Different additives have been used to prolong regional blockade. We designed a prospective, randomized, double-blind study to evaluate the effect of dexamethasone added to lidocaine on the onset and duration of axillary brachial plexus block. Sixty patients scheduled for elective hand and forearm surgery under axillary brachial plexus block were randomly allocated to receive either 34 mL lidocaine 1.5% with 2 mL of isotonic saline chloride (control group, n 30) or 34 mL lidocaine 1.5% with 2 mL of dexamethasone (8 mg) (dexamethasone group, n 30). Neither epinephrine nor bicarbonatewasaddedtothetreatmentmixture.Weused anervestimulatorandmultiplestimulationstechnique in all of the patients. After performance of the block, sensory and motor blockade of radial, median, musculocutaneous, and ulnar nerves were recorded at 5, 15, and 30 min. The onset time of the sensory and motor blockade was defined as the time between last injection and the total abolition of the pinprick response and complete paralysis. The duration of sensory and motor blockswereconsideredasthetimeintervalbetweenthe administration of the local anesthetic and the first postoperative pain and complete recovery of motor functions.Sixteenpatientswereexcludedbecauseofunsuccessful blockade. The duration of surgery and the onset times of sensory and motor block were similar in the twogroups.Thedurationofsensory(24276versus98 33 min) and motor (310 81 versus 130 31 min) blockade were significantly longer in the dexamethasone than in the control group (P 0.01). We conclude that the addition of dexamethasone to lidocaine 1.5% solution in axillary brachial plexus block prolongs the duration of sensory and motor blockade. (Anesth Analg 2006;102:263–7)

Dexamethasone added to lidocaine prolongs axillary brachial plexus blockade.

Background and objectiveDexamethasone has been shown to prolong the duration of postoperative analgesia when given as an adjunct for peripheral nerve blocks. However, it has not been evaluated when given in conjunction with bupivacaine and clonidine to provide blockade of the brachial plexus at the

Dexamethasone with bupivacaine increases duration of analgesia in ultrasound-guided interscalene brachial plexus blockade.

We systematically reviewed the safety and efficacy of perineural dexamethasone as an adjunct for peripheral nerve blockade in 29 controlled trials of 1695 participants. We grouped trials by the duration of local anaesthetic action (short- or medium- vs long-term). Dexamethasone increased the mean (95% CI) duration of analgesia by 233 (172-295) min when injected with short- or medium-term action local anaesthetics and by 488 (419-557) min when injected with long-term action local anaesthetics, p < 0.00001 for both. However, these results should be interpreted with caution due to the extreme heterogeneity of results, with I2 exceeding 90% for both analyses. Meta-regression did not show an interaction between dose of perineural dexamethasone (4-10 mg) and duration of analgesia (r2 = 0.02, p = 0.54). There were no differences between 4 and 8 mg dexamethasone on subgroup analysis.

https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/pdf/10.1111/anae.12823

A systematic review and meta-analysis of perineural dexamethasone for peripheral nerve blocks.

—The association between hypertension and insulin resistance might be explained by increased activity of the principal glucocorticoid, cortisol. Recent data show that the intensity of dermal vasoconstriction after topical application of glucocorticoids is increased in patients with essential hypertension. In this report, we examine whether increased glucocorticoid sensitivity or secretion is associated with insulin resistance and is a cause or consequence of hypertension. We studied 32 men (aged 47 to 56 years) from a cross-sectional study and 105 men (aged 23 to 33 years) in whom predisposition to high blood pressure has been defined by their own blood pressure and the blood pressures of their parents. In both populations, increased dermal glucocorticoid sensitivity was associated with relative hypertension, insulin resistance, and hyperglycemia. In young men with higher blood pressure whose parents also had high blood pressure, enhanced glucocorticoid sensitivity was accompanied by enhanced secretion of cortisol, enhanced ligand-binding affinities for dexamethasone in leukocytes, and impaired conversion of cortisol to inactive metabolites (cortisone and 5β-dihydrocortisol). Increased tissue sensitivity to cortisol, amplified by enhanced secretion of cortisol, is a feature of the familial predisposition to high blood pressure rather than a secondary effect of high blood pressure. It may be mediated by an abnormal glucocorticoid receptor, and it may contribute to the association between hypertension and insulin resistance.

Increased Glucocorticoid Activity in Men With Cardiovascular Risk Factors

Endothelial dysfunction may play a key role in keloid and hypertrophic scar pathogenesis - Keloids and hypertrophic scars may be vascular disorders.

Two currently used steroids (clobetasone butyrate and betamethasone valerate) reproducibly cause vasoconstriction on topical application to human forearm skin. Progesterone, deoxycorticosterone, testosterone, and estradiol, even at 100- to 200-fold higher concentrations, cause no vasoconstriction when applied alone. Applied with clobestasone butyrate, testosterone and estradiol are without antagonist effect; in contrast, both progesterone and deoxycorticosterone antagonize the vasoconstrictor response in a dose-related fashion, with a half-maximal effect at 20-30 times the concentration of clobetasone. Neither progesterone nor deoxycorticosterone affects the vasoconstriction produced by the intradermal injection of epinephrine. In most glucocorticoid-responsive systems, progesterone and deoxycorticosterone are glucocorticoid antagonists, and estradiol and testosterone are inactive. We interpret these studies as evidence that the vasoconstrictor effects of topical steroids are mediated by occupancy of classical glucocorticoid receptors, rather than by nonspecific pharmacological mechanisms.

Steroid-Induced Vasoconstriction: Glucocorticoid Antagonist Studies

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Steroid-Induced Vasoconstriction: Glucocorticoid Antagonist Studies