Transcutaneous oximetry in clinical practice: consensus statements from an expert panel based on evidence.

Transcutaneous oximetry (PtcO2) is finding increasing application as a diagnostic tool to assess the peri-wound oxygen tension of wounds, ulcers, and skin flaps. It must be remembered that PtcO2 measures the oxygen partial pressure in adjacent areas of a wound and does not represent the actual partial pressure of oxygen within the wound, which is extremely difficult to perform. To provide clinical practice guidelines, an expert panel was convened with participants drawn from the transcutaneous oximetry workshop held on June 13, 2007, in Maui, Hawaii. Important consensus statements were (a) tissue hypoxia is defined as a PtcO2 <40 mm Hg; (b) in patients without vascular disease, PtcO2 values on the extremity increase to a value >100 mm Hg when breathing 100% oxygen under normobaric pressures; (c) patients with critical limb ischemia (ankle systolic pressure of < or =50 mm Hg or toe systolic pressure of < or =30 mm Hg) breathing air will usually have a PtcO2 <30 mm Hg; (d) low PtcO2 values obtained while breathing normobaric air can be caused by a diffusion barrier; (e) a PtcO2 <40 mm Hg obtained while breathing normobaric air is associated with a reduced likelihood of amputation healing; (f) if the baseline PtcO2 increases <10 mm Hg while breathing 100% normobaric oxygen, this is at least 68% accurate in predicting failure of healing post-amputation; (g) an increase in PtcO2 to >40 mm Hg during normobaric air breathing after revascularization is usually associated with subsequent healing, although the increase in PtcO2 may be delayed; (h) PtcO2 obtained while breathing normobaric air can assist in identifying which patients will not heal spontaneously.

Wound oxygen levels during hyperbaric oxygen treatment in healing wounds.

Hyperbaric oxygen (HBO2) increases wound oxygen delivery, but few data quantify wound oxygen levels over the course of healing. We characterized these changes during and after HBO2 treatment in a rat wound model. The treatment group (n=7) received 2.0 ATA HBO2, 90 minutes BID for 15 days. Control rats (n=5) were only exposed to HBO2 during measurement. On days 5, 10, and 15, wound pO2 was measured before, during, and for an hour after HBO2 treatment. Both the peak pO2 and the pO2 one hour after HBO2 treatment were significantly greater than baseline on all days in both the treatment (p < .01) and control group (p < .05). The peak pO2 during HBO2 exposure and one hour after decreased significantly in the treatment group on day 15 compared to day 5 (p <.01, p <.05 respectively). No significant differences were found in pO2 values between days within the control group. These results demonstrate that both the peak wound oxygen levels and duration of elevation change significantly throughout the course of HBO2 treatment.

UHMS position statement: topical oxygen for chronic wounds.

