Fact or Fallacy: Dexmedetomidine Withdrawal in Critically Ill Adult Patients
by Meagan Macalalag, PharmD, Jeffrey Fish, PharmD, BCCCP, FCCM
Question: What is the incidence of dexmedetomidine withdrawal in critically ill adult patients? Should clonidine be used as a strategy to prevent dexmedetomidine withdrawal?
Since its introduction, the use of acting alpha-2 adrenergic receptor agonist, has considerably increased in the intensive care unit (ICU). The rise of dexmedetomidine is attributed to its promising pharmacologic profile. Unlike other sedatives used in the ICU, such as propofol and benzodiazepines, dexmedetomidine does not act via the gamma-aminobutyric acid (GABA)-mimetic system.
Since its introduction, the use of acting alpha-2 adrenergic receptor agonist, has considerably increased in the intensive care unit (ICU). The rise of dexmedetomidine is attributed to its promising pharmacologic profile. Unlike other sedatives used in the ICU, such as propofol and benzodiazepines, dexmedetomidine does not act via the gamma-aminobutyric acid (GABA)-mimetic system. Therefore, dexmedetomidine induces conscious sedation while preserving respiratory drive. Along with its sedative
effects, dexmedetomidine also possesses anxiolytic, analgesic, and sympatholytic properties, given its different mechanism of action and high selectivity for alpha-2 adrenergic receptors.
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2026 May/June Table of Contents
Question: What is the incidence of dexmedetomidine withdrawal in critically ill adult patients? Should clonidine be used as a strategy to prevent dexmedetomidine withdrawal?
Since its introduction, the use of acting alpha-2 adrenergic receptor agonist, has considerably increased in the intensive care unit (ICU). The rise of dexmedetomidine is attributed to its promising pharmacologic profile. Unlike other sedatives used in the ICU, such as propofol and benzodiazepines, dexmedetomidine does not act via the gamma-aminobutyric acid (GABA)-mimetic system.
Since its introduction, the use of acting alpha-2 adrenergic receptor agonist, has considerably increased in the intensive care unit (ICU). The rise of dexmedetomidine is attributed to its promising pharmacologic profile. Unlike other sedatives used in the ICU, such as propofol and benzodiazepines, dexmedetomidine does not act via the gamma-aminobutyric acid (GABA)-mimetic system. Therefore, dexmedetomidine induces conscious sedation while preserving respiratory drive. Along with its sedative
effects, dexmedetomidine also possesses anxiolytic, analgesic, and sympatholytic properties, given its different mechanism of action and high selectivity for alpha-2 adrenergic receptors.
Download PDF
2026 May/June Table of Contents