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Hyperbaric Medicine Team Joins War on Cancer

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The University of California, San Diego Medical Center’s Hyperbaric Medicine Center is part of a nationwide effort to compile and evaluate data in order to validate whether cancer patients being treated for radiation-related wounds heal more quickly and more thoroughly with hyperbaric oxygen therapy.

Each year in the United States, approximately 1.2 million Americans are diagnosed with cancer, half of whom receive radiation therapy. About five percent of those individuals develop problems or “late effect” wounds related to the radiation. Specialists say hyperbaric oxygen therapy is beneficial in managing radiation related injuries, and that a large-scale collection and analysis of data across treatment sites will help substantiate this working knowledge.

“As individual entities, it is difficult to know just how beneficial a therapy is until you can measure it across thousands of patients,” said Ian Grover, M.D., Medical Director, Hyperbaric Medicine Center at UC San Diego Medical Center. “So as health care professionals, it is very important to collaborate on our varying experiences through studies such as this registry.”

Radiation therapy can leave behind wounds on the skin, or cause blood in the urine or stool. The increased exposure to concentrated levels of oxygen through hyperbaric oxygen therapy helps re-generate blood vessels, thus delivering more oxygen to the wounded area and facilitating healing.

The information gathered at UC San Diego Medical Center will be merged with other leading centers across the U.S. The institutions have already shared findings from 2004 and 2005 and will be contributing data from 2006 and 2007 as well. The combined results will form a data base that will be used to demonstrate the merits of this therapy to other physicians and health care insurers.

“To ensure that this therapy becomes widely available, we must further define and demonstrate its benefits,” explained Robert Bartlett, M.D., President of the American College of Hyperbaric Medicine.

In 2006, Bartlett, along with Jeffrey Niezgoda M.D., Medical Director, Centers for Comprehensive Wound Care & Hyperbaric Oxygen Therapy, Aurora Health Care Hyperbaric & Wound Care Associates, in Milwaukee, Wisconsin designed a web-based registry to capture the success of U.S. doctors and nurses who employ this form of therapy.

“This will help us design the best course of treatment for these patients. And we can pass this information along to insurance companies, demonstrating that it is a valid, front-line therapy,” said Grover.

About the UC San Diego Hyperbaric Medicine Center

The UCSD Hyperbaric Medicine Center treats patients in accordance with the Undersea and Hyperbaric Medical Society guidelines for the use of hyperbaric oxygen therapy (HBOT).

HBOT is a form of medical treatment that grew from the experience gained by treating deep-sea divers with the “bends,” but now is primarily used to treat patients with problem wounds from radiation therapy and diabetes. The therapy’s purpose is to increase the amount of oxygen in the blood. During hyperbaric oxygen therapy, the patient breathes pure oxygen. At the same time, the pressure surrounding the patient’s body is slowly increased to two to three times the normal atmospheric pressure.

HBOT allows the blood to carry more oxygen to the tissues, promoting new tissue and blood vessel growth, and assisting in the healing process by permitting skin grafting or spontaneous healing. A high level of oxygen in the blood helps to fight infections caused by a variety of bacteria, some that only live in the absence of oxygen. It also enables white blood cells to destroy many kinds of bacteria more efficiently.

As the only hyperbaric chamber in San Diego County open 24 hours a day, seven days a week, UC San Diego Medical Center’s hyperbaric chamber plays a critical role in the San Diego County Emergency Medical System. The UC San Diego center is always available for emergency situations, such as diving accidents, carbon monoxide exposures or treatment for emergent ICU patients.

At UC San Diego Medical Center, HBOT is delivered by having a patient lie or sit in a large tube resembling a small submarine, lined inside with padded, bench-style seating for up to 12 people at a time, six on average. It is sealed and pressurized with air to a level several times normal atmospheric pressure. Once the patients are at “depth,” they are placed on 100% oxygen for a total of 90 minutes. Patients typically rest, read, watch television or sleep during this two hour treatment. On average, it takes 30 to 40 treatments over six weeks to see marked improvement in healing.

Initially used to treat diving complications, hyperbaric oxygen therapy is used for many indications from the specialties of: orthopedic surgery, general surgery, plastic surgery, maxillofacial and oral surgery, infectious disease, radiation oncology, and emergency medicine.

(NewsWise Press Release, Source: University of California, San Diego Health Sciences, June 16, 2008)


The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

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Interesting enough I work in a wound healing center where we have Hyperbaric oxygen therapy. I am actually going to be going to training in Idaho for this. Yes we do treat radiation wounds as well as radiation cystitis. I have seen lots of improvements with wound healing of many wounds with the chamber. If anyone would like information on this I have alot of info just PM me and I can mail them to you =)

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Radiation-induced necrosis is a serious reaction to radiation treatment. It may result from the death of tumor cells and associated reaction in surrounding normal brain or it may result from the necrosis of normal brain tissue surrounding the previously treated metastatic brain tumor. Such reactions tend to occur more frequently in larger lesions, either primary brain tumors or metastatic tumors.

