Radiation Necrosis Medication

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

Medication Summary

Medical therapy focuses on 2 mechanisms: controlling vasogenic edema and/or controlling vessel thrombosis.

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Corticosteroids

Class Summary

Steroid therapy has only a temporary role in relieving neurologic decompensation and deficits. It relieves any symptomology related to vasogenic edema and disruption of the blood-brain barrier. While administering steroid therapy, the clinician must implement another medical or surgical therapy to treat radiation necrosis and to protect the patient from long-term complications.

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Dexamethasone (Decadron, Dexasone)

 

Glucocorticoids such as dexamethasone have potent anti-inflammatory effects in many disorders. In addition to metabolic effects, they modify immune system response. Lacks salt-retaining property of hydrocortisone.

Patients can be switched from an IV to PO regimen in a 1:1 ratio.

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Anticoagulants

Class Summary

Because radiation necrosis pathophysiology involves vessel thrombosis and subsequent occlusion, anticoagulant use has been proposed.[19] To date, few case studies have addressed use in this condition; the evidence for anticoagulation is very limited. Patients with radiation necrosis may also be at risk of intracranial hemorrhage, further limiting the presumptive benefits of this therapy. In most of these studies, histologic verification of radiation necrosis was present. Patients received 6 mo of IV heparin, then warfarin with aPTT and PT adjusted to 1.5 times the control. Patients had significant resolution of deficits. When anticoagulation was stopped, symptoms reemerged. Almost immediate resolution of symptoms occurred when anticoagulation was restarted. Before starting anticoagulation therapy, careful diagnostic evaluation and management are needed.

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Heparin

 

Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis. Check aPTT after the first 6 h, then periodically q4-6h in early treatment. Dosage is therapeutic when aPTT is adjusted to 1.5 times normal.

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Warfarin (Coumadin)

 

Inhibits synthesis of vitamin K-dependent clotting factors (II, VII, IX, X) and anticoagulants (proteins C and S). Vitamin K is a cofactor for postribosomal synthesis of vitamin K-dependent clotting factors, which promote synthesis of gamma-carboxyglutamic acid (necessary for proper coagulation). Reportedly interferes with vitamin K epoxide regeneration. Peak anticoagulant effect is 72-96 h. Like other anticoagulants, warfarin has no effect on a preexisting thrombus.

Individualize dose in response to PT/INR and therapeutic goal. Periodic determination of PT/INR is required.

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Monoclonal antibodies

Class Summary

Agents in this category are used to decrease blood supply to a tumor by inhibiting angiogenesis.[20, 21]

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Bevacizumab (Avastin)

 

A recombinant, humanized antibody that inhibits vascular endothelial growth factor (VEGF). VEGF has a significant role in angiogenesis and maintenance of existing blood vessels. By inhibiting VEGF, the antibody would interfere with the blood supply to a tumor, which is thought to be critical to tumor metastasis. By preventing VEGF from reaching leaky capillaries that are associated with brain swelling, bevacizumab may also help in radiation necrosis.

Fifteen patients with malignant brain tumors were treated with bevacizumab or bevacizumab combination n in one study.

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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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