Clarity: The Importance of Patient Education

  • Darren Mazza, EMT, CHT
  • Volume 06 - Issue 1

One of the most important components of hyperbaric therapy is providing complete and informative patient education. Simply speaking to patients about risks and benefits alone doesn’t constitute thorough education or ensure that the patients understand their responsibilities. It is also necessary to educate patients on the importance of maintaining both good nutrition and hygiene, as they both have a direct impact on patient safety, health, and healing ability.

When possible, encourage a family member to participate in the patients’ education.  This can be a great way to encourage patient compliance. Family members are often times the only source of encouragement patients have aside from health care providers. Be clear when educating both the patients and their family members about safety measures.

As a CHT/safety director, I have an obligation to provide the safest environment possible for both the patients and staff in the clinic. Hyperbaric patients also have an obligation to both themselves and the clinic staff to comply with all aspects of the instructions provided to them. One of my goals is to encourage patients to take ownership of their health and their care to achieve their goals towards healing.

Always provide exceptional hyperbaric patient education. This lends the CHT credibility and demonstrates his or her competency and commitment to patient safety. This, in turn, gains patient trust and confidence in both the CHT and clinic.

One great example of providing good patient education is on the use of the air break line and mask. Don’t just hand the air break line and mask to the patient and send him into the chamber. The purpose of thorough patient education is to properly inform the patient of what the equipment is and how it works. The patient needs to be familiar as well as competent with the air break equipment. When teaching the patient how to properly use the air break equipment, instruct him to take two breaths from the air break line. Confirm that the mask creates an adequate seal and that the regulator provides proper air flow to the patient. This will ensure patient clarity and confirm that he has been prepared for treatment with adequate education and safety training.

Final Note: Don’t cut corners with patient education. It’s absolutely crucial for us as care providers to take the time and properly prepare patients for all aspects of the treatment they are about to receive.

About the Author

Darren-Mazza-Photo
Darren Mazza is the CHT and Safety Director at the Center for Wound Healing and Hyperbarics at Swedish/ Edmonds, located in the greater Seattle area. He has 20 years of experience in healthcare, which includes  8 years as an EMT in the greater Sacramento region. Darren also worked as a preceptor trauma tech in a Sacramento hospital for several years. After leaving California and moving to Idaho in 2005, his hyperbaric career began after becoming the department head of an outpatient wound care and hyperbaric center. His hobbies include fly fishing and fly tying.
 

 

 

Hyperbaric Safety

Clinic In Focus

  • Undersea and Hyperbaric Medical Society (UHMS)
  • Volume 06 - Issue 1

Continuing our series of interviews featuring outstanding hyperbaric and wound care centers around the world, we spoke with Courtney S. Hoffbauer, RN, MSN, Clinical Nurse Manager of the Orthopedic/Neurosurgery Unit, HBO, and Wound Care at Memorial Hospital, University of Colorado Health, which is accredited with distinction by the UHMS.

How has seeking UHMS accreditation affected your clinic?

Our accreditation raises the standard of practice to the next level. UHMS accreditation sets a standard for continuous improvement in regard to quality and patient care. Continuing education throughout the year is a mandate for all staff in order to continue accreditation. Quality improvement for patient care is at the forefront of accreditation. Memorial Hospital’s HBO department continues to not only meet our patients’ expectations, but exceed them.

What are the most common indications treated at your clinic?

The top five indications we treat most often are: diabetic foot wound, radionecrosis, carbon monoxide poising, necrotizing fasciitis, and decompression sickness.

What is the most memorable treatment success story that has come out of your clinic?

We treated a patient who demonstrated one of  the best limb salvage cases we have  seen.  As the nurse presented to the room for a consult, a surgeon was at the bedside informing the patient of the risks of refusing an amputation. The nurse vividly recalls the patient stating: “I have to keep trying before I opt to lose my leg.” It was that moment the nurse told the patient that, “We will do everything in our power to salvage your leg.” After a series of 30 daily treatments, this same nurse happened to encounter this patient several months later, as the patient walked by on both legs. The patient was so very grateful for one more chance.

Do you work with a management company?

We work with a consulting team from South Carolina, National Baromedical Services—the best in the country.

If you had to pick one thing to attribute your clinic’s success to, what would it be?

The team that works every day with the patients  in the unit is the leading factor of success for us. The team members know each other well and work side by side to ensure patients are receiving the best care. The team at the HBO unit has been working together for over five years, which is demonstrated by the cohesive nature of the group.

What is one marketing recommendation that you can make to help clinics increase their patient load?

Dr. Rob Price, our medical director, who also is an active-duty Lieutenant Colonel for the U.S. Army, plays a vital role in the success of our unit. One of his many strong attributes is the ability to network with and educate community physicians. We feel that community reputation is key to increasing patient census. We have a relationship with both the local U.S. Air Force Academy and Fort Carson Army Base to ensure we are available for their cadets or soldiers when in need.

Are there are any additional questions you’d like to answer, or is there any other information about your clinic you would like to showcase?

One of the most important facts about our HBO clinic is we are the only 24/7/365 HBO department left in the state of Colorado. Unfortunately, 24/7 HBO facilities are growing scarce; however, because of our relationship with our armed forces, we feel this is critical in our community.

CLINIC DETAILS
Memorial Hospital Wound Clinic/Hyperbaric Medicine Department
Printers Park Medical Plaza, 175 S. Union Blvd., Suite 305, Colorado Springs, CO 80910
Memorial Hospital Central, 1400 E. Boulder St., Colorado Springs, CO 80909
www.uchealth.org/southerncolorado
Wound Clinic: 719-365-6881 / HBO: 719-365-5920
Operating for over 10 years
Date of UHMS Accreditation: October 1, 2012 Number of chambers: 3
Chamber type: Monoplace
On staff: 4 nurses / 1 tech / 2 CHTs / 1 CHRN Dr. Rob Price, Medical Director

Our Wound Care Clinic saw a record 9,192 patients in 2014. The clinic has a variety of physician specialties available for our community, and in conjunction with HBO has saved many patients from losing limbs. The wound clinic uses cutting- edge technology to ensure we provide our patients with the very best. We were the first in the state  of Colorado to utilize Cellutome, which is a skin- grafting outpatient procedure.

