Dexmedetomidine (Dexdomitor) for Dogs and Cats: Sedation, Atipamezole, and the FDA Data
An evidence-based guide to dexmedetomidine (Dexdomitor, Sileo) for dogs and cats: how it works, its alpha-2 cardiovascular signature, atipamezole reversal, and FDA adverse event data.
Dexmedetomidine (marketed as Dexdomitor, Dexmedesed, Dexased, and as the oromucosal gel Sileo) is one of the most frequently utilized sedatives, pre-anesthetic medications, and analgesics in veterinary medicine. As a highly selective alpha-2 adrenergic agonist, its potency and rapid onset make it a cornerstone of veterinary clinical operations—from facilitating minor diagnostic procedures and managing aggressive or fearful patients to serving as a critical component of multimodal general anesthesia protocols.
However, the very mechanism that makes dexmedetomidine a highly effective sedative also drives a profound and predictable set of physiological alterations. The cardiovascular signature of alpha-2 agonists—characterized by initial hypertension, reflex bradycardia, peripheral vasoconstriction, and potential heart block—presents clear risk boundaries. Veterinary teams must understand these changes, not as side effects, but as the direct pharmacological action of the drug.
This monograph provides an in-depth review of dexmedetomidine’s pharmacology, clinical indications, dosing principles, cardiovascular effects, atipamezole (Antisedan) reversal mechanics, canine noise-aversion applications, and a reproducible analysis of the FDA's adverse event reporting database.
1. What is dexmedetomidine, and how does it work pre- and post-synaptically?
Dexmedetomidine is the active L-isomer of medetomidine, a racemic mixture developed in the late 1980s. By isolating the L-enantiomer, chemists removed the inactive D-enantiomer (levomedetomidine), resulting in a drug that acts as a highly selective agonist at alpha-2 adrenergic receptors. In fact, dexmedetomidine has an alpha-2 to alpha-1 selectivity ratio of approximately 1620:1, compared to clonidine’s 220:1 and xylazine’s 160:1.
The clinical effects of dexmedetomidine are mediated through its interactions with three distinct alpha-2 receptor subtypes (α₂A, α₂B, and α₂C) located within the central and peripheral nervous systems:
- Pre-Synaptic Activation (Central Nervous System): In the brain (specifically the locus coeruleus) and the spinal cord, dexmedetomidine binds to pre-synaptic alpha-2 receptors. This binding activates inhibitory G-proteins (Gᵢ/Gₒ), which inhibit adenylate cyclase and reduce intracellular cyclic AMP (cAMP). This limits calcium influx into the pre-synaptic terminal, preventing the exocytosis of vesicles containing norepinephrine. By suppressing norepinephrine release, dexmedetomidine halts the ascending arousal pathway, inducing a state of sleep-like sedation and anxiolysis.
- Spinal Cord Analgesia: In the dorsal horn of the spinal cord (specifically the substantia gelatinosa), activation of alpha-2 receptors decreases the release of excitatory neurotransmitters like substance P and glutamate from primary afferent nociceptors, while hyperpolarizing post-synaptic projection neurons. This interrupts pain transmission to the brain, providing significant somatic visceral analgesia.
- Post-Synaptic Activation (Peripheral Vasculature): On the smooth muscle cells of peripheral blood vessels, dexmedetomidine binds to post-synaptic α₂B receptors. This induces vasoconstriction, leading to a rapid and significant increase in systemic vascular resistance.
Because of this receptor-specific activity, dexmedetomidine achieves dose-dependent sedation, muscle relaxation, and analgesia without binding to other receptor classes (such as cholinergic, histaminergic, or GABAergic receptors).
2. How is dexmedetomidine dosed and administered in veterinary patients?
Dexmedetomidine is approved by the FDA Center for Veterinary Medicine (CVM) for use in dogs and cats. The labeled injectable formulations are typically supplied at a concentration of 0.5 mg/mL (500 mcg/mL).