A small body of literature has been published reporting the application of topical oxygen for chronic non-healing wounds . Frequently, and erroneously, this form of oxygen administration has been referred to as "topical hyperbaric oxygen therapy" or even more erroneously "hyperbaric oxygen therapy." The advocates of topical oxygen claim several advantages over systemic hyperbaric oxygen including decreased cost, increased safety, decreased complications and putative physiologic effects including decreased free radical formation and more efficient delivery of oxygen to the wound surface. With topical oxygen an airtight chamber or polyethylene bag is sealed around a limb or the trunk by either a constriction/tourniquet device or by tape and high flow (usually 10 liters per minute) oxygen is introduced into the bag and over the wound. Pressures just over 1.0 atmospheres absolute (atm abs) (typically 1.004 to 1.013 atm abs) are recommended because higher pressures could decrease arterial/capillary inflow. The premise for topical oxygen, the diffusion of oxygen into the wound adequate to enhance healing, is attractive (though not proven) and its delivery is certainly less complex and expensive than hyperbaric oxygen. When discussing the physiology of topical oxygen, its proponents frequently reference studies of systemic hyperbaric oxygen suggesting that mechanisms are equally applicable to both topical and systemic high pressure oxygen delivery. In fact, however, the two are very different. To date, mechanisms of action whereby topical oxygen might be effective have not been defined or substantiated. Conversely, cellular toxicities due to extended courses of topical oxygen have been reported, although, again these data are not conclusive, and no mechanism for toxicity has been examined scientifically. Generally, collagen production and fibroblast proliferation are considered evidence of improved healing, and these are both enhanced by hyperbaric oxygen therapy. Paradoxically, claims of decreased collagen production and fibroblast inhibition in wounds subjected to topical oxygen have been reported in studies of topical oxygen as a benefit of topical oxygen therapy. The literature on topical oxygen is mostly small case series or small controlled but not randomized trials. Moreover, the studies generally are not aimed at specific ulcer types, but rather at "chronic wounds." This non-specific approach is recognized as a major design flaw in any study of therapies designed to improve impaired wound healing. The only randomized trial for topical oxygen in diabetic foot ulcers actually showed a tendency toward impaired wound healing in the topical oxygen group. Contentions that topical oxygen is superior to hyperbaric oxygen are not proven. There are potentially plausible mechanisms that support both possibly beneficial and detrimental effects of topical oxygen therapy, and thus well designed and executed basic science research and clinical trials are clearly needed. There is some ongoing research in regard to the role of topical oxygen at established wound laboratories. Neither CMS nor other third party payors recognize or reimburse for topical oxygen. Therefore, the policy of the Undersea and Hyperbaric Medical Society in regard to topical oxygen is stated as follows: 1. Topical oxygen should not be termed hyperbaric oxygen since doing so either intentionally or unintentionally suggests that topical oxygen treatment is equivalent or even identical to hyperbaric oxygen. Published documents reporting experience with topical oxygen should clearly state that topical oxygen not hyperbaric oxygen is being employed. 2. Mechanisms of action or clinical study results for hyperbaric oxygen cannot and should not be co-opted to support topical oxygen since hyperbaric oxygen therapy and topical oxygen have different routes and probably efficiencies of entry into the wound and their physiology and biochemistry are necessarily different. 3. The application of topical oxygen cannot be recommended outside of a clinical trial at this time based on the volume and quality of scientific supporting evidence available, nor does the Society recommend third party payor reimbursement. 4. Before topical oxygen can be recommended as therapy for non-healing wounds, its application should be subjected to the same intense scientific scrutiny to which systemic hyperbaric oxygen has been held.

The role of nitric oxide in subcutaneous and transmural gut tissue oxygenation.

The influence of inhibiting the nitric oxide (NO) synthetase on tissue perfusion as indicated by tissue oxygen tensions was determined. Tissue oxygen probes were placed subcutaneously and on serosal and mucosal surfaces of colon of anesthetized adult rats. After a control period, the inhibitor of NO formation, N(G)-nitro-L-arginine methyl ester (L-NMMA), was given intravenously and followed 20 min later by infusion of substrate for NO synthetase, L-arginine. Mean arterial blood pressure (MAP), subcutaneous tissue oxygen tension (P(SQ)O2), serosal tissue oxygen tension (P SO(2)), and mucosal tissue oxygen tension (P(M)O2) were simultaneously measured. Baseline values for the measured parameters were MAP = 95 + or - 9 mmHg, P(SQ)O2 = 61 + or - 7 mmHg, P(S)O2 65 + or - 7 mmHg, and P(M)02 = 9 + or - 2 mmHg. The infusion of L-NMMA induced a significant increase in MAP to 123 + or - 7 mmHg (p < .001) and P(SQ)O2 to 72 + or - 7 mmHg (p < .001). P(S)O2 did not change significantly from baseline after L-NMMA infusion. A significant decrease in P(M)O2 to 4 + or - 2 mmHg was noted after L-NMMA infusion (p < .001). The administration of L-arginine promptly returned all measured parameters to baseline levels within 10 min of infusion. A transmural P(O2) gradient exists across the colon with P(M)O2 far lower than P(S)O2. P(SQ)O2 approximates P(S)O2 at baseline and P(S)O2 is not altered by inhibition of the NO synthetase. The 45% reduction in mucosal PO2 after L-NMMA, which was reversed by L-arginine infusion, suggests that nitric oxide participates in splanchnic vasomotor control with a preferential effect in the mucosal vasculature. The observed decrease in mucosal PO2 observed after inhibition of NO production is similar to the worsened hypoxia previously measured during hemorrhagic shock. Further work clarifying the local control mechanisms of gut tissue P02 can direct therapies to increase gut tissue oxygenation.

Postoperative pain management.

