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Article

December 1997

Transcutaneous monitoring of pO2 in the assessment of peripheral vascular disease

by Arnost Fronek
Blood gases/acid-base Hemoglobins
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There are several diagnostic approaches to identify and quantify different types of vascular disease. However, these methods usually do not reflect the condition of the cutaneous circulation. 

Because transcutaneous oxygen reveals the status of cutaneous circulation, it has been shown to be a powerful diagnostic tool in the evaluation of various aspects of arterial and venous diseases.

INTRODUCTION

There are several diagnostic approaches to identify and quantify different types of vascular disease, e.g. segmental pressure, doppler velocity, various types of plethysmography. 

In most cases they fulfill this goal as long as the prime objective of examination is the circulatory state of the skeletal muscle system. These methods, however, usually do not reflect the condition of the cutaneous circulation because it represents only about ­1/10 of the total limb circulation. 

Transcutaneous pO2 (tcpO2), on the other hand, reveals the status of cutaneous circulation. tcpO2 has been shown to be very useful in the evaluation of various aspects of arterial as well as venous disease.

Arterial Disease
Peripheral arterial occlusive disease (PAOD) is one of the most widely encountered impairments of the arterial system. It has been shown that the perfusion of the lower extremity has to be significantly compromised to affect a reduction of the skin circulation [1]. 

This explains why tcpO2 values reflect the degree of skin viability. Reduction in skin perfusion lead to a spectrum of different degrees of skin viability ranging from mild trophic changes (e.g. absence of hair, nail changes) to more severe complications such as non-healing ulcers. 

However, non-healing ulcers can also develop in the presence of an adequate arterial inflow (neuropathic ulcer) or due to a severe insufficiency of the venous system (venous ulcer).

Venous Disease
The efficiency of the venous circulation can be compromised by an insufficiency of the venous valvular system, an obstruction of the deep venous system (deep venous throm­bosis), or both. 

It has been documented that venous ulcers develop mainly if the site of venous pathology is below the knee [2,3]. From a hemodynamic point of view, distal valvular insufficiency, including the perforating venous system, is the most frequent cause of trophic changes of the skin culminating with the extreme form: venous ulcers.

Microvascular Disease
The definition of microvascular disease is equivocal. There is no question about there being a primary impairment of microcirculation, but there is a dilemma: Is the microvasculature dysfunctional and the large arterial system (> 1 mm diameter) intact? 

Or is the microcirculatory disturbance caused by a decreased arterial blood supply or increased venous pressure induced by venous disease? The ambiguity can be overcome by preceding any description of microvascular disease with an assurance that the large arterial or venous system functions within normal physiological limits.

PHYSIOLOGY OF THE SKIN

The skin consists of three different layers: epidermis, dermis, and subcutaneous tissue. Each one has specific functions:

Epidermis - is the outer layer which protects the body from the external environment. The cornified epidermis is a barrier to infection and a protection against water loss. It con­tains no vessels. Oxygen which diffuses from the capillaries has to traverse the epidermis to reach its surface.

Dermis - is the middle layer with a dense vascularization, mainly of arterioles, capillary loops and venules. In addition, it is the site of different types of glands, hair follicles and nerve fibers. The arterioles are very sensitive to temperature changes - an increase in temperature reduces the resistance, leading to an increased blood flow.

Subcutaneous tissue - sometimes defined as the hypodermis, contains different types of connective tissue cells especially fat cells - adipose tissue.

TRANSCUTANEOUS MEASUREMENTS

Evans and Naylor [4] demonstrated, for the first time, that it is possible to monitor pO2 of diffused oxygen from the surface of the skin by using a modified Clark-type electrode. The pO2 varied under these conditions between 0 - 3.5 mmHg. 

They proved, in addition, that with the removal of some superficial layers of epidermis (e.g. by stripping with tape) or with increasing skin blood flow (e.g. by using ultraviolet light), the recorded pO2 reached up to 30 mmHg. Heat-induced vasodilation was utilized by Huch et al [5] and Eberhard et al [6], demonstrating good arterializing by adding a heating element to the polarographic probe.