Dog Dosing (Body Surface Area vs. Body Weight)
For dogs, the official FDA-approved label doses are calculated based on body surface area (BSA) rather than strictly by body weight. This is because smaller dogs have a higher metabolic rate relative to their body mass than larger dogs. Dosing solely by body weight in micrograms per kilogram (mcg/kg) would result in under-sedating toy breeds or over-sedating giant breeds.
- Labeled Intravenous (IV) Dose: 375 mcg/m²
- Labeled Intramuscular (IM) Dose: 500 mcg/m²
In clinical practice, veterinarians frequently adapt these to weight-based charts for convenience, though standardizing by BSA remains the most precise method to ensure consistent sedation depth. Weight-based dosing for premedication typically ranges from 1 to 10 mcg/kg IM or IV, depending on the other drugs in the pre-anesthetic cocktail (e.g., opioids like torbugesic, methadone, or hydromorphone).
Cat Dosing
For cats, dexmedetomidine is approved for intramuscular use to achieve sedation and analgesia, or as a pre-anesthetic.
- Labeled Intramuscular (IM) Dose: 40 mcg/kg
At this dose, sedation onset occurs within 10 to 15 minutes, with peak effects at 30 minutes, lasting roughly 1 to 2 hours.
Constant Rate Infusion (CRI)
For anxious, painful, or emergence-delirious inpatients in the intensive care unit (ICU), dexmedetomidine is frequently administered as a Constant Rate Infusion (CRI). A CRI provides stable plasma concentrations, avoiding the cardiovascular spikes associated with bolus dosing.
- CRI Dosing Range: 0.5 to 3.0 mcg/kg/hour (often initiated after a low-dose loading bolus of 0.5 to 1.0 mcg/kg given slowly).
- Clinical Monitoring during CRI: CRIs should be delivered via automated syringe pumps. Heart rate, respiratory rate, and blood pressure must be assessed every 1 to 2 hours. Inpatients receiving a CRI should have active warming (e.g., Bair Hugger or warm water circulating blankets) adjusted to keep rectal temperature above 99.5°F.
Micro-Dosing in Geriatric or Debilitated Patients
While labeled for healthy animals, low doses of dexmedetomidine (referred to as "micro-doses") are sometimes used in compromised patients under intense monitoring. Doses as low as 0.1 to 0.5 mcg/kg IV can provide significant anxiolysis and synergize with opioids without triggering the massive vasoconstrictive spikes seen with standard clinical doses. This approach requires careful patient-by-patient risk analysis and a dedicated syringe pump.
3. Why does dexmedetomidine slow the heart and pale the gums?
The cardiovascular response to dexmedetomidine is classic, triphasic, and highly reproducible. Understanding this pathophysiology is essential for safe monitoring and patient selection.
[ Dexmedetomidine Injection ]
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(Peripheral Alpha-2B Activation)
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Peripheral Vasoconstriction (Spasm)
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Systemic Hypertension (Spike)
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(Aortic Baroreceptor Stimulation)
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Vagal Nerve Stimulation
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Vagal Bradycardia (HR drop) AV Block (1st/2nd Deg)
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Central Norepinephrine Suppression
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Mild Vasodilation (Later)
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Normotension / Hypotension
Phase 1: Vasoconstriction and Hypertension
Within minutes of injection (IV or IM), peripheral α₂B receptor activation causes severe vasoconstriction. Systemic vascular resistance spikes. As a result, blood pressure rises dramatically (hypertension), with systolic pressures sometimes exceeding 200 mmHg.
Phase 2: Vagal Bradycardia and Arrhythmias
The aortic and carotid baroreceptors detect this sudden rise in pressure and trigger a compensatory vagal (parasympathetic) reflex. The brain tells the heart to slow down to protect vital organs from hypertensive damage.
