Clonidine Toxicity

Updated: Dec 15, 2017
  • Author: David Riley, MD, MSc, RDMS, RDCS, RVT, RMSK; Chief Editor: Michael A Miller, MD  more...
  • Print

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.




United States

In the 2016 Annual Report of the American Association of Poison Control Centers' National Poison Data System, 5351 single exposures to clonidine were reported. Of those, 3504 were unintentional toxicities and 106 were reported as an adverse reaction. [4]


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 5351 reported toxic exposures to clonidine in 2016, 3858 were treated in a health care facility. Of this subset of patients, 972 had no significant outcome, 1192 had minor effects, 1748 had moderate morbidity, and 139 had major morbidity. No deaths were reported. [4]


Of the 5351 reported toxic exposures to clonidine in 2016, 1760 were in patients younger than 6 years, 2106 were in patients 6-19 years old, and 1315 were in patients 20 years of age and older. [4]