01Approach to the Critical Patient/attcp70

Immediate priorities

›Airway and breathing assessment

›Airway compromise indications for immediate action

›Obtundation or GCS < 8

›Inability to protect airway from secretions or vomiting

›RSI preferred; avoid succinylcholine if rhabdomyolysis or hyperkalemia suspected

›Oxygenation targets

›SpO2 >= 94% on supplemental oxygen

›If unable to maintain, escalate to high-flow nasal cannula or intubation

›Ventilation considerations

›Tachypnea from metabolic acidosis may require ventilatory support

›Avoid respiratory alkalosis-induced arrhythmia

›Circulation and hemodynamic priorities

›Hypertensive emergency recognition

›SBP >180 mmHg with end-organ damage

›Targets: reduce MAP by no more than 25% in first hour

›Cardiovascular collapse triggers

›Takotsubo cardiomyopathy

›Refractory ventricular arrhythmia

›Consider VA-ECMO for refractory cardiogenic shock

›IV access and monitoring

›Two large-bore IVs

›Continuous cardiac monitoring and pulse oximetry

›12-lead ECG immediately for chest pain or arrhythmia

›Hyperthermia management

›Core temperature threshold for critical intervention

›Temperature >40°C is rapidly life-threatening

›Rectal temperature preferred for accuracy

›Cooling priority

›Aggressive external cooling — ice water immersion or evaporative cooling

›Cooling rate >0.15°C/min associated with improved survival

›Antipyretics (acetaminophen) are ineffective — hyperthermia is not hypothalamic

›Adjunct benzodiazepines

›Reduce psychomotor agitation contributing to heat generation

›Agitation and seizure priorities

›Agitation immediate approach

›Low-stimulus environment, verbal de-escalation first

›Benzodiazepines first-line; do not delay chemical sedation

›Avoid prolonged physical restraint without chemical sedation

›Associated with sudden death from positional asphyxia and hyperthermia

›Seizure management

›Benzodiazepines first-line for toxin-induced seizures

›Avoid phenytoin — ineffective for toxin-induced seizures

Monitoring and targets

›Monitoring bundle

›Continuous cardiac monitoring for arrhythmia detection

›QTc prolongation from antipsychotic adjuncts

›Ventricular tachycardia and fibrillation risk

›Serial vital signs every 15–30 minutes in agitated patient

›Core temperature trend

›Blood pressure trend response to treatment

›Urine output monitoring

›Target UOP 1–3 mL/kg/hr in rhabdomyolysis

›Foley catheter if output not assessable

›Escalation triggers

›ICU escalation

›Persistent hyperthermia >40°C

›Refractory agitation requiring continuous sedation infusion

›Mechanical ventilation requirement

›Toxicology consultation triggers

›Diagnostic uncertainty about toxidrome

›Refractory symptoms not responding to standard therapy

›Suspected body packing or polydrug ingestion

Consult triggers

›Critical consultation indications

›Toxicology for refractory symptoms or diagnostic uncertainty

›Available via phone 24/7 through Poison Control Center

›Cardiology for ACS, new cardiomyopathy, or arrhythmia

›STEMI pathway activation if indicated

›Neurosurgery for intracranial hemorrhage

›Emergent CT head without contrast first

›Psychiatry for persistent psychosis beyond 24–48 hours or suicidality

›Addiction medicine for all patients with methamphetamine use disorder

02History/hx56

Substance use history

›Drug exposure characterization

›Route of administration

›Smoked or IV — fastest onset (minutes), highest peak levels, greatest toxicity risk

›Oral or intranasal — onset 30 minutes, lower peak, longer duration

›Amount used and time of last use

›Half-life approximately 5–30 hours; toxicity may be prolonged

›Binge use pattern and duration of current episode

›Sleep deprivation (days without sleep) increases severity

›Co-ingestants

›Opioids (methamphetamine present in 63% of opioid-related deaths)