- Heart Rate Drop: Heart rate frequently drops by 50% to 70% of baseline. In dogs, rates of 30 to 50 beats per minute (bpm) are common; in cats, rates may drop to 80 to 120 bpm.
- Cardiac Conduction Blocks: The high vagal tone frequently induces first-degree or second-degree atrioventricular (AV) blocks. First-degree AV block and Mobitz Type I (Wenckebach) second-degree AV block — where P-waves progressively delay and occasionally fail to conduct, producing a dropped beat — are common, expected physiological responses under dexmedetomidine that typically resolve without treatment as long as perfusion is maintained. High-grade or Mobitz Type II second-degree AV block (sudden, non-conducted P-waves without prior delay) is not benign; it warrants closer monitoring and, if perfusion is compromised, reversal with atipamezole.
- Mucous Membrane Color: The peripheral vasoconstriction causes blood to shunt away from the skin and mucous membranes to the core. This produces the characteristic pale or grey mucous membranes that owners and technicians observe. Capillary refill time (CRT) is prolonged.
Phase 3: Normotension to Hypotension
As the initial peripheral vasoconstriction begins to wear off, and central norepinephrine suppression continues to prevent sympathetic outflow, blood pressure decreases. Over the subsequent 1 to 2 hours, the patient transitions from hypertension to normotension or mild hypotension, while bradycardia often persists.
The Anticholinergic Controversy: Why NOT to Give Atropine
A common mistake in veterinary medicine is administering an anticholinergic (like atropine or glycopyrrolate) to treat dexmedetomidine-induced bradycardia.
- The Danger: Anticholinergics force the heart rate to increase by blocking parasympathetic input. However, they do not resolve the peripheral vasoconstriction. Forcing a bradycardic heart to pump rapidly against extremely high vascular resistance dramatically increases myocardial work and oxygen consumption, which can precipitate myocardial ischemia, severe tachyarrhythmias, or cardiovascular collapse.
- The Rule: If the heart rate is low but blood pressure is adequate, do not treat the bradycardia. If the patient is cardiovascularly compromised (hypotensive, poor perfusion, poor ventilation), do not use an anticholinergic—reverse the dexmedetomidine with atipamezole.
4. Which patients should NOT receive dexmedetomidine?
Because of its heavy cardiovascular toll, dexmedetomidine is not a safe choice for every patient. Patient selection must strictly follow cardiac and metabolic criteria.
| Patient Category | Suitability | Clinical Rationale |
|---|---|---|
| Healthy Young to Middle-Aged (ASA I-II) | Excellent Fit | High cardiovascular reserve; easily tolerates transient hypertension and bradycardia. |
| Cardiovascular Disease | Strictly Contraindicated | Cannot tolerate increased afterload, bradycardia, or decreased cardiac output. Risk of congestive heart failure. |
| Severe Respiratory Disease | Strictly Contraindicated | Dexmedetomidine causes mild to moderate respiratory depression; compounds hypoxemia. |
| Hepatic or Renal Impairment | Contraindicated / Cautious | Metabolism occurs in the liver; excretion via kidneys. Clearance is significantly prolonged. |
| Pre-existing Bradycardia / Hypotension | Strictly Contraindicated | Worsens underlying conduction blocks, low heart rate, and tissue perfusion. |
| Endocrine / Debilitated / Shock | Contraindicated | Compromised compensatory mechanisms; high risk of cardiovascular collapse. |
| Seizure History | Cautious Use | Dexmedetomidine can lower the seizure threshold in susceptible individuals. |
Species-Specific Cautions
- Cats and Emesis: Dexmedetomidine stimulates the chemoreceptor trigger zone (CRTZ) in the brainstem. In cats, this is heavily mediated by alpha-2 receptors. Intramuscular injection of dexmedetomidine will induce vomiting in approximately 50% to 80% of cats. This can be useful if foreign-body emesis induction is needed, but is a hazard in patients with an unprotected airway, increased intraocular pressure, or a risk of aspiration pneumonia.
