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  • Blood Levels of medicine after injections

  • Coccyx Trabecular Fractures


When do peak blood levels occur after a facet or trigger point injection? (steroid)

Peak serum levels of injected medications typically occur within 24 hours for corticosteroids used in lumbar facet joint injections, though the exact timing varies by medication type and injection site.

For triamcinolone acetonide administered via intra-articular lumbar facet joint injections, peak median serum concentration (3.6 ng/mL) was detected within 24 hours after injection.

[1]

 This study also found a prolonged terminal elimination half-life of 213 hours, with serum cortisol suppression lasting an average of 4.4 days.

[1]

For trigger point injections, the pharmacokinetics depend on the specific agent used. When local anesthetics like lidocaine or bupivacaine are injected into trigger points, absorption into the bloodstream occurs more rapidly than with depot corticosteroid preparations.

[2-3]

 However, specific peak concentration timing for trigger point injections is not well-characterized in the medical literature.

The clinical significance of systemic absorption varies by medication. With corticosteroids, the prolonged half-life and endocrine effects could increase the risk for drug-drug interactions in patients taking medications that inhibit corticosteroid metabolism.

[1]

 For local anesthetics used in trigger point injections, systemic absorption is generally rapid but the clinical impact is typically minimal when appropriate doses are used.

[2-3]

Would you like me to summarize the comparative pharmacokinetics and systemic effects of different corticosteroids and local anesthetics used in these injections, to help guide agent selection based on patient-specific risk factors?

1.

Corticosteroid and Cortisol Serum Levels Following Intra-Articular Triamcinolone Acetonide Lumbar Facet Joint Injections.

Pain Practice : The Official Journal of World Institute of Pain. 2018. Dickson RR, Reid JM, Nicholson WT, Lamer TJ, Hooten WM.

2.

Trigger Point Injections.

Physical Medicine and Rehabilitation Clinics of North America. 2022. Appasamy M, Lam C, Alm J, Chadwick AL.

3.

Guideline Update for the Performance of Fusion Procedures for Degenerative Disease of the Lumbar Spine. Part 13: Injection Therapies, Low-Back Pain, and Lumbar Fusion.

Journal of Neurosurgery. Spine. 2014. Watters WC, Resnick DK, Eck JC, et al.Guideline


When do peak blood levels occur after an epidural steroid injection?  (steroid)

Peak serum levels of corticosteroids after epidural steroid injection typically occur within 24 hours, though the specific timing varies by corticosteroid formulation.

For triamcinolone acetonide, peak serum concentrations of 4.1 ng/mL were detected within 24 hours after lumbar interlaminar epidural injection, with a similar peak of 5.4 ng/mL occurring at 22.1 hours following cervical interlaminar epidural injection.

[1-2]

 The terminal elimination half-life was prolonged at 523 hours for lumbar and 219 hours for cervical administration.

[1-2]

For dexamethasone, pharmacokinetic studies show that epidural administration results in approximately 50% lower peak plasma concentrations compared to intravenous administration, though the total systemic exposure (AUC) is equivalent.

[3]

 The lower peak concentration reflects slower absorption from the epidural space.

Methylprednisolone demonstrates similar rapid systemic absorption, with maximal cortisol suppression occurring by day 1 post-injection and serum cortisol levels below normal in 87% of patients at day 7.

[4]

 Cortisol suppression persisted for a median of 14 days, indicating sustained systemic steroid exposure.

[4]

The clinical significance is that particulate corticosteroids (triamcinolone, methylprednisolone) cause more prolonged HPA axis suppression than non-particulate formulations (dexamethasone, betamethasone).

[5]

 Particulate steroids produced average cortisol reductions of 41.0-41.6% at 3 weeks, whereas non-particulate formulations showed no significant cortisol suppression compared to local anesthetic alone.

[5]

Would you like me to summarize the comparative risks and benefits of particulate versus non-particulate corticosteroids for epidural injection, particularly regarding safety profiles and clinical outcomes?

1.

Serum Triamcinolone Levels Following Interlaminar Epidural Injection.

Regional Anesthesia and Pain Medicine. 2015. Hooten WM, Nicholson WT, Gazelka HM, et al.

2.

Serum Triamcinolone Levels Following Cervical Interlaminar Epidural Injection.

Pain Research & Management. 2017. Lamer TJ, Dickson RR, Gazelka HM, et al.

3.

The Pharmacokinetics and Pharmacodynamics of Dexamethasone Following Epidural SP-102 or Intravenous Dexamethasone Sodium Phosphate Injection in Subjects With Lumbosacral Radicular Pain.

International Journal of Clinical Pharmacology and Therapeutics. 2022. Yee S, Robson R, Stannard E, Lal R, Lissin D.

4.

Hypothalamic Pituitary Adrenocortical Axis Suppression Following a Single Epidural Injection of Methylprednisolone Acetate.

Pain Physician. 2017. Abdul AJ, Ghai B, Bansal D, et al.

5.

Systemic Effects of Epidural Steroid Injections for Spinal Stenosis.

