An Introduction to hyperbaric oxygen therapy
Hello! I am Dr. Jeffrey Niezgodo, the Medical Director for the Center for Comprehensive Wound Care and Hyperbaric Oxygen Therapy located at St. Lukes Medical Center in Milwaukee, Wisconsin. I would like to thank you for joining me in this presentation entitled 'An Introduction To Hyperbaric Oxygen Therapy.
As a starting point, I would like to provide a brief overview of this lecture. First, we will start by discussing compromised wound healing. We need to understand what compromises healing in our patients and how oxygen and wound healing are interdependent before understanding the role of hyperbaric oxygen therapy in the management of patients with compromised wounds. WE will discuss hyperbaric oxygen therapy in detail after we build a foundation for understanding how oxygen plays an important role in wound healing. We will define hyperbaric oxygen therapy, discuss in detail the physiology of this therapeutic mechanism, we will discuss the indications and contraindications for the use of hyperbaric therapy in our patients, and finally I will provide a brief history tour of how hyperbaric therapy has been used over the years.
So, let us start by discussing compromised wound healing. Here is a photograph of a patient of mine who certainly meets the criteria for compromised wound healing. He had a chronic wound based on multiple processes. He presented with a necrotizing soft tissue infection. These _______ incisions exit through the plantar surface of his foot. You can see the Penrose drain draining through the plantar wound. He had underlying osteomyelitis and he has already lost his great toe to the ravages of diabetes. This patient clearly is going to be difficult from the healing standpoint.
Often times, the patients who have compromised wound healing can become patients with chronic wounds as we often see these wounds can be present for weeks to years and understanding the basic physiology of the underlying wound healing processes is important in the management of these patients in helping them to heal.
Let us discuss the physiology of wound healing. Going back to our early school days, we understand that there are phases of wound healing. The first phase of wound healing is the phase of hemostasis. This primarily involves platelets and it is the phase where the active bleeding is controlled. The platelets then release the signals and they call into play the white blood cells, the neutrophils, and we enter the phase of inflammation or the inflammatory phase. This phase often lasts for several days. Again through chemical signaling, we then enter the proliferative phase. The main cells active here are the fibroblasts, their role is to lay down a rich collagen and matrix network. The proliferative phase will last for several days to several weeks. Following the proliferative phase, we then enter the maturation phase and this phase goes on from several weeks to several years. Often times, we forget that the wounds continue to heal beyond the time they show epithelialization and we are often too frequent to discharge these patients only to have them come back with occurrence of their wounds due to a traumatic injury and disruption of the new epithelium.
The patients without chronic medical problems such as diabetes or those patients that are not smokers are considered to be noncompromised hosts. An acute wound in these patients, the non-compromised patient, often progress through the phases of healing especially the last 3 phases, without significant delay.
When we are caring for a patient with a chronic wound, often a patient that is compromised from a healing standpoint, we find that this patient will often stagnant between the inflammatory or the proliferative phase never reaching the maturation phase thus never healing their wound. Question often arises, is the commonality between these patients with chronic wounds? Why do they stagnate between the inflammatory and proliferative phase? Is their common factor? I think there is, and I would like to explain to you my rationale for stating that an oxygen deficit is a very common finding in patients with chronic wounds.
Let us discuss oxygen and wound healing, why is oxygen so important in the wound healing process. First, all phases of wound healing are oxygen dependent. Next, we understand that in the early phase of healing, the metabolic demands of tissue can increase significantly, some authors report, by a factor of 20 or more. Next, hypoxic tissue is not in the environment that is conducive to fibroblasts. Tissue oxygen tensions above 30 mmHg are required for fibroblasts to replicate and to perform their metabolic activity of laying down a collagen matrix. Oxygen is important in the development of new blood vessels or angiogenesis, and finally oxygen is important for killing microbes or the antimicrobial activity that is very important in wound healing. Oxygen has been shown to be both bacteriostatic as well as bacteriocidal.
Oxygen is important for collagen synthesis. We stated earlier that oxygen is important for the replication of fibroblasts, however it is also important for metabolic activity. Oxygen is required for messenger RNA to be translated into procollagen peptides. In addition, oxygen is a cofactor in the hydroxylation and glycosylation of procollagen peptides to form the triple-helix procollagen.
