The Pivotal Role of Oxygen in Pressure Injury Etiology and Prevention

  • Glenn Butler, CHT; Jody C. DiGiacomo, MD, UHM, FACS; Edward Golembe, MD, UHM, FACCWS; Scott Gorenstein, MD, UHM, FACEP; Bok Lee, MD, FACS
  • Volume 07 - Issue 2

In an effort to safely provide adjunctive hyperbaric oxygen therapy to a larger population of sick and postsurgical patients with compromised flaps/grafts, Life Support Technologies (LST) developed a research program to better understand the etiology of pressure injury (ulcers). (Note: The National Pressure Ulcer Advisory Board has elected to use the term “injury” rather than “ulcer” to describe the initial postischemic injury phase that may lead to an ulcer.)

During hyperbaric therapy, patients must lie on special hyperbaric chamber mattresses that are not as pressure relieving as hospital-provided bed systems that are powered, alternating, or low-air-loss system designs.

To better understand the biomechanical and biochemical mechanisms relating to pressure injury, LST developed systems that combined mattress interfacial pressure mapping with spectrographic oximetry. This new technology provided simultaneous real-time pressure and deep-tissue blood perfusion as measured by multiple, near-infrared sensors for tissue hemoglobin saturated oxygen or rSO2. We utilized this technology to evaluate 16 powered and nonpowered clinical mattress systems dominating the medical market. The human subject research portion of the program to date has involved more than 200 clinical evaluations using male and female subjects ranging in age from 18 to 65 years old.

Off-Loading Technologies, Inc. (OLT) then utilized this technology to design, evaluate, and patent the OXY-MAT™ series of offloading systems engineered to naturally optimize patient blood-perfusion and deep-tissue oxygen tensions over a wide range of patient/mattress interface pressures.

Traditional Pressure Mapping

In developing the system, we first turned to the industry standard of pressure-mapping systems available on the market. This basic technology has been used over the past 50 years to design and promote commercially available clinical and retail mattress systems.

Commercial pressure-mapping systems often contain transient data variables that make them a concern for the reliable evaluation of pressure-offloading measurement. As Figure 1 shows, we placed a 240-pound male on a nonpowered mattress equipped with a conventional commercial pressure-mapping system. In only 30 seconds, we inadvertently adjusted the electronic gain up 200 percent and noted the changes in recorded interface pressure.

FIGURE 1. Effect of Gain


This event represented an unacceptable opportunity for experimental error. Our modified pressure-mapping system has been designed to eliminate any ability to change adjustments between baseline and serial measurements.

Traditionally, to evaluate mattress systems, pressure data have been extrapolated over time using empirical algorithms (Hunt et al.) to estimate time-to-tissue ischemia and to predict pressure-injury (ulcer) development. In an effort to better understand and measure internal tissue pressure changes, several invasive or indirect methods have been used.

Invasive pressure-sensing catheters are unsuitable for use in human volunteers. Indirect methods include ultrasonic and magnetic resonance with chemical tagging where the displacement of tag lines allows one to calculate internal tissue pressure deformation.

Classical teaching states approximately 30 mmHg tissue pressures would result in capillary blood vessel collapse, a reduction of blood flow carrying nutrients (i.e., oxygen), eventually leading to ischemia. Using these new evaluation technologies, however, we often see much higher interfacial pressures in basically healthy individuals without developing any pressure injury, while many compromised patients with comorbidities begin to have ischemic changes almost immediately despite best efforts to offload the patient.

Clearly, a lot more is going on than we fully understand.

Deep-Tissue Oxygen Tensions

We soon realized measuring pressure alone was not a meaningful predictor of tissue ischemia — reperfusion (I/R) injury leading to a pressure injury. Deep-tissue blood perfusion as measured by oxygen tensions is the only reliable real-time indicator of relative tissue ischemia leading to a true reperfusion injury, pressure injury and ulcer development.

Colin, Loyant, et al. measured transcutaneous oxygen tensions on the sacrum of 20 healthy individuals positioned on 5 different mattress types. That study demonstrated lower oxygen tensions as compared with a control as subjects were exposed first to a standard mattress and then several other mattresses. Oxygen tensions improved on foam and maximized on a water-equalizing mattress.

Pressure is only one of the contributors to the pathophysiology and relative risk of pressure ulcer development. Factors such as microvascular disease, blood perfusion, BMI, nutrition, and comorbidities affecting nitric oxide (NO) autoregulation/vasodilatation and the physiological management of reactive oxygen species (ROS) all play an important part in relative pressure injury risk.