Pictured below: The staff at Memorial Hospital Wound Clinic/Hyperbaric Medicine Department in Colorado Springs, Colorado.

clinic-in-focus-6-1

Free Mini-Course: The Business of Wound Care and Hyperbaric Medicine

Join us for this free 4-part mini-course and jump start your clinic business today! 
  • Are you a clinic manager or medical director who wants to increase patient load and referrals but has no money for marketing?
  • Could you be losing money due to incorrect billing and coding?
  • Do you want to become a profit center for the hospital but inefficient business operations are holding your clinic back?

If you don't know where to start, how to start, or what you need to know to take your clinic to the next level, this free 4-part mini-course is for you.

This mini-course is taught by Dr. Michael White, MD, MMM, CWS, UHM and course director for the live two-day workshop, The Business of Wound Care and Hyperbaric Medicine.

You Will Learn:

Lesson 1: [Video] How to create a strong (or stronger) foundation for your clinic business

  • How to identify where your patient referrals are coming from (or should be coming from).
  • How to create an action plan for effective, efficient marketing.
  • How to become a profit center for the hospital.

Lesson 2: [Video] The explosion of chronic wounds in the U.S. and the opportunity for wound care and hyperbaric medicine clinics to serve more patients.

Lesson 3: 4 Easy steps to market your clinic.

Lesson 4: How key are front office operations to the wound clinic business?

  • Learn the two key considerations for creating efficient front office operations that contribute to the achievement of your clinic's overall financial goals.
Join us for this free 4-part mini-course and jump start your clinic business today! 

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Oxygen, Hyperbaric Oxygen, and Free Radicals Wound Management Considerations

  • Michael B. Strauss, MD and Stuart S. Miller, MD
  • Volume 06 - Issue 1

Introduction

No one questions the roles oxygen has in wound healing. In almost every aspect of wound healing, from the inflammatory process to remodeling and from tissue survival to infection control, adequate tissue oxygen tensions are essential. The roles of hyperbaric oxygen (HBO), however, are not as well defined. When wound healing is not progressing in a normal fashion and ischemia/hypoxia is a contributing factor, it makes sense to use HBO as an adjunct to manage this aspect of the problem. Even more controversial is the role of free radicals in wound healing and whether the production of free radicals by HBO is detrimental to healing and survival. This article addresses these three aspects of the oxygen molecule spectrum and dispels misconceptions about the harmful nature of free radicals.

Things to Know about Oxygen

The chemical element oxygen has many unique features. It has the ability to oxidize almost any organic substance to modify it. It does this by “gob- bling up” electrons from the compound, which defines oxidation. It also actively forms oxides with inorganic elements such as iron, which results in the rusting process. No other element is so active in the degrading/oxidizing process. As “destructive” as oxygen is, life as we know it would not exist on earth without oxygen. The question is how is this paradox resolved? The answer is that defenses against oxygen were developed as evolution of life on Earth progressed. As Nick Lane said in Oxygen: The Molecule that Made the World, oxygen is the "elixir of life —and death."1  Much is known about the role of oxygen in wound healing. A gradient exists from inspired oxygen tensions of 160 mmHg while breathing air to 0.5 mmHg in the mitochondria (Table 1). This is a 99.7 percent decrease in oxygen tensions from the start to the end of the gradient. Without the 0.5 mmHg oxygen tensions in the mitochondria, energy for cell metabolism will not occur. Consequently, any interference in the oxygen tension at each step of the gradient can be detrimental to mitochondrial function. Clinical conditions that ultimately interfere with oxygen delivery to the mitochondria occur at each level of the gradient (Table 2).

Table 1: Oxygen Fall-off from Inspired Air to the Mitochondria

6-1-Oxygen-HBO-table-1

The chemical structure of oxygen is such that its nucleus of 8 protons and 8 neutrons sits in a protective shell (also seen in helium, calcium, nickel, tin, lead, and other heavier elements), which makes its molecular form very stable and prevents decay into other elements. This accounts for oxygen being the third most common element in the universe, second only to hydrogen and helium.
What is more pertinent with respect to oxygen’s reactivity is its electron cloud. The lowest tier energy level, the s-shell, is spherical and filled with two electrons. The next energy level/shell, the p- shell, can hold 8 electrons. However, in oxygen’s case, it has 6 electrons. Consequently, it aggressively seeks 2 additional electrons to fill this shell and stabilize the shell’s energy state. This makes oxygen the most active chemical element in “gobbling up” electrons to combine with or to degrade other elements and compounds.
In contrast, carbon forms bonds with itself and other elements because carbon (element 6) has 4 electrons left over and needs 4 more electrons to fill its p-shell. This explains the variety of permutations and combinations of carbon bonding and the ability to form an almost infinite number of organic compounds.

From the wound healing consideration, the tissue fluid oxygen tension is the one that is so critical for healing. Hunt (1969) confirmed that in order for fibroblasts to function and for wounds to heal, the tissue oxygen tension needs to be in the 30- 40 mmHg range (Figure 1).2 Healing is unlikely to occur below 30 mmH; above 40 mmHg healing is likely. Failure for wounds to heal with oxygen tensions 40 mmHg or greater indicate that other potential causes of non-healing, such as bioburden, deformity, inadequate protection/stabilization, malnutrition, cicatrix/bursa barriers to angiogenesis, matrix metalloproteins, and/or inadequate protection/stabilization, are also present.