This slide is courtesy of Dr. T. K. Hunt. Dr. hunt is well known across the world for his basic science research looking at oxygen and its role in wound healing. This is some of Dr. Hunts work where he looked at collagen deposition versus different oxygen tensions and as you will see in this slide, the more hypoxic the environment i.e. the 2% and 5% oxygen tissue tension environment lay down much less collagen versus as what you would see in the normal oxygen tissue tension environment of 20% oxygen.
I stated earlier that oxygen has an important role in the development of angiogenesis or the development of new blood vessels. Tissues with low oxygen tension actually release angiogenic growth factor. VEGF or vascular endothelial growth factor has an important role in the stimulation of new budding capillaries. Tissues with low oxygen tensions or hypoxic tissues demonstrate a diminished angiogenesis. This is because oxygen is again important for fibroblasts to lay down a collagen matrix and this matrix is important for endothelial cells to proliferate.
Is oxygen important in the postoperative wound healing patient, for example a patient such as this has had a rotational tissue muscle flap as well as coverage with split thickness skin grafting, a surgical insult such as this clearly increases demands on this tissue and therefore the demands of oxygen. If oxygen is important in this patient, clearly would also be important in those patients with other compromising factors.
Let us look a little bit more closely on our patient that has had an insult causing vascular compromise. What is the pathophysiology that compromises this would healing. When we have a sudden occlusion of the arterial blood supply, whether this is from a surgical insult, from a pressure etiology, or some other compromise, we start to develop tissue ischemia. The tissue is starved of blood, thus starved of oxygen. The tissue ischemia results in tissue hypoxia as well as the buildup of carbon dioxide and other metabolic byproducts. These toxins cause insult on the microcirculation and changes to the microcirculation. We start to have loss of vascular membrane integrity. Once this occurs, we start to have leakage of the intravascular fluids to the extravascular tissue. This results in tissue edema. Now, if we reach a point in the algorithm, we start developing tissue edema, we will have further extrinsic compression of this limited arterial blood supply causing a viscous downward spiral and unless we are able to intervene and correct, we will often have loss of tissue or loss of limb.
So, in summary, a patient with an arterial vascular compromise leads to tissue hypoxia caused by compromised oxygen supply. This results in compromised wound healing.
When we are managing the patient with a chronic wound or the patient that is compromised from a wound-healing standpoint, we typically can identify that this patient has an oxygen deficit. We need to correct this through one of several techniques of oxygen augmentation. The first thing that must be addressed is the patients vascularity. Often times, significant peripheral vascular disease can be addressed through percutaneous techniques and angioplasty. The patients that cannot be addressed through an endovascular technique often requires the talented skills of a vascular surgeon and revascularization techniques. By decreasing tissue edema, we can decrease the intrinsic compression on small blood vessels and thus increase distal flow. By decreasing tissue demands, we can increase oxygen delivery. The patients that have significant bacterial colonization or tissue infections can be improved by controlling their infection and thus decreasing the demands on the tissue. We can also maximize delivery by treating anemia and other delivery systems and finally we can look at adjunctive techniques of adding oxygen to the tissue adjunctive augmentation as seen in hyperbaric oxygen therapy.
So, now that we have looked at the role of oxygen in wound healing and demonstrated how important oxygen is to the patient with a chronic wound, let us now look at how we can assist these patients from a augmentation standpoint utilizing hyperbaric oxygen therapy. First, let us define hyperbaric oxygen.
When defining hyperbaric oxygen therapy, I find it is often easier to understand what is not hyperbaric oxygen therapy. This is not hyperbaric oxygen therapy. The oxygen boot and the oxygen butt bag are also not hyperbaric oxygen therapies.
This is an oxygen extremity chamber often promoted by the vendors as being topical hyperbaric oxygen therapy. This is purely topical oxygen. There is no hyperbaric component here at all. The pressures generated inside this chamber are so small they can barely be measured.