OBJECTIVES: To examine the relationship between analgesia and clinical outcome and to review new methods of delivering opioid analgesics and new pharmacologic analgesic agents. DATA SOURCES: A computer-assisted search of the literature on postoperative pain management, and a review of those areas in which new approaches have led to a change in clinical practice. RESULTS: Current research focuses on the ability of analgesia to decrease perioperative complications. Recent advances allow enhanced postoperative analgesia with a low incidence of side effects. Administration of opioids via a patient-controlled device or via an epidural catheter yields excellent analgesia with a low rate of side effects compared with intramuscular opioids. Several non-narcotic, parenteral drugs, including ketorolac tromethamine and alpha 2-adrenergic agonists are now available. These drugs decrease opioid requirement, and thus the rate of serious side effects, including respiratory depression. Moreover, because these drugs act at sites other than opioid receptors, they may enhance the quality of analgesia at the same time they decrease opioid requirement. CONCLUSIONS: New technology and new agents allow more rational management of postoperative pain. Use of these techniques results in increased patient satisfaction and may improve clinical outcome.

Transmural gut oxygen gradients in shocked rats resuscitated with heparan.

OBJECTIVES: To develop a reproducible model to measure transmural gut tissue PO2, to determine the gradient from serosa to mucosa during normovolemia and hypovolemia, and to determine the effect of resuscitation with heparan sulfate (danaparoid sodium) on this gradient. DESIGN: Fluorescent tissue oxygen sensors were placed onto serosal and mucosal surfaces of rat colon. Hemorrhagic shock was induced using a fixed pressure (mean arterial pressure, 40 mm Hg) model and resuscitated with either saline solution or heparan. RESULTS: Control animals had stable mean (+/- SD) serosal and mucosal tissue oxygen tensions (PO2) of 64 +/- 4 and 10 +/- 2 mm Hg, respectively. In shocked animals, baseline serosal PO2 decreased to 37 +/- 2 mm Hg at a mean (+/- SD) of 19 +/- 7 minutes after the initiation of hemorrhage. Mucosal values decreased to a minimum of 4 +/- 2 mm Hg at 45 +/- 15 minutes after the initiation of hemorrhage. Serosal PO2 returned to baseline during resuscitation in both control and heparan-resuscitated animals. Mucosal PO2 did not return to baseline in the shock/no heparan group. In the heparan-resuscitated animals, however, mucosal PO2 increased above baseline (13 +/- 3 mm Hg at 3 hours after completion of hemorrhage). CONCLUSIONS: A transmural gradient of PO2 exists across the colon with mucosal PO2 far lower than serosal PO2. Both serosal and mucosal PO2 decrease during hypovolemia. During hypovolemia, the PO2 of the entire gut wall is in a range in which phagocytic killing is impaired by hypoxia. Heparan improved mucosal PO2 and it may restore and/or protect gut function by oxygen-related mechanisms.

Cigarette smoking decreases tissue oxygen.

Subcutaneous wound-tissue oxygen (PsqO2) tension in eight volunteers fell rapidly and significantly in response to smoking, and remained low for 30 to 50 minutes. Sham "smoking" had no effect. These data suggest that a typical "pack-per-day" smoker experiences tissue hypoxia during a significant portion of each day. The degree of hypoxia found in these subjects has been associated with poor wound healing in animal and human studies. The onset and duration of tissue hypoxia paralleled the well-established plasma pharmacokinetics of nicotine. This suggests that peripheral vasoconstriction, induced by the adrenergic effects of nicotine, may contribute to the observed decrease in PsqO2.

Perioperative collagen deposition in elderly and young men and women.

