The role of steroids in the management of brain metastases: a systematic review and evidence-based clinical practice guideline

Abstract

QuestionDo steroids improve neurologic symptoms in patients with metastatic brain tumors compared to no treatment? If steroids are given, what dose should be used? Comparisons include: (1) steroid therapy versus none. (2) comparison of different doses of steroid therapy.Target populationThese recommendations apply to adults diagnosed with brain metastases.RecommendationsSteroid therapy versus no steroid therapyAsymptomatic brain metastases patients without mass effectInsufficient evidence exists to make a treatment recommendation for this clinical scenario.Brain metastases patients with mild symptoms related to mass effectLevel 3 Corticosteroids are recommended to provide temporary symptomatic relief of symptoms related to increased intracranial pressure and edema secondary to brain metastases. It is recommended for patients who are symptomatic from metastatic disease to the brain that a starting dose of 4–8 mg/day of dexamethasone be considered.Brain metastases patients with moderate to severe symptoms related to mass effectLevel 3 Corticosteroids are recommended to provide temporary symptomatic relief of symptoms related to increased intracranial pressure and edema secondary to brain metastases. If patients exhibit severe symptoms consistent with increased intracranial pressure, it is recommended that higher doses such as 16 mg/day or more be considered.Choice of SteroidLevel 3 If corticosteroids are given, dexamethasone is the best drug choice given the available evidence.Duration of Corticosteroid AdministrationLevel 3 Corticosteroids, if given, should be tapered slowly over a 2 week time period, or longer in symptomatic patients, based upon an individualized treatment regimen and a full understanding of the long-term sequelae of corticosteroid therapy.Given the very limited number of studies (two) which met the eligibility criteria for the systematic review, these are the only recommendations that can be offered based on this methodology. Please see “Discussion” and “Summary” section for additional details.

Use of Dexamethasone in Patients with High-Grade Glioma: A Clinical Practice Guideline

“…In a study reporting the results of two consecutive randomized trials involving 96 patients with brain metastases, Vecht et al 3 Retrospective studies and reviews report that the most common starting dose of dexamethasone ranges between 8 mg and 16 mg daily 5,6,8,12 . In a recent review of the role of steroids in the management of brain metastases, Ryken and colleagues concluded that symptomatic patients should be treated with a starting dose of 4-8 mg daily; if the patient exhibits severe symptoms associated with increased intracranial pressure, a dose of 16 mg daily or higher could be considered 9 . Two recent comprehensive reviews recommend an initial intravenous loading dose of 10-20 mg dexamethasone when a patient presents with acute neurologic symptoms caused by a brain tumour or spinal cord lesion; the loading dose should be followed by maintenance dosing with oral or intravenous dexamethasone in divided doses totalling to 4-24 mg daily 13,14 .…”

“…In general, the tapering schedules most commonly reported involve a gradual decrease in the dose or dosing interval over a period of 2-4 weeks to prevent rebound symptoms, with longer periods for symptomatic patients 3,7,8,9,15 . Some publications favour tapering until a physiologic dose equivalent to 20 mg of cortisol daily is achieved, which might be 0.25 mg dexamethasone daily 18,19 .…”

Application of Computed Tomography for Differential Diagnosis of Glioma Stoke and Simple Cerebral Hemorrhage

“…The studies demonstrated that about 5% patients with gliomas can encounter apoplectic hemorrhage, especially those with glioblastoma (Barkovich et al, 1998;Fiveash et al, 2003;Pina et al, 2014;Ryken et al, 2014;Wang et al, 2014). Glioma hemorrhage is mainly caused by the following factors: a. tumor vascular occlusion and distal vascular necrosis caused by vascular endothelial proliferation, hemangiectasis and vascular distension due to tumor growth as well as invasion of tumor on blood vessels; b. degeneration and necrosis of adjacent tissue structures resulted from tumor infiltration and oppression as well as extended tumor vessels; c. local blood stasis and increased press caused by tumors oppressing adjacent regurgitant vessels; d. changes of tumor haemodynamics due to head trauma and radiotherapy (Fraum et al, 2011;Jo et al, 2014).…”

Letter to the Editor: “The role of imaging in the management of progressive glioblastoma. A systematic review and evidence-based clinical practice guideline” [J Neurooncol 2014; 118:435–460]

“…We have read with interest the review by Ryken et al [1] about the role of imaging in the management of progressive glioblastoma. In general, we agree with this review but we cannot support the opinion that the routine use of Positron-Emission-Tomography (PET) to identify progression of glioblastoma is not recommendable.…”