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HBOT for Radiation-induced Necrosis

gdpawel's picture
gdpawel
Posts: 549
Joined: May 2001

HBO Therapy For Radiation-induced Necrosis

Radiation-induced necrosis has been estimated to occur in 20% to 25% of patients for cancerous tumors in the brain. Some studies say it can develop in at least 40% of patients irradiated for tumors following large volume or whole brain radiation and possibly 3% to 9% of patients irradiated focally (as in stereotactic radiation) for brain tumors (in reality, they just don't know). Even with more localized use of radiation, significant neurological deficits can result.

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 and T1-SPECT studies are useful in differentiating radiation-induced necrosis from recurrent tumor.

PET is useful in a variety of therapy-monitoring applications, including distinguishing between radiation necrosis and recurrence; determining the resectability of a recurrence; and evaluating response to chemotherapy or radiation therapy. This is because effective therapy leads to rapid reductions in the glucose uptake levels of tumors. PET tracers can easily reveal this drop in metabolic activity and show - sometimes within minutes or hours - whether a patient is responding positively to a particular course of treatment. With this information, physicians can quickly modify less effective therapy, thereby improving patient outcomes and reducing the cost of ineffective treatment.

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.

Hyperbaric Oxygen Therapy (HBOT) is now a useful terapeutic option for patients with confirmed symptomatic radiation necrosis. I've received a number of emails from radiation necrosis patients who had HBO Therapy, and (the good news is) it works!

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.

http://anesthesia.duhs.duke.edu/divisions/hyperbarics.html

sbiw3momof2
Posts: 3
Joined: Jul 2006

My 31 yr. old daughter had a brain tumor, radiation and chemo when she was 16. Currently, she is suffering from "episodes" where her speech becomes slow, sounds "retarded" (forgive my use of that word)and frequently feels extremely tired. Are these symtoms that you recognize?

gwmmedical
Posts: 2
Joined: Nov 2010

Sir,

Great Post re Radiation Necrosis and HBOT.

I have an Oligodendroglioma BT. The current est. stage is 2/3. I have had same tumor at some level for 20 years, being treated with Antineoplastins and Surgery.

Have you come across anything in your reading re Brain Tumors and HBOT or Cancer and HBOT. I am not very interested in adjunct info and post radiation info.

Thanks.

KMPonder's picture
KMPonder
Posts: 102
Joined: Dec 2009

Just this past week, after a cold PET on 10/22, hubby had experienced vision issues in the periphery of both eyes. We got him to an amazing neuro ophthalmologist on Tuesday who suspected radiation necrosis. Duke sent his medical records overnight. On the 10/21 MRI it shows a "new enhancement on the optic chiasm." Yet on the 10/22 PET, it was completely cold. Since it is most unlikely to be a malignant tumor, they are suspecting most highly radiation necrosis. His radiation oncologist says he was nowhere near the optic chiasm. He did have whole brain/spine radiation in 1987 for his first malignant tumor. No problems until August 2009, when he developed radiation-induced AAs.

They began Avastin yesterday. They are going to do five days of a steroid push all next week. They cannot biopsy the optic chiasm or he would definitely go blind. N ophth also said that HBOT is not good, as it can induce malignant tumors, so since he's just got a cold PET in October, she's ruling that out for now.

We hope the Avastin along with the steroid push can stop the progression and reverse the loss.

I have come to the conclusion that radiation can be really, really harmful. Unfortunately, when you have two bouts of brain cancer in your lifetime, it seemed the best course of treatment at both times. It's been discouraging news to receive, just three weeks after a completely negative PET. We remain hopeful this new course of treatment will help this issue.

Beckymarie
Posts: 358
Joined: Aug 2009

I agree with your opinion on radiation. My husband had a GBM and had the standard 6week protocal of radiation. He was never the same after the radiation, extreme fatigue, steroid myopathy in his legs, confusion. Granted some this was from the inflammation and pressure of the tumor but he was better before the radiation than after. In hindsight I am not sure we would follow the same path of treatment as the outcome radiation vs non-radiation would be the same. He was also on Avastin and did get some good benefits from the Avastin. I wish him the best with his treatment.

