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Desflurane

A Review of its Pharmacodynamic and Pharmacokinetic Properties and its Efficacy in General Anaesthesia

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An Erratum to this article was published on 01 December 1995

Abstract

Synopsis

Desflurane is a halogenated ether inhalation general anaesthetic agent with low solubility in blood and body tissues, and approximately one-fifth the potency of isoflurane. The pharmacodynamic properties of desflurane generally resemble those of isoflurane; thus, it produces dose-dependent depression of the central nervous and cardiorespiratory systems, and tetanic fade at the neuromuscular junction.

The alveolar equilibration of desflurane is rapid (90% complete at 30 minutes compared with 73% for isoflurane). Both desflurane and isoflurane are distributed to various tissues to a similar extent. Desflurane is resistant to chemical degradation and undergoes negligible metabolism (≈10% of that seen with isoflurane). Desflurane ‘wash-out’ is ≈2 to 2.5 times faster than that of isoflurane in the first 2 hours after discontinuation of anaesthesia.

The low solubility of desflurane facilitates a rapid induction of anaesthesia and precise control of the depth of anaesthesia (during maintenance). Results from a few clinical studies indicate that emergence from desflurane is significantly earlier (by ≈2 to 6 minutes) than that from propofol anaesthesia, whereas other studies do not concur. In comparison with isoflurane, emergence from desflurane anaesthesia is significantly earlier (by 5 minutes) after ambulatory and ≈50% earlier (also significant) after nonambulatory surgical procedures. Limited comparative studies with halothane or sevoflurane also suggest an earlier time of emergence from desflurane anaesthesia.

Comparative studies of desflurane and propofol, and other inhalation agents, indicate that the times to toleration of oral fluids, sitting and discharge from recovery room are similar, regardless of the general anaesthetic agent administered. However, some limited data in elderly patients (aged >65 years) suggest that this patient group spends a significantly shorter time in the postanaesthesia care unit after desflurane than after isoflurane anaesthesia.

Differences, if any, in the recovery of cognitive and psychomotor functions after desflurane or propofol anaesthesia remain unclear. However, in comparison with isoflurane anaesthesia, recovery of these functions (up to 45 minutes post-operatively) occurs earlier after desflurane. Significantly fewer patients are subjectively impaired (i.e. drowsy, clumsy, fatigued or confused) upon recovery from desflurane than from isoflurane anaesthesia. Likewise, significantly fewer adult patients are delirious when recovering from desflurane than from isoflurane anaesthesia, though in paediatric patients delirium is more likely when recovering from desflurane than from halothane anaesthesia.

Haemodynamic stability during coronary artery surgery is as well maintained with desflurane as with isoflurane, and the drug does not worsen the adverse postoperative outcomes. Moreover, desflurane appears to be better than isoflurane at blunting the haemodynamic response after sternotomy and other noxious stimuli. The incidence of myocardial ischaemia during coronary artery surgery is similar with either desflurane or isoflurane anaesthesia.

Transient airway irritant effects are the most common adverse events during induction of anaesthesia with deseflurane; therefore, this agent is not recommended for induction of anaesthesia in paediatric patients. The incidence of intraoperative cardiovascular events during desflurane anaesthesia is similar to that reported with isoflurane. The incidence of postoperative nausea and vomit-ing after desflurane anaesthesia is higher than after propofol but similar to that after other inhalation agents. Hepatic or renal function is not adversely affected after desflurane anaesthesia.

Overall, although desflurane is generally not well tolerated during induction of anaesthesia, it embodies many of the desirable feature s of an ideal agent, which include stability to chemical degradation, low solubility in blood and body tissues, negligible metabolism and low potential for hepato-renal toxicity. These favourable physical and pharmacokinetic characteristics should present desflurane as a valuable inhalation anaesthetic agent for the maintenance of general anaesthesia in ambulatory surgery (complementary to intravenous induction with propofol) as well as in nonambulatory surgical procedures.

Pharmacodynamic Properties

Desflurane is a halogenated ether inhalation general anaesthetic agent with low solubility in blood and body tissues and low potency [minimum alveolar concentration (MAC) value ranging from 4.58 to 7.25%, depending on the stimulus used]. It is approximately one-fifth as potent as isoflurane.

The cerebrovascular and cardiorespiratory effects of desflurane essentially parallel those of isoflurane. It produces dose-dependent decreases in cerebrovascular resistance and cerebral metabolic rate of oxygen consumption, increases in intracranial pressure at 0.5 to 1.5 MAC doses and impairment of cerebral autoregulation.

