Sir, Awake fiberoptic intubation (AFOI) is recommended for patients with anticipated difficult airway, failed intubation, and unstable cervical spine injury where optimum positioning for laryngoscopy is difficult to achieve. Preparation includes obtundation of airway reflexes, adequate sedation, and anxiolysis along with preservation patent airway and adequate ventilation. Dexmedetomidine produces hypnosis, amnesia, analgesia, anxiolysis, sympatholysis, and antisialogogue effects; all of them are desired during AFOI.[1] Administration of dexmedetomidine through inhalational route could be a new promising noninvasive method. The bioavailability of dexmedetomidine is 65% and 82% through nasal and buccal mucosa, respectively, following nebulization.[2] Here, we reported a series of four cases of patients with difficult airway in which dexmedetomidine was used as adjuvant to lignocaine nebulization before awake fiberoptic bronchoscope-guided nasotracheal intubation. Written consent was taken from all patients. All these patients were scheduled for mandibular excision and reconstruction under general anesthesia. After shifting the patients to operating room, standard ASA monitor was connected and baseline was taken. Injection glycopyrrolate 0.2 mg i.m., intranasal xylometazoline 0.1%, was given 15 min prior to nebulization to each patient. Patients were nebulized with mixture of 4% lignocaine 10 ml and dexmedetomidine 1 μg/kg by using ultrasonic nebulizer for 15 min followed by fiberoptic bronchoscope-guided nasotracheal intubation. All patients received supplemental oxygen (2 l/min) through the working channel of the bronchoscope. Following intubation, general anesthesia was induced. The parameters observed include heart rate, mean arterial pressure, oxygen saturation at 0, 5, 10, 15 (end of nebulization), and 20 min (just after intubation). Other parameters were observed such as cough and gag reflexes [severity graded as no cough, slight ≤2 coughs, moderate (3–5 coughs), severe (>5 coughs)], patient comfort (cooperative, restless/minimal resistance, severe resistance/requirement for immediate general anesthesia), and signs of lignocaine toxicity. Discussion There were bradycardia and hypotension noted during nebulization in case 2 and 3 as shown in Table 1. Tachycardia was noted at 20 min in case 2 and 4. One episode of cough and gag reflex was noted in case 2. No cough, gag, and other adverse effects such as bronchospasm, seizures due to lignocaine toxicity, and oversedation were recorded in rest of cases as shown in Table 1. Patients were comfortable throughout the procedure.Table 1: Shows vitals parameter and cough/gag reflexes during intubationBrummett et al.[3] studied the effect after perineural dexmedetomidine injection and they attributed to the increased duration of analgesia to the local action of dexmedetomidine. The analgesic effect of dexmedetomidine was not reversed by a ∞2-adrenoceptor antagonist (prazosin or idazoxan), hence confirming its local site of action. Hence, we hypothesize that dexmedetomidine nebulization provides surface analgesia to airway mucosa in addition to its systemic effect due to its effects on peripheral nerve endings. We could not measure systemic levels of the drugs due to lack of this facility in our institute. Hence, we limited the maximum dose of lignocaine to 400 mg and dexmedetomidine 1 μg/kg. For validation of our hypothesis, we further require randomized controlled studies. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
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Aug 1, 2024
Joshua Eaton + 6
Open Access
