Initial bolus of conventional versus high-dose dexamethasone in metastatic spinal cord compression

Neurology ◽  
1989 ◽  
Vol 39 (9) ◽  
pp. 1255-1255 ◽  
Author(s):  
Ch. J. Vecht ◽  
H. Haaxma-Reiche ◽  
W. L. J. van Putten ◽  
M. d. Visser ◽  
E. P. Vries ◽  
...  
2017 ◽  
Vol 7 (3) ◽  
pp. 272-279 ◽  
Author(s):  
Gordon D. Skeoch ◽  
Matthew K. Tobin ◽  
Sajeel Khan ◽  
Andreas A. Linninger ◽  
Ankit I. Mehta

Study Design: Narrative review. Objective: Metastatic spinal cord compression (MSCC) is a very frequent complication among cancer patients. Presenting commonly as nocturnal back pain, MSCC typically progresses to lower extremity paresis, loss of ambulatory capabilities, and paraplegia. In addition to standard treatment modalities, corticosteroid administration has been utilized in preclinical and clinical settings as adjunctive therapy to reduce local spinal cord edema and improve clinical symptoms. This article serves as a review of existing literature regarding corticosteroid management of MSCC and seeks to provide potential avenues of research on the topic. Methods: A literature search was performed using PubMed in order to consolidate existing information regarding dexamethasone treatment of MSCC. Of all search results, 7 articles are reviewed, establishing the current understanding of metastatic spine disease and dexamethasone treatment in both animal models and in clinical trials. Results: Treatment with high-dose corticosteroids is associated with an increased rate of potentially serious systemic side effects. For this reason, definitive guidelines for the use of dexamethasone in the management of MSCC are unavailable. Conclusions: It is still unclear what role dexamethasone plays in the treatment of MSCC. It is evident that new, more localizable therapies may provide more acceptable treatment strategies using corticosteroids. Looking forward, the potential for more targeted, localized application of the steroid through the use of nanotechnology would decrease the incidence of adverse effects while maintaining the drug’s efficacy.


1989 ◽  
Vol 70 (6) ◽  
pp. 920-925 ◽  
Author(s):  
Jean Yves Delattre ◽  
Ehud Arbit ◽  
Howard T. Thaler ◽  
Marc K. Rosenblum ◽  
Jerome B. Posner

✓ In order to assess the clinical and biological effects of glucocorticoids in the therapy of epidural spinal cord compression, the T8–10 epidural space of 50 rats was implanted with Walker 256 tumor. The rats were studied 10 to 20 days later when they became paraparetic. The regional blood-spinal cord transport constant (K, a function of the blood-spinal cord barrier) of 14Carbon-labeled aminoisobutyric acid was measured with quantitative autoradiography 6 hours after intravenous injection of low-dose (0.1 mg/kg), intermediate dose (1 mg/kg), and high-dose (10 mg/kg) dexamethasone. The effects of dexamethasone in these doses on the clinical signs and water content of the compressed cord were also evaluated 40 hours after treatment began. The K factor increased 730% in compressed compared with noncompressed spinal cords (p < 0.001). Dexamethasone induced a dose-related reduction of both K (p = 0.007) and water content of the compressed cord (p < 0.0001). Stabilization or, more rarely, improvement of weakness at 24 and 40 hours posttreatment correlated with the dose of dexamethasone (r = 0.88, p < 0.001). This study demonstrates that dexamethasone has a dose-related beneficial clinical effect associated with an improvement of blood-spinal cord barrier breakdown and a reduction of the water content of the compressed cord. This study supports the use of high-dose dexamethasone for the initial treatment of epidural spinal cord compression.


2018 ◽  
Vol 7 (5) ◽  
pp. 719-726 ◽  
Author(s):  
Helga Schultz ◽  
Svend Aage Engelholm ◽  
Eva Harder ◽  
Ulrik Pedersen-Bjergaard ◽  
Peter Lommer Kristensen

Background The risk of developing diabetes mellitus (DM) during treatment with high-dose glucocorticoids is unknown and monitoring of glucose is random in many settings. Objective To determine incidence of and risk factors for induction of DM during high-dose glucocorticoid therapy of metastatic spinal cord compression (MSCC) in patients referred to radiotherapy. Furthermore, to describe the time course of development of DM. Subjects and methods 140 patients were recruited (131 were included in the analysis) with MSCC receiving high-dose glucocorticoid ≥100 mg prednisolone per day were included in a prospective, observational cohort study. The primary endpoint was development of DM defined by two or more plasma glucose values ≥11.1 mmol/L. Plasma glucose was monitored on a daily basis for 12 days during radiotherapy. Results Fifty-six of the patients (43%; 95% CI 35–52%) were diagnosed with DM based on plasma glucose measurements during the study period. Sixteen patients, 12% (95% CI 6–18%), were treated with insulin. At multivariate analysis, only high baseline HbA1c predicted the development of insulin-treated DM. An HbA1c-value <39 mmol/mol was associated with a negative predictive value of 96% for not developing DM needing treatment with insulin. The diagnosis of diabetes with need for insulin treatment was made within 7 days in 14 of the 16 (88%; 95% CI 72–100%) patients. Conclusion The risk of developing DM during treatment with high-dose glucocorticoids in patients with MSCC referred to radiotherapy is high in the first treatment week. Only referral HbA1c predicts the development of DM.


2007 ◽  
Vol 67 (1) ◽  
pp. 256-263 ◽  
Author(s):  
Dirk Rades ◽  
Peter J. Hoskin ◽  
Johann H. Karstens ◽  
Volker Rudat ◽  
Theo Veninga ◽  
...  

2016 ◽  
Vol 28 ◽  
pp. S2
Author(s):  
A. Cole ◽  
J. O'Hare ◽  
K. Harpur ◽  
C. O'Brien ◽  
N. Evans ◽  
...  

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