HYPOTHESIS: Women deposit more collagen after major abdominal surgery than men. DESIGN: A post hoc analysis of data obtained from 2 prospective, randomized, double-blind clinical trials. SETTING: University hospital general surgical service. PATIENTS: One hundred sixteen patients undergoing colon resection. MAIN OUTCOME MEASURES: Protein and hydroxyproline (collagen) deposition during the first 7 postoperative days in expanded polytetrafluoroethylene implants positioned subcutaneously. RESULTS: On univariate analysis, men and women deposited comparable amounts of collagen (257 +/- 120 vs 281 +/- 117 ng/mm, respectively). When potential confounding factors were entered into a generalized mixed-effects model, only the interaction between age and sex was a significant factor (P = .047). Collagen deposition decreased with age in men, being 317 +/- 133 ng/mm in men younger than 45 years, but only 238 +/- 113 ng/mm in those older than 45 years (P = .03). In contrast, collagen deposition was virtually identical in women younger than 45 years (280 +/- 133 ng/mm) and in those older than 45 years (281 +/- 110 ng/mm). Only 3 of these women were receiving hormone replacement therapy. CONCLUSIONS: Collagen deposition after surgery decreased significantly with age in men, while remaining unchanged in women. Younger men and women deposited similar amounts of collagen. Therefore, older men made less collagen after surgery than older women, perhaps explaining the consistent observation that wound dehiscence is twice as common in men than in women. Our results differ from previous studies conducted in healthy, nonsurgical volunteers, which showed that (1) young women made significantly more collagen than young men and (2) collagen deposition was reduced in postmenopausal women, but deposition returned to premenopausal values with hormone replacement therapy. Differences between our results and those reported previously likely stem from the populations studied. In particular, multiple perioperative factors decrease collagen deposition, which apparently obscures the differences observed previously in healthy, unstressed volunteers.

Subcutaneous perfusion and oxygen during acute severe isovolemic hemodilution in healthy volunteers.

HYPOTHESIS: Acute severe isovolemic anemia (to a hemoglobin [Hb] concentration of 50 g/L) does not decrease subcutaneous wound tissue oxygen tension (PsqO(2)). SETTING: University hospital operating room and inpatient general clinical research center ward. SUBJECTS: Twenty-five healthy, paid volunteers. METHODS: Subcutaneous oxygen tension and subcutaneous temperature (Tsq) were measured continuously during isovolemic hemodilution to an Hb level of 50 g/L. In 14 volunteers (initially well-perfused), "normal" perfusion (Tsq >34.4 degrees C) was achieved by hydration and systemic warming prior to starting isovolemic hemodilution, while in 11 volunteers (perfusion not controlled [PNC]), no attempt was made to control perfusion prior to hemodilution. MAIN OUTCOME MEASURES: Measurements of PsqO(2), Tsq, and relative subcutaneous blood flow (flow index). RESULTS: While PsqO(2), Tsq, and flow index were significantly lower in PNC vs well-perfused subjects at baseline, there was no significant difference between them at the Hb of 50 g/L (nadir). Subcutaneous PO(2) did not decrease significantly in either group. Arterial PO(2) was not different between the groups, and did not change significantly over time; Tsq and flow index increased significantly from baseline to nadir Hb in both groups. CONCLUSIONS: The level of PsqO(2) was maintained at baseline levels during hemodilution to Hb 50 g/L in healthy volunteers, whether they were initially well-perfused or mildly underperfused peripherally. Given the significant increase in Tsq and flow index, this resulted from a compensatory increase in subcutaneous blood flow sufficient to maintain oxygen delivery. Wound healing depends to a large extent on tissue oxygen delivery, and these data suggest that even severe anemia by itself would not be sufficient to impair wound healing. Thus, transfusion of autologous packed red blood cells solely to improve healing in surgical patients with no other indication for transfusion is not supported by these results.

Effect of hyperoxia on vascular endothelial growth factor levels in a wound model.

HYPOTHESIS: Hyperbaric oxygen (HBO) therapy increases vascular endothelial growth factor (VEGF) levels in wounds. DESIGN: Wounds were monitored for oxygen delivery during HBO treatment, and wound fluids were analyzed for VEGF and lactate on days 2, 5, and 10 following wounding. SETTING: Experimental animal model. INTERVENTIONS: Rats were randomized to HBO therapy and control groups. The HBO therapy was administered for 90 minutes, twice daily with 100% oxygen at 2.1 atmospheres absolute. Treatment was administered for 7 days following wounding. MAIN OUTCOME MEASURES: Vascular endothelial growth factor, PO(2), and lactate levels in wound fluid were measured on days 2, 5, and 10. RESULTS: Wound oxygen rises with HBO from nearly 0 mm Hg to as high as 600 mm Hg. The peak level occurs at the end of the 90-minute treatment, and hyperoxia of lessening degree persists for approximately 1 hour. The VEGF levels significantly increase with HBO by approximately 40% 5 days following wounding and decrease to control levels 3 days after exposures are stopped. Wound lactate levels remain unchanged with HBO treatment (range, 2.0-10.5 mmol/L). CONCLUSIONS: Increased VEGF production seems to explain in part the angiogenic action of HBO. This supports other data that hypoxia is not necessarily a requirement for wound VEGF production.