- Feline Polypharmacy Safety: While not observed in feline field trials, sudden deaths have been reported in cats receiving dexmedetomidine in complex combinations alongside ketamine and butorphanol (the popular "DKB" cocktail). Feline patients must be closely monitored during induction and recovery.
- Thermoregulation: Dexmedetomidine depresses the thermoregulatory center in the hypothalamus. Combined with sedation-induced immobility, this leads to rapid hypothermia. Supplementary active warming is mandatory for all sedated patients.
5. How does atipamezole (Antisedan) reverse dexmedetomidine, and what does it NOT reverse?
One of the greatest clinical advantages of dexmedetomidine is its rapid and complete reversibility. Atipamezole hydrochloride (Antisedan) is a highly selective alpha-2 adrenergic antagonist designed specifically to displace dexmedetomidine from receptor sites.
Pharmacodynamics of Reversal
Atipamezole binds competitively to alpha-2 receptors, blocking dexmedetomidine and restoring normal norepinephrine release.
- Onset: Reversal is typically evident within 5 to 10 minutes after intramuscular (IM) injection.
- Administration Route: Atipamezole should be administered intramuscularly (IM). While intravenous (IV) administration is possible in dire emergencies (e.g., cardiopulmonary arrest under sedation), IV use can cause rapid vasodilation, profound hypotension, reflex tachycardia, and severe central nervous system excitement (delirium, thrashing).
Dosing of Atipamezole
To ensure complete receptor displacement, atipamezole is dosed relative to the amount of dexmedetomidine administered. Because atipamezole is formulated at 5.0 mg/mL (5000 mcg/mL) and dexmedetomidine at 0.5 mg/mL (500 mcg/mL), they are designed for an equal volume ratio in dogs.
- Dog Reversal Dose: The FDA-approved dose (NADA 141-033) is based on body surface area, matching the agonist volume:
- If Dexdomitor was given at 375 mcg/m² IV, Antisedan is dosed at 3750 mcg/m² IM.
- If Dexdomitor was given at 500 mcg/m² IM, Antisedan is dosed at 5000 mcg/m² IM.
- In weight-based terms, this equals a 10:1 ratio of atipamezole to dexmedetomidine (e.g., if a dog received 10 mcg/kg of dexmedetomidine, it receives 100 mcg/kg of atipamezole).
- Cat Reversal Dose: The use of atipamezole in cats is considered off-label in the United States, though it is standard practice globally. The typical feline dose is half of the dog ratio (a 5:1 ratio of atipamezole to dexmedetomidine, or half the volume of the injected sedative).
Key Reversal Caveats
- Reversal of Analgesia: Atipamezole does not selectively reverse sedation while leaving pain relief intact; it reverses both. If a patient underwent a painful procedure (e.g., laceration repair or dental extraction) under dexmedetomidine sedation, reversing the sedative will instantly remove all alpha-2-mediated analgesia. Veterinarians must ensure alternative analgesic coverage (e.g., local nerve blocks, NSAIDs, or pure mu opioids) is active before reversing.
- Sedation Relapse (Resedation): The half-life of atipamezole is shorter than the half-life of dexmedetomidine in some patients. This is particularly true if dexmedetomidine was given intravenously. As atipamezole concentrations drop, remaining dexmedetomidine can re-bind to receptors, causing the patient to slide back into a sedated, bradycardic state. Patients must be monitored in a quiet area until recovery is confirmed stable.
- Feline Dyspnea Reports: Feline pharmacovigilance reports contain cases of transient dyspnea, tachypnea, or open-mouth breathing immediately following atipamezole administration. While usually self-limiting, cats must be observed closely post-reversal.
6. What is Sileo oromucosal gel, and how is it used for noise aversion?
In 2016, the FDA approved Sileo (dexmedetomidine oromucosal gel) at a concentration of 0.09 mg/mL. It represents a unique formulation and clinical application of the drug.