Measurement Technique

  1. Calibration - following the calibration instructions recommended by manufacturer.

  2. Site selection - an ideal site would be located over a homogenous capillary bed without large veins, skin defects, or hair. Placing it directly over bone may also give erroneous results, especially if a change in body position causes skin to be pulled against a protruding bone.

  3. Site preparation - To improve oxygen diffusion and to standardize the mea­surement technique it is recommended that excessive skin cells be removed by stripping the skin 10-15 times with an adhesive tape (e.g. 3MTM filament tape), using a fresh tape section each time.

  4. Probe placement - Place the probe on the selected site immediately after calibration is completed. To prevent strain or tension on the probe, secure the cord against the skin by using standard medical tape.

  5. Measurement - It takes about 15 minutes after the probe has been placed on the skin for the tcpO2 to become stabilized.

Factors Influencing tcpO2 Values

  • Probe temperature (due to the affect on microvasculature and on the oxy­hemoglobin dissociation curve).

  • Arterial pO2. 

  • Metabolic consumption of O2 by the dermal tissue.

  • Oxygen consumption by the electrodes.

  • Skin thickness and skin resistance to O2 diffusion (more pronounced to dynamics).

  • Capillary density and rate of cutaneous blood flow.

TRANSCUTANEOUS pO2 IN ARTERIAL DISEASE

Resting Values in Arterial Occlusive Disease
Numerous studies have documented that tcpO2 values are usually reduced in severe PAOD, especially in critical ischemia[1,8,9,10,11,12,13], but the separation between normal and ischemic skin is not reliable, except in critical ischemia. 

Hauser et al [14] introduced the “regional perfusion index (RPI)” which relates the limb tcpO2 to that of the chest. It proved to be especially useful during exercise testing. In order to increase the sensitivity of the test, various sensitizing procedures, which are described below, have been proposed and tested.

In order to increase the sensitivity and specificity of tcpO2 methodology, a number of “sensitizing” procedures have been applied. This applies not only to the improvement of diagnostic accuracy but also to better utilization of this methodology to prog­nosticate normal healing and optimal amputation level determination.

Sensitizing Maneuvers
Leg position - in normal lower extremities tcpO2 values decrease with leg dependency if the skin temperature is maintained at 37 oC [15]. 

In patients with severe peripheral arterial occlusive disease (PAOD), an increase is usually observed. From a practical point of view the results with a 44 oC  heated probe are more relevant. An average increase of 15.1 mmHg was observed in normal subjects when changing from a supine to sitting position, whereas in patients with PAOD the increase was significantly higher, 28.1 mmHg.

The effect of leg position was described by Becker et al [16] as a useful test to classify the severity of PAOD. Only 5 % of PAOD patients required amputation if forefoot tcpO2 (44 oC) was > 40 mmHg in the sitting position, while patients with <10 mmHg could expect a 85 % chance of amputation. 

These findings were recently confirmed by Scheffler et al [17], who could objectively identify critical ischemia if tcpO2 in sitting position was found to be less than 40 mmHg.

Transitional Occlusion (Post Occlusive Reactive Hyperemia PORH)
The well described PORH response observed in flow studies, can be reproduced with tcpO2 measurement with a probe temperature of only 37 oC [18] but, as described above, the results at this probe temperature, are not very reliable.

On the other hand, when the standard 43 oC or 44 oC probe temperature is used, the “overshoot” is not recorded (probably due to local vasodilatation) but the rate of circulatory recovery measured as tcpO2, T/2 (the time it takes to reach 50 % of the initial tcpO2 value) after a 4-minute occlusion can be easily measured: 87.1 seconds in control subjects and 136.1 seconds in patients with severe PAOD [19]. 

Similar results were reported by Kram et al [20] and Slagsvold et al [21].

Effect of Exercise

Exercise has been used to “sensitize” the investigative methods to separate claudicants from normal subjects. Standardized treadmill protocols were used by Hauser and Shoemaker [14] and Holdich et al [22], but the correlation of tcpO2 with pain-free walking distance was not satisfactory. 