It is remarkable that oxygen and its compounds carbon dioxide and water are the critical substances that maintain the higher forms of life on Earth. While oxygen is necessary for generating energy through ATP (adenosine triphosphate) as is needed for all cellular processes in higher organisms, its waste product is carbon dioxide.
It is almost mind-boggling that carbon dioxide, water, and sunlight are the essential ingredient of photosynthesis, and the end products of photosynthesis are oxygen and glucose. A structure somewhat analogous to the mitochondrion, the chloroplast, a member of the plasmid family, is responsible for this remark- able conversion. Chloroplasts are the energy generating organelles of plants and generate energy by chemiosmotic mechanism similar to mitochondria. Consequently, while oxygen is essential for animal metabolism, carbon dioxide is essential for plants. Together, they help maintain the Earth’s oxygen/carbon dioxide atmosphere in balance.

 

Table 2: Conditions that Interfere with Oxygen Availability to the Mitochondria

Tissue Level Conditions
Lungs Ventilation-perfusion inequalities, obstructive lung disease
Arteries Atherosclerosis, vasoconstriction, shunting, anemia
Capillaries/Red Blood Cells Thickening of the basement membrane, sludging, hemoglobinopathies
Tissue fluids Relative barriers; e.g., edema, cicatrix, bursa, exudates
Cells Neoplasms

 

Oxygen, the “elixir of life,”  is  not  only  required for wound healing—its intracellular tensions and radicals  generated  by  biochemical  reactions are an integral part of many other cellular processes. These range from maintaining consciousness to initiating angiogenesis and from intermediary metabolism (Krebs cycle) to white blood cell oxidative killing. For example, during the oxidative burst in the neutrophil phagocytic vesicle, oxygen consumption increases 100-fold or more to kill bacteria through the generation of superoxides and peroxides.3,4 Oxygen is carried to every cell in the body by the bloodstream through a “loose” attachment to the iron in the hemoglobin molecule. With high oxygen tensions, as in the lungs, oxygen attaches to the hemoglobin molecule. In the tissues, oxygen diffuses through the capillary to the lower oxygen tension tissue fluids and into the cell. The physiology is explained by the Henderson-Hasselbalch equation and the biochemistry by oxygen attachment to iron to convert it to the ferric state in the oxygen-rich lung environment and release of oxygen and conversion to the ferrous state because of the lower oxygen tension tissue fluids.

As the “elixir…of death,” oxygen, when not physiologically regulated, is harmful and can kill every cell in the body. Obviously, too low oxygen tensions result in interference with cell function, which has important ramifications for wound healing. With low oxygen tensions, the cell  goes  into  a  state of suspended animation (hibernation). While not dead, it is not functioning at a level where it can continue its physiological functions. For the fibroblast, this means the arrest of wound healing; however, with restoration of adequate oxygen tensions it can recover these functions. This, of course, is the justification for revascularization and hyperbaric oxygen therapy (discussed in the next section). Oxygen tensions below a certain point for a sustained period of time result in cell death and no chance of return of function. A big question is whether oxygen utilization for metabolism, analogous to combustion, is ultimately responsible for the cell’s death just as after the consumption of all combustible material, the fire ceases to burn. Cells are programmed to die, i.e., apoptosis, at specific times. Is this because oxidation eventually “burns out” every cell in the body and results in the death of the organism?

Oxygen percentages over 17 percent are required for a fire to burn regardless of the oxygen tension. This contrasts to the extraction of oxygen from inhaled air in the lungs, where the partial pressure of oxygen (reflected in the number of molecules breathed) is essential for adequate oxygenation of tissues. The following examples further illustrate this chemistry and physiology.
In 1967 three astronauts were cremated when the space module (which was on the ground  at the time) was pressurized with pure  oxygen at 0.4 ATA (atmospheres absolute), and a spark set off an explosion from the combustible materials in the capsule. Not only did the combustible articles burn in the pure oxygen environment, they were explosive even though the partial pressure of oxygen was 0.4 of an atmosphere. The reason for using hypobaric pure oxygen was to reduce the additional weight of the 80 percent nitrogen contained in air.
In contrast, for diving studies at a thousand- foot depth, 1 percent oxygen is breathed while the remainder of the gas mixture is helium with a little added nitrogen At this depth the partial pressure of oxygen is more than 160 mmHg— sufficient to meet the lungs’ requirement for ventilation. Conversely, it would not be possible to kindle a flame in this 1 percent oxygen mixture.

Figure 1: Oxygen Tensions Necessary for Wound Healing

6-1-Oxygen-HBO-Figure-1

Legend: Oxygen is required for fibroblasts to elaborate their functions of secretion and collagen formation. If deficient, the fibroblast may remain viable but not function for angiogenesis, a matrix needs to be generated by the fibroblast so capillary budding can grown into it and advance the blood supply.

Things to Know about Hyperbaric Oxygen

Too much oxygen is likewise harmful, the other aspect of the “elixir…of death.” Sustained periods of breathing 100 percent oxygen can cause pulmonary edema. Hyper-physiological doses of oxygen, as achieved with hyperbaric oxygen, are toxic to every cell in the body. The target tissue for this side effect is the brain, and the consequence of this toxic insult is the oxygen-induced seizure. Intermittent exposures and air breaks while breathing HBO mitigate this side effect. Why seizures occur with increased oxygen tensions of the brain is not clear. Some attribute it to hyper-metabolism just as increased oxygen percentages cause a fire to burn more vigorously. Another idea (which will be further elaborated later) is that the scavengers of the reactive oxygen species are overwhelmed by the free radicals generated by the hyperbaric oxygen exposure.