Pain. 2018. Friedly JL, Comstock BA, Heagerty PJ, et al.


Blood levels of local anesthetic vary significantly by injection site. (LA = local anesthesia)

Blood levels of local anesthetic vary significantly by injection site, with the highest systemic absorption occurring after intercostal nerve blocks and the lowest after subcutaneous administration.

[1-2]

 For the specific procedures you asked about, here's what the medical literature shows:

Epidural injections produce peak plasma levels of lidocaine at 30-45 minutes after injection.

[3]

 Following 75 mg of epidural lidocaine (2% solution), the maximum venous plasma concentration averages 0.41 ± 0.07 mcg/mL.

[4]

 The rate of vascular absorption from the epidural space is significantly faster than from the subarachnoid space, with higher plasma concentrations at 2, 5, and 10 minutes post-injection.

[4]

Trigger point injections have not been extensively studied for systemic absorption kinetics in the medical literature. However, given that trigger point injections typically use small volumes (often 0.5-3 mL) of dilute local anesthetic solutions and involve intramuscular administration, systemic absorption would be expected to fall between subcutaneous (lowest) and intercostal (highest) routes.

[1-2]

Facet joint injections similarly lack robust pharmacokinetic data in the literature. Intra-articular facet injections typically use volumes of 0.25-1.5 mL, with joint capsule capacity of 1.0-2.0 mL.

[5]

 The small volumes and confined anatomical space suggest limited systemic absorption, though capsular rupture with larger volumes can lead to extravasation and potentially increased systemic uptake.

For reference, objective adverse CNS manifestations become apparent with venous plasma levels above 6 mcg free base per mL of lidocaine.

[1]

 The addition of epinephrine reduces peak plasma concentrations and slows absorption rates across all injection sites.

[3][6]

Would you like me to summarize the comparative risk of systemic toxicity (e.g., local anesthetic systemic toxicity, LAST) for these injection techniques, including any reported cases or thresholds from the literature?

1.

Lidocaine Hydrochloride. FDA Drug Label.

Food and Drug Administration. Updated date: 2026-01-01.

2.

LIDOCAINE HCl and EPINEPHRINE. FDA Drug Label.

Food and Drug Administration. Updated date: 2021-09-08.

3.

MLK F4 Kit. FDA Drug Label.

Food and Drug Administration. Updated date: 2026-01-08.

4.

Absorption of Lidocaine Following Subarachnoid and Epidural Administration.

Anesthesia and Analgesia. 1979. Giasi RM, D'Agostino E, Covino BG.

5.

Consensus Practice Guidelines on Interventions for Lumbar Facet Joint Pain From a Multispecialty, International Working Group.

Regional Anesthesia and Pain Medicine. 2020. Cohen SP, Bhaskar A, Bhatia A, et al.Guideline

6.

Clinical Pharmacokinetics of Local Anaesthetics.

Clinical Pharmacokinetics. 1979. Tucker GT, Mather LE.


Coccyx trabecular fracture - microscopic fracture in the trabecular (cancellous) bone

A coccyx trabecular fracture is a microscopic fracture within the trabecular (cancellous) bone of the coccyx, distinct from fractures involving the cortical shell or complete displacement of coccygeal segments.

While most literature on coccyx fractures focuses on macroscopic fractures classified by mechanism (flexion, compression, or extension types), trabecular microfractures represent a form of microscopic tissue damage within the internal bone structure.

[1]

 Research on vertebral loading demonstrates that trabecular microfracture can occur in cancellous bone before overt cortical shell failure.

[2]

 Under cyclic compressive loading, trabecular microfractures appear as the primary form of microdamage in vertebral cancellous bone, with few microcracks observed.

[2]

In the clinical context of coccyx trauma, such microscopic trabecular damage may not be readily visible on standard radiographs, which typically identify displaced fractures, luxations, or hypermobility.

[3]

 Cross-sectional imaging like MRI or CT may be more sensitive for detecting subtle trabecular injury, though the term "trabecular fracture" is not commonly used in standard coccyx fracture classifications.

These microfractures could potentially contribute to coccydynia (coccyx pain) even when conventional imaging appears normal or shows only subtle findings. The clinical significance lies in understanding that bone damage at the microscopic level may explain persistent symptoms in some patients with coccygeal trauma.

Would you like me to review the available evidence on the sensitivity and specificity of MRI and CT for detecting coccyx trabecular fractures, and how imaging findings correlate with clinical outcomes such as persistent coccydynia?

1.

Classification of Fractures of the Coccyx From a Series of 104 Patients.

European Spine Journal : Official Publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society. 2020. Maigne JY, Doursounian L, Jacquot F.

2.

Trabecular Microfracture Precedes Cortical Shell Failure in the Rat Caudal Vertebra Under Cyclic Overloading.

Calcified Tissue International. 2009. Kummari SR, Davis AJ, Vega LA, et al.

3.

Causes and Mechanisms of Common Coccydynia: Role of Body Mass Index and Coccygeal Trauma.