A more severe exercise protocol was probably the reason for a better correlation obtained by Schmidt et al [23]. Byrne et al [8] found 20 % of claudicants with normal tcpO2 values. However, they showed a significant decline after exercise (treadmill at a speed of 1.5 miles/hr and 20 degrees incline).

Oxygen Inhalation
Similar to leg dependency, oxygen inhalation helps to unmask hidden oxygen reserves by increasing O2 saturation in the arterial blood. Under normal conditions, following inhalation of 100 % oxygen,  tcpO2 values from the foot increase by approximately 230 % [24]. 

This response is significantly reduced in patients with arterial disease [25,26].

Determination of Optimal Amputation Level
There is a relatively wide range of critical tcpO2 values that separate successful from unsuccessful amputation stump healing. The majority of researchers consider 30 mmHg as the critical dividing line [27,28,29,30,31]. Kram and coworkers [20], using the calf/brachial tcpO2 ratio, concluded that a ratio >0.20 predicts successful stump healing. 

Franzeck et al [19] originally considered 10 mmHg as a dividing line but in view of some primary stump healing occurring below 10 mmHg as well, they decided to apply oxygen inhalation as a “sensitizing” factor. 

In subsequent studies from the same group, the 10 mmHg dividing line was reconfirmed, but the accuracy was increased if an increase of tcpO2 beyond the 10 mmHg with oxygen inhalation was con­sidered to predict successful amputation stump healing [25,32]. McCollum et al [24] prefer the determination of rate of change of tcpO2 during oxygen inhalation. A rate of increase of 9 mmHg/min is considered a dividing line.

Currently, it is difficult to explain the relatively wide range of tcpO2 “dividing lines” separating potential successful from un­successful stump healing. A number of factors have to be considered: the average experience of the surgical group, electrical specifications of the probes and especially oxygen consumption of the probe. It seems useful that each institution, together with the instrumentation used, establish its own exact criteria.

Predicting Wound Healing
Patients with severe arterial occlusive disease may develop a poorly healing wound even after a small trauma. In the most severe stage (Fontaine IV), spontaneously developing ulcera usually resist standard conservative treatment. 

Under these conditions very low tcpO2 values are recorded; usually between 10-20 mmHg. A 10 mmHg level is generally considered to be incompatible with spon­taneous or conservatively treated healing process. With leg dependency, a value of 40 mmHg can be considered as a discriminant value [17].

Diabetic Neuropathy
Gaylarde et al [33] have shown that at 37 oC, tcpO2 in the legs and feet of diabetic patients with peripheral neuropathy was significantly higher than in control subjects and diabetic patients without neuropathy. 

After a probe temperature increase to 44 oC, tcpO2 increased in all three groups, but the increase was smallest in diabetics with neuropathy. These results are consistent with a loss of vasoconstrictor tone. Similar results were reported earlier by Weindorf et al [34] using heat or rubefacients.

Therapeutic Control Using tcpO2
Effect of Drugs
It is important to recognize that at probe temperature of 41 oC, local vasodilator administration does not increase tcpO2 value [35]. It is therefore not surprising that studies using various vasodilator agents sometimes yielded confusing and even decreasing tcpO2 values, especially in patients with arterial disease [36,37,38]. 

Positive results have been obtained, however, when probe temperature was kept at 37 oC [39,40]. Under this condition it could be shown that there was a significant increase in tcpO2 (at 37 oC) after an i.v. infusion of prostaglandin E in patients with critical ischemia.

Effect of Balneologic Treatment
Exposure to CO2-containing water increased tcpO2 (44 oC) from 63.8 mmHg to 71.3 mmHg (after 20 minutes) in patients with arterial occlusive disease. The effect of temperature was ruled out by a placebo study using standard water[41].

TRANSCUTANEOUS pO2 IN VENOUS DISEASE

Most investigators have found tcpO2 to be reduced in extreme cases of venous disease (e.g. in venous ulcers), while the results are normal in the unaffected skin. This is dis­tinctly different in arterial disease, where reduced tcpO2 can be detected in a sig­nificantly wider area. 