The mechanisms of hyperbaric oxygen are support- ed by physics and physiology.5.6 Hyperbaric oxygen at 2 ATA (33 FSW) increases the inhaled oxygen partial pressure tenfold from 160 mmHg partial pressure of oxygen to over 1600 mmHg. This increases the oxygen diffused from the alveolus to the plasma of the alveolar capillary tenfold but does not change the hemoglobin-carried oxygen of the red blood cell since in the absence of lung disease and/or red blood cell diseases, it would already be approaching 100 percent.

In room air, 97.5 percent of the oxygen in the blood is carried by the hemoglobin in the red blood cell and 2.5 percent is physically dissolved in plasma. With hyperbaric oxygen, the tenfold increase in plasma oxygen adds 25 percent to the blood’s oxygen carrying capacity. All oxygen delivery (as well as nutrients) to cells, be it from hemoglobin or physically dissolved in the plasma, must first diffuse through the capillary, then through tissue fluids, to the cell. The oxygen diffusion is in response to gradients, which are high in the blood, lower in the tissue fluids, and lowest in the cell. With HBO the tenfold increase in plasma oxygen content supplements the hemoglobin-carried oxygen and mitigates conditions where blood flow, hemoglobin-carried oxygen, or diffusion distance problems interfere with oxygen delivery to the cell (Figure 2). Under HBO conditions enough oxygen is physically dissolved in the tissue fluids to meet cellular oxygen requirements in the absence of hemoglobin-carried oxygen.

Another method of increasing the partial pressures of oxygen above physiological levels is through SCUBA diving. SCUBA diving to 100 feet of sea water (fSW) increases the oxygen partial pressure of the inhaled air fourfold,  which is nearly equivalent to breathing pure oxygen at sea level. While this is tolerated for the relatively short durations of the SCUBA dive, saturation diving (in an underwater habitat) at 100 fSW requires reducing the oxygen percentages of the breathing gas in order to prevent oxygen toxicity.
With closed circuit rebreathers the likelihood of oxygen toxicity, especially seizures, is much greater. When breathing pure oxygen in a re- breather unit, depth and time durations are strictly limited. for example, a 30 fSW dive is limited to 30 minutes, while shallower dives can have longer durations.
Mixed-gas closed circuit rebreathers are designed to provide a constant partial pressure of oxygen regardless of the depth. To accommodate the increased ambient pressures with descent, increased percentages of the diluent gas are added to the breathing loop. Seizures may occur from errors in setting the oxygen partial pressures. In addition, the breathing mixture may be switched to pure oxygen near the surface to has- ten off-gassing of the inert gas. However, if done prematurely, for example at a depth greater than 30 fSW, an oxygen seizure may occur.
In 1959 Boerema et al. demonstrated that piglets who had their red blood cells removed could be kept alive and functioning for brief periods (15 minutes) with physically dissolved oxygen in their plasma.7 The end-point of the study was carbon dioxide accumulation rather than oxygen deficiency.
This study dispelled the “Haldane hex,” which contended that cells could only utilize oxygen that was hemoglobin borne. Boerema’s study gave the use of hyperbaric oxygen a solid physiological basis and ushered in the modern area of HBO therapy. for this seminal contribution, we refer to Dr. Boerema as the father of hyperbaric medicine.

Oxygen diffuses through relative barriers poorly, especially as compared to carbon dioxide. Carbon dioxide’s ability to diffuse through tissue fluid is 20-times greater than that of oxygen. Commonly encountered relative barriers include atherosclerotic vessels, which interfere with perfusion; thickened capillary membranes, which slow diffusion through the endothelium; edema fluid, which increases the diffusion distance from the capillary to the cell; and cicatrix, which acts as an obstruction (Table 2). The tenfold increase in tissue fluids achieved with HBO promotes oxygen tissue diffusion through these barriers, which are considered relative because they can vary in extent from inconsequential to totally obstructing oxygen availability to the cell.

An example of a relative barrier is that of edema associated with stasis ulcers. The more severe the edema, the more likely a stasis ulcer will develop. The pathophysiology of the ulcer etiology can be multifactorial such as from trauma, venous stasis disease, atrophic/friable skin, loss of skin elasticity with aging, hemosiderin deposition in the subcutaneous tissues, cicatrix formation from ischemia/hypoxia of the underlying tissues, and/or insufficient perfusion to allow healing.
 
Regardless of the cause, a primary intervention in managing the stasis ulcer is that of reducing edema through use of elastic wraps, elastic support hose, leg compression pumps, and/or diuretics. The reduction of edema reduces the distance oxygen has to diffuse through tissue fluids to reach the ulcer wound bed.
 
While everyone attests to the benefit of edema reduction in managing stasis ulcers, the beneficial role of reducing oxygen diffusion distance through tissue fluids to improve oxygen delivery to the ulcer and promote healing must not be overlooked.

Figure 2: Blood Oxygen Content, Hyperbaric Oxygen and "Life without Blood"

Oxygen-HBO-figure-2

Legend: The physically dissolved oxygen from the hyperbaric oxygen exposure adds to the hemoglobin-carried oxygen. Once the hemoglobin-carried oxygen becomes fully saturated it cannot carry additional oxygen. At about a 2000 mmHg oxygen partial pressure there is enough oxygen content in the plasma to meet oxygenation requirements without hemoglobin-carried oxygen. This was demonstrated by Boerema's "Life without Blood" experiment.

