Attention-Deficit/Hyperactivity Disorder (ADHD)

Know which drug is on board - Methylphenidate and amphetamine salts arrive with tachycardia and hypertension. Atomoxetine inhibits the norepinephrine transporter. Clonidine and guanfacine do the reverse and bring sedation, bradycardia and hypotension. Confirm the agent and the last dose before you plan your hemodynamics, because the autonomic starting point is opposite between the two groups.

Cardiac screen before a stimulant patient - Sudden death has been reported in children and adults with pre-existing structural cardiac abnormality taking stimulants, and both methylphenidate and amphetamine carry that warning. Take a history for family sudden death or ventricular arrhythmia, get a baseline ECG, and add an echo when the history or exam suggests structural disease. Stimulants are avoided outright in known cardiomyopathy, serious rhythm abnormality or coronary disease.

Holding the stimulant on the day of surgery - Stopping a stimulant is not dangerous: stimulant withdrawal is mild, vital functions are preserved, and it is treated with observation. A missed morning dose costs nothing physiologically, while a taken dose brings the tachycardia and hypertension the drug is designed to produce. Clonidine and guanfacine are the exception and get continued.

Do not stop clonidine abruptly - Abrupt clonidine discontinuation causes rebound hypertension and withdrawal symptoms. Continue it through the perioperative period rather than holding it with everything else on the morning of surgery.

MAOIs and hypertensive crisis - Methylphenidate is contraindicated with monoamine oxidase inhibitors, and amphetamine plus an MAOI can produce hypertensive crisis. At least 14 days must separate an MAOI from a stimulant. If both appear on the medication list, resolve it before induction rather than at the head of the bed.

Vasopressor choice after chronic heavy exposure - Stimulant tolerance comes from downregulated postsynaptic receptors and depleted presynaptic neurotransmitter stores. In a patient with heavy or diverted stimulant use, an indirect-acting pressor has less stored catecholamine to release, so a direct-acting agent titrated to effect is the more predictable choice.

Seizure threshold - Evidence is mixed but methylphenidate may lower the seizure threshold, and it is stopped outright if seizures develop on therapy. Relevant if the patient also has epilepsy or is on another agent that does the same.

Emergence agitation in children - Emergence delirium is common after sevoflurane and desflurane in children, and preoperative anxiety and distress at induction predict it along with maladaptive postoperative behavior. Dexmedetomidine 0.5 mcg/kg given immediately after induction reduces the incidence and spares volatile; below 0.5 mcg/kg it does not consistently prevent it, and above 1 mcg/kg it prolongs emergence and PACU time. Giving it just before emergence delays awakening instead. Propofol and ketamine also reduce the incidence. Score it with the Pediatric Anesthesia Emergence Delirium (PAED) scale so the diagnosis is not just an impression.

Behavioral plan at induction - Impulsivity and poor cooperation make a mask induction harder in a child. Premedication and a parent or child-life presence smooth it, and since preoperative distress feeds emergence delirium, the effort spent before induction pays out in PACU.

If the picture is sympathomimetic toxicity - Hyperthermia, tachycardia, tachypnea, mydriasis, tremor, seizures and altered mental status point to stimulant excess, not light anesthesia. Benzodiazepines control agitation and seizures, propranolol handles tachyarrhythmias, nitroprusside starting at 0.5 to 1 mcg/kg/min treats severe hypertension, and IV fluid plus active cooling addresses hyperthermia and protects the kidneys from rhabdomyolysis.

Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder of inattention, hyperactivity and impulsivity tied to catecholamine signaling in the brain. What reaches the operating room is usually the pharmacology, not the behavior. Methylphenidate blocks the dopamine transporter and also acts indirectly through the vesicular monoamine transporter; amphetamine and dextroamphetamine are non-catecholamine sympathomimetic amines that drive dopamine and norepinephrine out of presynaptic terminals into the synapse, raising both systolic and diastolic blood pressure and acting as a weak bronchodilator and respiratory stimulant.

The non-stimulants pull the other way. Atomoxetine is a selective presynaptic norepinephrine reuptake inhibitor. Clonidine and guanfacine are alpha-2 agonists that inhibit norepinephrine release in the rostral ventrolateral medulla and locus coeruleus, reducing sympathetic tone and producing sedation, hypotension and bradycardia. Same diagnosis, opposite autonomic starting points.