Dosing and Administration
Sileo is indicated for the treatment of noise aversion in dogs—specifically fears triggered by fireworks, thunderstorms, construction, or transport.
- Mechanism: Unlike the injectable form, Sileo is administered oromucosally (applied to the oral mucosa between the dog's cheek and gum). It is absorbed across the mucous membranes.
- Bioavailability: Oromucosal absorption bypasses first-pass hepatic metabolism, achieving a bioavailability of approximately 28%.
- Critical Warning: Sileo must NOT be swallowed. If a dog swallows the gel, it undergoes first-pass hepatic metabolism and the product may not be effective — in pharmacokinetic studies, gastrointestinal administration produced no measurable blood levels. It must absorb locally through the gums.
Sileo Syringe Mechanics and Safety Dial
Sileo is packaged in a specialized multi-dose syringe equipped with a dial-ring. The ring must be turned to lock at the specific dot increment matching the dog's prescribed dose (measured in "dots" based on body weight). If the ring is not locked, or if the plunger is pushed without locking, the dog may receive a massive overdose. Owners must receive a demonstration in the clinic before using Sileo at home.
Calming Without Heavy Sedation
The therapeutic goal of Sileo is anxiolysis without recumbent sedation. By delivering a micro-dose (125 mcg/m² oromucosally, which is roughly one-quarter of the injectable IM sedative dose), Sileo suppresses the central fear response (norepinephrine surge) without causing severe motor impairment or recumbency. Dogs remain ambulatory and responsive but calm.
- Onset: Typically 30 to 60 minutes.
- Redosing: May be repeated at approximately 2-hour intervals as the noise event continues, up to a maximum of 5 doses per event.
- Age Limit: Not evaluated or approved for dogs younger than 16 weeks of age.
7. What do the FDA adverse event reports actually show for dexmedetomidine?
To build a realistic safety profile, we queried the FDA's openFDA Animal and Veterinary Adverse Event database (extract dated July 5, 2026) — the same public pharmacovigilance system that captures voluntary adverse-drug-event reports from veterinarians, manufacturers, and owners.
Methodology and Filter Scope
- Filter Rule: We extracted every report whose active-ingredient field contained "dexmedetomidine" (capturing dexmedetomidine hydrochloride and combination products such as dexmedetomidine-ketamine-butorphanol protocols).
- Deduplication: Because a single report can list several drugs and several reactions, each report was counted once using its unique adverse-event-report identifier — so a dog that experienced both bradycardia and emesis counts as one report in each of those categories, not twice in a total. (The openFDA
report_idfield is a coarser submission key that groups many individual reports; the per-report identifier is the correct denominator.) - Denominator: The query identified 8,616 unique adverse-event reports involving dexmedetomidine in this extract.
Key Adverse Event Findings
The data strongly corroborates the labeled alpha-2 pharmacology: a dominant profile of excessive or prolonged sedation and lack of efficacy, layered over a clear cardiovascular, central nervous system, and gastrointestinal signature.
+------------------------------------+----------------------------------------+
| Clinical Category | Unique Reports (n=8,616) |
+------------------------------------+----------------------------------------+
| Lack of efficacy / ineffective | 2,413 (28.0%) |
| Sedation (excessive/prolonged) | 1,544 (17.9%) |
| Vomiting / emesis | 780 (9.1%) |
| Bradycardia | 719 (8.3%) |
| Lethargy | 651 (7.6%) |
| Cardiac arrest | 485 (5.6%) |
| Seizure | 343 (4.0%) |
| Hypersalivation | 279 (3.2%) |
| Apnoea | 265 (3.1%) |
| Tachycardia | 247 (2.9%) |
| Ataxia | 245 (2.8%) |
| Hypothermia | 232 (2.7%) |
| Pale mucous membrane | 231 (2.7%) |
| Hypotension | 150 (1.7%) |
| Arrhythmia | 147 (1.7%) |
| Tremor | 106 (1.2%) |
| Heart block / AV block | 104 (1.2%) |
| Hypoglycaemia | 58 (0.7%) |
+------------------------------------+----------------------------------------+
Read the cardiovascular row as the drug's mechanism made visible: bradycardia, cardiac arrest, tachycardia, hypotension, arrhythmia, and heart block together account for a large share of reports, and they map directly onto the triphasic blood-pressure and conduction profile described in Section 3. "Lack of efficacy" leading the table is consistent with real-world under-dosing or tolerance rather than pharmacologic failure, and is one reason clinicians combine dexmedetomidine with opioids rather than pushing the alpha-2 dose higher.
