The Comparison of the Efficacy of Lidocaine, Paracetamol, and Dexmedetomidine in Preventing Rocuronium Injection Pain

General anesthesia induction is initiated with propofol, and after loss of consciousness is achieved, rocuronium is administered to provide muscle relaxation. Propofol and rocuronium may cause pain during intravenous injection, with an incidence ranging from 20% to 100% for propofol and from 22% to 84% for rocuronium. The current hypothesis regarding the mechanism of pain associated with intravenous drug injection is that stimulation of polymodal nociceptors triggers the release of endogenous pain mediators such as prostaglandins. This stimulation is thought to be related to the non-physiological osmolarity or pH of the drug solution.

The pain that occurs during anesthesia induction may lead to undesirable reflex movements, which can result in accidental dislodgement of the intravenous catheter. In addition, in response to strong nociceptive stimulation, it may also contribute to the development of increased arterial blood pressure and tachycardia. Various pharmacological and non-pharmacological strategies have been investigated to reduce the incidence and severity of injection pain. Among the most commonly used agents for this purpose are lidocaine, various opioids, magnesium, sodium bicarbonate, ketamine, paracetamol, and dexmedetomidine.

Although lidocaine is frequently used to prevent propofol/rocuronium injection pain during anesthesia, propofol or rocuronium pain can still occur in up to 30% of cases, even with lidocaine administration. Therefore, there is currently no pharmacological agent in the literature that has been definitively confirmed to reduce propofol/rocuronium pain.

Paracetamol is a widely used agent for pain management and as an antipyretic, although its precise molecular mechanism of action is not fully understood. However, the antinociceptive effects of paracetamol are thought to occur through both peripheral and central mechanisms via inhibition of cyclooxygenase-2 (COX-2). With its peripheral effects, paracetamol is thought to reduce propofol- and rocuronium-induced injection pain and the associated involuntary withdrawal movements . In addition, paracetamol has been shown to selectively suppress peripheral PGE₂ release and to increase COX-2 gene expression in an acute inflammation model. Another study reported that paracetamol exhibits selectivity in inhibiting the synthesis of prostaglandins and related factors. Furthermore, although paracetamol does not inhibit COX enzymes at therapeutic concentrations in vitro, it has been reported to inhibit a variant of COX enzymes in vivo.

Dexmedetomidine is an α₂-adrenergic receptor agonist with supraspinal, spinal, and peripheral effects, possessing strong sedative, analgesic, and sympatholytic properties. Alpha-2 receptors are found in blood vessels and inhibit the release of norepinephrine. Although some studies in the literature have reported that dexmedetomidine reduces propofol- and rocuronium-induced pain, there are also studies that do not support this finding. Moreover, the effective optimal dose of this agent has not yet been clearly established.