An exception represents the liposclerotic skin where the overall tcpO2 is reduced, but to a lesser degree than in the immediate proximity of the ulcer. It has to be pointed out that there is a pronounced overlap with normal values, except at the edge of ulcers where the tcpO2 values are homogeneously lower.

An interesting explanation for the heterogeneity of tcpO2 results was recently given by Roszinski and Smaller [42] who compared noninvasive tcpO2 with invasive (needle electrodes) pO2 determinations in the tissue. 

While the results varied very little in normal patients when moving the needle in 1 mm intervals, the same movements of the needle in patients with venous trophic changes yielded alterations of 10-30 mmHg, depending on the severity of the condition. 

The reduced tcpO2 values in venous disease, reported by a number of investigators [43,44,45,46,47,48,49] can also be explained by the results obtained with a transparent tcpO2 probe that permits simultaneous vital microscopy [11].

The correlation of tcpO2 and morphologic characteristics also offers an explanation of the overlap reported by many authors. Franzeck et al [11] and, later, Hoffmann et al [50] demonstrated a direct correlation of tcpO2 values with microvascular density. 

At sites of white atrophy (atrophie blanche) there was also an unmeasurable tcpO2 level which grew with the increasing numbers of capillaries. Moosa et al [51] confirmed the low tcpO2 values close to venous ulcers, but could demonstrate a significant increase after oxygen inhalation. 

Though the increase percentagewise was higher around the ulcers than in the healthy tissues, the final tcpO2 values were still lower. This was interpreted by the authors as a confirmation of the “fibrin cuff” theory, which explains the trophic changes in venous disease by a layer of fibrin surrounding the capillaries thus compromising oxygen diffusion [52].

The lower post-oxygen inhalation tcpO2 values can, however, also be explained by a decreased capillary density as discussed above. Partsch [53] argues that since oxygen inhalation leads to a higher tcpO2 increase in the vicinity of venous ulcers than in the vicinity of arterial ulcers, the factor of di­minished blood supply may be less of a contributing factor.

Effect of Drugs on tcpO2 in Venous Disease
Neumann and van den Brock [54] observed a slight but statistically significant increase in tcpO2 in patients with moderate degrees of venous insufficiency, after administration of O-rutosides. Similar results were reported previously by Belcaro et al [55].

Factors Affecting tcpO2 in Venous Disease

Edema
Edema reduction achieved for instance by external intermittent compression [56] did not influence the tcpO2 reading which could be interpreted to mean that edema per se has no effect on tcpO2. This question does not seem to be settled because Kolari et al [39] found an increase in tcpO2 after edema reduction. 

Similarly, Creutzig et al [38] recorded an increase in tcpO2 (close to the ulcer) after compression (bandaging).

Elastic Compression
An interesting method to estimate a so-called venomotor index by comparing tcpO2 values was obtained by Rooke et al [57] with two different temperatures (42 oC and 45 oC): the ratio of these two values represents the index. 

They found in stasis dermatitis a decreased tcpO2 and a decreased “venomotor” index which improved with elastic compression.