KMPonder's picture
KMPonder
Posts: 102
Joined: Dec 2009

Thank you. I think I fear the idea of radiation now more than ever. I never dreamed my husband could potentially lose his sight. I never dreamed he'd have brain cancer twice in a lifetime, either.

We've just had the one Avastin treatment, but he tolerated it just fine, thankfully. They say there are really no side effects. He also did well with the Temodar, except for fatigue. Cognitively, I can see very minor changes. Confusion is only slight and mostly when he's very tired. Most of the time, he's still as sharp as a tack. I feel we've been blessed in so many ways. He has fought so hard to overcome this battle. I just wish I could snap my fingers and make it all go away.

Are you holding up well? I sure hope so. Your responses to me and others are encouraging to us, and I hope it helps with your healing.

gdpawel's picture
gdpawel
Posts: 549
Joined: May 2001

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

Rory1987's picture
Rory1987
Posts: 122
Joined: Nov 2009

HBOT looks promising in treating radiation-induced necrosis, IS there any update as to the use of this therapy to treat radiation induced necrosis?

KMPonder's picture
KMPonder
Posts: 102
Joined: Dec 2009

We've just returned from Duke, and my hubby will likely start HBOT in about a month for radiation necrosis. They are pretty certain the enhancement is necrosis vs. a new tumor. They cannot biopsy it, because it's on the optic chiasm and he'd go blind. Our doctor at Duke has had a patient who began being unable to swallow due to radiation necrosis, and after 30 treatments of HBOT, symptoms reversed. He's now singing in his church choir again. I haven't had time to do actual research, but she feels confident about it and we may have no other choice to try and save his vision. Other than this, he's feeling great!

Remaining hopeful...always.

Rory1987's picture
Rory1987
Posts: 122
Joined: Nov 2009

thats a good sign that someone who has radiation induced necrosis recovered. it would be great if you could update us from time to time about the progress of your husband's HBOT treatment. God bless and good luck to your husband

By the way, you mentioned that your husband underwent WBR back in 1987, if you don't mind me asking, how was his side effects after getting WBR? my dad's friend had completed WBR a few months ago and your husband's story could definitely be useful in informing him with the effects of WBR. THanks

rory

KMPonder's picture
KMPonder
Posts: 102
Joined: Dec 2009

Hi Rory.

He had no side effects a few months after his WBR and spine radiation too in 1987, except 22 years later we know these AA tumors diagnosed in 2009 were caused by the radiation he had.

Thanks for the articles. We have to run to his Avastin treatment this morning, but I do plan to look at these later today.

I will definitely keep you updated as to his HBOT. We don't expect that to start for another month. We are stopping by our wound center this morning to see if they can handle the daily schedule. I think they only have one chamber.

Kim

Rory1987's picture
Rory1987
Posts: 122
Joined: Nov 2009

thank you, the updates will definitely help those who have fears about radionecrosis and give them options for treatments and can provide some doctors who haven't heard about this treatment for radionecrosis some infomration.

Rory1987's picture
Rory1987
Posts: 122
Joined: Nov 2009

I did some research about using HBOT in treating Radionecrosis and I found a few good articles that seem to provide some good info on the effectiveness of HBOT.. maybe you could read them too.

http://www.tbims.org/combi/ubb/Forum4/HTML/000056.html
http://healthnews.uc.edu/publications/findings/?/1917/1921/
http://www.radiationnecrosistherapy.com/technical/headneck.html#treatment

tomkat26
Posts: 1
Joined: Jul 2012

Hi,
How did the treatments go? My husband had WBR 10/2011. After he finished he returned to his Gamma Knife Dr. and he said the tumors were gone and nothing had changed since mid Sept. he felt he did not really need the WBR, but after a siesure from scare tissue a DR.(from the hospital) convinced my husband to have WBR. I was there for the consultation----not clear at all about side effects-especially for someone over 60 yrs. Anyway, many days he can not sit-up, urinates and is mentally not there. He is in pretty good shape for a few days, walks around, uses the bathroom etc. Within 6 wks after the WBR major fatigue/depression set in and never went away. Every so often I give him a half of Decadron and the next day he is normal, he is on other steriods but I found this by accident to help.
Any feedback or direction would be welcomed as I get the same ole run around from all the Docs involved, no one ever brings up WBR side effects!!! Thanks, Kath

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