Do Age and Comorbidity Affect Risk?

Our test-data trending demonstrates young and healthy individuals are able to sustain higher tissue pressures longer and still demonstrate normal active hyperemic response and blood-oxygen tensions above the ischemic threshold of 40 mmHg and with a reliable return to baseline oxygen tensions. Conversely, some older patients with comorbidities that can compromise blood autoregulation appear to lose tissue-oxygen tensions faster under moderate pressure (60 mmHg) and do not demonstrate a normal active hyperemic response. They tend to maintain lower pressure tissue-oxygen levels than starting tensions. Research continues to evaluate this trend.

Pathophysiology of Pressure Ulcer Development

The prime causal factor for the development of pressure injury and subsequent ulcers consists of excessive tissue pressure-loading sustained for time periods sufficient to cause pressure-prone tissue to become ischemic, then hypoxic, leading to reperfusion injury.

Since nearly all patients are in bed for eight hours or more, the mattress system selected for clinical use becomes a significant variable in the reduction and/or relief of pressure on the patient’s body, particularly over bony prominences. Any increase in mechanical stress (pressure and shear) further affects the availability of nutrients, such as oxygen, to susceptible tissues.

Ischemia leading to hypoxic injury is the result of decreased blood flow to cutaneous tissue after prolonged periods of elevated tissue interface pressure. The resulting reperfusion injury causes neutrophil capillary endothelium adherence, cell rolling, sludging, and clotting that inhibits/occludes blood nutrient and oxygen supply.

This ischemia–reperfusion injury cycle (Figure 2) decreases blood flow and increases the hypoxic biochemical cascade that forces tissue cells to use anaerobic pathways to produce ATP energy. This causes more lactic acid to accumulate, resulting in greater acidosis, as well as increased quantities of hydrogen ions and potassium around the cell.


FIGURE-2US and Foreign Patents Pending - Offloading Technologies, Inc.- Copy Rights 2016

In normal individuals, this biochemical cascade of metabolites and oxygen radicals should lead to nitric oxide release and up-regulates other vessel vasodilators (active hyperemia)that promote increased fresh blood flow with oxygen and other nutrients to the tissues.

A review of these physiological mechanisms helps us to appreciate why deep-tissue oxygen tensions are the only meaningful real-time indicator for pressure injury risk and prevention.

The Pressure/Oxygen Relationship

It is generally understood there is a close correlation between an increase in tissue pressure and a reduction in blood flow, with approximately 30 mmHg pressure resulting in capillary vessel collapse.

Our testing has demonstrated an increase in tissue pressure and that tissue’s blood flow as measured by oxygen saturation often did not inversely correlate. A high interface pressure often did not result in a lower tissue-oxygen saturation value leading to ischemia and a lower tissue interface pressure did not always result in better blood perfusion and higher oxygen saturation.

Simultaneous Pressure and Oxygen Measurements

— A More Complete Picture

Simultaneous measurement of both pressure and deep-tissue oxygen tensions provide a more complete picture of the effects of pressure and blood-flow reduction resulting in lower oxygen tensions leading to ischemia. To develop a dependable system, we modified and integrated near infrared spectrographic oximetry used to measure brain oxygen during anesthesia (tissue-oxygen saturation) into our existing, improved pressure-mapping system. This served as an indicator of blood perfusion by the direct measurement of tissue-oxygen tension. The combination of simultaneous pressure and oxygen tension has permitted us to evaluate offloading mattress system designs and to safely determine a given patient’s tolerance to pressure without risking pressure injury development.

After substantial evaluation and human testing, we have demonstrated that tissue pressure and oxygen tensions are not necessarily inversely proportional and near normal perfusion can exist under high interfacial tissue pressures (>100 mmHg) as could be clinically experienced in healthy individuals.

Weight Redistribution Analysis

Figure 3 is an example of an LST pressure-only weight distribution map on the same subject and mattress system lying down and then sitting with the bed raised to a 45-degree position.



These two maps depict the weight transfer from the torso in the supine (laying down) position and weight transfer down to the sacrum and ischium when in a 45-degree sitting position. With many bedded and wheelchair patients spending a majority of time in a sitting or upright position, the sacrum, ischium and heels are a primary concern.

But what is actually happening to the blood perfusion and/or any ischemic changes taking place in these at-risk tissues? Is there any difference in blood perfusion values and pressure injury risk between a 45-year-old brittle diabetic motorcycle rider (smoker) with a broken hip and a healthy 86-year-old who slipped on ice and broke a hip?