References
  1. Kvernebo K, Megerman J, Hamilton G et al. Response of skin photoplethysmography, laser doppler flowmetry and transcutaneous oxygen tensiometry to stenosis-induced reductions in limb blood flow. Eur J Vasc Surg, 1989; 3: 113-20.
  2. Partsch H. Transcutaneous pO2 measure­ments in the surrounding of venous and neutrophic ulcers. In: Ehrly AM, Hauss J, Huch R, eds. Clinical Oxygen Pressure Measurement. Berlin: Springer-Verlag, 1987: 156-61.
  3. Shull KC, Nicolaides AN, Fernandes é Fernandes J et al. Significance of popliteal reflux in relation to ambulatory venous pressure and ulceration. Arch Surg 1970; 114: 1304-06.
  4. Evans NT, Naylor PF. The systemic oxygen supply to the surface of human skin. Resp Physiol 1967; 3: 21-27.
  5. Huch A, Huch R, Lübbers DW. Quantitive polarographische Sauerstoffdruckmessung auf der Kopfhaut des Neugeborenen. Arch Gynaekol 1969; 207: 443.
  6. Eberhard P, Hammacher K, Mindt W. Perkutane Messung des Sauerstoff partial­druckes. Proc “Medizin-Technik” 1972; Stuttgart 26.
  7. Rolfe P. Arterial oxygen measurement in the newborn with intravascular transducers. In: Hill DW, Watson BW, eds. IEE Medical Electronics Monographs. London: Peter Perigrinns Ltd 1976; 126-58.
  8. Byrne P, Provan JL, Ameli FM et al. The use of transcutaneous oxygen tension measure­ments in the diagnosis of peripheral vascular insufficiency. Ann Surg 1984; 200: 159-65.
  9. Clyne CA, Ryan J, Webster JH et al. Oxygen tension on the skin of ischemic legs. Am J Surg 1982; 143: 315-18.
  10. Dowd GS, Provan JL, Ameli FM. Measurement of transcutaneous oxygen pressure in normal and ischaemic skin. Brit J Bone Joint Surg 1983; 65: 79.
  11. Franzeck UK, Bollinger A, Huch R et al. Transcutaneous oxygen tension and capillary morphologic characteristics and density in patients with chronic venous incompetence. Circulation 1984; 70: 806-11.
  12. Spence VA,  Walker VF. Tissue oxygen tension in normal and ischaemic human skin. Cardiovasc Res 1984; 18: 140-44.
  13. Toennesen KH. Transcutaneous oxygen tension in imminent foot gangrene. Acta Anaesth Scand 1978; (Suppl 68): 107-10.
  14. Hauser CJ, Shoemaker WC. Use of a transcutaneous pO2 regional perfusion index to quantify tissue perfusion in peripheral vascular disease. Ann Surg 1983; 197: 337-43.
  15. Caspary L, Creutzig A, Alexander K. Comparison of laser-doppler-flux and tcpO2 in healthy probands and patients with arterial ischemia. In: Huch A, Huch R, Rooth G, eds. Continuous transcutaneous monitoring. Advances in Experimental Medicine & Biology. New York: Plenum Press, 1987: 220.
  16. Becker F et al. Predictive value of tcpO2 in chronic severe ischemia of the lower limbs. Int J Microcirc: Clin Exp 1988; 7: 261-71.
  17. Scheffler A, Eggert S, Rieger H. Influence of clinical findings, positional manoeuvers, and systolic ankle arterial pressure on trans­cutaneous oxygen tension in peripheral arterial occlusive disease. Eur J F Clin Invest 1992; 22: 420-26.
  18. Ewald U, Tuvemo T, Rooth G. Early reduction of vascular reactivity in diabetic children detected by transcutaneous oxygen electrode. Lancet I 1981: 1287-88.
  19. Franzeck UK, Talke P, Bernstein EF, Golbranson FL et al. Transcutaneous pO2 measurements in health and peripheral arterial occlusive disease. Surgery 1982; 91: 156-63.
  20. Kram HB, Appel P, White RA et al. Assessment of peripheral vascular disease by postocclusive transcutaneous oxygen recovery time. J Vasc Surg 1984; 1: 628-34.
