Fentanyl-induced cough during general anesthesia: a different perspective

Abstract

We refer to the recently published article by Yu and co-workers [1] titled ''Premedication with intravenous dexmedetomidine-midazolam suppresses fentanyl-induced cough''.In this article, the authors observe incidences of fentanyl-induced cough (FIC) between 0 and 63.6 %. In our experience, the incidence FIC is much lower. In fact, we rarely observe coughing during induction of general anesthesia in our practice. Typically, we administer an intravenous preinduction bolus dose of 100 lg via a peripheral intravenous cannula to our adult patients. This equates to approximately half the dose quoted by the authors (1.5 vs. 3.0 lg/kg), based on a standard 70 kg patient. The apparent lower incidence of FIC observed in our practice is at least partly supported by Phua and coauthors [2], who have demonstrated that the injection of fentanyl 1.5 lg/kg via a peripheral venous line elicits cough in just 28 % of patients. A similar incidence of FIC (33 %) is documented by Shen et al. [3] following a bolus of fentanyl 2 lg/kg.A recently published randomised controlled trial by QiFeng Tang and co-workers [4] involving 400 patients demonstrated that a priming lower dose of fentanyl is effective to suppress FIC. They recommend using a priming dose of 0.5 lg/kg to suppress cough during the induction of anesthesia. In addition, they found the incidence of FIC to be positively correlated with the dose of fentanyl used, as suggested by our observations. However, there are cases where FIC is particularly undesirable such as in patients with cerebral aneurysms, brain trauma, open eye injury, dissecting aortic aneurysm, pneumothorax and hypersensitive airway disease [5]. In such cases, perhaps the method used by QiFeng Tang and co-workers is more suitable as it involves the administration of a single agent, thus avoiding any potential complications resulting from polypharmacy. In fact, a known side effect of pretreatment with dexmedetomidine involves the induction of bradycardia and hypotension [6].Conflict of interest None.

Effect of intravenous dexmedetomidine-midazolam on fentanyl-induced cough

“…We read with great interest the recent letter by Lawlor et al [1] published in Irish Journal of Medical Science, referring to our original article [2] entitled ''Premedication with intravenous dexmedetomidine-midazolam suppresses fentanyl-induced cough''. And we thank Lawlor et al for his interest in our article and appreciate the opportunity to discuss the incidence of fentanyl-induced cough during general anesthesia.…”

“…In Lawlor and co-workers's [1] experience, they rarely observed coughing during induction of general anesthesia administering an intravenous preinduction bolus dose of 100 lg via a peripheral intravenous cannula to their adult patients. This method could be optional in clinic.…”

Comparing the different oxycodone doses of prevent oxycodone for prevention of preventing fentanyl‐induced cough during induction of general anaesthesia

“…However, intravenous oxycodone 0.075 and 0.100 mg/kg was found to reduce FIC incidence significantly; the inhibitory effect was dose‐dependent. Regarding previous literature, the mechanism of cough incidence suppression may be explained by the fact that when oxycodone was given, some cough‐related receptors could be occupied, thereby blocking its combination with fentanyl 14‐16 . On the one hand, this mechanism was speculated to directly inhibit the excitement of the medulla oblongata cough centre, thereby producing the antitussive effect.…”

“…Regarding previous literature, the mechanism of cough incidence suppression may be explained by the fact that when oxycodone was given, some cough-related receptors could be occupied, thereby blocking its combination with fentanyl. [14][15][16] On the one hand, this mechanism was speculated to directly inhibit the excitement of the medulla oblongata cough centre, thereby producing the antitussive effect. On the other hand, it may act on the trachea and bronchial tree muon through κ receptors, with suppression of the reflex tube contraction producing the antitussive effect.…”