Desflurane suppresses EEG activity at ≥1.24 MAC, and it is not epileptogenic either at deep anaesthetic levels or under hypocapnic conditions. There is a dose-dependent suppression of somatosensory-evoked potentials at 0.5 to >1.5 MAC in healthy volunteers, while sub-MAC concentrations suppress intermediate-latency auditory-evoked responses.

Cardiac output is maintained in humans despite dose-dependent depression of cardiovascular function and myocardial contractility during desflurane anaesthesia with controlled ventilation. Tachycardia may be more prominent with desflurane than isoflurane at >1.0 MAC. Adequate myocardial tissue perfusion is maintained despite a decline in perfusion pressure during desflurane anaesthesia. Prolonged anaesthesia (up to 7 hours) appears to result in cardiovascular, but not cerebral, tolerance in humans. Desflurane, like isoflurane, is a coronary vasodilator, but it does not appear to induce the ‘coronary steal’ phenomenon in a canine model.

A rapid increase in end-tidal concentrations of desflurane (at ≥1.0 MAC) in patients and healthy volunteers results in transient sympathetic-mediated cardiovascular stimulation which is significantly more pronounced than that observed with isoflurane. This sympathoexcitation is absent with sevoflurane.

Dose-dependent respiratory depressant effects of desflurane (at ≤1.24 MAC), such as decrease in tidal volume and increase in ventilation rate, are similar to those of isoflurane. Desflurane produces neuromuscular relaxation and therefore potentiates skeletal muscle relaxation induced by neuromuscular blocking agents.

Pharmacokinetic Properties

Equilibration between inspired and tissue concentrations of desflurane is rapid compared with that of other inhalation anaesthetic agents. Alveolar equilibration of desflurane is ≈90% complete in healthy volunteers within 30 minutes compared with isoflurane (73%) or halothane (58%). The estimated tissue distribution of desflurane is generally similar to that of isoflurane.

Desflurane is eliminated ≈2 to 2.5 times more quickly than isoflurane or halothane in the first 2 hours after discontinuation of anaesthesia. Pulmonary clearance of desflurane is 4.11 L/min (vs 3.94 L/min for isoflurane and halothane) and total body clearance is 4.60 L/min (vs 4.00 and 3.94 L/min for isoflurane and halothane, respectively).

Desflurane is resistant to in vitro degradation in moist soda lime at ≤60°C, although there is slight degradation at 80°C (0.45% per hour). Desflurane undergoes negligible metabolism (≈10% that of isoflurane) in vivo, although the precise mechanism is unknown.

Clinical Evaluation

A number of studies in ambulatory patients report a statistically significant earlier emergence from desflurane than from propofol or isoflurane anaesthesia (≈2 to 6 and 5 minutes earlier, respectively), although some studies have not found this difference between desflurane and propofol anaesthesia. Emergence from desflurane anaesthesia in this group of patients appears to be significantly more rapid than emergence from sevoflurane or halothane anaesthesia. The times to toleration of oral fluids, sitting and readiness for discharge from the recovery room are comparable, regardless of the general anaesthetic administered.

In the early postoperative period up to 90 minutes, psychomotor and cognitive functions are less impaired after desflurane than after isoflurane ambulatory anaesthesia, whereas such differences are less apparent when desflurane is compared with propofol. Generally, these functions return to their baseline levels within 2 hours postoperatively regardless of the anaesthetic background. Subjective impairment (i.e. drowsiness, clumsiness, fatigue or confusion) is significantly less upon recovery from desflurane than from isoflurane anaesthesia.

Emergence from nonambulatory anaesthesia with desflurane is ≈50% significantly earlier than that with isoflurane. In addition, up to 45 minutes postoperatively, cognitive and psychomotor function recovery occurs earlier after desflurane than after isoflurane anaesthesia, although this difference is not apparent 60 minutes after cessation of administration.

Elderly patients (aged >65 years) recovering from nonambulatory desflurane anaesthesia tend to spend a shorter time in the postanaesthesia care unit compared with those who received isoflurane anaesthesia (80 vs 128 minutes).

Desflurane does not worsen the adverse postoperative outcomes after coronary artery surgery, and haemodynamic stability during desflurane anaesthesia is similar to that during isoflurane or opioid anaesthesia. Compared with isoflurane, desflurane is better at blunting the haemodynamic response after sternotomy and other noxious stimuli. There is no difference between desflurane and isoflurane anaesthesia with respect to the incidence of ECG changes indicative of myocardial ischaemia during coronary artery surgery. However, when desflurane is compared with opioid anaesthesia, conflicting results with respect to the incidence of myocardial ischaemia upon induction, but not during maintenance of anaesthesia, were reported. Changes in the depth of anaesthesia in response to surgical stimuli are more rapidly controlled with desflurane than with isoflurane.