Key: A-V O2 = arterial-venous oxygen extraction, HBO = hyperbaric oxygen, Rx = treatment, w/o = without

 

In our experience, there are three fundamental reasons why wounds, especially diabetic foot ulcers, do not heal in the usual and customary fashion.8 These are failure to address adequately the underlying deformity; persistence of deep infection of bone, cicatrix, and/or bursa; and ischemia/hypoxia. Of the three, the confirmation of ischemia/ hypoxia is perhaps the easiest. This can be ascertained with the clinical exam (e.g., palpable pulses, Doppler pulses, skin coloration and temperature, and capillary refill time), imaging studies, and juxta-wound transcutaneous oxygen measurements (TCOMs). As mentioned before, tissue fluid oxygen tensions in the 30-40 mmHg range are needed for wounds to heal.2 Juxta-wound TCOMs measure and reflect the tissue fluid oxygen tensions and can be used as a guide to determine whether the ischemic/hypoxic wound will heal or if measures to increase perfusion/oxygenation are needed.

Hyperbaric oxygen is an intervention to increase wound oxygenation (in addition to revascularization, edema reduction, improved cardiac function, and pharmacological agents).9 The value of using TCOMs to predict healing with use of HBO as an adjunct to manage wound hypoxia and achieve healing is established. We reported that hypoxic wounds (that is, wounds with juxta-wound TCOM levels in room air of less than 40 mmHg) heal in 87 percent of cases if the TCOMs increase to 200 mmHg or greater with HBO exposure and HBO treatments are subsequently used in wound management.12 This information using TCOMs objectifies the indications for HBO in problem wounds.

The origin of the 200 mmHg oxygen tension with HBO for predicting healing of the hypoxic wound is attributed to Dr. George B. Hart. In the 1990s TCOMs became available but predictions for healing with HBO ranged from 300 to 900 mmHg oxygen tensions.
In the late 1990s Dr. Hart was queried as to what juxta-wound TCOM value was needed for healing to occur with HBO treatments. from his keen observations he gave the number of 200 mmHg. In the 1997 and 1998 Annual Undersea and Hyperbaric Medical Society meetings we presented posters from our observations demonstrating the validity of the 200 mmHg number in increasing series of patients.11,12 This work culminated in our 2002 Foot & Ankle International prospective peer reviewed publication with a study group of 82 patients who had TCOMs less than 30 mmHg in room air.12
In reviewing the history of the predictive value of the 200 mmHg number for healing of the hypoxic wound with HBO, we found that this value was also used in a paper by fife et al. in 2002.12 In their review of over 1100 patients with many permutations such as using 100 percent surface oxygen, leg elevations tests, etc., it was unclear how they derived the 200 mmHg number stated in their conclusions.

Hyperbaric oxygen has applications to many other medical conditions in addition to hypoxic wounds. The indications for using HBO in other conditions are based on its mechanisms. We divide the mechanisms into primary and secondary.5,6 The primary mechanisms hyperoxygenation and pressurization (to reduce bubble size) are immediate and act in  a drug dose-duration fashion. Applications in addition to decompression sickness and arterial gas embolism include threatened flaps, acute blood loss anemia, acute peripheral ischemia, burns, crush injuries and compartment syndromes, and central retinal artery occlusions. Secondary mechanisms occur as a result of hyperoxygenation and pressurization acting on body tissues and microorganisms. In contrast to the dose-duration effects of the primary mechanisms, the effects of the secondary mechanisms tend to be additive and require repetitive HBO treatments. They include edema reduction, stimulation of host healing responses (including fibroblast function and angiogenesis), gas washout (for carbon monoxide poisoning and decompression sickness), reperfusion injury, delayed radiation damage of soft tissue and bone, cerebral abscess, refractory osteomyelitis, gas gangrene, and necrotizing soft tissue infections. Awareness of the mechanisms of HBO helps justify its use. In addition, mechanisms of HBO may have applications to current off-label uses of HBO such as acute brain and spinal cord events, sports injuries, osteonecrosis, and fracture healing.

Things to Know about Free Radicals and Hyperbaric Oxygen

For decades researchers have known that highly reactive molecules called free radicals cause ag- ing by damaging the DNA (deoxyribonucleic acid) of cells and thus disturbing the carefully regulated functions of tissues and organs. Free radical formation is an integral part of intermediary metabolism (Krebs cycle) and, with glucose plus oxygen, provides the energy for cell metabolism, cell/tissue function, and generation of cell products. In addition, free radicals generated by the phagosomes in the neutrophil kill bacteria. How- ever, reactive oxygen species in the wrong place  or in super-physiological numbers damage tissues. This is observed with radiation injury and ischemia-reperfusion injury. There is increasing recognition that cardiovascular diseases, neurodegenerative diseases such as Alzheimer’s and chronic inflammation, apoptosis, and necrosis have oxidative stress components.

With evolution, cells have generated antioxidants (oxygen radical scavengers) to mitigate oxidative stresses. This phenomenon is so important that Lane asserts that life would not have evolved to its present form without the generation of antioxidants to “tame” the highly reactive oxygen radicals it generates.1 Defenses to mitigate the oxidative stresses include vesicles such as the mitochondrion shell, which contains the reactive oxygen species as glucose is metabolized to generate energy, and allows the train of reactions to proceed in a regulated fashion. The other mechanism to handle reactive oxygen species is the generation of antioxidants such as glutathione peroxidase and superoxide dismutase.

While HBO is believed to generate reactive oxygen species, oxygen is required for the generation of oxygen radical scavengers.14 Consequently, in the hypoxic environment insufficient oxygen to generate the oxygen radical scavengers may cause damage such as cell death and tissue necrosis, which is always of concern in problem wounds. Much is known about oxygen radical scavengers/ antioxidants, oxygen transporters, and reactive oxygen species.15 For example, 84 genes in the human genome are related to oxygen stresses.

A number of vitamins have been promoted as antioxidants and purported to be useful in preventing aging such as vitamins E, C, and A. Vitamin E in particular was promoted for this purpose. It also had been used in conjunction with HBO treatments to prevent oxygen seizures.
Vitamin E is no longer recommended for preventing seizures with HBO, because seizure rates are so low with clinical HBO treatments that they are almost a non-occurrence. When a seizure does occur, it is usually associated with hypoglycemia in the diabetic patient or non- therapeutic doses of anticonvulsants in the patient with a seizure history.