Here is another example of the misuse of the term topical hyperbaric oxygen therapy. Clearly, this extremity bag delivering oxygen to the extremity alone is purely topical oxygen and does not meet the criteria for hyperbaric oxygen therapy.
Misunderstandings, misrepresentations, and misconceptions about hyperbaric oxygen therapy have been around for a long time. Here is a copy of an old newspaper article that describes the amazing oxygen chamber curing almost everything. Clearly, this is not what hyperbaric oxygen therapy is it will not cure everything.
This is also not hyperbaric oxygen therapy. Misuse of a treatment modality such as hyperbaric oxygen therapy such as demonstrated here clearly hinders our ability to deliver this therapy in the patients that are truly deserving and truly needing this treatment modality.
So what is the textbook definition of hyperbaric oxygen therapy? Hyperbaric therapy is simply defined as inhaled 100% oxygen delivered to the patient while the patient is completely enclosed in a pressurized environment. This oxygen can be delivered by either mask, hood, respirator device, or an endotracheal tube for those patients that are intubated.
To have a better understanding of the mechanism of action of hyperbaric oxygen therapy, let us look at the basic science and the physiology behind this treatment in a little more detail. At sea level, a patient has an external force applied to them of 1 atmosphere. This is the weight of the atmosphere actually bearing down on the body. If you were to go out to the ocean and began to do some scuba diving, every 33 ft that you descend below the surface of the water, you pick up another atmosphere equivalent. So, at 33 ft of sea level, you have the weight of the atmosphere bearing down plus the weight of 33 feet column of seawater, so you would have 2 ATA at 33 ft. If you go to 66 ft, you now have 2 columns of water each measuring 33 ft plus the atmosphere itself plus 3 ATA.
If we again look at our patient at sea level, breathing air, breathing air at 1 ATA, we notice that all bindings sites through our red cells, all hemoglobin binding sites are saturated. We know that each red cell has 4 hemoglobin bindings sites and as you will note from this cartoon, all of the sites are saturated. We carry very little oxygen actually physically dissolved in the plasma. Breathing air at 1 ATA level, we only carry 0.3 volume percent oxygen actually dissolved in plasma.
When our patient is pressurized to 3 ATA and placed on 100% oxygen, we have some interesting things that happen. First of all, you will notice that we have not changed the binding of oxygen molecules to the red cells at all but you will notice there is significant increase in the amount of oxygen that is actually physically dissolved in the plasma. At 3 ATA on 100%, we can physically dissolve 6.9 volume percent of oxygen into the plasma surrounding the red blood cells. This is the benefit of hyperbaric oxygen therapy, 6.9 volume percent is actually enough oxygen to sustain life. This is a significant amount of dissolved oxygen.
Let us know look at how these pressure and gas relationships influence our cells at the end arterial level. To again look at our patient breathing air at 1 ATA, we see that the PaO2 at the end arterial level is approximately 100 mmHg. The oxygen that is dissolved in the plasma as well as that carried on the red cells can diffuse away from the artery approximately 64 microns. The diffusion gradient is somewhat less at the venous end.
However, when we pressure our patients to 3 ATA and place them on 100% oxygen, you remember the previous slide showing the marked increase in dissolved plasma, it does several things, you could see what happens to the arterial PaO2 goes up significantly over 2000 mmHg and again that extra oxygen that is in the bloodstream can diffuse out to a much greater level. In fact there is a five-fold increase in the diffusion radius to 247 microns. Again, the numbers were somewhat less at the venous level.
When our patients are in hyperbaric environment breathing oxygen, they have oxygen administered for approximately 90 minutes. However, that is not the end of hyperbaric treatment. You will notice from this cartoon that the blood levels go up precipitously and fall precipitously based on the length of the time the patient is on oxygen but what is most important is that there are slow on take and release tissues such as muscle and subcutaneous tissues, there you see that the level of the oxygen rise somewhat slower than what you see in the blood, however most importantly when the patient comes out of the hyperbaric chamber that these tissues have to off gas again at a slower rate and so that patient actually sees oxygen at the subtle level through these slower off gassing tissues for a much greater length of time. The patient actually experiences increased oxygen for almost 2 to 3 hours following the treatment.