  21. Slagsvold CE, Rosen L, Standen E. The relation between changes in capillary morphology induced by ischemia and post-ischemic transcutaneous pO2 response. Int J Microcirc: Clin Exp 1991; 10: 117-25.
  22. Holdich TA et al. Transcutaneous oxygen tension during exercise in patients with claudication. Brit Med J 1986; 292: 1625-28.
  23. Schmidt JA, Bracht C, Leyhe A et al. Transcutaneous measurement of oxygen and carbon dioxide tension (tcpO2 and tcpO2) during treadmill exercise in patients with arterial occlusive disease (AOD) - stages I and II. Angiology 1990; 4: 547-52.
  24. McCollum PT, Spence VA, Walker WF. Oxygen inhalation induced changes in the skin as measured by transcutaneous oxymetry. Br J Surg 1986; 73: 882-85.
  25. Harward TR, Volny J, Golbranson F et al. Oxygen inhalation-induced transcutaneous pO2 changes as a predictor of amputation level. J Vasc Surg 1985; 2: 220-28.
  26. Caspary L, Creutzig A, Alexander K. Variability of tcpO2 - measurements at 37 °C and 44 °C in patients with claudication in consideration of provocation tests. VASA 1993; 22: 129-36.
  27. Burgess EM, Matsen FA, Wyss CR et al. Segmental transcutaneous measurements of pO2 in patients requiring below-the-knee amputation for peripheral vascular in­sufficiency. J Bone and Joint Surg 1982; 64 - A: 378-82.
  28. Cina C, Katsamouris A, Megerman J et al. Utility of transcutaneous oxygen tension measurements in peripheral arterial occlusive disease. J Vasc Surg 1984; 1: 362-71.
  29. Katsamouris A, Brewster DC, Megerman J et al. Transcutaneous oxygen tension in selection of amputation level. Am. J. Surg. 1984; 147: 510-17.
  30. Ratliff DA, Clyne CA, Chant AD et al. Prediction of amputation wound healing: the role of transcutaneous pO2 assessment. Br J Surg 1984; 71: 219-22.
  31. White RA, Nolan L, Long J et al. Noninvasive evaluation of peripheral vascular disease using transcutaneous oxygen tension. Am J Surg 1982; 144: 68-75.
  32. Oishi C, Fronek A, Golbranson FL. The role of noninvasive vascular studies in determining levels of amputation. Am J Bone & Joint Surg 1988; 70: 1520-30.
  33. Gaylarde PM, Fonseca VA, Llewellyn G et al. Transcutaneous oxygen tension in legs and feet of diabetic patients. Diabetes 1988; 37: 714-16.
  34. Weindorf N, Schultz-Ehrenburg U, Altmeyer P. Diagnostic assessment of diabetic microangiopathy by tcpO2 stimulation tests. Adv Exptl Med Biol 1987; 220: 83-86.
  35. Svedman P, Holmberg J, Jacobsson S et al. On the relation between transcutaneous oxygen tension and skin blood flow. Scand J Plast Reconstr Surg 1982; 16: 1331.
  36. Svedman P, Jacobsson S, Lindell SE et al. Measurement of transcutaneous oxygen tension: A method for studying the blood supply of the skin. IRCS Med Sci 1978; 6: 339.
  37. Creutzig A, Alexander K. Drug induced alterations in muscle tissue oxygen pressure in patients with arterial occlusive disease. Int J Microcirc 1985: Clin Ex; 4: 173-81.
  38. Creutzig A., Caspary L, Ranke C et al. Transkutaner pO2 und laser Doppler flux bei steigenden Dosierungen von intrarteriell und intravenous appliziertem Prostaglandin E. VASA  1987; 16: 114-18.
  39. Creutzig A, Wuppermann T, Hanauske U et al. Sauerstoffdruckfelder in Unterschenkel­geschwüren. Der Hausartzt 1985a; 36: 612-16.
  40. Creutzig A, Dau D, Caspary L et al. Transcutaneous oxygen pressure measured at two different electrode core temperatures in healthy volunteers and patients with arterial occlusive disease. Int J Microcirc 1987a; Clin Exp 5: 373-80.
