Use of Dexmedetomidine in Cardiothoracic and Vascular Anesthesia

Is Dexmedetomidine the Key for Reducing Acute Kidney Injury After Cardiac Surgery?

“…Dexmedetomidine also may provide anti-inflammatory benefits in response to surgical stress through cytokine inhibition and suppression of adrenoceptor-mediated vascular constriction in the renal structures. 7,8 These effects perhaps explain the Peng et al findings of reduced AKI with dexmedetomidine use, specifically in the preoperative and intraoperative settings, irrespective of postoperative use. With the temporal insult of cardiopulmonary bypass, early preservation of the renal vasculature may serve as a mechanism for prevention of phenotypic AKI in the post-bypass setting.…”

“…A similar hypothesis has been proposed for early prophylactic dexmedetomidine application in sepsis to protect against intestinal injury. 7,8 The Peng et al study is not without limitation. The 9 studies included in the analysis spanned nearly a decade, and therefore several different definitions were used to characterize AKI.…”

“…6 Dexmedetomidine has become an increasingly popular anesthetic in the critically ill because of its ability to facilitate sedation in nonintubated patients; allow for intubated patients to be more interactive; shorten mechanical ventilatory durations; reduce incidences of delirium; and provide opioid-sparing effects, reducing postoperative pain. 7 Because of its sympatholytic properties, dexmedetomidine may result in additive hemodynamic instability-which is already a known risk factor for postoperative AKI-raising concern for potential renal hypoperfusion from hypotensive effects with its use. 2,7 Despite this, Peng et al did not find any differences in hypotension or bradycardia or the need for vasopressors with dexmedetomidine use.…”

“…7 Because of its sympatholytic properties, dexmedetomidine may result in additive hemodynamic instability-which is already a known risk factor for postoperative AKI-raising concern for potential renal hypoperfusion from hypotensive effects with its use. 2,7 Despite this, Peng et al did not find any differences in hypotension or bradycardia or the need for vasopressors with dexmedetomidine use. These findings are likely a result of relatively lower doses of dexmedetomidine used in the included studies (<0.8 mg/kg/h) and omission of bolus administration.…”

“…Interestingly, dexmedetomidine-mediated sympathetic inhibition has been suggested to reduce local norepinephrine activity in the renal vasculature, promoting vasodilation of the renal artery. 7 Other putative effects to the kidney include reduced sodium reabsorption and inhibited vasopressin secretion, preserving the glomerular filtration rate. Dexmedetomidine also may provide anti-inflammatory benefits in response to surgical stress through cytokine inhibition and suppression of adrenoceptor-mediated vascular constriction in the renal structures.…”