Simultaneous Pressure/Oxygen Measurements in Humans

Figure 4 shows an example of an LST simultaneous interface pressure/tissue oxygen analysis. For clarity in this graph, we are looking only at ischium pressure and oxygen values. Our standard studies simultaneously include scapula, ischium, sacrum, trochanter, and heels.


In Figure 4, the subject goes from a standing position to supine for a 20-minute period, then is elevated to a 70-degree reclining position for an additional 20 minutes and then returns to a standing position.

Note that in both standing and supine positions, ischial tissue oxygen averages 55 percent, while ischial pressure averages 26 mmHg in the supine position. In the 70-degree position, the subject’s weight transfers to the ischium and the average interface pressure rises to 99 mmHg, while the ischium oxygen tension only decreases to 51 percent.

The net pressure increase from the supine to sitting position is more than 280 percent, but the oxygen tension only decreases by 6.5 percent from the supine position. This is an effect of the human body’s ability to autoregulate blood perfusion as measured by oxygen saturation.

This is a typical example of how pressure and blood perfusion are not inversely proportional in healthy subjects able to carry out normal autoregulation/active hyperemia. Conversely, it helps us better understand how age and comorbidities compromise blood perfusion autoregulation, hyperemia, I/R, and pressure injury development.

Active Hyperemia

Active hyperemia is a normal physiological process that automatically compensates for reductions in blood flow due to transient vessel occlusions or increased tissue- interface pressures, such as prolonged sitting in healthy persons. As we sit, receptors sense our muscles becoming ischemic and congested with metabolic byproducts. We then unconsciously shift our weight to allow normal active hyperemia to vasodilate the muscles and flush the tissues with fresh blood. We can repeat this process hundreds of times a day without long-term effect.

As persons become older, develop comorbidities such as diabetes, associated neuropathy, paraplegias or compromised mentation, they become less able to initiate normal autonomic active hyperemia vasodilatation and become more susceptible to pressure-related ischemia leading to hypoxia, reperfusion injury and necrosis.

Reactive Hyperemia

Reactive hyperemia occurs after the normal physiological mechanisms of active hyperemia are exhausted. Reactive hyperemia is the transient uncontrolled increase in blood flow that occurs following some prolonged period of ischemia as might occur after the removal of a tourniquet.

The only meaningful variables seem to be patient comorbidities that down-regulate autonomic vasodilation and tissue-oxygen tension-recovery times that allow tissues to become ischemic long enough to induce a true reperfusion injury.

When Repetitive Hyperemia Leads To Ischemia

If the patient’s position is changed often enough after a mild ischemic incident (two-hour nursing repositioning), some focal tissue pressure will be released and there will be moderate active hyperemia and blood-vessel dilation.

This increased blood flow flushes out metabolites/free radicals, and a normal blood flow due to autoregulation will resume. This is a normal process.

Excessive and repetitive ischemia, hypoxia, and then repetitive reactive hyperemia will lead to a true ischemic / reperfusion injury and neutrophil adherence to the capillary endothelium that then result in cell rolling, sludging and progressive blood flow reduction/occlusion.

This ischemic/reperfusion injured tissue becomes increasingly compromised and more susceptible to pressure injury/ulcer development upon repeating this pressure reinjury cycle.

For patients with comorbidities, the anatomical areas most susceptible to pressure and shear are the scapula, sacrum, ischium, trochanter and heel. For seated and wheelchair patients, the areas most impacted are the buttocks and the ischium.

The role of shear forces developed in sitting with respect to tissue trauma in the region of the ischial tuberosities may be significant in pressure ulcer causation. Prior study results have shown that cutaneous pulsatile flow measured at the buttocks of the geriatric hospitalized patient and seated paraplegics is considerably reduced compared with that of healthy subjects.

Average skin shear values developed by a geriatric hospitalized group were three times that of a young, healthy group. It also has been shown that the sitting shear force developed by paraplegics is considerably greater than corresponding measurements of normal subjects. We think this is due in part to neuropathy effecting muscle tone and normal active hyperemia vasodilation.

Reactive Hyperemia Demonstrated

Using our simultaneous Near-Infrared Spectrographic Tissue Oximetry/Interface Pressure System, we have noted that about 80 percent of normal test subjects demonstrated some reactive hyperemia (RH) of the sacrum, in particular, upon standing after being supine on a mattress surface for a 90-minute test period.