Analysis of Outcomes
Across the 8,616 unique reports, 1,240 recorded a fatal outcome in the outcomes field — 969 categorized as "Died" and 274 as "Euthanized" (a small number of reports list both). For comparison, 3,091 reports recorded a complete recovery to normal, 1,749 were ongoing, and 1,203 had an unknown outcome at the time of reporting. The FDA's serious-adverse-event flag was set to true in 3,556 of the reports.
Important Data Caveats
When reviewing this FDA data, readers and clinical teams must apply the following limitations:
- Passive Surveillance Limitation: Adverse drug event reporting to the FDA is voluntary for veterinarians and pet owners. These counts represent passive pharmacovigilance reports and do not establish incidence rates or prove direct causality. The denominator of total animals safely administered dexmedetomidine is unknown but represents many millions of doses; the percentages above are shares of reports, not of exposed animals.
- Polypharmacy Confound: The fatal reports overwhelmingly involved complex anesthetic cocktails (combinations of dexmedetomidine with ketamine, butorphanol, propofol, tiletamine, zolazepam, or inhaled gas anesthetics). These fatalities reflect critical, high-risk, or emergency procedures in hospitalized veterinary patients rather than adverse reactions to standalone dexmedetomidine used for routine sedation.
- Species Attribution: Reports were predominantly canine (5,407) and feline (2,806), with a small number involving exotic species and roughly 55 accidental human exposures — a reminder of the handling warning on the Sileo syringe covered in the FAQ below.
8. How does dexmedetomidine compare to other sedatives like acepromazine, trazodone, or gabapentin?
Veterinarians have several options for sedation and chemical restraint. The table below compares dexmedetomidine to other common agents used in veterinary clinics.
| Drug | Class | Primary Mechanism | Reversible? | Main Cardiovascular Effect | Primary Clinical Use |
|---|---|---|---|---|---|
| Dexmedetomidine | Alpha-2 Agonist | Norepinephrine suppression | Yes (Atipamezole) | Hypertension, vasoconstriction, bradycardia | Procedural sedation, pre-med, noise phobia |
| Acepromazine | Phenothiazine | Dopamine (D₂) & α₁ blockade | No | Vasodilation, hypotension | Pre-medication, travel anxiety (adjunct) |
| Trazodone | SARI | Serotonin receptor modulator | No | Mild hypotension, minimal change | Situational anxiety, post-op cage rest |
| Gabapentin | Ca-Channel Modulator | Excitatory transmitter reduction | No | Minimal to none | Chronic pain, fear-free vet visit sedation |
- Dexmedetomidine vs. Acepromazine: Acepromazine provides reliable sedation but causes vasodilation and hypotension without analgesia. Because it is not reversible, its effects last 4 to 8 hours. Dexmedetomidine provides shorter, reversible sedation with significant analgesia, but carries a higher initial vasoconstrictive workload.
- Dexmedetomidine vs. Gabapentin/Trazodone: Gabapentin and trazodone are oral medications used for mild to moderate situational anxiety, taking 1 to 2 hours to take effect. They do not provide the heavy, recumbent chemical restraint required for clinical procedures, which is the primary domain of injectable dexmedetomidine.