Wound hypoxia and acidosis limit neutrophil bacterial killing mechanisms.

BACKGROUND: "Respiratory burst" activity, ie, O2- production, is dependent on PO2, temperature, pH, and glucose concentrations within the physiologic range. OBJECTIVES: To determine whether environmental conditions characteristic of wounds may limit human neutrophil respiratory burst metabolism and to clarify the degree to which bactericidal oxidant production depends on local PO2. METHODS: Human blood and wound neutrophils were stimulated with phorbol myristate acetate. Oxygen consumption and superoxide production were measured over a range of 30 to 300 mm Hg PO2, 0 to 40 mmol/L glucose, pH 6.0 to 8.0, and 30 degrees C to 37 degrees C. The apparent Michaelis Menten constant for oxidant production with respect to PO2 was calculated. RESULTS: Oxygen consumption and O2- production were dependent on PO2 throughout the range tested. Half-maximal oxidant production occurred in the range of 45 to 80 mm Hg PO2 and maximal at PO2 higher than 300 mm Hg. These data agree with the highest previous estimates. Oxidant generation was also dependent on pH, temperature, and glucose concentration, but to a lesser extent. CONCLUSIONS: Leukocyte bacterial killing capacity as measured by oxygen consumption and superoxide production are substantially impaired at the low oxygen tensions often found in wounds. Changes in pH, temperature, and glucose concentration have lesser but nonetheless significant consequences. The data provide a plausible mechanism for the vulnerability of some wounds to infection and for the previous finding that increasing oxygen tension at wound sites enhances bactericidal function. Thus, the data serve as a basis for future studies on prevention of wound infection.

Wound tissue oxygen tension predicts the risk of wound infection in surgical patients.

OBJECTIVE: To test the hypothesis that subcutaneous wound oxygen tension (PsqO2) has a predictive relation to the development of wound infection in surgical patients. DESIGN: A noninterventional, prospective study. SETTING: A university department of surgery. PATIENTS: One hundred thirty operative general surgical patients at notable risk of infection as predicted by an anticipated Study on the Effect of Nosocomial Infection Control (SENIC) score of 1 or greater. OUTCOME MEASURES: PsqO2 was measured perioperatively. Its relation to the subsequent incidence of surgical wound infection was then determined and compared with the SENIC score as a criterion standard. RESULTS: Although the SENIC score and PsqO2 are inversely correlated, PsqO2 is the stronger predictor of infection. Low PsqO2 identified patients at risk and concentrated them in a cohort that was about half the size of that identified by the SENIC score. CONCLUSIONS: Subcutaneous perfusion and oxygenation are important components of immunity to wound infections. The SENIC score identifies systemic physiological variables that are important to the development of wound infection. Nevertheless, PsqO2 is the more powerful predictor of wound infection. Moreover, PsqO2 can be manipulated by available clinical means, and thus may direct interventions to prevent infection.

Local radiant heating increases subcutaneous oxygen tension.

BACKGROUND: We evaluated a novel bandage that incorporates a thermostatically controlled radiant heater. We first determined optimal bandage temperature, based on increases in subcutaneous oxygen tension, a measure correlating well with resistance to infection and wound strength. We then tested the hypothesis that prolonged radiant heating would increase collagen deposition in experimental thigh wounds. METHODS: The experimental bandages were positioned on the anterior thigh of 8 volunteers, and heated for 2 hours at 38 degrees C, 42 degrees C, or 46 degrees C, in a random order. Subcutaneous oxygen tension under the bandage was recorded from an electrode positioned within a subcutaneous tonometer. We studied 10 volunteers in the second protocol. For 1 week, the experimental bandage was continuously applied to one thigh, and heated to 38 degrees C using a 2-hour on/off cycle. On the alternate week, a standard gauze bandage was applied to the contralateral thigh. Treatment order was randomly assigned. Wound collagen deposition under each bandage was evaluated with subcutaneous polytetrafluoroethylene tubes, which were removed and assayed for hydroxyproline on the eighth day. Data are presented as means +/- SDs. RESULTS: Skin temperature during heating ranged from 36 degrees C to 37.5 degrees C. Oxygen tension increased approximately 50% during heating, but the increase was comparable at the three tested temperatures. Even after heating was discontinued, subcutaneous oxygen tension remained elevated for the remaining 3 study hours. Collagen deposition after 1 week of active heating was 3.4 +/- 1.0 microg/ cm. After 1 week of control treatment, collagen deposition was 3.2 +/- 1.1 microg/cm (P = not significant). CONCLUSIONS: Our data suggest that radiant heating at 38 degrees C significantly increases subcutaneous oxygen tension, and presumably resistance to infection. However, prolonged heating at this temperature does not increase wound collagen deposition.

