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Delayed Hypertension and Bradycardia With Intranasal Dexmedetomidine and Oxymetazoline
Smith T, Ramamurthi R
Lucile Packard Children's Hospital Stanford, Palo Alto, CA, USA
Intranasal dexmedetomidine is used in the pediatric population for ease of noninvasive administration. Rate to peak serum concentrations is variable ranging from 15-60 minutes with an average of 38 minutes3. It is primarily an alpha adrenoreceptor agonist with high alpha-2 affinity (1620:1). Alpha-2 receptor agonism in the locus coeruleus causes sedation and decreased sympathetic outflow with minimal effects on respirations. Common adverse side effects include transient hypertension, hypotension and bradycardia with IV bolus. Often an attractive choice because it has minimal drug-drug interactions, case reports of untoward events sound a tone of caution2. We present a case of delayed hypertension and bradycardia with co-administration of dexmedetomidine and oxymetazoline.
A 5-year-old 15 kg male with history of chronic cough and asthma presented for microdirect laryngoscopy and fiberoptic bronchoscopy. Preoperative vital signs were within normal limits. Preoperatively, 75mcg dexmedetomidine was given via nasal atomizer. Following inhalational induction, anesthesia was maintained utilizing TIVA with remifentanil and propofol infusions. Thirty minutes after surgical administration of nasal oxymetazoline, MAP began to slowly increase to a peak of 122 with a coinciding HR nadir of 55 recorded in PACU as the patient slept comfortably. Vital signs normalized spontaneously over 40 minutes and the patient was discharged home.
The side effects of hypertension and bradycardia are known for both dexmedetomidine and oxymetazoline. For dexmedetomidine, hypertension with bradycardia is reported as a transient immediately following IV bolus, but not after intranasal administration1. Similarly for oxymetazoline, hypertension and bradycardia is reported as abrupt soon after administration4. These associations are very unlike what was seen during this case where there was a delayed and slow rise of MAP peaking at 80 minutes post dexmedetomidine and 60 minutes post oxymetazoline administration. The mechanisms behind the delayed hypertension and bradycardia remain unclear. The exact interplays are impossible to know, but the authors would suggest that a possible higher than intended dosing with a slow rate of nasal absorption combined with dual activation of postsynaptic alpha receptors (perhaps via some unknown synergistic mechanism) may have caused the exaggerated and delayed response seen in this case.
1. A comparison of intranasal dexmedetomidine for sedation in children administered either by atomizer or by drops. Li BL, Zhang N, Huang JX, Qiu QQ, Tian H, Ni J, Song XR, Yuen VM, Irwin MG. Anaesthesia. 2016 May;71(5):522-8.
2. An exaggerated hypertensive response to glycopyrrolate therapy for bradycardia associated with high-dose dexmedetomidine. Mason KP, Zgleszewski S, Forman RE, Stark C, DiNardo JA. Anesth Analg. 2009 Mar;108(3):906-8.
3. Bioavailability of dexmedetomidine after intranasal administration. Iirola T, Vilo S, Manner T, Aantaa R, Lahtinen M, Scheinin M, Olkkola KT. Eur J Clin Pharmacol. 2011 Aug;67(8):825-31.
4. Oxymetazoline and hypertensive crisis in a child: can we prevent it? Latham GJ, Jardine DS. Paediatr Anaesth. 2013 Oct;23(10):952-6.
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