9. What is the clinical monitoring checklist for veterinary teams?
When administering dexmedetomidine in the clinic, the following monitoring protocols should be enforced:
- ECG Monitoring: Standard leads should monitor for second-degree AV blocks and bradycardia. Ensure the rate matches the patient's size and perfusion status.
- Blood Pressure: Oscillometric cuffs should measure mean arterial pressure (MAP). Be prepared for high initial readings (Phase 1) followed by normotension.
- Pulse Oximetry (SpO₂): Place a probe on the tongue or vulva/prepuce. Note that peripheral vasoconstriction can sometimes cause probe failure due to poor local perfusion.
- Active Warming: Circulating water blankets, forced-air warmers, or warm IV fluids should be initiated immediately upon sedation to combat hypothermia.
- Quiet Environment: Alpha-2 sedated patients remain sensitive to auditory stimuli. Sudden loud noises can cause a sudden, temporary arousal, presenting a safety risk to the clinical team.
FAQs
Can the effects of dexmedetomidine be reversed if a pet is over-sedated?
Yes. The effects of dexmedetomidine can be rapidly and completely reversed using the antagonist atipamezole (Antisedan). Administered via intramuscular injection, it typically restores normal alertness, heart rate, and reflexes within 5 to 10 minutes. However, it also reverses any pain relief provided by the sedative.
Why do cats sometimes have trouble breathing after atipamezole?
Pharmacovigilance reports and the Antisedan label note cases of cats exhibiting transient dyspnea, tachypnea, or open-mouth breathing shortly after receiving atipamezole. Atipamezole is not FDA-approved for use in cats, and although reversal is common in practice, this reaction — usually mild and self-limiting — is one reason cats must be kept under close observation in a quiet space until their respiratory pattern has returned to normal.
Is Sileo the same drug as Dexdomitor, and can I use it for everyday anxiety?
Sileo and Dexdomitor both contain the active ingredient dexmedetomidine, but they are very different formulations. Dexdomitor is a high-dose injectable sedative for clinic use. Sileo is a low-dose, slow-absorbing gel applied to the gums to treat acute noise aversion (e.g., during fireworks or storms). It is not approved or appropriate for daily management of generalized anxiety.
Why does my dog's gums look pale after a dexmedetomidine sedation?
Dexmedetomidine activates receptors on blood vessels, causing them to constrict (vasoconstriction). This narrows the blood vessels in the gums and skin, shifting blood flow to the body's core. The pale or grayish appearance of the gums is a direct result of this decreased peripheral blood flow and is expected under this medication.
What should I do if Sileo accidentally gets on my skin or is swallowed by a person?
Human exposure to dexmedetomidine can cause bradycardia, hypotension, sedation, and dizziness. In case of skin or mucosal contact, wash the area immediately with soap and water. If swallowed or absorbed, seek medical attention immediately. Keep the Sileo syringe out of reach of children.
Sources
- FDA CVM NADA 141-033 Freedom of Information Summary: Antisedan (atipamezole hydrochloride) for Dogs
- DailyMed Prescribing Label: Antisedan (atipamezole hydrochloride) Injection for Dogs
- Clinician's Brief Review: Dexmedetomidine & Atipamezole Dosing and Mechanics
- Zoetis Sileo Product Launch and Information: Sileo (dexmedetomidine oromucosal gel) for Noise Aversion
- FDA CVM NADA 141-456 Freedom of Information Summary: Sileo (dexmedetomidine oromucosal gel) — 125 mcg/m² oromucosal dose, 28% oromucosal bioavailability
- DailyMed Prescribing Label: Sileo (dexmedetomidine oromucosal gel) for Dogs
- VCA Animal Hospitals Guide: Dexmedetomidine (Dexdomitor) Reference
- openFDA Animal and Veterinary Adverse Events Database: US FDA Adverse Event Reports (2026-07-05 run)