Limited data suggest that desflurane (1 to 4.5%) in oxygen provides well tolerated and effective obstetric analgesia during vaginal delivery. Likewise, caesarean section surgery can be performed without excessive uterine bleeding when desflurane 3% (end-tidal concentration) is administered.

Tolerability

The pungency of desflurane is reflected in its transient airway irritant effects during induction of anaesthesia at concentrations >6%. These effects (commonly seen in adults) include coughing, excitatory effects, breath-holding, excessive secretions and laryngospasm. The airway irritant effects are not well tolerated by paediatric patients, in whom excitatory effects (51 %) and coughing (29%) are the most commonly reported reflexes. Other adverse events include apnoea, pharyngitis and oxyhaemoglobin desaturation (SpO2 <90%).

Haemodynamic stability during maintenance of anaesthesia with desflurane is generally well preserved and similar to that during isoflurane, propofol or halothane anaesthesia. The incidence of a number of cardiovascular events occurring during desflurane anaesthesia, namely, tachycardia, bradycardia, hypertension, hypotension and nodal arrhythmias, is not significantly different from that with isoflurane.

Postoperative nausea is reported in 10 to 54% of adult and paediatric patients after desflurane anaesthesia, whereas vomiting occurs in 7 to 33% of patients. Significantly fewer adult patients experience delirium when recovering from desflurane anaesthesia than when recovering from isoflurane anaesthesia (0 to 13% vs 44 to 75%). In contrast, paediatric patients tend to be delirious more frequently after emergence from desflurane than from halothane anaesthesia.

Hepatic or renal function is not affected by desflurane anaesthesia up to 7.35 MAC-hours. Desflurane, given at 2.8 to 3% for 2.0 to 2.5 hours, does not worsen chronic hepatic or renal disease. To date, malignant hyperthermia has not been reported with desflurane anaesthesia in humans.

Dosage and Administration

Inspired concentrations of 4 to 11 % desflurane usually produce surgical anaesthesia in adult patients, with or without premedication with opioids, in 2 to 4 minutes. Induction of anaesthesia with desflurane is not recommended in paediatric patients aged <12 years.

Surgical anaesthesia in adult patients may be maintained with concentrations of 2 to 6% desflurane with concomitant use of nitrous oxide and 2.5 to 8.5% when oxygen is used concomitantly. Surgical anaesthesia in paediatric patients may be maintained with concentrations of 5.2 to 10% desflurane with or without the concomitant use of nitrous oxide.

Concentrations of 1 to 4% desflurane in nitrous oxide-oxygen are recommended for maintenance of anaesthesia in patients with chronic renal or hepatic impairment and during renal transplantation surgery.

Desflurane is currently not recommended for administration to neurosurgical patients (except in the US, where it is authorised for this patient group, provided it is administered at ≤0.8 MAC), during pregnancy, or in patients with known or suspected genetic susceptibility to malignant hyperthermia.

Nitrous oxide, opioids, benzodiazepines and other sedative agents reduce the MAC of desflurane. Desflurane potentiates the pharmacological activity of neuromuscular blocking agents in a dose-dependent manner.

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    Sanjay S. Patel & Karen L. Goa

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Various sections of the manuscript reviewed by: R.R. Bartkowski, Department of Anesthesiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania, USA; AM. Breckenridge, Department of Pharmacology and Therapeutics, The University of Liverpool, Liverpool, England; P.J. Davis, Department of Anesthesiology and Critical Care Medicine, Children’s Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, Pennsylvania, USA; C. Diefenbach, Klinik für Anaesthesiologie und Operative Intensivmedizin der Universität zu Köln, Cologne, Germany; E.I. Eger, Department of Anesthesia, University of California, San Francisco, California, USA; P. Flynn, Anaesthetics Unit, The Royal London Hospital, London, England; M.I. Gold, Department of Anesthesiology, University of Miami School of Medicine, Miami, Florida, USA; J.M. Hunter, University Department of Anaesthesia, Royal Liverpool University Hospital, Liverpool, England; R.M. Jones, Department of Anaesthetics, St Mary’s Hospital Medical School, Imperial College of Medicine, London, England; J. Lerman, Department of Anaesthesia, The Hospital for Sick Children, University of Toronto Faculty of Medicine, Toronto, Ontario, Canada; C.A. Lien, Department of Anesthesiology, The New York Hospital-Cornell University Medical Center, New York, New York, USA; S. Oshita, Department of Anesthesiology, Yamaguchi University Hospital, Ube, Yamaguchi, Japan; D.C. Warltier, Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.

An erratum to this article is available at http://dx.doi.org/10.1007/BF03259621.

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Patel, S.S., Goa, K.L. Desflurane. Drugs 50, 742–767 (1995). https://doi.org/10.2165/00003495-199550040-00010

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