Reactive oxygen species may have salubrious effects with respect to longevity and disease prevention. There is increasing appreciation of noncoding DNA sequences (epigenes, or “junk” genes) as being able to influence genetic information through the expression of DNA. The physiological reactive oxygen species generated by HBO could be one of the “missing links” in our understanding of how they are beneficial to the organism. Reactive oxygen species may remove damaged DNA segments that lead to aging, diseases, neoplasms, or prevent wound healing.

A “take home” observation of this is seen in the exuberant callus formation that recurs debridement after debridement, especially in the diabetic foot ulcer. Even after the wound heals, the exuberant callus returns as if the message system to form callus persists, suggesting that epigenes have influenced the DNA associated with callus formation.

Animal studies have shown that longevity is in- creased in animals genetically altered and missing antioxidant enzymes.16 In addition, those animals that overproduced superoxides lived 32 percent longer than the controls. The longest living rodent, the naked mole rat, is able to survive 25 to 30 years, has lower levels of antioxidants than similar sized rodents, and remains disease free eight times longer. The hypothesis to explain this observation was that the mole rat accumulates more oxidative damage to their tissues at an earlier age, so only the most healthy individuals survive. A herbicide that generates free radicals resulted in worms living 58 percent longer than untreated animals.

This may support the “survival of the fitness” concept, that the young organism should be exposed to a constellation of diseases to “train” their immune systems. Epigenes may influence DNA to generate the antibodies, etc., and free radicals may “turn on” the epigenes so at a young age the organism becomes immunologically privileged, ensuring the longest possible survival.

Conclusions

Oxygen is a remarkable molecule; too little is lethal and too much is lethal. Organisms have generated remarkable mechanisms to maintain oxygen in physiological settings. Hyperbaric oxygen may alter these protective responses on one hand and on the other may make them more effective. The role of reactive oxygen in wound healing has hardly been addressed, but much is known about its role in killing bacteria. We are not quite ready to recommend sleeping in the pressurized HBO chamber, but if HBO modestly generates reactive oxygen species to turn on epigenes to influence DNA messaging which, in turn, mitigate disease processes, many new roles for HBO can be expected.

References

  1. Lane N. Oxygen: The Molecule that made the World. New York: Oxford University Press; 2002. P. 1-15.
  2. Hunt TK, Zederfeldt B, Goldstick TK. Oxygen and healing. Am J Surg. 1969;118:521-5.
  3. Sabarra AJ, Karnovsky MI. The biochemical basis of phagocytosis. I. Metabolic changes during the ingestion of particles by polymorphonuclear leu- kocytes. J Biol Chem. 1959; 234(6):1355–62.
  4. Sabarra AJ, Karnovsky MI. The biochemical basis of phagocytosis. II. Incorporation of C14-labeled building blocks into lipid, protein, and glycogen of leukocytes during phagocytosis. J Biol Chem. 1960; 235(8):2224-9.
  5. Strauss MB, Hart GB, Miller SS, et al. Mechanisms of hyperbaric oxygen. Part 1 primary: hyperoxygenation and pressurization. Wound Care & Hyperbaric Medicine. 2012; 3(3):27-42.
  6. Strauss MB, Hart GB, Miller SS, et al. Mechanisms of Hyperbaric Oxygen. Part 2 secondary: consequences of hyperoxygenation and pressurization. Wound Care & Hyperbaric Medicine. 2012; 3(4):45-63.
  7. Boerma I, Meyne MG, Brummelkamp  WK,  et al. Life without blood. A study  of the influence of high atmospheric pressure and hyperthermia on dilution of the blood. J Cardiovas Surg. 1960; 1:133-46.
  8. Strauss MB, Aksenov IV, SS Miller. MasterMinding Wounds. North Palm Beach, FL: Best Publishing Company; 2012. P. 27-8.
  9. Strauss MB, Miller SS, Aksenov IV, Manji K. Wound oxygenation and an introduction to hyperbaric oxygen therapy: interventions for the hypoxic/ischemic wound. Wound Care & Hyperbaric Medicine. 2012; 3(2):36-52.
  10. Strauss MB, Breedlove JW, Hart GB. Use of Transcutaneous oxygen measurements to predict healing in foot wounds. Undersea Hyperb Med. 1997; 24(Abst 40):15.
  11. Strauss MB, Winant DM, Breedlove JW, et al. The predictability of transcutaneous oxygen measurements for wound healing. Undersea Hyperb Med. 1998; 25(Abst 28):16.
  12. Strauss MB, Bryant BJ, Hart GB. Transcutaneous oxygen measurements under hyperbaric oxygen conditions as a predictor for healing of problem wounds. Foot Ankle Intl. 2002; 23:933-7.
  13. Fife CE, Buyukcakir C, Otto G, et al. The predictive value of transcutaneous oxygen tension measurements in diabetic lower extremity ulcers treated with hyperbaric oxygen therapy: a retrospective analysis of 1144 patients. Wound Repair Regen. 2002; 10:198-207.
  14. Ferrari R, Ceconi C, Curello S, et. al. Oxygen- mediated myocardial damage during ischaemia and reperfusion: role of the cellular defences against oxygen toxicity. J Mol Cell Cardiol. 1985 Oct;17(10):937-45.
  15. Oxidative stress and antioxidants as biomarkers, [This email address is being protected from spambots. You need JavaScript enabled to view it.], 25 FEB 2015.
  16. Moyer MW. The myth of antioxidants. Scientific American. 2013;308(2): 62-7.

About the Authors

Drs. Strauss and Miller are physicians at the Hyperbaric Medicine Department at Long Beach Memorial Medical Center. Additional biographical information can be found after their diving article on page 33. The authors would like to acknowledge Dr. Phi-Nga Jeannie Le for her editorial contribution to this article.