As an extreme example of this phenomenon, the LST lab group tested a standard, first-generation, three-inch, monolithic memory foam mattress designed for use in monoplace hyperbaric chambers. This testing was initiated because of LST’s clinical concerns regarding this mattresses’ ability to adequately offload compromised patients receiving hyperbaric oxygen therapy over a two-hour supine period. (Figure 5)



US and Foreign Patents Pending - Offloading Technologies, Inc. - Copy Rights 2016

The degree of reactive hyperemia was sometimes significant. For example, Subject #4 of eight subjects tested in this series went from a pretest sacral area oxygen saturation value of 76 percent, then down to an averaged value of 45 percent over a 90-minute period while the subject remained supine and as immobile as possible to simulate a paraplegic/insensate patient. Many subjects (70 percent) experienced ever- increasing to eventual pain/spasms in the sacral area during this 90-minute supine and immobile test period.

Upon standing, Subject #4’s sacral oxygen levels went up immediately to more than 95 percent oxygen saturation (instrument full scale) and remained in that fulminant reactive hyperemic level for a 13-minute period before normalizing (autoregulation) back to 65 to 68 percent (below test-start oxygen baseline). On standing, the subject noted an extreme sensation of heat and interruption of pain. The sacral oxygen tension eventually stabilized at 62 percent. This was typical of tests repeatedly demonstrating lower baseline oxygen and is considered the hallmark of a true ischemic reperfusion injury.

Compromised Patients are at Greater Risk

During this same test series, a paraplegic subject’s sacrum became so ischemic we had to interrupt the test after only a 30-minute period. We again attribute this to neuropathy affecting muscle tone and normal active hyperemia vasodilation. This subject had no pain sensation. This further demonstrates that neurologically compromised and paraquadriplegic patients are physiologically incapable of functional active hyperemia beyond any sensation of ischemic pain. We postulate that this magnitude reactive hyperemia is a hallmark of reperfusion injury and an early indicator of pressure injury development.

Repetitive Ischemia/Reperfusion Injury Syndrome

We theorize that significant and repetitive changes (>30 percent) in oxygen tensions can induce a reactive hyperemia and will likely — over time — result in a repetitive ischemic/reperfusion injury syndrome that forces tissues into anaerobic cell respiration pathways, pressure injury and eventual necrosis. Figure 6 represents a theoretical progression of I/R over patient turning cycles.

The three peaks on the right side of the graph are extrapolated from actual test results depicted in the two graph peaks at the left side of the graph. These two events (the first peak is from Figure 5) were 90 minutes apart with a 13-minute and then a 17-minute uncontrolled reactive hyperemia of the subject’s sacrum.

Based on our other test results to date, we believe that this extrapolated data is representative of the actual progression of repetitive ischemia leading to significant I/R injury and neutrophil adherence to the capillary endothelium. The authors are presently developing an animal model to further demonstrate and research this phenomenon.

Whole Body Active Hyperemia

Another test program was designed to compare sacral oxygen tensions on the same subject while lying on six different mattress systems. Each test subject demonstrated a unique pattern of somatic active hyperemia (SAH) when going from a standing to a supine position, then sitting in a 70-degree position and back to standing.

This pattern was unique to each subject, and the autoregulation wave pattern results were also constant, regardless of the bed surface. Only the oxygen-tension shifted based on the mattress type being tested. Note the unique signature waveform regardless of the mattress type being tested.

Example: Subject B’s sacral oxygen saturation has the same pattern signature on each of six different types/manufacturer mattress surfaces. Figure 6 shows standing time before the 20-minute supine test measurement, then test measurements over a 20-minute period while in the 30-degree position, and then again when standing.






  1. The preponderance of the literature and our research support our conclusion that pressure alone has demonstrated not to be a reliable real-time indicator of mattress design superiority or to measurably reduce pressure injury risk or ulcer incidence.

  2. The pathophysiology of pressure ulcer development is just beginning to be understood. The true dynamics of repetitive ischemia/reperfusion injury as they relate to deep-tissue oxygen/nutrient supply and cell metabolite management are critical to pressure injury prevention, ulcer development and wound care.

  3. Reactive hyperemia must be avoided. The time and tissue interface pressures required to induce an ischemic/ reperfusion (I/R) event vary significantly from patient to patient with age, comorbidities and functional circulatory autoregulation.

  4. Repetitive I/R injury syndrome data support the hypothesis that repetitive reactive hyperemia inducing I/R produces ever-increasing neutrophil adherence to capillary endothelium that progressively reduces tissue- perfusion and tissue-oxygen tensions. This time and pressure is very variable and requires additional study.

  5. Repetitive ischemic/reperfusion injury syndrome is a term the authors developed to describe the cyclic changes in blood flow in an immobile patient’s tissue contact area under repeated pressure and offloading cycles when a patient is periodically turned. This phenomenon can also be induced by a misadjusted alternating mattress.