Wound healing and wound infection. What surgeons and anesthesiologists can do.

Wound healing can be enhanced and wound infections prevented, often by simple, inexpensive, readily available means. Preoperative evaluation for impediments to healing, such as malnutrition, vasoconstriction, hyperglycemia, and steroid use, allows correction prior to operation. Intraoperatively, the surgeon should concentrate on surgical technique, appropriate antibiotic use, and prevention of vasoconstriction (volume, warming). Postoperatively, the focus should be on prevention of vasoconstriction through pain relief, warming, and adequate volume resuscitation and on maintaining nutrition and normoglycemia. These approaches apply as well to chronic wounds. Additionally, maintenance of a moist environment, correction of local vasospasm with sympathetic blockade or warming, and stimulation of angiogenesis through aggressive debridement or hyperbaric oxygen therapy enhance healing of chronic wounds.

Pulsed microamperage stimulation: a controlled study of healing of surgically induced wounds in Yucatan pigs.

BACKGROUND AND PURPOSE: Microamperage direct current and microamperage electromagnetic stimulation are used to accelerate healing in bone. Although many clinicians are using microamperage stimulation to relieve pain and facilitate wound healing, there is significant question regarding whether this low-intensity direct current significantly accelerates soft tissue wound repair. The purpose of this study was to determine whether low-voltage pulsed microamperage current (100 microA, 60 V, 0.1 Hz) enhances the healing of superficial, full-thickness, or incisional wounds created to simulate acute abrasions, ulcers, and lacerations. SUBJECTS: Ten adult Yucatan mini pigs served as the subjects for this study. METHODS: Variables associated with healing were measured in 60 matched pairs of surgically induced partial-thickness, full-thickness, and incisional wounds after either sham or anodal (positive-polarity) stimulation with pulsed microamperage current (100 microA) was administered for 1 hour per day for 5 days. Sterile, disposable electrodes (2 x 4 cm) were placed over each wound, which was kept wrapped and protected throughout the study. RESULTS: At 7 days postinjury, all wounds were healing well with no signs of infection. There were no differences in tensile strength, collagen density, maturity, or deposition (hydroxyproline), wound size, or visual appearance between the sham treatment and treatment lesions. No changes in local subcutaneous oxygen or temperature were found in the swine during or after microamperage stimulation. CONCLUSION AND DISCUSSION: This study did not provide any evidence to support the use of microamperage stimulation to accelerate wound healing. No negative effects, however, were found. Further research is needed to determine whether there is a critical interaction between the size of the electrode relative to the wound, the density of the current, the duration of the treatment, the polarity of the treatment electrode, and the acuity or chronicity of wounding and the effectiveness of microcurrent stimulation for wound healing.

Comparison of Clark electrode and optode for measurement of tissue oxygen tension.

Measurement of PsqO2 has proven clinically valuable. The optode is more stable and reliable than the Clark electrode, does not consume oxygen, measures temperature, and is relatively simple to use. The good correlation between values obtained by the Clark electrode and the optode in this study demonstrate that the optode may replace the Clark electrode without loss of prior data.

Adjuncts to preparing wounds for closure: hyperbaric oxygen, growth factors, skin substitutes, negative pressure wound therapy (vacuum-assisted closure).

Achieving closure in a chronic wound requires provision of adequate oxygen delivery to the tissue, adequate protein and other nutritional factors, a moist environment, an appropriate inflammatory milieu, dèbridement, and correction of contributing medical diagnoses. In some patients, these conditions are achieved easily, whereas in others, greater effort is required. Adjunctive treatments, including HBO2, growth factors, skin substitutes, and negative-pressure wound therapy (e.g., V.A.C.) can provide the proper conditions for healing in appropriately selected patients.

Tissue oxygenation, anemia, and perfusion in relation to wound healing in surgical patients.