Spine. 2000. Maigne JY, Doursounian L, Chatellier G.

Conservative management is the first-line treatment for coccyx trabecular fractures, with interventional techniques and coccygectomy reserved for refractory cases. Most fractures heal with conservative therapy, though instability or persistent pain may require escalation.

[1-2]

Initial conservative treatment includes NSAIDs, analgesics, sitting cushions (donut-shaped or wedge cushions), pelvic-floor training, and physical therapy.

[2-4]

 Manual therapies such as pelvic-floor training and elastic therapeutic tape have shown limited to clinically relevant efficacy.

[2]

 For patients with persistent symptoms after initial conservative measures, coccygeal corticosteroid injection is typically the next step, though patients often require repeat injections over time.

[3-4]

Additional conservative modalities may provide benefit in select cases. Acupuncture combined with Tai Chi has demonstrated pain reduction and functional improvement in case reports.

[5]

 Laser acupuncture produced analgesic effects and facilitated bone healing in one patient with refractory post-traumatic coccydynia.

[6]

 Intranasal calcitonin has been used to treat acute pain from coccyx fractures, with decreased pain levels and minimal adverse events in a small case series.

[7]

Manual therapy combined with steroid injection achieved complete pain relief in 61.9% of patients with persistent coccydynia, compared to only 17.4% with steroid injection alone, with no relapses in the combined therapy group versus a 56.5% relapse rate with injection alone.

[8]

 Other interventional options include ganglion impar block, radiofrequency ablation, and extracorporeal shock wave therapy, though high-quality evidence is limited.

[2][9-10]

Coccygectomy should be considered for intractable cases with demonstrated instability after failure of conservative and interventional treatments.

[2][4][11]

 In a meta-analysis, 84% of patients obtained pain relief and 76% returned to work, with mean pain relief rated 5.4 on a 1-10 scale after at least 36 months.

[2]

 However, wound dehiscence occurs in 5% of patients, wound infections in 14-27%, and 3% require repeat surgery.

[2-3][12]

 Total coccygectomy appears superior to partial resection, with partial procedures associated with poorer outcomes.

[11]

 For patients with posterior coccyx dislocations, coccygectomy may be considered more rapidly given the association with unfavorable conservative treatment outcomes.

[4]

Duration of conservative treatment before considering surgery typically ranges from 6 months to 2 years, though longer symptom duration is associated with worse outcomes.

[4][11]

 High-quality comparative studies are lacking to definitively guide treatment selection and timing.

[9-10]

Would you like me to summarize the comparative effectiveness and safety profiles of the various interventional treatments—such as ganglion impar block, radiofrequency ablation, and extracorporeal shock wave therapy—specifically for coccyx trabecular fractures, based on the latest available evidence?

1.

Classification of Fractures of the Coccyx From a Series of 104 Patients.

European Spine Journal : Official Publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society. 2020. Maigne JY, Doursounian L, Jacquot F.

2.

Coccygodynia: Diagnosis and Treatment.

Deutsches Arzteblatt International. 2025. Benditz A, Thoma R.New

3.

A Treatment and Outcomes Analysis of Patients With Coccydynia.

The Spine Journal : Official Journal of the North American Spine Society. 2004. Hodges SD, Eck JC, Humphreys SC.

4.

Conservative Treatment for Chronic Coccydynia: A 36-Month Prospective Observational Study of 115 Patients.

European Spine Journal : Official Publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society. 2021. Charrière S, Maigne JY, Couzi E, et al.

5.

Acupuncture Combined With Tai Chi in the Treatment of a Patient With Coccyx Fracture: A Case Report.

Medicine. 2025. Bai X, Tian Y, Wang C, et al.New

6.

Laser Acupuncture for Refractory Coccydynia After Traumatic Coccyx Fracture: A Case Report.

Medicine. 2020. Lin CH, Wu SY, Hu WL, et al.

7.

Coccyx Fractures Treated With Intranasal Calcitonin.

Pain Physician. 2014. Foye PM, Shupper P, Wendel I.

8.

Management of Persistent Coccydynia With Transrectal Manipulation: Results of a Combined Procedure.

European Spine Journal : Official Publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society. 2018. Seker A, Sarikaya IA, Korkmaz O, et al.

9.

A Review of Current Treatment Options for Coccygodynia.

Current Pain and Headache Reports. 2018. Elkhashab Y, Ng A.

10.

The Interdisciplinary Management of Coccydynia: A Narrative Review.

PM & R : The Journal of Injury, Function, and Rehabilitation. 2022. White WD, Avery M, Jonely H, et al.

11.

Acute Traumatic Instability of the Coccyx: Results in 28 Consecutive Coccygectomies.

European Spine Journal : Official Publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society. 2013. Ramieri A, Domenicucci M, Cellocco P, Miscusi M, Costanzo G.

12.

Coccygectomy for Coccygodynia: A Single-Center Experience.

Medicine. 2023. Izci EK, Keskin F.


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