  6. Medical institutions are being sold an ever-growing array of increasingly complicated and costly powered mattress systems ostensibly developed to further reduce pressure injury ulcer risks with each new design. New mattress designs are still based on interface pressure mapping and have not been able to produce measurable improvements in patients’ deep-tissue, oxygen-saturation levels, improved patient comfort or reduced insomnia.

  7. All types of mattress systems must be designed to either permit patients to induce normal active hyperemia by patient movement or to simulate movement in insensate/ nonmoving patients to induce normal active hyperemia for them. It is estimated that more than 90 percent of hospital and long-term-care facility patients are capable of normal active hyperemia and should be placed on nonpowered equalizing mattress systems.

  8. A unique somatic active hyperemia signature was observed in each of our test subjects as they were placed in supine, sitting and standing positions. This could be repeated one year later and the subject identified solely by the shape of their oxygen saturation curves.

  9. Powered mattress systems were compared with the Oxy- Mat™ in independent clinical trials. Oxy-Mat™ has been credited with improved patient sleep, some reduction in pain medication and the improved ability to participate in P/T rehabilitation.

  10. The overutilization of powered mattress systems likely represents a significant unnecessary cost in health care and may be a contributing factor in clinical outcomes and longer length of stay due to sleep deprivation.



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About the Authors


GLENN BUTLER (Founder/CEO LST) has more than 45 years of experience in military and commercial diving and clinical hyperbaric operations. He has developed and/or operated more than 20 major hospital-based hyperbaric medicine programs internationally.

The Life Support Technologies group (LST) provides hospital-based elective and emergency wound care and hyperbaric medicine services around the New York Tri-State area. Butler was the principal consultant when LST was sole-sourced by NASA’s Johnson Space Center to engineer zero-gravity simulation breathing systems and develop new oxygen safety standards for the astronaut training program. He continues to lead the group’s efforts in its ongoing role with NASA.

He was a founding member of the National Board Certification for Hyperbaric Technologists and is a member of the UHMS Hyperbaric Safety Committee. He has authored 12 HBO2-related U.S. patents and published more than 45 related documents. He is a founding partner of Off- Loading Technologies Inc, the design/manufacturing group for the OXY-MAT products.



DR. BOK LEE (Chairman of Clinical Research and Development) is a distinguished, internationally recognized vascular surgeon with more than 200 published scientific articles and 9 books to his credit. His latest books are The Wound Management Manual (McGraw- Hill, 2005) and The Spinal Cord Injured Patient (Second Edition, Demos, 2002). Lee served on the Board of Governors of the American College of Surgeons for 1993 to 1999. He has been professor of surgery (NY Medical College, Valhalla, NY), director of Surgical Research (Sound Shore Medical Center, New Rochelle, NY) and adjunct professor (Rensselaer Polytechnic Institute, Troy, NY). Lee is actively involved in conducting hyperbaric research with the LST team.



EDWARD GOLEMBE (Skin Integrity Service, Westchester Medical Center, NY) is board certified in plastic surgery and hyperbaric medicine. He belongs to the American Society of Plastic Surgeons, New York Regional Society of Plastic and Reconstructive Surgeons, Medical Society of the County of Kings, Undersea and Hyperbaric Medical Society, and the New York State Hyperbaric Medical Society. He is also scuba certified and a DAN referral physician.



JODY CHRISTOPHER DIGIACOMO (director of Surgical Critical Care, associate director of Trauma, Nassau University Medical Center, NY) has been board certified in hyperbaric medicine since 2004. He has published more than 33 medical articles. DiGiacomo’s academic appointments include associate professor of surgery at St. George’s University School of Medicine (Grenada); associate professor of surgery at State University of New York, Stony Brook; adjunct clinical associate professor of surgery at the New York College of Osteopathic Medicine; and assistant professor of surgery at the University of Pennsylvania School of Medicine (Philadelphia, PA). He is also a Fellow of the American College of Surgeons.


SCOTT GORENSTEIN (clinical director, Division of Regenerative Medicine Winthrop University Hospital Mineola, NY) is board certified in emergency medicine and hyperbaric medicine. He is clinical director, Division of Regenerative Medicine at Winthrop University Hospital in Mineola, NY, and assistant clinical professor of surgery at Stony Brook University in Stony Brook, NY. He is a Fellow of the American College of Emergency Physicians, president-elect of the Northeast Chapter of the Undersea and Hyperbaric Medical Society (UHMS) and a Fellow of the American Professional Wound Care Association.






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