The diagnosis of radiation-induced necrosis is difficult to confirm. Many patients have a mixture of tumor and radiation necrosis and a biopsy may be necessary to distinguish it. Neither symptoms nor radiographic findings clearly distinguish radiation-induced necrosis from tumor. However, the FDG-PET Scan (which measures cellular metabolism) and T1-SPECT studies are useful in differentiating radiation-induced necrosis from recurrent tumor.

Hyperbaric Oxygen Therapy (HBOT) is a useful therapeutic option for patients with confirmed symptomatic radiation necrosis. Until the new millenium, the only treatment for patients was pentoxifyline or heparin therapy, and it was almost always unsuccessful. Both Duke University for Hyperbaric Oxygen Therapy and the University of Cincinnati previously had clinical trials on this science.

The most common condition treated at some Hyperbaric Oxygen Therapy Centers is tissue injury caused by brain radiation therapy for cancer. Wound healing requires oxygen delivery to the injured tissues. Radiation damaged tissue has lost blood supply and is oxygen deprived. Chronic radiation complications result from scarring and narrowing of the blood vessels within the area which has received the treatment. Hyperbaric Oxygen Therapy provides a better healing environment and leads to the growth of new blood vessels in a process called re-vascularization. It also fights infection by direct bacteriocidal effects. Using hyperbaric treatment protocols, "most" patients with chronic radiation injuries can be cured.

Hyperbaric oxygen therapy is administered by delivering 100 percent oxygen at pressures greater than atmospheric (sea level) pressure to a patient in an enclosed chamber. Hyperbaric oxygen acts as a drug, eliciting varying levels of response at different treatment depths, durations and dosages, and has been proven effective as adjunctive therapy for specifically indicated conditions.

Oxygen is a natural gas that is absolutely necessary for life and healing. Purified oxygen is defined as a drug but is the most natural of all drugs. Oxygen under pressure is still the same gas but is more able to penetrate into parts of the body where the arterial flow is hindered, producing ischemia (loss of blood flow) and hypoxia (lack of oxygen). When oxygen under pressure is breathed by a patient in a sealed chamber, it is termed a hyperbaric oxygen treatment (HBOT).

In addition to raising the arterial levels of oxygen 10 to 15 times higher than that produced by normal atmospheric pressure, the pressure exerted within the body can and does exert therapeutic benefits on acute and chronically traumatized and swollen tissus.

If on medicare, the approved course is 2.0 atm (two times above atmospheric pressure) for 90 minutes 20-30 sessions. For hyperbaric oxygen therapy to be covered under the Medicare program in the United States, the physician must be in constant attendance during the entire treatment. This is a professional activity that cannot be delegated in that it requires independent medical judgment by the physician. The physician must be present, carefully monitoring the patient during the hyperbaric oxygen therapy session and be immediately available should a complication occur. This requirement applies in all settings and no payment will be made by Medicare unless the physician is in constant attendance during the procedure.

Who Should Avoid This Therapy?

Avoid these treatments if you have a seizure disorder, emphysema, a high fever, or an upper respiratory infection. Do not undergo them if you have a severe fluid build-up in the sinuses, ears, or other body cavities. Forego them if you've had surgery for optic neuritis, or have ever had a collapsed lung. Avoid them, too, if you are taking doxorubicin (Adriamycin), cisplatin (Platinol), disulfiram (Antabuse), or mafenide acetate (Sulfamylon).

Pregnancy was once considered a contraindication for hyperbaric therapy. However, it's now deemed acceptable if a condition will cause long-term damage to the mother or fetus. For example, the treatments are given to pregnant women with carbon monoxide poisoning, which is toxic to both mother and child.

What Side Effects May Occur?

Seizures, a result of the direct effect of oxygen on the brain, are the most serious side effect associated with hyperbaric therapy. The risk is estimated at one in 5,000. Every chamber is equipped with a quick-release mechanism. If a seizure occurs, the oxygen will be immediately released and the seizure will subside.

Minor side effects include popping of the ears similar to that experienced in a descending aircraft. Sinus pain, earache, and headache are other possible side effects. In fact, pain may occur in any body cavity where air can get in but can't get out. For example, dental pain may occur if a filling has trapped air beneath it. In rare cases, pressurized oxygen may rupture an eardrum.





http://www.baromedical.com/about_hyperb ... dicine.asp

http://www.spinalrehab.com.au/Updates/H ... ments%20ca n%20help%20patients%20with%20radiation-induced%20brain%20injuries.htm

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  • 1 year later...

When brain tumors are treated with radiation therapy, there is always a risk of radiation-induced necrosis of healthy brain tissue. Insidious and potentially fatal, radiation necrosis of the brain may develop months or even years after irradiation.

This poorly understood side effect can occur even when the most stringent measures are taken to avoid exposing healthy tissue to harmful levels of radiation. In most cases, radiation necrosis of the brain occurs at random, without known genetic or other predisposing risk factors. The only treatment options typically available for radiation necrosis of the brain are surgery to remove dead tissue and use of the steroid dexamethasone to provide limited symptom control. But clinicians have not found a way to stop the progression of necrosis, despite having tested a range of therapies including anticoagulants, hyperbaric oxygen, and high-dose anti-inflammatory regimens.

