Corticosteroids in the Treatment of Spinal Cord Injuries: Difference between revisions
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After the initial tissue damage the inflammatory sequelae is controllable. The inflammatory response is illustrated through tissue ischemia, oxidative stress, inflammatory, and immune responses. Steroids such as Methyl prednisone are utilized in the reduction of oxidative stress | After the initial tissue damage associated with a spinal cord injury, the inflammatory sequelae is controllable. The inflammatory response is illustrated through tissue ischemia, oxidative stress, inflammatory, and immune responses. Steroids such as Methyl prednisone are utilized in the reduction of oxidative stress as it is a primary degenerative event post trauma<ref name=":0">Manchikanti, L., Cash, K. A., Pampati, V., & Falco, F. J. (2014). Transforaminal epidural injections in chronic lumbar disc herniation: A randomized, double-blind, active-control trial. Retrieved from <nowiki>https://www.ncbi.nlm.nih.gov/pubmed/25054399</nowiki></ref><ref name=":1">Singh, P. L., Agarwal, N., Barrese, J. C., & Heary, R. F. (2012). Current therapeutic strategies for inflammation following traumatic spinal cord injury. ''Neural Regeneration Research'', ''7''(23), 1812–1821. <nowiki>http://doi.org/10.3969/j.issn.1673-5374.2012.23.008</nowiki></ref>. Additionally, higher doses have illustrated neuroprotective and immunosuppressive capacities through the release of interleukins, reducing Ca2+ aggregation, and necrosis limiting the progression of ischemia<ref name=":0" /><ref name=":1" /> | ||
Oral and intravenous are prescribed for systemic disorders such as arthritis, blood disorders, allergic reactions, and immune disorders <ref name=":1" /> .The biological half-life is also to be considered as the therapeutic range as is between 1.8 and 5.2 hours <ref name=":2">Ciccone, C. D. (2016). ''Pharmacology in rehabilitation'' (5th ed.). Philadelphia: F.A. Davis Company.</ref>. | ==== '''Pharmacokinetics''' ==== | ||
Oral and intravenous forms are prescribed for systemic disorders such as arthritis, blood disorders, allergic reactions, and immune disorders<ref name=":1" />. The biological half-life is also to be considered as the therapeutic range as is between 1.8 and 5.2 hours<ref name=":2">Ciccone, C. D. (2016). ''Pharmacology in rehabilitation'' (5th ed.). Philadelphia: F.A. Davis Company.</ref>. Other modes of administration such as spinal, inhaled, and local injections are prescribed to SCI and patients with tendinopathies to limit systemic leakage of the steroid <ref name=":0" /><ref name=":1" />. | |||
Noted complications such as wound infections, sepsis, and pneumonia are prevalent. Gastrointestinal and collagenous tissue disruption have been exhibited | ==== '''Adverse Effects''' ==== | ||
Noted complications such as wound infections, sepsis, and pneumonia are prevalent in patients with spinal cord injuries. Gastrointestinal and collagenous tissue disruption have been exhibited with long-term use of MP<ref name=":1" />. The catabolic effects of glucocorticoids on various tissue such as bone, ligament, and tendon are well-documented. Reduction of bone density in both patients with osteoporosis and arthritis is common<ref name=":2" /><ref name=":3">Hachemi Y, Rapp AE, Picke AK, Weidinger G, Ignatius A, Tuckermann J. Molecular mechanisms of glucocorticoids on skeleton and bone regeneration after fracture. ''J Mol Endocrinol''. 2018;61(1):R75-R90.</ref>. In addition, this class of steroids may lead to muscle atrophy, hypertension, diabetes exaggeration, glaucoma, and cataracts<ref name=":1" />. These side effects emphasize the need for the PT to maintain a watchful eye and communicate with the physician if there is a need to limit glucocorticoid therapy. | |||
The therapist must be mindful of the systemic effects and their respective presentation. Osteoporosis patients that are prescribed glucocorticoids have an increased incidents of compression fractures <ref name=":3" />. This limits the interventions to the | ==== '''Physical Therapy Implications''' ==== | ||