›Alcohol, GHB, benzodiazepines

›Cocaine (relevant for beta-blocker contraindication)

Presenting symptoms

›Cardinal sympathomimetic symptoms

›Chest pain

›Character, radiation, onset — distinguish ACS from dissection

›Palpitations and racing heart

›Headache — worst of life raises concern for intracranial hemorrhage

›Shortness of breath and dyspnea

›Agitation, paranoia, and hallucinations

›Visual, auditory, and tactile (formication — "meth bugs")

›Associated features

›Bruxism and diaphoresis

›Tremor and repetitive behaviors

›Anorexia and insomnia

›Dark or cola-colored urine suggesting rhabdomyolysis

›Decreased urine output

03Physical Exam/exam38

Vital signs

›Critical vital sign thresholds

›Temperature >40°C — immediately life-threatening; rectal measurement preferred

›SBP >180 mmHg — hypertensive emergency with end-organ damage

›Heart rate >150 bpm — assess for SVT, AF, or VT

›Respiratory rate >30 — metabolic acidosis or pulmonary involvement

›SpO2 <94% — hypoxia requiring supplemental oxygen

Neurologic exam

›Pupillary assessment

›Mydriasis — sympathomimetic toxidrome

›Anisocoria or unreactive pupils — intracranial emergency

›Mental status and agitation scoring

›Level of consciousness (GCS or AVPU)

›RASS or Sedation-Agitation Scale (SAS) to quantify agitation for pharmacotherapy titration

›Orientation, coherence, psychosis assessment

›Motor and reflex exam

›Hyperreflexia — sympathomimetic or serotonin syndrome

›Clonus — serotonin syndrome concern

›Focal weakness or facial droop — stroke

›Tremor and rigidity

›Cerebellar exam

›Ataxia or dysmetria — intoxication vs. posterior fossa pathology

Cardiovascular exam

›Cardiac auscultation

›New murmur — endocarditis (tricuspid most common in IV users)

›Irregular rhythm — atrial fibrillation

›Muffled heart sounds — pericardial effusion

›Peripheral perfusion

04Differential Diagnosis/ddx43

Sympathomimetic toxidromes

›Cocaine toxicity

›ICD-10: T40.5X1A

›Similar presentation; co-ingestion common

›Shorter duration of action than methamphetamine

›Key implication: avoid pure beta-blockers in cocaine co-ingestion

›Synthetic cathinone toxicity ("bath salts")

›ICD-10: T43.641A

›Urine drug screen may not detect; clinical diagnosis

›MDMA (ecstasy) toxicity

›ICD-10: T43.621A

›Hyponatremia risk from excess free water intake

›Serotonergic component more prominent

›PCP (phencyclidine) toxicity

›ICD-10: T40.991A

›Nystagmus, dissociative features, extreme agitation

Toxidromes that mimic sympathomimetic

›Anticholinergic toxidrome

›ICD-10: T44.3X1A

›Key differentiator: dry skin, urinary retention, absent bowel sounds

›Tachycardia and hyperthermia overlap — skin moisture is key

›Serotonin syndrome

›ICD-10: G25.82

›Clonus, hyperreflexia, and diarrhea distinguish from pure sympathomimetic

›Hunter Criteria for diagnosis

›Neuroleptic malignant syndrome

›ICD-10: G21.0

›Recent antipsychotic use, lead-pipe rigidity, bradykinesia

05Laboratory Tests/lt43

Core laboratory panel

›Basic metabolic panel

›Electrolytes — hyponatremia (MDMA co-use), hyperkalemia (rhabdomyolysis)

›Renal function — AKI from rhabdomyolysis or renal vasoconstriction

›Glucose — hypoglycemia mimicking altered mental status

›Complete blood count

›Leukocytosis from sympathomimetic state (stress leukocytosis, not infection)

