JB, Seong YJ, Lee HJ, et al. Foot screening techniques in a diabetic population. J Korean Med Sci. 2000;15:78-82.

24. Lundin M, Wilksten JP, Perakyla T, et al. Distal palpation: is it reliable? World J Surg. 1999;23:252-255.

25. Criqui MH, Fronek A, Klauber, MR, et al. The sensitivity, specificity, and predictive value of traditional clinical evaluation of peripheral arterial disease: results from noninvasive testing in a defined population. Circulation. 1985;71:516-522. 

26. Ho M, Veale D, Eastmond C, et al. Macrovasular disease and systemic sclerosis. Ann Rheum Dis. 2000;59:39-43.

27. Hamalainen H, Ronnemaa T, Halonen, JB Toikka T. Factors predicting lower extremity amputation in patients with type 1 or type 2 diabetes mellitus. J Intern Med. 1999;246:97-103.

28. Papamichael CM, Lekakis JP, Stamatelopoulos KS, et al. Ankle brachial index as a predictor of the extent of coronary atherosclerosis and cardiovascular events in patients with coronary artery disease. Am J Cardiol. 2000; 86:615-618.

29. Feinglass J, McCarthy WJ, Slavensky R, et al. Functional status and walking ability after lower extremity bypass grafting or angioplasty for intermittent claudication. J Vasc Surg. 2000;31:93-103.

30. Naschitz JE, Ambrosio DA, Chang JB. Intermittent claudication: Predictors and outcome. Angiology. 1988;39:16-22.

31. Harris JP, Finn WR, Rudo ND, et al. Assessment of donor limb hemodynamics in femorofemoral bypass for claudication. Surgery. 1981; 90:764-773.

32. Stein M, Amelfi MF, Gray R, et al. Angiographic assessment of arterial outflow: predictive value of a new classification. J Vasc Interv Radiol. 1991; 2:365-370.

33. Dudley NJ, Green IR, Griffiths PA. Monitoring recovery following exercise in the Doppler evaluation of lower extremity arterial disease. Clin Phys Physiol Meas. 1990;11:193-199.

34. Feinberg RL, Gregory RT, Wheeler JR, et al. The ischemic window: a method for the objective quantification of the training effect of exercise therapy for intermittent claudication. J Vasc Surg. 1992;16:244-250.

35. Desvaux B, Abraham P, Colin D, et al. Ankle to arm index following maximal exercise in normal subjects and athletes. Med Sci Sports Exerc. 1996;28:836-39.

36. Perakayla T. Lindholm T, Lepantalo M. Can reactive hyperemia be used instead of exercise test in assessment of mild intermittent claudication? Ann Chir Gynaecol. 1999;88:276-279.

37. Jonason T, Ringqvist I. Factors of prognostic importance for subsequent rest pain in patients with intermittent claudication. Acta Med Scan. 1985;218:27-33.

38. Yataco AR, Gardner AW. Acute reduction in ankle brachial index following smoking in chronic smokers with peripheral arterial occlusive disease. Angiology. 1999;50:355-360.

39. Cronenwett JL, Warner KG, Zelenock GB, et al. Intermittent claudication: current results of nonoperative management. Arch Surg. 1984; 119:430-436.

40. Pollack EW, Chavis P, Wolfman EF. The effect of postural changes upon the ankle arterial perfusion pressure. Vasc Surg. 1976;10:219-222.

41. Coni NK. Posture and the arterial pressure in the ischaemic foot. Age Aging. 1983;12:151-154.

42. Aikens JE. Thermal biofeedback for claudication in diabetes: a literature review and case study. Altern Med Rev. 1999;4:104-110.

43. Rofsky NM. MR angiography of the aortoiliac and femoropopliteal vessels. Magn Reson Imaging Clin N Am. 1998;6:371-384.

44. Rich K. Transcutaneous oxygen measurements: implications for nursing. J Vasc Nurs. 2001;19:55-61.

45. Ballard, JL, Eke, CC, Bunt TJ, Killeen JD. A prospective evaluation of transcutaneous oxygen measurements in the management of diabetic foot problems. J Vasc Surg. 1995;22:485-490.

46. Benscotter EL, Gerber A, Friedberg J. Transcutaneous oxygen measurement as a non-invasive indicator of level of tissue healing in patients with PVD and projected amputations. J Am Osteopath Assoc. 1984;83:560-574.

47. Franzeck UK, Rayman GA. Assessment of microvascular function and tissue viability. In: Tooke JE, Low GD, eds. A Textbook of Vascular Medicine. London, England: Arnold, 1996;127.

48. Scholten P, Bever A, Turner K, Warburton L. Graduated elastic compression stockings on a stroke unit: a feasibility study. Age Aging. 2000;29:357-359.