Clonidine Toxicity Treatment & Management

Provide aggressive supportive care because patients may rapidly decompensate. Address airway, breathing, and circulation (ABCs) as usual. Intravenous access with crystalloid and pressor support with dopamine may be necessary.

If a clonidine patch is present on the skin, remove it and wash the exposed area. Initiate standard naloxone therapy and blood glucose checks.

Continuous electrocardiographic (ECG) monitoring should carry over to the emergency department (ED).

Prehospital ipecac syrup administration is contraindicated.

Focus initial treatment on the ABCs. Clonidine toxicity can cause serious respiratory depression and apnea requiring immediate endotracheal intubation and mechanical ventilation. Once the airway is secure, place the patient on continuous ECG, blood pressure, and oxygen saturation monitoring. Place at least one large-bore IV line. Consider central venous pressure (CVP) monitoring in patients who are markedly hypotensive.

Clonidine toxicity can cause serious respiratory depression and apnea requiring immediate endotracheal intubation and mechanical ventilation.

Hypotension is very common with clonidine toxicity; initially treat the patient with aggressive crystalloid infusion. If aggressive volume resuscitation fails to raise blood pressure, consider pressors such as dopamine and epinephrine. Maintain good urine output because clonidine is excreted at least 50% unchanged in the urine.

Bradycardia, either sinoatrial (SA) nodal or AV nodal, has been reported with clonidine toxicity. ^[7] Atropine is the first-line drug of choice. Consider dopamine if atropine fails with SA nodal, first-degree, or Mobitz I AV nodal block; however, in Mobitz II and third-degree AV nodal block, atropine is only temporizing until definitive pacing is initiated.

Transcutaneous pacing is quicker to initiate, but causes the patient more discomfort than transvenous pacing. Consider transvenous pacing in patients with massive ingestions who have third-degree AV nodal block.

Hypertension may occur initially from peripheral alpha1-agonist activity and vasoconstriction. This hypertension is usually transient and does not require treatment; if hypertension is severe, symptomatic, and prolonged, treatment with a short-acting agent such as intravenous nitroprusside can be considered.

Administer activated charcoal by mouth or nasogastric tube for clonidine toxicity in a 1-g/kg dose (standard for toxic ingestions). If significant CNS depression exists, intubate before administering activated charcoal to prevent aspiration. The clinician should be aware that even intubated patients are at risk of activated charcoal aspiration. Lavage is controversial; yet consider it if ingestion is significant and occurred less than an hour before arrival.

Naloxone (Narcan) may treat clonidine toxicity. It improves the mental status of adults and children who have ingested toxic amounts of clonidine; this, however, has not been universal and naloxone can cause hypotensive and hypertensive responses. ^[8] Naloxone can also has been reported to cause severe hypertension. ^[9]

The American Academy of Pediatrics ^[10] recommends a dose of naloxone of 0.1 mg/kg for infants and children up to age 5 years or weighing 20 kg. Children older than 5 years or weighing more than 20 kg may be given 2 mg of naloxone. Adults with isolated clonidine toxicity may be given 2 mg doses of naloxone, titrated to effect. The clinician should be aware that naloxone administration in chronic opioid users can precipitate withdrawal with consequent vomiting and risk of aspiration.

Provide symptomatic and supportive care, the main therapy for clonidine toxicity. Passively warm patients who have hypothermia. Most comas resolve with supportive measures.

Two case reports document yohimbine reversal of clonidine toxic states. ^[11] Yohimbine is a central alpha2-adrenergic antagonist with effects that directly oppose clonidine, making it a theoretically useful antidotal agent. ^[11]

Admit significantly symptomatic patients with clonidine toxicity to the intensive care unit (ICU). A ward admission on a monitor is probably reasonable for minimal symptoms if the patient has been observed for several hours with improvement or without worsening. Remember that patients demonstrating clonidine toxicity, secondary to transdermal exposure, may experience a prolonged period of symptoms from a prolonged half-life secondary to a "depot" effect in the subdermal tissues.

Transfer patients with clonidine toxicity if the potential benefits outweigh the risks.

Patients with suspected clonidine ingestion may be discharged if they remain asymptomatic for 4-6 hours and have normal vital signs. Obtain a psychiatric evaluation before discharge for patients with suspected intentional ingestion.

Unless the treating physician has extensive experience with acute poisonings or if significant toxicity manifests, contacting a poison control center for advice and feedback is reasonable. A formal toxicology team may provide valuable input.

In general, treat with supportive care. Administer activated charcoal to all patients at risk for aspiration after intubation. Temporary support for symptomatic cardiovascular effects of clonidine also may be necessary.