 

 

 

How to Make Your Hyperbaric Medicine Practice Stand out from the Pack

  • Best Publishing Company DEPTH Blog
  • Volume 06 - Issue 1

Each of us in the field of hyperbaric medicine wants to create an exceptional practice. Part of creating a practice that makes you “stand out from the pack”  is finding a continuing education program to keep you up-to-date on cutting edge medical advances in hyperbaric medicine and growing your network of industry colleagues to help take your practice to the next level of success.

Our colleagues at the Mayo Clinic have organized a team of experts in hyperbaric medicine for a unique two-day 16.0 hour CME/MOC accredited event on April 17-18, 2015 in Rochester, Minnesota titled Hyperbaric Medicine 2015.

CONFERENCE DETAILS
Hyperbaric Medicine 2015
April 17-18, 2015
Mayo Clinic, Rochester, MN
Website: https://ce.mayo.edu/preventive-medicine/node/1825
Phone: 800-323-2688
email: This email address is being protected from spambots. You need JavaScript enabled to view it.

The Mayo Clinic in Minnesota has been recognized as the best hospital in the nation for 2014-15 by U.S. News and World Report. They are a nonprofit worldwide lead- er in medical care, research, and education for people from all walks of life.

Conference topics will include:

  • HBO2 therapy in lower limb crush injury, compromised flaps, and deep tissue infections
  • Osteomyelitis and infected prosthetic materials
  • ICU equipment support (ventilators, monitors, and IV pumps)
  • The integration of hyperbaric safety checklists and procedures in electronic medical record systems

Participants will enjoy two bonuses included free with their registration:

  • Tour of Mayo Clinic's multiplace program and interactive session of sharing best practices in hyperbaric medicine
  • Access to the course material, which includes a full conference slide set for your clinic's educational use, for up to 1 year after the course

from Paul Claus, MD, UHM, course director for Hyperbaric Medicine 2015:

“Our speakers are leading experts in the field of hyperbaric medicine as well as specialized prac- tices of plastic /transplant surgery, critical care / anesthesia, hyperbaric nursing, biomedical equip- ment modification, and evidence-based medicine research. You will leave with a greater network  of hyperbaric colleagues, the knowledge to take your clinical practice to the next level of success AND a full conference educational slide set for use in your own staff educational tool chest!”

If you’re serious about taking your practice to the next level in 2015, we encourage you to consider attending this conference. Registration is open now!

CME - AMA PRA Category 1 Credits™ - maximum of 16 (Program) and 5 (Self-assessment) American Academy of Family Physicians - up to 16.00 prescribed credit(s).

MOC/ABPM – This activity is approved by the American Board of Preventive Medicine (ABPM) for Maintenance of Certification (MOC) credit for a maximum of 16.0 LLSA/MOC credits.

NBDHMT - Approved by the National Board of Diving & Hyperbaric Medical Technology for 16 Category ‘A’ credits.

Sinus and Ear Disorders that Take Place during Hyperbaric Oxygen Therapy

  • Emanuele Nasole, MD; Antonio Paoli, MD, BSc; Gerardo Bosco, MD, PhD; and Enrico Camporesi, MD
  • Volume 06 - Issue 1


Sinus and internal and external ear disorders are the most common side effects of hyperbaric oxygen therapy (HBO).1 These spaces are the cranium’s pneumatic sockets and, particularly those of the middle and inner ear, are most frequently involved in the pressure stress caused by compression and decompression maneuvers during exposure to altered pressures in the hyperbaric chamber. Barotrauma is the mechanical tissue damage produced by environmental pressure variation, and the middle ear is the most frequently involved structure in this kind of damage. According to Boyle’s law (the product of pressure and volume is a constant for a given mass of confined gas) it is easy to understand why all enclosed air cavities are more susceptible to this kind of lesion. Barotraumas can occur due to an increase or decrease of gas volume. To avoid gas volume decrease during the compression phase, the patient must perform some compensatory maneuvers aimed at inhaling and forcing gas (air or oxygen) into the nasal and sinus cavities. During decompression in the chamber or even underwater, the body’s gas expands and is expelled from cavities to the outside, usually without any active maneuvers.

It is essential to teach the patient about the functions of the hyperbaric chamber and the correct maneuvers of baro compensation. In this article, we will describe the main barotraumas that can occur during HBO2.

External Ear Barotrauma (EEB)

In normal conditions, the caliber of the external auditory canal is sufficient to allow immediate pressure compensation. An EEB can only happen if the external auditory meatus is blocked by an obstacle, such as impacted earwax, external otitis, or ear plugs, during chamber compression. In this case during compression the obstacle prevents the equilibration between outside and inside pressure. During the compression phase there is a reduction of volume both in the plugged external ear and in the middle ear spaces. This leads  to edema and petechial hemorrhages of the auditory tube, middle ear, and tympanic membrane. Rare complications include ear bleeding and tympanic perforation. Symptoms include acute pain, deafness, vertigo, nausea, and ear bleeding. The treatment therapy consists of antibiotics and topical steroids.

Middle Ear Barotrauma (MEB)

The most common side effect of HBO2 is middle ear barotrauma.2,3 MEB is more common during compression, while during decompression it is less likely to be reported. MEB during compression is a more pathological event and is related to a failed compensatory maneuver to relieve pressure between the middle ear and Eustachian tubes. The incidence of reported MEB varies between different hyperbaric centers from 5 to 66.7 percent.4,5 This difference is due to the heterogeneous population sample (intubated patients vs. spontaneous breathing patients) or to other causes.