›Anemia in chronic users from poor nutrition

›Creatine kinase

›Rhabdomyolysis threshold: CK >1,000 U/L warrants IV fluids; CK >5,000 associated with AKI risk

›Serial CK every 6 hours if elevated

›Troponin

›Myocardial injury from vasospasm, ACS, or demand ischemia

›Serial high-sensitivity troponin at 0 and 3 hours if chest pain

›Lactate

›Elevated in tissue hypoperfusion, seizure activity, or shock

›Lactate >=2 mmol/L warrants investigation

Toxicology

›Urine drug screen

›Amphetamines positive 1–4 days after last use

›False positives: pseudoephedrine, some antihistamines, buproprion

›Does not distinguish methamphetamine from amphetamine or MDMA

›Serum ethanol

›Co-ingestion common; lowers seizure threshold

›Acetaminophen and salicylate levels

›Routine screen in altered mental status or intentional ingestion

›Quantitative serum amphetamine level

›Not routinely available; rarely alters acute management

06Diagnostic Tests/dt58

Scoring Systems

›Sedation-Agitation Scale (SAS) or RASS

›SAS score 1–7; target SAS 3–4 (calm and cooperative) with treatment

›RASS score -5 to +4; target 0 to -1 for sedated patients

›Guides pharmacotherapy titration and escalation decisions

›Stimulant Overdose Observation Scale (SOOS)

›Tool for serial monitoring of stimulant toxicity severity

›Useful for disposition decisions and treatment response assessment

›Richmond Agitation-Sedation Scale (RASS)

›Validated in ICU and emergency settings

›Score every 30 minutes during active agitation management

›Modified Glasgow Coma Scale

›Baseline neurologic assessment

›GCS <13 warrants CT head to exclude intracranial hemorrhage

MRI

›Brain MRI indications

›Subacute focal neurologic deficits where CT was negative

›Posterior fossa and brainstem ischemia better visualized on MRI

›Persistent altered mental status beyond expected drug effect duration

›MRI with DWI sequences for ischemic stroke detection

›Sensitivity >95% for ischemic stroke vs. <80% for CT in early hours

›Methamphetamine-induced leukoencephalopathy

›White matter changes in chronic users on T2/FLAIR sequences

›MRI limitations in acute setting

›Requires patient cooperation — agitated patients unable to complete

›CT head without contrast is first-line in acute emergency

›MRI deferred until patient is stabilized

07Disposition/dispo34

ICU admission criteria

›Indications for ICU-level care

›Hyperthermia >40°C

›Hypertensive emergency with end-organ damage (stroke, ACS, aortic dissection)

›Seizures or status epilepticus

›Rhabdomyolysis with AKI or CK >5,000 U/L

›Intracranial hemorrhage

›Refractory agitation requiring continuous sedation infusion

›Cardiac arrhythmias requiring continuous management

›Mechanical ventilation requirement

›Cardiogenic shock or hemodynamic instability

Observation criteria

›Indications for 6–8 hour emergency department observation

›Moderate agitation responding to benzodiazepines

›Mild-moderate hypertension trending down with treatment

›Awaiting serial troponin or CK results

›Psychosis beginning to clear with treatment

›No end-organ damage identified on initial workup

Discharge criteria

›Safe discharge requirements

›Vital signs normalized and stable for >=1 hour off medications

›Agitation and psychosis resolved

›Ambulating, tolerating oral intake, normal mental status

›No evidence of end-organ damage (normal troponin, CK, renal function)

›Safe disposition — not suicidal or homicidal, able to care for self

›Follow-up plan established

›Discharge contraindications

›Persistent QTc prolongation from antipsychotic treatment

08Treatment/t106

Agitation — stepwise approach

›Step 1: Non-pharmacologic

›Low-stimulus environment with reduced light and sound

›Verbal de-escalation

›Avoid prolonged physical restraint without chemical sedation

›Associated with sudden death from positional asphyxia and hyperthermia

›Step 2: Benzodiazepines (first-line pharmacotherapy)

