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Pain Fellows Lecture Series: Pharmacology of Injections

Pain Fellows Lecture Series: Pharmacology of Injections. Contrast Agents. Why do we use them? Localize precise anatomic locations Prevent aberrant spread of injectate Reduce fluorscopic time (reduce exposure). When do we use them?. Exclude intravascular or intrathecal injection

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Pain Fellows Lecture Series: Pharmacology of Injections

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  1. Pain Fellows Lecture Series:Pharmacology of Injections

  2. Contrast Agents • Why do we use them? • Localize precise anatomic locations • Prevent aberrant spread of injectate • Reduce fluorscopic time (reduce exposure)

  3. When do we use them? • Exclude intravascular or intrathecal injection • Dilineate anatomy – SI joints, epidural spaces, LSBs, SGBs, discograms

  4. Classification • Positive Agents • Absorb xrays • Creates darker shadow • Negative Agents • More transparent than tissue • Creates light shadow • Air, nitrogen, co2, helium, xenon

  5. Classification • Non Ionic - hydrophillic • Less toxic • Does not combine with other molecules • Lower osmolality

  6. Classification • Ionic • More toxic due to presence of negatively charged free ends • Able to combine with other molecules and form or break bonds  tissue toxicity

  7. Contrast Agents • 1st generation • Iodinated – tri-iodinated benzoate anion • Limited by high osmolar concentration • Up to 8x physiologic level • Higher osmolality  toxicity (hemodynamic & discomfort)

  8. Contrast Agents • 2nd generation • Labeled as “non-ionic”; actually just less free iodine • Higher iodine:particle ratio (lower osmolality) • Rapidly absorbed into systemic circulation • Minimal metbolism • >90% renally excreted

  9. Nomenclature • Name + number • The name is the iodinated particle • Number is the concentration of the iodinated particle • Ex omnipaque 180 = 180mg/ml of iodine • Recommended daily limit is 3 grams/day

  10. Commonly used contrast agents Normal serum osm = 300 mOsm/kg H20

  11. Adverse reactions • 90% occur within 15 minutes (recommend observation 30-60 mins post procedure) • Must have resuscitation equipment and drugs available • Incidence is 5-12% w/ionic agents • Most frequent = headache, nausea, vomiting

  12. Adverse reactions • Allergic • Vasomotor • Cutaneous • Bronchospasm • Cardiovascular • Vasovagal • anaphylactoid

  13. Adverse reactions (cont) • Chemotoxic • Thyrotoxicosis – rare • Nephrotoxicity • Arrhythmias

  14. Adverse reactions • Hyperosmolality • Erythrocyte damage • Endothelial damage & thrombosis • Vasodilation • Hypervolemia • Cardiac depression

  15. Renal Toxicity • Risk factors • Ionic agents • DM • Dehydration / pre-renal azotemia • CRI

  16. Pre-treatment Recommendations • 12 Hours prior • Predinisone 20 to 50mg PO • Zantac 50 mg • Diphenhydramine 25 to 50 mg po • 2 hours prior • Prednisone 20 to 50 mg PO • Zantac 50 mg po • Diphenhydramine 25 to 50 mg PO • Immediately before • 25 mg IV

  17. Corticosteroids • Mineral corticoids vs. Glucocorticoids vs. adrenal androgens • We use glucocorticoids • All are chemical modifications of Cortisol

  18. MOA • Anti-inflammatory • ? Radiculopathy may represent toxic spill of anti-inflammatory mediators from the disc • Disc contains PLA-2, interleukins and prostaglandins • McCarron demonstrated that only a small amount of NP material was needed to cause a a severe inflammatory response and increase in nerve root size

  19. Anti-inflammatory effects • They induce the lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substratearachidonic acid. • The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect.

  20. MOA • Decreased spontaneous ectopic discharge rate • Reversible inhibition of C-fiber transmission (not A-B) – direct membrane stabilization • Glucocorticoid receptors found in Substantia Gelatinosa - ? Modulate input from peripheral nociceptors?

  21. Immunosuppressive • Immunosuppressive mechanism • Glucocorticoids suppress the cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-γ, the most important of which is the IL-2. Smaller cytokine production reduces the T cell proliferation. • Glucocorticoids also suppress the humoral immunity, causing B cells to express smaller amounts of IL-2 and of IL-2 receptors. This diminishes both B cell clone expansion and antibody synthesis.

  22. Corticosteriods

  23. Corticosteroids

  24. Why particulate? • The premise behind sustained relief from epidural steroid injections is that particulates precipitate out onto the nerve roots. • Non-particulates rapidly disperse away from the nerves and therefore are very short lived in their effects.

  25. Adverse reactions • Fluid retention • Hypertension • Hyperglycemia • Erythema/facial flushing • Menstrual irreg • Gastritis / PUD • Adrenal suppresion • Cushings syndrome • Bone demineralization • Steroid myopathy • Allergic reactions (succinate salts) • Brief euphoric/manic episodes

  26. The most dreaded complication • Lower thoracic / upper lumbar • Transforaminal ESI • Intravascular injection • Cord ischemia  paralysis

  27. References • Image Guided Spine Intervention – Douglas Fenton • Use of Radiopaque Contrast Agents for the Interventional Pain Physician – Chopra, P and Smith, H; PainPhysician Journal, Oct 2004

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