Effect of Pharmacological Agents Administered for Attenuating the Extubation Response on the Quality of Extubation: A Systematic Review

Abstract

Background Several drugs have been tried to obtund the hemodynamic extubation response but all have variable side effects that may affect the quality of short-term recovery. Objective Our primary objective was to evaluate the effect of pharmacological agents, such as dexmedetomidine, local anesthetics, and so on, administered for attenuating the extubation response on the quality of extubation, as judged by the presence or absence of cough, sedation, and laryngospasm/bronchospasm in adult patients who had undergone general anesthesia. A secondary objective was to evaluate the effect of these drugs on other immediate postextubation complications such as respiratory depression, desaturation, bradycardia, hypotension, and nausea and vomiting (PONV). Methods This is a systematic review of (randomized controlled trials) RCTs with meta-analysis. The Medical Literature Analysis and Retrieval System Online (MEDLINE), Cumulative Index of Nursing and Allied Health Literature (CINAHL), and Cochrane Central Register of Controlled Trials (CENTRAL) databases were searched for RCTs on the effect of pharmacological agents on both the hemodynamic extubation response as well as the quality of extubation. Results Fourteen out of 24 included studies were subjected to a meta-analysis. The risk of cough was less likely in the intervention group as compared to control groups (OR 0.26, 95% CI 0.15 to 0.46, p<0.00001, I 2 =35%). Sedation, hypotension (OR= 10.47; 95% CI: 1.86, 58.80, p=0.008, I 2 =0%), and bradycardia (OR= 6.57; 95% CI: 2.09, 20.64, p=0.001, I 2 =0%) were reported with dexmedetomidine. Only one study reported laryngospasm with dexmedetomidine and two studies with opioids.

Compound Lidocaine cream combined with tetracaine prevents cough reaction of patients with general anesthesia caused by extubation: a randomised controlled trial

“…Our study showed that the compound Lidocaine cream also can signi cantly reduce the incident of cough caused by endotracheal extubation about 35% compared NS control group, but there are still 61% patients who have a cough response, perhaps this is because younger patients were more responsive to tracheal tube stimulation of the airway mucosa than older patients [20]. A review study also showed that local anesthetics did not attenuate cough associated with extubation [21], but another eta-study showed that topical airway anesthesia demonstrated better than placebo or no medication in reducing immediate post-extubation cough/bucking [22]. It is well known that tetracaine has a very strong mucosal penetration and can play a better mucosal surface anesthesia [7].…”

Anesthetic management for inhibiting sympathetic activation in an adolescent patient diagnosed with catecholaminergic polymorphic ventricular tachycardia and undergoing left cardiac sympathetic denervation: A case report

“…22,23 As extubation itself can also be physically stressful, increasing BP and HR, consideration should be given to smooth extubation by preventing airway irritation and cough in addition to pain control for gentle recovery from anesthesia. [29][30][31] Several options have been introduced for this, including deep extubation, exchanging the endotracheal tube to a laryngeal mask airway prior to extubation, and limiting unnecessary stimulation on emergence such as the "No-Touch technique". 30,32,33 Pharmacologic interventions such as intravenous remifentanil, dexmedetomidine, or lidocaine can be added to facilitate these techniques.…”

Effect of dexmedetomidine on hemodynamics in patients undergoing hysterectomy: a meta-analysis and systematic review

“…It mainly acts on α2 receptors in the spinal cord and locus coeruleus to inhibit neuronal discharge and sympathetic outflow and reduce sympathetic nerve activity, leading to a reduced perioperative stress response and consequent sedative and analgesic effects. 20 When dexmedetomidine enters the body, it binds to α2 receptors, reducing sympathetic tone and strengthening vagus nerve activity, while inhibiting adenylate cyclase activity and adenosine cyclophosphate synthesis, and reducing the influx of calcium ions to the nerves. The release of transmitters thus reduces hyperpolarization of the presynaptic and postsynaptic membranes, thereby contributing to sedation and the anti-stress response.…”

“…The release of transmitters thus reduces hyperpolarization of the presynaptic and postsynaptic membranes, thereby contributing to sedation and the anti-stress response. 4 , 20 …”