Oxygen tension and collagen deposition were measured in standardized, subcutaneous wounds in 33 postoperative surgical patients. Pertinent clinical and wound parameters were analyzed by Pearson's correlation test and sequential linear regression analysis. Collagen deposition was directly and significantly proportional to wound oxygen tension and measures of perfusion. There were no significant correlations with hematocrit, estimated blood loss, length of operation, smoking, age, weight, sex, or urine output. This study in humans confirms animal experiments showing that collagen deposition and tensile strength in wounds are limited by perfusion and tissue oxygen tension. It appears unnecessary to maintain hemoglobin at normal levels to support repair, provided that peripheral perfusion can be maintained at a high level in compensation for anemia. These circumstances reflect the fact that although oxygen is essential to many aspects of healing, and must be delivered at adequate partial pressures, reparative tissue consumes relatively little of it.

Use of tissue oxygen tension measurements during resuscitation from hemorrhagic shock.

BACKGROUND: Tissue oxygen tension can be measured directly in selected organ beds, and these measurements may be more sensitive in assessing the adequacy of resuscitation than global physiologic parameters. We hypothesized that heart tissue oxygen tension would be an important marker for the severity of ischemic insult to the heart during hemorrhagic shock. We further hypothesized that gut oxygen tension measured in the jejunum would prove to be a better measure of splanchnic hypoperfusion than intramucosal pH (pHi). METHODS: Tissue oxygen probes were inserted directly into the myocardium of the left ventricle and into the lumen of the proximal jejunum in 10 anesthetized swine. A pHi catheter was introduced into the stomach. The animals were subjected to a controlled hemorrhage of 50% of estimated blood volume. Gut and cardiac oxygen were monitored continuously during hemorrhage and resuscitation, which was performed with shed blood and crystalloid. RESULTS: While gut O2 and pHi trended together, we were unable to establish a correlation between changes in these two variables during hemorrhage and resuscitation. Heart PO2 decreased significantly during hemorrhage, but surpassed baseline values after resuscitation, a finding not seen in gut PO2. No standard physiologic variables reliably predicted changes in heart PO2 during these experiments. CONCLUSIONS: Tissue oxygen tensions measurements are highly responsive to changes induced during graded hemorrhagic shock and resuscitation. Gut PO2 and pHi appear to be measuring different physiologic processes in the gastrointestinal tract. The compensatory ability of the heart far exceeds that of the gut after ischemic insult. This hemorrhagic shock model appears feasible for the study of various methods of resuscitation.

Centrally and locally mediated thermoregulatory responses alter subcutaneous oxygen tension.

Mild perianesthetic hypothermia decreases resistance to infections. Decreased resistance likely results in part from direct immune inhibition. However, decreased tissue oxygen partial pressure also decreases resistance to infection by impairing oxidative killing by neutrophils and collagen deposition. Thermoregulatory vasoconstriction decreases skin blood flow and may also decrease subcutaneous tissue oxygen tension. Accordingly, we determined the influence of centrally and locally mediated thermoregulatory vasomotion on subcutaneous oxygen tension. We also compared subcutaneous oxygen tension to other potential markers of tissue perfusion: laser Doppler flowmetry and transcutaneous oxygen tension. Arterial oxygen tension was maintained near 325 mm Hg in five volunteers. Control subcutaneous oxygen tension values were recorded after 1 hour of euthermia (no sweating or vasoconstriction). Volunteers were then cooled with a circulating-water mattress positioned under the trunk and legs. After 1.5 hours of cooling sufficient to produce shivering, the right upper arm was covered for 1 hour with a small circulating water blanket set to 40 degrees C while systemic cooling continued. The volunteers were then systematically warmed to produce sweating, and the right arm was locally cooled. There was no correlation among laser Doppler flowmetry, transcutaneous oxygen tension, and subcutaneous oxygen tension. Systemic cooling significantly decreased subcutaneous oxygen tension, but subcutaneous oxygen tension in the right arm returned to control values during local heating. Systemic warming significantly increased subcutaneous oxygen tension, and 1 hour of local cooling failed to fully reverse the increase. These data indicate that thermoregulatory vasoconstriction significantly decreases tissue oxygen availability. Decreased subcutaneous oxygen tension may be one mechanism by which mild perianesthetic hypothermia facilitates development of surgical wound infections.