  41. Hartman B, Drews B, Burnus C et al. Zunahme von Fussrücken - Hautdurchblutung und - transkutanem Sauerstoffpartialdruck während Unterschenkel-Immersion in CO2 - Wasser bei Patienten mit arterieller Verschlus­skrankheit. VASA 1991; 20: 382-87.
  42. Roszinski S, Schmeller W. Invasive (intrakutane) und nichtinvasive (transkutane) Messung des Sauerstoffpartialdrucks der Haut bei Patienten mit chronischer Veneninsuf­fizienz. Phlebologie  1995; 24: 1-8.
  43. Clyne CA, Ramsden WH, Chant AD et al. Oxygen tension on the skin of the galter area of limbs with venous disease. Br J Surg 72: 644-47.
  44. Kolari P, Pekanmäki JK, Pohjola RT. Transcutaneous oxygen tension in patients with post-thrombotic leg ulcers: treatment with intermittent pneumatic compression. Cardiovasc Res 1988; 22: 138-41.
  45. Mannarino El, Pasqualini L, Maragoni G et al. Chronic venous incompetence and trans­cutaneous oxygen pressure: a controlled study. VASA 1988; 17: 159-61.
  46. Neumann HA, van Leeuwen M, van den Broek MJ et al. Transcutaneous oxygen tension in chronic venous insufficiency syndrome. VASA 1984; 13: 213-19.
  47. Sindrup JH, Avnstrop C, Steenfors HH et al. Transcutaneous pO2 and laser doppler blood flow measurements in 40 patients with venous leg ulcers. Acta Derm Venereol (Stockholm) 1987; 67: 160-63.
  48. Mani R, White JE, Barrett DF et al. Tissue oxygenation, venous ulcer and fibrin cuffs. J Royal Soc Med 1989; 82: 345-46.
  49. Belcaro G, Rulo A, Vasdekis S, et al. Combined evaluation of postphlebitic limbs by laser doppler flowmetry and trans­cutaneous pO2/pCO2 measurements. VASA 1988; 17: 259-61.
  50. Hoffmann U, Franzeck UK, Speiser E et al. Microangiopathie bei chronischer Veneninsuffizienz. Phlebol Protokol 1990; 19: 10-15.
  51. Moosa HH, Falanga V, Steed DL et al. Oxygen diffusion in chronic venous ulceration. J Cardiovasc Surg 1987; 28:464-67.
  52. Browse NL, Burnand KG. The cause of venous ulceration. Lancet 1982; 2: 243-45,
  53. Partsch H. Investigations on the pathogenesis of venous leg ulcers. Acta Chir Scand 1988; 544 Suppl: 25-29.
  54. Neumann HA, van den Broek MJ. Evaluation of O-(b-hydroxyethyl)-rutosides in chronic venous insufficiency by means of noninvasive techniques. Phlebology 1990; 5: 13-20.
  55. Belcaro G, Rulo A, Caniani C. Evaluation of the microcirculatory effects of Venoruton  in patients with chronic venous hypertension by laser-Doppler flowmetry, transcutaneous pO2 and pCO2 measurents, leg volumetry and ambulatory venous pressure measurements. Phlebology 1989; 4: 23-29.
  56. Nemeth AJ, Falanga V, Alstadt SP et al. Ulcerated edematous limbs: effect of edema removal on transcutaneous oxygen mea­surements. J Am Acad Dermatol 1989; 20: 191-97.
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References
  1. Kvernebo K, Megerman J, Hamilton G et al. Response of skin photoplethysmography, laser doppler flowmetry and transcutaneous oxygen tensiometry to stenosis-induced reductions in limb blood flow. Eur J Vasc Surg, 1989; 3: 113-20.
  2. Partsch H. Transcutaneous pO2 measure­ments in the surrounding of venous and neutrophic ulcers. In: Ehrly AM, Hauss J, Huch R, eds. Clinical Oxygen Pressure Measurement. Berlin: Springer-Verlag, 1987: 156-61.
  3. Shull KC, Nicolaides AN, Fernandes é Fernandes J et al. Significance of popliteal reflux in relation to ambulatory venous pressure and ulceration. Arch Surg 1970; 114: 1304-06.
  4. Evans NT, Naylor PF. The systemic oxygen supply to the surface of human skin. Resp Physiol 1967; 3: 21-27.
  5. Huch A, Huch R, Lübbers DW. Quantitive polarographische Sauerstoffdruckmessung auf der Kopfhaut des Neugeborenen. Arch Gynaekol 1969; 207: 443.
