Clonidine Toxicity

Updated: May 30, 2020
  • Author: David Riley, MD, MSc, RDMS, RDCS, RVT, RMSK; Chief Editor: Michael A Miller, MD  more...
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Practice Essentials

Clonidine is a central alpha-agonist that is used as an antihypertensive agent. Other reported clinical uses include treatment of opiate and alcohol withdrawal [1] and control of atrial fibrillation with a rapid ventricular rate. It is also used for the following:

  • Pediatric preanesthesia

  • Pediatric postoperative pain

  • Migraine headaches

  • Nicotine addiction

  • Menopausal flushing

  • Attention deficit disorder [2]

  • Tourette syndrome [3]

  • Pediatric panic and anxiety disorders

At therapeutic doses (0.2-0.9 mg/d), clonidine is commonly associated with adverse effects such as dry mouth, sedation, dizziness, and constipation. While generally safe, at toxic doses clonidine can cause serious cardiopulmonary instability and central nervous system (CNS) depression in children and adults.

Clonidine is available in a weekly transdermal patch (Catapres TTS: 0.1 mg, 0.2 mg, or 0.3 mg/d, with each patch containing 2.5 mg, 5 mg, and 7.5 mg of clonidine, respectively) and in tablet form (Catapres: 0.1 mg, 0.2 mg, and 0.3 mg; Combipres includes 15 mg of chlorthalidone diuretic). An ophthalmic solution is occasionally used in the treatment of glaucoma.



Clonidine is an imidazole derivative and was first used as a nasal decongestant. Decongestants containing tetrahydrozoline, also an imidazole derivative, can result in the same signs and symptoms as clonidine poisoning when ingested, especially in children.

Clonidine acts primarily as a presynaptic CNS alpha2-agonist, stimulating receptors in the nucleus tractus solitarii of the medulla oblongata. This inhibits sympathetic outflow, which results primarily in a reduction of sympathetically mediated vasoconstriction, cardiac inotropy, and chronotropy.

Clonidine also has peripheral alpha1-agonist activity, which may produce transient vasoconstriction and hypertension early in overdose when peripheral drug levels may be transiently higher than levels in the CNS.

Clonidine is rapidly absorbed from the gastrointestinal tract and has excellent CNS penetration because of lipid solubility. Peak plasma concentrations are reached 3-5 hours after a single oral dose. Dermal application may take several days to reach steady state levels. No known pharmacologically active metabolites exist. Plasma half-life is 12-16 hours, with the antihypertensive effects occurring within 30-60 minutes of ingestion. Clonidine is excreted unchanged in the urine and is metabolized by the liver.



In the 2018 Annual Report of the American Association of Poison Control Centers' National Poison Data System, 5439 single exposures to clonidine were reported. Of those, 3418 were unintentional toxicities. In 2018, 1616 were in patients younger than 6 years, 2337 were in patients 6-19 years old, and 1402 were in patients 20 years of age and older. [4]



Prognosis is generally good for patients who present early and have had prompt and proper treatment. Mortality is rare with a small number of reported deaths. Morbidity, in terms of cardiorespiratory and CNS dysfunction, generally tends to be more severe in young persons than in adults.

Of the 5439 reported toxic exposures to clonidine in 2018, 3853 were treated in a health care facility. Of this subset of patients, 982 had no significant outcome, 1135 had minor effects, 1758 had moderate morbidity, and 200 had major morbidity. No deaths were reported. [4]


Patient Education

Children may be easily affected by relatively small doses of clonidine. Educating patients about the importance of keeping clonidine and all drugs out of children's reach is critical.

For patient education resources, see the Drug Overdose Center and Poisoning - First Aid and Emergency Center, as well as PoisoningDrug OverdoseActivated Charcoal, and Poison Proofing Your Home.