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Case Reports  |   September 2004
Dexmedetomidine as a Total Intravenous Anesthetic Agent
Author Affiliations & Notes
  • Michael A. E. Ramsay, M.D., F.R.C.A.
    *
  • David L. Luterman, M.D.
  • *Chairman, Department of Anesthesiology & Pain Management and †Attending Staff, Department of Pulmonary Medicine, Baylor University Medical Center, Dallas, Texas.
Article Information
Case Reports
Case Reports   |   September 2004
Dexmedetomidine as a Total Intravenous Anesthetic Agent
Anesthesiology 9 2004, Vol.101, 787-790. doi:
Anesthesiology 9 2004, Vol.101, 787-790. doi:
DEXMEDETOMIDINE is a highly selective α2adrenoceptor agonist that has sedative and analgesic properties with associated reduction in opioid and anesthetic requirements.1–11 One significant advantage of dexmedetomidine is that in the clinical dose range there is no respiratory depression.12–14 The agonistic action on the α2adrenoceptors in the sympathetic ganglia modulates the release of catecholamines, resulting in a sympatholytic effect and reports of bradycardia and hypotension.15–19 As the dose of dexmedetomidine is increased, there is a direct action on the blood vessels causing vasoconstriction and a possible increase in blood pressure.3,18 This report describes three patients who presented for surgery with potential airway management challenges. Dexmedetomidine was administered to these patients in increasing doses until general anesthesia was attained. The effects of these high doses of dexmedetomidine on respiratory function and hemodynamics are described. The rate of dexmedetomidine infusion was administered based on actual patient body weights.
Case Reports
Case 1
A 66-yr-old, 85-kg woman presented with inspiratory stridor and was found to have a severe subglottic stenosis of her trachea. The stenosis was measured to be 1.5 cm below the vocal cords and to have a lumen diameter of 4 mm. Neodymium:yttrium-aluminum-garnet laser destruction of the tracheal stenosis was scheduled emergently. The patient was brought to the operating room and peripheral intravenous and arterial cannulae were inserted and electrocardiogram electrodes and pulse oximetry sensor were applied. A loading dose of dexmedetomidine 1 μg/kg was infused over 10 min and then an infusion of 0.7 μg·kg−1·h−1was delivered but rapidly increased over 10 min to 10 μg·kg−1·h−1to attain an acceptable level of anesthesia that would allow the airway to be instrumented by direct laryngoscopy. Topical lidocaine was applied to the nasal mucosa, the back of the pharynx, and the upper surface of the glottis. A fiberoptic bronchoscope was passed through the nose and the tracheal stenosis was visualized. No supplemental oxygen was supplied. When the patient was completely unresponsive approximately 20 min after induction the laser was powered and the tracheal stenosis was ablated. The procedure took 30 min and during that time the airway had to be supported with a chin lift. The blood pressure declined from 150/80 mm Hg to 110/60 mm Hg and pulse rate was maintained between 70 and 75 beats/min. (figs. 1 and 2) After 20 min the infusion of dexmedetomidine was reduced to 5 μg·kg−1·h−1, but the patient began to exhibit signs of lightening from anesthesia and so the infusion was increased back to 10 μg·kg−1·h−1. The oxygen saturations were maintained at greater than 90% except when the upper airway was obstructed and a chin lift was necessary. (  fig. 3) Once the chin lift was applied the saturations quickly returned to normal concentrations, and no supplementary oxygen was delivered. An arterial blood gas analysis performed in the middle of the procedure revealed an arterial partial pressure of carbon dioxide (Paco2) of 43 mm Hg and a partial pressure of oxygen (Pao2) of 82 mm Hg.
Fig. 1. Blood pressure changes during anesthesia in patient in Case 1. 
Fig. 1. Blood pressure changes during anesthesia in patient in Case 1. 
Fig. 1. Blood pressure changes during anesthesia in patient in Case 1. 
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Fig. 2. Pulse rate changes during anesthesia in patient in Case 1. 
Fig. 2. Pulse rate changes during anesthesia in patient in Case 1. 
Fig. 2. Pulse rate changes during anesthesia in patient in Case 1. 
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Fig. 3. Oxygen saturation changes during anesthesia in patient in Case 1. 
Fig. 3. Oxygen saturation changes during anesthesia in patient in Case 1. 
Fig. 3. Oxygen saturation changes during anesthesia in patient in Case 1. 
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The patient was taken to the recovery room and became immediately responsive to a loud audible stimulus or light glabellar tap (Ramsay Sedation Score of 4). She remained at this level of sedation for an hour and then reached a Ramsay Sedation Score of 3. When aroused the patient exhibited signs of good cognition, but quickly fell back to sleep when the stimulation ceased. She remained hemodynamically stable and at an Ramsay Sedation Score of 3 for another hour before fully recovering and being ready for discharge from the recovery room after a total time of 2 h.
Case 2
A 65-yr-old, 50-kg man was admitted with acute exacerbation of chronic respiratory failure secondary to emphysema. He required mechanical ventilation for 5 days and was then weaned to spontaneous ventilation and the endotracheal tube was removed. While breathing room air, his arterial Pao2was 55 mm Hg and Paco2was 60 mm Hg. He was then scheduled to have extensive resections of facial skin cancers with full-thickness skin graft reconstruction. The patient arrived in the operating room tachycardic and hypertensive and vigorously refused local anesthesia. Sedation with dexmedetomidine was attempted with a loading dose of 1 μg/kg followed by an infusion of 0.7 μg·kg−1·h−1. This did not provide adequate anesthesia so the infusion was increased to 5 μg·kg−1·h−1, and after a further 10 min the patient was anesthetized deeply enough to allow the surgery to take place. No supplemental oxygen was administered because of the close proximity of the electrical cautery.
