Radiation Necrosis Treatment & Management

  • Author: Michael J Schneck, MD; more...
 
Updated: Apr 19, 2011
 

Medical Care

Probably the most important factor in providing good care is the clinician's confidence of diagnosis. Exposing a patient with radiation necrosis to unwarranted antineoplastic treatment is not desirable.

  • A conservative option in treating a patient with radiation necrosis is observation. This may be appropriate for a patient found to have an asymptomatic necrotic mass on follow-up MRI. If the patient is asymptomatic and definitive diagnosis of radiation necrosis or recurrent glioma does not make a difference in clinical management, the patient should be monitored clinically and with serial MRI scans.
  • For patients with signs and symptoms of mass effect, increased intracranial pressure, or neurologic disability, consider other treatment options. Consider surgical evaluation, steroids, anticoagulation, or hyperbaric oxygen therapy separately or in combination.[17, 18]
  • Hyperbaric oxygen promotes perfusion and angiogenesis.
    • Oxygen is delivered at 20-24 atm for 20-30 sessions. Each session lasts approximately 90-120 minutes.
    • Hyperbaric oxygen therapy is expensive, time-consuming, and not readily available at most medical centers.
    • Efficacy is not well documented.
    • Small case studies exist, but many of these patients also were receiving concomitant steroid therapy. These clinical series showed resolution of a lesion on MRI.[17]
    • Hyperbaric oxygen can be provided in conjunction with anticoagulation.
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Surgical Care

In addition to providing potential histologic diagnosis, surgery has other therapeutic benefits. Surgical debulking of the lesion can relieve increased intracranial pressure and improve disability. Patients with obstructive hydrocephalus may require a shunting procedure. Surgery, however, is associated with a high risk of complications or neurologic deficit and should be reserved for symptomatic patients in whom medical therapy fails.

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Contributor Information and Disclosures
Author

Michael J Schneck, MD  Associate Professor, Departments of Neurology and Neurosurgery, Stritch School of Medicine, Loyola University; Associate Director, Stroke Program, Director, Neurology Intensive Care Program, Medical Director, Neurosciences ICU, Loyola University Medical Center

Michael J Schneck, MD is a member of the following medical societies: American Academy of Neurology, American Society of Neuroimaging, Neurocritical Care Society, and Stroke Council of the American Heart Association

Disclosure: Boehringer-Ingelheim Honoraria Speaking and teaching; Sanofi/BMS Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; UCB Pharma Honoraria Speaking and teaching; Talecris Consulting fee Other; NMT Medical Grant/research funds Independent contractor; NIH Independent contractor; Sanofi Grant/research funds Independent contractor; Boehringer-Ingelheim Grant/research funds Independent contractor; Baxter Labs Consulting fee Consulting

Coauthor(s)

Anna Janss, MD, PhD  Associate Professor of Pediatric Neuro-oncology, Emory University School of Medicine; Consulting Neuro-oncologist, Children's Healthcare of Atlanta

Anna Janss, MD, PhD is a member of the following medical societies: American Academy of Neurology, American Association for Cancer Research, American Medical Association, Children's Oncology Group, International Association for the Study of Pain, Pennsylvania Medical Society, Society for Neuro-Oncology, and Society for Neuroscience

Disclosure: Nothing to disclose.

Specialty Editor Board

Frederick M Vincent Sr, MD  Clinical Professor, Department of Neurology and Ophthalmology, Michigan State University Colleges of Human and Osteopathic Medicine

Frederick M Vincent Sr, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners, American College of Legal Medicine, American College of Physicians, and Michigan State Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Jorge Kattah, MD  Head, Program Director, Professor, Department of Neurology, University of Illinois College of Medicine at Peoria

Jorge Kattah, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, and New York Academy of Sciences

Disclosure: Biogen Honoraria Consulting; Bayer Corporation Honoraria Consulting

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MRI of a patient with symptoms of gait unsteadiness 1 year after being diagnosed with a posterior fossa primitive neuroectodermal tumor (PNET). Treatment during the 1-year interval prior to this MRI consisted of surgical resection, craniospinal radiation of 2340 cGy, boost dose given to the posterior fossa for a total of 5500 cGy, chemotherapy (vincristine, cis-platinum, and cyclohexylchloroethylnitrosurea [CCNU]), and dexamethasone therapy.
Positron emission tomography with [18F]-labeled fluorodeoxyglucose (PET-FDG) performed following the MRI of a patient with symptoms of gait unsteadiness 1 year after being diagnosed with a posterior fossa primitive neuroectodermal tumor (PNET). Treatment during the 1-year interval prior to these studies consisted of surgical resection, craniospinal radiation of 2340 cGy, boost dose given to the posterior fossa for a total of 5500 cGy, chemotherapy (vincristine, cis-platinum, and cyclohexylchloroethylnitrosurea [CCNU]), and dexamethasone therapy. PET-FDG demonstrates hypometabolism consistent with probable radiation necrosis. Four years later, the patient is stable and without evidence of tumor progression.
 
 
 
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