Hyperbaric oxygen therapy can be delivered to patients in one of two fashions. They can be treated in a multi-place hyperbaric chamber or in mono-place chambers. Let us look at the differences between the 2 chambers types in a little more detail.
First, let us look at multi-place chambers. Multiplace chambers are large pressure chambers. This chamber at Travis Air Force Base California is capable of treating 18 patients at one time. Multiplace chambers are pressurized with air and the patients' breath oxygen via hood tent or mask. At Travis Air force Base, they use hood tent as demonstrated here. Again, the oxygen is delivered systemically as the patient inhales the gas delivered through this hood tent.
Treating a patient in a monoplace hyperbaric chamber accomplishes the same end result as those patients treated in a multiplace chamber, however there are some differences. Based on the name monoplace, obviously typically the treatments are on single patient. There is no hands on care as the patient is enclosed in this acrylic tube. If they require intermediate assistance from the nurse or the physician, the chamber must decompress before this can be accomplished. The entire monoplace chamber is pressurized with 100% oxygen and the patient then breathes that ambient environment. Again, this is different from the multiplace in that the multiplace is pressurized with air and the patients' breath the oxygen through a breathing device. For excellent intercoms for communication, the patients are monitored continuously during the entire treatment and can communicate with the outside attendant at any time. The patients truly enjoy the monoplace environment as typically the stereo and TV hook up outside the chambers allows for them to watch their favorite TV shows or movies during the treatment.
Here you see a picture of a patient enjoying a hyperbaric session in a monoplace chamber. You see that his eyes are focused on the monitor on the wall playing his favorite soap opera.
Regardless of the setting, whether it is multiplace or monoplace, all patients truly enjoy their hyperbaric experience.
There are several manufacturers of monoplace chambers. Perry has introduced a chamber that you see pictured here. This chamber is several inches larger than for example chambers produced by Sechrist. This does not seem like a big issue, however those few inches provides the patient added comfort and clearly has had a positive effect in decreasing issues related to claustrophobia that some patients experience in the monoplace chamber.
Let us look at the indications for hyperbaric oxygen therapy. This can be broken into 3 groups: Emergent indications, routine indications, and experimental. Let us look at each of these in some more detail.
Let us first look at the emergent indications for hyperbaric oxygen therapy. An emergent indication is typically indication where the patient should be treated as soon as possible. The first emergent indication is acute carbon oxide poisoning. Typically, whenever you think about carbon oxide poisoning, you should also think about cyanide poisoning especially as seen in patients with house fires and smoke inhalation. Decompression illness or The Bends is also emergent indication. Air or gas embolism often seen in diving accidents but also witnessed in the hospital due to iatrogenic events. Gas gangrene, necrotizing fasciitis again are 2 emergent processes that are emergent indications. Crush injuries and exceptional blood loss anemia comprise the list of emergent indications.
Next, let us look at the routine indications for hyperbaric. The most common routine indication is patients with problem or compromised wounds. Often times, these patients are compromised due to acute arterial insufficiency. Osteomyelitis or bone infection is another routine indication. Patients that suffer the ravages of radiation and develop problem such as soft tissue radionecrosis or osteoradionecrosis are also candidates for hyperbaric. Compromised flaps and grafts, burns and intracranial abscess comprise the remainder of the list of routine indications.
There are number of experimental indications for hyperbaric therapy. I think it is a reasonable summary to say that the jury is still out regarding the efficacy of hyperbaric in each of these categories but they are listed here for academic purposes. The first experimental indication is Lyme disease. Sickle cell disease and priapism have also been looked at. There is a lot of interest right now in looking at utilizing hyperbaric therapy for the treatment of the patient with cerebral palsy or anoxic brain injury, however no definitive data has proven this indication. Myocardial infarction as well as brain infarction is also been actively studied, and finally brown recluse spider bite completes our list of experimental indications.