Hemodynamically he became stable with heart rate slowing from 120 beats/minute to 65 beats/minute and blood pressure declining from 220/120 mm Hg to 120/65 mm Hg. Oxygen saturation, measured by a pulse oximeter, was maintained above 90% and respiratory rate declined from 30 breaths/min to 16 breaths/min. At the conclusion of the procedure local anesthesia was infiltrated into the surgical sites. The patient required no analgesia in the postanesthesia recovery unit and remained hemodynamically stable. He was discharged from the unit 2 h postoperatively.
Case 3
A 50-yr-old, 80-kg man presented for an evaluation of an upper airway obstruction. He had an artificial upper trachea in the form of a silastic Montgomery tracheal stent. This was placed 10 yr ago, after he had sustained multiple traumas that included a severe tracheal injury. The stent had been replaced approximately every year since then, and the tracheal stoma débrided at the same time. He required treatment for chronic pain and was receiving long-term opioid therapy. Previous anesthetics had been complicated by difficulties with airway management, as the upper airway was severely distorted by scar tissue. Postoperative pain management also was challenging because of his chronic opioid use.
The patient was brought to the operating room, routine monitors were applied, and peripheral venous and arterial cannulae were inserted. Dexmedetomidine was administered with a loading dose of 1 μg/kg followed by an infusion of 0.7 μg·kg−1·h−1. The infusion was increased over 5 min to 5 μg·kg−1·h−1and maintained at this rate for a further 5 min before the patient would tolerate the surgery. The patient then underwent rigid and fiberoptic bronchoscopy together with a laryngoscopy. The tracheal prosthesis was removed and the trachea was débrided. The patient breathed room air spontaneously throughout this part of the procedure and oxygen saturations were maintained above 92%. A new tracheal stent was inserted without difficulty. The patient then underwent bronchopulmonary lavage with saline to irrigate profuse purulent material present in the bronchi. Supplemental oxygen was required during this part of the procedure. The patient recovered comfortably, without requiring any opioid therapy and with hemodynamic stability. He was discharged home 3 h later from the recovery room.
Discussion
These case reports demonstrate that dexmedetomidine may be used as a total intravenous anesthetic agent in certain patients if doses are increased to a high enough level. Previous studies on assessing dexmedetomidine as a general anesthetic found that supplementary agents were necessary, but the doses of dexmedetomidine had not reached the high levels of administration reported here.20 In the first case reported here, the dexmedetomidine was supplemented with topical anesthesia before surgical intervention. In the second patient, postoperative analgesia was supplemented with infiltration of local anesthesia. The attributes of dexmedetomidine of sedation, analgesia, and no respiratory depression demonstrated at lower doses appear to be sustained at anesthetic doses. However, control of the airway was lost in the first patient, requiring manual support in the form of a chin lift, although respiratory drive was maintained. The level of sedation at which airway control is lost has not been well studied; this may occur at lower doses of dexmedetomidine. The advantage in these patients was that the airway was maintained easily together with adequate respiratory drive such that supplemental oxygen was not required. There was no demonstrable respiratory depression as measured by pulse oximetry in the patients breathing room air; however, airway support was required in the first patient. The lack of respiratory depression was confirmed in patient 1 by an arterial blood gas analysis that recorded a normal Paco2in the middle of the procedure. The blunting of the sympathetic nervous system in these patients produced satisfactory hemodynamics. No patient experienced hypotension or severe bradycardia, as has been reported.19 This may have been that all three patients were extremely anxious initially and exhibited tachycardia and hypertension before induction of anesthesia. There was also no evidence of vasoconstriction and hypertension as the dose of dexmedetomidine was increased to high levels, as has also been reported.3 The dexmedetomidine infusion was increased rapidly over 5 to 10 min to gain faster control of the patients. The plan was to titrate the dose back down once good anesthesia had been obtained. However, it was not possible to achieve this in any of the patients, and patient 1 had to have the infusion increased back up to 10 μg·kg−1·h−1to allow the procedure to be completed.
The preservation of respiratory drive offers the opportunity that this anesthetic technique may present another method for providing anesthesia for the patient with a difficult airway. This needs to be studied more thoroughly, as the data available on dexmedetomidine mainly relates to its use as an anesthetic and opioid-sparing agent at much lower doses and when used in combination with other anesthetic, sedative, and analgesic agents. At these high doses there were no airway concerns other than one patient requiring a chin-lift, and no opioids were required even in the patient who was a chronic opioid user. The recovery period required for these patients was not significantly prolonged when compared to many conventional anesthetic techniques; it was between 2 and 3 h. All three patients were hemodynamically stable in the recovery unit. The cost of this technique is also potentially higher than that of conventional anesthetics, but the advantage of no loss of respiratory drive and good analgesia without the need for opioids may well justify this expense.
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Fig. 1. Blood pressure changes during anesthesia in patient in Case 1. 
Fig. 1. Blood pressure changes during anesthesia in patient in Case 1. 
Fig. 1. Blood pressure changes during anesthesia in patient in Case 1. 
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Fig. 2. Pulse rate changes during anesthesia in patient in Case 1. 
Fig. 2. Pulse rate changes during anesthesia in patient in Case 1. 
Fig. 2. Pulse rate changes during anesthesia in patient in Case 1. 
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Fig. 3. Oxygen saturation changes during anesthesia in patient in Case 1. 
Fig. 3. Oxygen saturation changes during anesthesia in patient in Case 1. 
Fig. 3. Oxygen saturation changes during anesthesia in patient in Case 1. 
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