  6. Eberhard P, Hammacher K, Mindt W. Perkutane Messung des Sauerstoff partial­druckes. Proc “Medizin-Technik” 1972; Stuttgart 26.
  7. Rolfe P. Arterial oxygen measurement in the newborn with intravascular transducers. In: Hill DW, Watson BW, eds. IEE Medical Electronics Monographs. London: Peter Perigrinns Ltd 1976; 126-58.
  8. Byrne P, Provan JL, Ameli FM et al. The use of transcutaneous oxygen tension measure­ments in the diagnosis of peripheral vascular insufficiency. Ann Surg 1984; 200: 159-65.
  9. Clyne CA, Ryan J, Webster JH et al. Oxygen tension on the skin of ischemic legs. Am J Surg 1982; 143: 315-18.
  10. Dowd GS, Provan JL, Ameli FM. Measurement of transcutaneous oxygen pressure in normal and ischaemic skin. Brit J Bone Joint Surg 1983; 65: 79.
  11. Franzeck UK, Bollinger A, Huch R et al. Transcutaneous oxygen tension and capillary morphologic characteristics and density in patients with chronic venous incompetence. Circulation 1984; 70: 806-11.
  12. Spence VA,  Walker VF. Tissue oxygen tension in normal and ischaemic human skin. Cardiovasc Res 1984; 18: 140-44.
  13. Toennesen KH. Transcutaneous oxygen tension in imminent foot gangrene. Acta Anaesth Scand 1978; (Suppl 68): 107-10.
  14. Hauser CJ, Shoemaker WC. Use of a transcutaneous pO2 regional perfusion index to quantify tissue perfusion in peripheral vascular disease. Ann Surg 1983; 197: 337-43.
  15. Caspary L, Creutzig A, Alexander K. Comparison of laser-doppler-flux and tcpO2 in healthy probands and patients with arterial ischemia. In: Huch A, Huch R, Rooth G, eds. Continuous transcutaneous monitoring. Advances in Experimental Medicine & Biology. New York: Plenum Press, 1987: 220.
  16. Becker F et al. Predictive value of tcpO2 in chronic severe ischemia of the lower limbs. Int J Microcirc: Clin Exp 1988; 7: 261-71.
  17. Scheffler A, Eggert S, Rieger H. Influence of clinical findings, positional manoeuvers, and systolic ankle arterial pressure on trans­cutaneous oxygen tension in peripheral arterial occlusive disease. Eur J F Clin Invest 1992; 22: 420-26.
  18. Ewald U, Tuvemo T, Rooth G. Early reduction of vascular reactivity in diabetic children detected by transcutaneous oxygen electrode. Lancet I 1981: 1287-88.
  19. Franzeck UK, Talke P, Bernstein EF, Golbranson FL et al. Transcutaneous pO2 measurements in health and peripheral arterial occlusive disease. Surgery 1982; 91: 156-63.
  20. Kram HB, Appel P, White RA et al. Assessment of peripheral vascular disease by postocclusive transcutaneous oxygen recovery time. J Vasc Surg 1984; 1: 628-34.
  21. Slagsvold CE, Rosen L, Standen E. The relation between changes in capillary morphology induced by ischemia and post-ischemic transcutaneous pO2 response. Int J Microcirc: Clin Exp 1991; 10: 117-25.
  22. Holdich TA et al. Transcutaneous oxygen tension during exercise in patients with claudication. Brit Med J 1986; 292: 1625-28.
  23. Schmidt JA, Bracht C, Leyhe A et al. Transcutaneous measurement of oxygen and carbon dioxide tension (tcpO2 and tcpO2) during treadmill exercise in patients with arterial occlusive disease (AOD) - stages I and II. Angiology 1990; 4: 547-52.
  24. McCollum PT, Spence VA, Walker WF. Oxygen inhalation induced changes in the skin as measured by transcutaneous oxymetry. Br J Surg 1986; 73: 882-85.
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No portrait of author Arnost Fronek

 

Department of surgery 
University of California 
San Diego 
California 
USA
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