As with any medical therapy, hyperbaric oxygen therapy is not without side effects, let us discuss these now. The first concern for a physician monitoring the patient in hyperbaric environment is that of barotrauma, changes due to a pressure alteration. We can see the effect of pressure in the ears, lungs and sometimes in teeth abscess or teeth cavities and these must be monitored closely. There are techniques to ensure that the patient has very minimal effects of pressure but again this must be monitored. The next area of concern is giving oxygen to patients, clearly oxygen in significant doses can be toxic especially to the CNS, however oxygen can also effect on the pulmonary structures and eyes and again this is monitored closely. The patients that undergoing hyperbaric treatment have been shown to develop occasional hypoglycemic episodes. It is unclear whether the hyperbaric is stimulating extra endogenous insulin production or whether it is stimulating the receptor sites for insulin and thus when patient is administered exogenous insulin, will become at more risk for hypoglycemia if the receptors are activated. Claustrophobia is an issue especially in the monoplace setting. This can often times be easily managed with anti-anxiolytic medications. Congestive heart failure is also a very rare side effect. We can push the patients who are out on the outer bounce of the starling curve further out and hence place them at risk for congestive heart failure and we monitor this closely.
Next, let us discuss the contraindications to hyperbaric oxygen therapy. There is only one absolute contraindication and that is of an untreated pneumothorax. Clearly an untreated pneumothorax place the patient at risk for tension pneumothorax especially on a cent and pneumothorax must be controlled prior to decompressing the patients. There are several relative contraindications. The patients with fever often are at increased risk for oxygen toxicity and oxygen seizures and fever must be controlled prior to hyperbaric treatment. Severe claustrophobia is also a possible contradiction. We do not want to force patients to have this therapy and as I mentioned earlier, claustrophobia can often times be managed very easily with anxiolytic medications and gentle sedatives. COPD and congestive heart failure are also need to be monitored closely giving increased doses of oxygen to patients that are emphysematous or severe COPD oxygen dependent can have risks and this need to be mentored closely and as I mentioned earlier we often times are very cautious in those patients with a history of congestive heart failure as we can exacerbate this condition. Finally, the patient that have been maintained on high FiO2, those patients are intubated in the intensive care unit that are maintained on high concentrations of oxygen for a period of time are certainly at risk for increased pulmonary toxicity due to the administration of oxygen in the hyperbaric environment, and finally there are certain chemotherapeutic agents that can be potentiated when they are administered conjointly with hyperbaric therapy and be very cautious to take a full history of the current medication regimen to the patients prior to that treatment.
Now that we have a better understanding of what hyperbaric oxygen therapy is, some of the indications, contraindications, and what patients can expect in the hyperbaric environment, let us take a brief history tour and see where the field of hyperbaric medicine has evolved from and where it is heading.
Hyperbaric oxygen has been around for a longtime. In 1862, Dr. Jourdanet operated this hyperbaric chamber facility, the sliding door mechanism that you see illustrated in the photograph is still used currently in a number of chambers produced today.
In 1875, Dr. Forlanini operated this hyperbaric facility. Here in this illustration, you see a cutaway of the inside showing the lady of the times being treated in very luxurious surroundings.
In 1879, Dr. Fontaine was reported to have used the first mobile hyperbaric operating room. To the right of this illustration, you can see the _______ apparatus that supply the compression and the pressurization for the chamber. This is where the intern of the time was actually tasked and obtained his or her first medical experience. As you will notice in this history tour, the philosophy for utilizing interns for this type of work has not changed very much in over the years.
In 1880s, Dr. Paul Bert made a significant impact in the field of hyperbaric oxygen therapy. Dr. Bert experimented and reported extensively on the pressure changes and effects of oxygen under pressure. Dr. Bert is often times referred to as the father of pressure physiology.
As I mentioned earlier, Dr. Bert experimented extensively. He gave a significant insight and worked out many of the early laws regarding oxygen toxicity. Here you see a photograph/illustration of Dr. Bert in one of his chambers actually doing an experimentation on himself inhaling oxygen under pressure.
In the 1920s, Dr. Orville J. Cunningham left his mark in the field of hyperbaric medicine. In Cleveland, Ohio, Dr. Cunningham constructed this monstrous 10 story hyperbaric hotel.