Other common causes of MEB include the presence of diseases of the upper respiratory tract that generate obstructions of the Eustachian tube (e.g., infectious rhinitis and allergic and nonallergic rhinitis; ingestion of alcohol, which causes nasal congestion; large nasal polyps; large septal deviations; tobacco smoke; use of beta blockers and parasympathomimetic drugs; etc.) and incorrect or delayed compensation techniques.

Depression of the middle ear tympanic membrane during the chamber  compression  begins to appear at a pressure of 1.2–1.3 atmospheres absolute (ATA) with reduction of the volume of endotympanic gas by 20-30 percent of the initial volume. There is a retraction of the tympanic membrane with pain, hyperemia, and edema of the ME mucosa that could lead to hemorrhage and cause the tympanic membrane to rupture. This generally produces a grade 1 or 2 MEB (according to the Teed classification) in more than 90 percent  of patients; about 20 percent of patients with ear pain show tympanic membrane alterations short of perforation (MEB >grade 1).

MEB is prevented in most patients by teaching autoinflation techniques or by use of tympanostomy tubes for those who cannot autoinflate their middle ear compartment. A prospective study in patients treated with HBO2 demonstrated that many patients develop serous otitis media  during serial treatments. A history of Eustachian tube dysfunction predicted serous otitis media.6 Pseudoephedrine has been demonstrated to be effective in preventing barotitis media in a double-blind randomized controlled clinical trial in underwater divers.7 Conversely, topical nasal oxymetazoline hydrochloride was found to be ineffective in preventing middle ear barotrauma during HBO2.8

Other Complications

Sinus squeeze is the second most common in- chamber complication4 and usually occurs in patients with upper respiratory tract infections or allergic rhinitis. Usually a program of decongestant nasal spray, antihistamines, and/or steroid nasal spray just before compression allows the hyperbaric therapy to continue.

Serous otitis has been reported in patients receiving HBO2 therapy.8 Although once thought to be due to reduced middle ear pressure by oxygen resorption, there is evidence to suggest that HBO2 might cause a reversible derangement in a middle ear chemoreceptor reflex arc that may regulate middle ear aeration.9

Hyperbaric Experience in Monoplace Chambers

Specific considerations for patients treated in monoplace chambers have been recently summarized in an analysis of adverse events using data from all Diversified Clinical Services centers operating for the period of 2009–2010.1 Diver- sified Clinical Services (now Healogics) provides management services to 340 hospital-based out- patient wound care centers, of which 89 percent provide outpatient hyperbaric oxygen  treatment to diagnoses limited to those listed in the UHMS Hyperbaric Oxygen Therapy Indications. Adverse event data was collected concurrently in a central proprietary database.1

The primary adverse event categories were ear pain, confinement anxiety, hypoglycemic events, shortness of breath, seizures (including both oxygen toxicity and hypoglycemic event seizures), sinus pain, and chest pain. Reporting data was reviewed from 463,293 monoplace hyperbaric oxygen treatments provided in hospital-based outpatient settings involving 17,267 patients (an average of 27 treatments per patient). The majority of these patients received hyperbaric oxygen treatment for diabetic limb salvage or complications associated with prior radiation therapy.

In 2009 there were 916 adverse events reported for 207,479 treatments in 7,871 patients, an overall adverse event rate of 0.44 percent. In 2010 there were 954 adverse events reported for 255,814 treatments in 9,396 patients, an overall adverse event rate of 0.37 percent. In order of decreasing rate of occurrence were ear pain (of any description), confinement anxiety, hypoglycemic events, shortness of breath, seizures (including both oxygen toxicity and hypoglycemia- related seizures), sinus pain (of any description), and shortness of breath. There was no significant difference in the number or ranking of adverse events between 2009 and 2010. In this series of treatments, all patients received a standardized medical evaluation prior to initiating treatment, standardized pretreatment education, and a standardized assessment prior to each treatment. The consistent attention to detail may be the cause of such a low rate of complications.

References

  1. Beard T, Watson B, Barry R, Steward D, Warriner R. Analysis of adverse events occurring in patients undergoing adjunctive hyperbaric oxygen treatment: 2009-2010 (Abstract). Undersea Hyperb Med. 2011;38(5):455.
  2. Davis JC, Dunn JM, Heimbach RD. Hyperbaric medicine: patient selection, treatment procedures, and side effects. In: Davis JC, Hunt TK, eds. Problem wounds: the role of oxygen. New York: Elsevier; 1988. P. 225-35.
  3. Davis JC. Hyperbaric oxygen therapy. J Intensive care Med 1989; 4:55-7.
  4. Bessereau J, et al. Middle-ear barotrauma after hyperbaric oxygen therapy. Undersea Hyperb Med. 2010. 37(4): 203-8.
  5. Karahatay S, et al. Middle ear barotrauma with hyperbaric oxygen therapy: effect on middle ear and Eustachian tube function. Laryngoscope 1992;102:48-52.
  6. Brown M, Jones J, Krohmer J. Pseudoephedrine for the prevention of barotitis media: a controlled clinical trial in underwater divers. Ann Emerg Med. 1992; 21:849-52.
  7. Carlson S, Jones J, Brown M, Hess C. Prevention of hyperbaric-associated middle ear barotrauma. Ann Emerg Med. 1992; 21:1468-71.
  8. Shupak A, Atias J, Aviv J, Melamed Y. Oxygen diving induced middle ear under-aeration. Acta Otolaryngol Stockh. 1995;115: 422-26.

 

About the Authors

Emanuele Nasole, MD, hyperbaric physician, Peschiera, Verona, Italy

Antonio Paoli, MD, BSc Associate Professor

Gerardo Bosco MD, PhD, Assistant Professor, Environmental Physiology and Medicine lab, Department of Biological Sciences, University of Padova, Italy

Enrico M. Camporesi MD, TeamHealth Anesthesia, Research Institute, Tampa General Hospital

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