The therapist must be mindful of the systemic effects and their respective presentation. Osteoporosis patients that are prescribed glucocorticoids have an increased incidents of compression fractures<ref name=":3" />. This limits the interventions available to the therapist, particularly high-velocity manipulations. Tendon and ligament ruptures are prevalent as collagen synthesis is disturbed<ref name=":3" />. To limit the accompanying adverse effects, strengthening bone and musculature through weight bearing activities is recommended. | |||
== Back to [[Pharmacological Management of Spinal Cord Injuries]]. == | == Back to [[Pharmacological Management of Spinal Cord Injuries]]. == | ||
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Revision as of 05:29, 1 December 2018
After the initial tissue damage associated with a spinal cord injury, the inflammatory sequelae is controllable. The inflammatory response is illustrated through tissue ischemia, oxidative stress, inflammatory, and immune responses. Steroids such as Methyl prednisone are utilized in the reduction of oxidative stress as it is a primary degenerative event post trauma[1][2]. Additionally, higher doses have illustrated neuroprotective and immunosuppressive capacities through the release of interleukins, reducing Ca2+ aggregation, and necrosis limiting the progression of ischemia[1][2]
Pharmacokinetics[edit | edit source]
Oral and intravenous forms are prescribed for systemic disorders such as arthritis, blood disorders, allergic reactions, and immune disorders[2]. The biological half-life is also to be considered as the therapeutic range as is between 1.8 and 5.2 hours[3]. Other modes of administration such as spinal, inhaled, and local injections are prescribed to SCI and patients with tendinopathies to limit systemic leakage of the steroid [1][2].
Adverse Effects[edit | edit source]
Noted complications such as wound infections, sepsis, and pneumonia are prevalent in patients with spinal cord injuries. Gastrointestinal and collagenous tissue disruption have been exhibited with long-term use of MP[2]. The catabolic effects of glucocorticoids on various tissue such as bone, ligament, and tendon are well-documented. Reduction of bone density in both patients with osteoporosis and arthritis is common[3][4]. In addition, this class of steroids may lead to muscle atrophy, hypertension, diabetes exaggeration, glaucoma, and cataracts[2]. These side effects emphasize the need for the PT to maintain a watchful eye and communicate with the physician if there is a need to limit glucocorticoid therapy.
Physical Therapy Implications[edit | edit source]
The therapist must be mindful of the systemic effects and their respective presentation. Osteoporosis patients that are prescribed glucocorticoids have an increased incidents of compression fractures[4]. This limits the interventions available to the therapist, particularly high-velocity manipulations. Tendon and ligament ruptures are prevalent as collagen synthesis is disturbed[4]. To limit the accompanying adverse effects, strengthening bone and musculature through weight bearing activities is recommended.
Back to Pharmacological Management of Spinal Cord Injuries.[edit | edit source]
- ↑ 1.0 1.1 1.2 Manchikanti, L., Cash, K. A., Pampati, V., & Falco, F. J. (2014). Transforaminal epidural injections in chronic lumbar disc herniation: A randomized, double-blind, active-control trial. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/25054399
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Singh, P. L., Agarwal, N., Barrese, J. C., & Heary, R. F. (2012). Current therapeutic strategies for inflammation following traumatic spinal cord injury. Neural Regeneration Research, 7(23), 1812–1821. http://doi.org/10.3969/j.issn.1673-5374.2012.23.008
- ↑ 3.0 3.1 Ciccone, C. D. (2016). Pharmacology in rehabilitation (5th ed.). Philadelphia: F.A. Davis Company.
- ↑ 4.0 4.1 4.2 Hachemi Y, Rapp AE, Picke AK, Weidinger G, Ignatius A, Tuckermann J. Molecular mechanisms of glucocorticoids on skeleton and bone regeneration after fracture. J Mol Endocrinol. 2018;61(1):R75-R90.