However, recent studies at M. D. Anderson have shown that the monoclonal antibody bevacizumab (Avastin) may be able to stop radiation necrosis of the brain and allow some of the damage to be reversed. Victor A. Levin, M.D., a professor in the Department of Neuro-Oncology and the senior researcher on the studies, said the findings suggest that radiation necrosis of the brain can be successfully managed—and perhaps even prevented—with bevacizumab or similar drugs.

The need for such a breakthrough is as old as radiation therapy for cancers in the brain. “No matter what we do or how good we do it, we know a small percentage of patients who receive radiation therapy to the central nervous system will suffer late-occurring radiation necrosis,” Dr. Levin said. “We used to think it was the dose that was causing problems. Then we did a study and found that there was little to no relation to radiation dose or radiation volume—the necrosis occurred simply by chance. So it is impossible to say which patients will develop this problem; we just have to monitor them and hope for the best.”

Like necrosis, the discovery that bevacizumab has an effect on necrosis can also be attributed to chance. Bevacizumab, a newer drug that prevents blood vessel growth in tumors by blocking vascular endothelial growth factor (VEGF), was originally approved in the United States for the treatment of metastatic colon cancer and non–small cell lung cancer. An M. D. Anderson group that included Dr. Levin decided to test the drug in patients who had VEGF-expressing brain tumors. “Some of these patients also had necrosis from prior radiation therapy, and we were struck by the positive response of those patients to bevacizumab,” Dr. Levin said. “We had never seen such a regression of necrotic lesions with any other drug like we did in those patients.” The observation prompted the researchers to design a placebo-controlled, double-blind, phase II trial sponsored by the U.S. Cancer Therapy Evaluation Program in which bevacizumab would be tested specifically for the treatment of radiation necrosis of the brain.

The trial is small, having accrued 13 of a planned 16 patients, and is limited to those with progressive symptoms, lower-grade primary brain tumors, and head and neck cancers. But the results have been unlike anything the researchers have seen before in radiation necrosis therapy. All of the patients receiving bevacizumab responded almost immediately to treatment, with regression of necrotic lesions evident on magnetic resonance images, while none of the patients receiving the placebo showed a response. The results were striking, and all of the patients who switched from placebo showed a response to bevacizumab as well. So far, responses have persisted over 6 months even after the end of bevacizumab treatment.

Side effects seen in the trial so far included venous thromboembolism in one patient, small vessel thrombosis in two patients, and a large venous sinus thrombosis in one patient. Dr. Levin is unsure whether the side effects were caused by therapy or the radiation necrosis itself. “We’re also not absolutely sure what is causing the positive effects against the radiation necrosis,” he said. “We presume it’s related to the release of cytokines like VEGF, since bevacizumab is very specific and only reduces VEGF levels. We think aberrant production of VEGF is involved with radiation necrosis of the brain, and the fact that even short treatment with bevacizumab seems to turn off the cycle of radiation damage further confirms the central role of VEGF in the process.”

The multidisciplinary research team has also postulated that radiation therapy damages astrocytes, a cell type involved in various brain functions, and causes them to leak VEGF. This leaked VEGF might then cause further damage to brain cells and further leakage of VEGF. “It gets to be a very vicious cycle,” Dr. Levin said. “The question is, is that all that’s going on?”

Dr. Levin hopes that the answers to that question and others may lead to preventive measures against radiation necrosis, beyond what is already done to control the development of radiation itself. Perhaps bevacizumab can be given in low doses before radiation or intermittently afterward to reduce VEGF levels and protect the brain from abnormally high levels of the protein. He hopes such approaches can be tested in future studies. “Just the fact that bevacizumab works has helped us understand so much more about what happens in radiation necrosis,” he said. “Everything we’ve tried up until now has been a brick wall.”

Source: OncoLog, May 2009, Vol. 54, No. 5

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This is very interesting and hopeful.

An answer to prevention of radiation necrosis in brain tissue would be wonderful, and truly a godsend.

Let's hope they are on the right track with Avastin. I remember Bill having that particular regimen (Avastin), and wondering at the time if it would enter the brain through the blood/brain barrier.

Of course, I wasn't apprised of this aspect.


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I've just discovered this recently and I'm going to look into it further, since treatment for radiation-induced necrosis was a subject dear to me. I think Avastin and radionecrosis may dovetail with some current work in cell function analysis.

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Yes, Greg, the subject is close to my heart, as well.

Much of what occurs with WBR happens at the long end of things. I guess when they tell people about the side effects they don't think in terms of long-term survivors.

Bill had some rather difficult times with finding words, formulating ideas, and some others that occurred after the two-year mark.

Still, he was Bill, and I was very grateful to have most of his original self at the end. His dry humor was there to the last.

Here's to hope in finding solutions.


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