Sinus arrest with intrathecal dexmedetomidine.

Abstract

Sir, Dexmedetomidine, a highly selective α2 adrenoceptor agonist, is being increasingly used as an adjuvant in neuraxial blocks as it prolongs the sensory and motor block in a dose-dependent manner.[1] Severe bradycardia and cardiac arrest has been reported with the intravenous use of dexmedetomidine.[23] However, severe bradycardia progressing to sinus arrest after intrathecal administration of dexmedetomidine has not been reported. A 40-year-old female, 155 cm in height and weighing 65 kg, was scheduled for total abdominal hysterectomy. She had been operated for myomectomy under spinal anaesthesia 5 years back. Her general physical examination and all routine investigations were unremarkable. Upon arrival in the operating room, monitors were attached and her vitals were recorded. A peripheral venous access was established and pre-loaded with 500 mL of Ringer lactate. The subarachnoid space was reached in the L2-L3 interspace using a 25G Quincke's needle with the patient in the left lateral position. After ensuring free flow of cerebrospinal fluid, 2.5 mL of hyperbaric bupivacaine with 10 μg of dexmedetomidine was administered. The patient was positioned supine and oxygen was administered via a face mask at a rate of 5 L/min. The level of sensory block to pinprick was T10 after 2 min, and T6 was the highest level of sensory block achieved. The surgery commenced and the patient's heart rate remained in the range of 50-60/min, with the blood pressure at around 130/80 mmHg. After about 70 min, when the surgeons were suturing the peritoneum, there was a sudden drop in her heart rate to 40/min. Immediately, the surgical handling was stopped and injection atropine 0.6 mg was given intravenously, to which there was no response for 3 min. Meanwhile, she complained of some discomfort in her epigastrium and her heart rate further dropped to 34/min while her blood pressure was 124/76 mmHg with SpO2 of 99%. Another dose of inj. atropine 0.6 mg was given intravenously but her heart rate dropped to 18/min over 5 s followed by sinus arrest. Then, the third dose of inj. atropine 0.6 mg was given, which led to an increase in her heart rate to 86/min. The level of sensory blockade was T10 at this time and the SpO2 was consistently 99%. The surgery was completed in the next 15 min uneventfully and the estimated blood loss was around 200 mL. The patient remained comfortable with a heart rate of around 74/min and blood pressure of 124/86 mmHg. Her post-operative Holter monitoring and echocardiography were unremarkable. Intrathecal dexmedetomidine when combined with spinal bupivacaine produces earlier onset and prolonged duration of sensory and motor block with excellent quality of post-operative analgesia without significant haemodynamic alterations.[14] Although episodes of sinus arrest and severe bradycardia progressing to asystole have been reported in patients receiving intravenous dexmedetomidine,[23] no severe cardiovascular complications have been observed with intrathecal dexmedetomidine. Two cases of bradycardia (heart rate 50/min) have been observed by Gupta et al. when they used 5 μg of dexmedetomidine as an intrathecal adjuvant for post-operative analgesia.[5] The two very unusual features observed in our case were the time to the occurrence of sinus arrest and the high dose of atropine required for its treatment. As 1 h had elapsed between the intrathecal administration of drugs and the sinus arrest, sinus arrest due to sympathetic blockade due to bupivacaine was less likely. The level of sensory block had also receded to T10 by that time. We therefore speculate that a centrally mediated decrease in sympathetic outflow and increase in parasympathetic outflow due to dexmedetomidine may be the cause. The patient's autonomic response to peritoneal stretching could also be a contributing factor responsible for the severe bradycardia in this case. However, the bradycardia did not respond to the cessation of surgical handling and the usual dose of atropine. A fall in blood pressure and heart rate has been reported with various interventions like displacement of liver, insertion of hand into the peritoneal cavity, placement of packing and retraction of the wound edges. A vagally mediated reflex has been implicated in most cases, but exact pathways have not been established so far.[6] To conclude, although dexmedetomidine is an attractive intrathecal adjuvant for post-operative analgesia, we recommend meticulous use of this drug with vigilant monitoring in the operating room as well as in the post-anaesthesia care unit keeping in mind the possibility of delayed occurrence of severe bradycardia.