Dr. Cunninghams hyperbaric hotel was spectacular. The accommodation is again very luxurious and accommodated for the patients. Here you see the library room where the residents of the hotel were to join after dinner for an enjoyable book and a cigar. Dr. Cunningham was treating a variety of patients and was actually drummed out of the medical association when he began treating patients with uremia and syphilis in this hyperbaric facility. The chamber itself was eventually sold for scrap iron during the war.
In 1965, herald the beginning of hyperbaric medicine in Milwaukee, Wisconsin. Here you see Bonnie, a larger chamber being lowered into its place in the basement of the hospital. St. Lukes Medical Center was actually built around and on top of our hyperbaric facility.
Here, you see a picture of Clyde, our second multi chamber also being lowered into place in the basement of St. Lukes Medical Center.
Bonnie and Clyde have rested in their original positions over the past 35 years and have treated thousands of patients. The hospital has grown around these chambers. My office is actually located just to the left of the Bonnie. My nurses told me that my office is not much cleaner today.
The hyperbaric facility at St. Lukes Medical Center has been operational since 1969. Bonnie and Clyde continue in their operational status serving the patients of the Milwaukee in greater Wisconsin area. This hyperbaric facility has treated literally tens of thousands of patients over the past 35 years and has been a leader in the area of clinical hyperbaric medicine as well as investigational research and experimental areas of hyperbaric medicine.
The largest multiplace facility in the United States is located at Travis Air Force Base in California. Travis Air Force base boasts a triple lock chamber or actually 3 hyperbaric chambers interconnected together. Each chamber can be operated independently or together. Largest chamber in the background is a 21-foot in diameter sphere.
Here you see the inside of the large chamber at Travis. This chamber is actually capable of treating 18 patients at one time.
I hope you enjoyed your brief history tour of hyperbaric oxygen therapy across the years and across the United States. Let us now turn our attention to the effects of hyperbaric oxygen therapy on our patients. By delivering oxygen under pressure, we can cause tissue hyperoxygenation. This is very important in tissues that are marginal from a survival standpoint due to tissue hypoxia and ischemia. We can increase salvage rates in these tissues. In addition, tissues that are compromised will have increased metabolic demands. We can meet these demands through tissue hyperoxygenation. Hyperbaric therapy has also been demonstrated to cause angiogenesis or the development of new blood vessels. Hyperbaric therapy also causes a mild vasoconstriction and thus decreases the tissue edema. Increased oxygen clearly has an antimicrobial role. Hyperbaric therapy is used often in those diseased states that are related to infectious processes. More recent research has demonstrated that hyperbaric oxygen therapy can cause an up regulation of growth factor receptor sites and finally hyperbaric oxygen therapy has an antioxidant effect on tissues.
There is much basic science and research that has been accomplished in the field of hyperbaric oxygen therapy. I wanted to share with you a study that I accomplished a few years ago and published in the Journal of Plastic And Reconstructive Surgery. In this study, we recruited human volunteers. We performed this study in a prospective and double-blinded fashion. This study was performed at Travis Air Force Base the chamber that demonstrated just a little area. We created UV blister wounds on the forearms of our volunteers and then we looked at these patients over several days. What we noticed in this study is that the group that was treated with hyperbaric oxygen therapy had a decrease in tissue edema to a statistically significant number as well as decreased fluid exudation also to a p value of less than 0.5, we noticed a trend toward increased epithelialization, however, we did quite reach statistical significance. I think this study speaks well to the fact that hyperbaric oxygen therapy does have a positive impact on many clinical factors.
As we mentioned earlier, hyperbaric therapy can stimulate angiogenesis or development of new blood vessels. Marx in the American Journal in 1990 published results where he looked at irradiated rabbit mandibles. Marx was able to demonstrate a statistically increase in the vascularity visualized in microangiograms in the rabbits that were treated with hyperbaric oxygen. Similarly, Gibson in Surgical Forum in 1997, reported stastically greater
angiogenesis in mice with implanted Matrigel plugs when they were treated with hyperbaric oxygen therapy.
We also know that capillary density increases when hyperbaric oxygen is breathed. The study several years ago by Smith and Ketchum demonstrated this phenomenon.
In this experiment, they created full thickness burns on the back of rats. They then treated a group with hyperbaric oxygen therapy and held another group as control. Here you see a picture of the angiograms of the burn area in the group of animals on the left treated with hyperbaric as compared to the control group that was not treated with hyperbaric on the right. You can see a marked increase in the area of angiogenesis in those animals that were treated with hyperbaric oxygen therapy.
Exciting new research has been published by John and Wendy Burrows. John and Wendy have looked at cellular proliferation of human fibroblasts. They have taken fibroblasts from human and cultured them. They then challenged one of the cell lines with a dose of hyperbaric oxygen. Here you see the graph of the results. The group in red is the group that was treated with hyperbaric and you notice there was a significant increase in the proliferation of these fibroblasts that have been exposed to hyperbaric oxygen therapy.
The _______ have also published several studies demonstrating that hyperbaric oxygen increases growth factor receptor expression again the study with human dermal fibroblasts. Here you see the control group that has been stained with immunofluorescent stain for growth factor receptors. They then took a similar line of fibroblasts, challenged this cell line with a single dose of hyperbaric oxygen 2.5 ATA per 90 minutes and as you will see from this staining, there is a significant increase in
growth factor receptor expression thus demonstrating very nicely that hyperbaric does in fact increase growth factor receptor expression.
That concludes our presentation and Introduction to Hyperbaric Oxygen Therapy. I hope you found this presentation valuable and interesting as well as entertaining. Should you have any other questions regarding the use of hyperbaric oxygen therapy, please do not hesitate to contact me. It has been my pleasure to spend time with you.
|Goals and Objectives|
After participating in this activity, the viewer should be better able to:
1. Describe what compromised wound healing is.
2. Explain the role of oxygen in wound healing.
3. Describe the definition and physiology of hyperbaric oxygen therapy.
4. Recognize the indications for hyperbaric oxygen therapy.
Estimated time to complete this activity is 49 minutes.
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We may target our advertising or marketing depending on information we have about you. For example, a user that is a healthcare professional who treats diabetes may receive advertising for new diabetes therapies (although in neither case will the advertiser have access to any individually identifiable information about you). We may also personalize our Web site based on your interests. For example, you may see different articles in different places on our Web site based on information you have shared with us, or information we have gained by observing your previous behavior, or information we may have gained from your interactions with a third party that shares information with us. We use information for our own internal marketing, research, and related purposes. Third Parties In addition to aggregate information (discussed previously), we may share some kinds of personally identifiable information with third parties as described below.
Other Companies: We have strategic relationships with other companies who offer products and services on our Web sites. When you are interacting with those companies, different rules and privacy policies may apply. We do not control the collection or use of information you provide to these companies, but we do require that those companies clearly state their policies so you can decide whether to give them any information.
Promotional Offers: Sometimes we send offers to selected groups of customers on behalf of other businesses. When we do this, we do not give that business your name and address. We provide a variety of mechanisms for you to tell us you do not want to receive such promotional offers. For example, we may provide an opt-in box for consumers to receive an email from another business, and we make clear that by opting in you are submitting your data to a third party.
Protection of Information
We have implemented technology and security policies, rules and other measures to protect the personal data that we have under our control from unauthorized access, improper use, alteration, unlawful or accidental destruction, and accidental loss. We also protect your information by requiring that all our employees and others who have access to or are associated with the processing of your data respect your confidentiality. We use security methods to determine the identity of its registered users, so that appropriate rights and restrictions can be enforced for that user. Reliable verification of user identity is called authentication. We use both passwords and usernames, as well as double opt-n verification, to authenticate users. Users are responsible for maintaining their own passwords.
Access to Information and Choices
Correction of Information We Have About You
If you believe that registration information collected by our Web site(s) is in error, you may edit your personal profile any time that you like. You can directly edit most of your user profile on the Web site on which you initially registered. Information that you can not edit may only be changed by contacting Web Customer Support (see CONTACTS). Requests for deletion of your record may result in your removal from the registry, but we may keep certain demographic information about you for product improvement purposes. You may contact Web Customer Support and ask for the changes that you would like to make.
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