›Midazolam 5–10 mg IM or IV

›Onset: 3–5 minutes IM, 1–2 minutes IV

›Repeat every 5–10 minutes as needed

›Lorazepam 2–4 mg IV or IM

›Duration 4–6 hours

›Repeat every 10 minutes if needed

›Diazepam 5–10 mg IV

›Long duration useful for prolonged agitation

›Evidence level: Class I recommendation (AHA 2023)

›Step 3: Antipsychotics (adjunct for psychosis or refractory agitation)

›Droperidol 2.5–5 mg IM or IV

›More rapid sedation than lorazepam in one RCT

›Monitor QTc

›Olanzapine 5–10 mg IM

›Avoid IV route with benzodiazepines (respiratory depression risk)

›Aripiprazole — least QTc effect among antipsychotics

›Step 4: Ketamine for refractory agitation

›Ketamine 4 mg/kg IM when IV access not possible

›Dissociative dose; onset 1–3 minutes IM

›Useful for severely combative patient prior to IV access

›Step 5: ICU-level sedation for refractory cases

›Propofol infusion — start 5–10 mcg/kg/min; titrate to effect

›Dexmedetomidine infusion — 0.2–1.5 mcg/kg/hr

›Alpha-2 agonist; reduces sympathomimetic tone

›No respiratory depression at usual doses

Hyperthermia management

›External cooling (priority intervention)

›Ice water immersion — fastest cooling method

›Cooling rate >0.15°C/min associated with improved survival

›Evaporative cooling with fans and misting — alternative if immersion not available

›Cold IV fluids (1–2 L 0.9% NaCl at 4°C)

›Target temperature <38.5°C

›Adjunct pharmacotherapy

›Benzodiazepines — reduce psychomotor heat generation

›Avoid antipyretics (acetaminophen, ibuprofen)

›Hyperthermia is not from hypothalamic set-point elevation

›Antipyretics are ineffective and may delay cooling

›Muscle relaxation for refractory hyperthermia

›Neuromuscular blockade with intubation if temperature >41.1°C refractory to above

›Non-depolarizing agent preferred (rocuronium 0.6–1.2 mg/kg IV)

Hypertensive emergency

›Step 1: Benzodiazepines first

›Treat agitation — often normalizes blood pressure

›Lorazepam 2–4 mg IV or midazolam 5 mg IV

›Step 2: Antihypertensive agents if persistent

›Nicardipine infusion 5 mg/hr IV; titrate 2.5 mg/hr every 5–15 minutes

›Maximum 15 mg/hr

›Preferred for methamphetamine-associated hypertension (dihydropyridine CCB)

›Phentolamine 2.5–5 mg IV bolus — alpha-1 antagonist

›Useful if pure beta-blockers being avoided

›Sodium nitroprusside 0.3–0.5 mcg/kg/min IV

›Titrate to effect; maximum 10 mcg/kg/min

›Risk of cyanide toxicity with prolonged use >72 hours

›Nitroglycerin 10–20 mcg/min IV if cardiac ischemia present

›Titrate by 5 mcg/min every 3–5 minutes

›Beta-blockers — evidence and controversy

›ASAM/AAAP guideline recommends labetalol or carvedilol if benzodiazepines fail

›Combined alpha-1 and beta-blockade avoids unopposed alpha stimulation

›Concerns about "unopposed alpha stimulation" with pure beta-blockers repeatedly debunked for methamphetamine (NEJM Evidence 2023)

›Avoid pure beta-blockers if cocaine co-ingestion suspected

›Avoid long-acting antihypertensives — risk of hemodynamic collapse as drug wears off

›Blood pressure targets

›Reduce MAP by no more than 25% in first hour to avoid watershed ischemia

›Further reduction over next 2–6 hours if clinically stable

Seizure management

›First-line treatment

›Benzodiazepines: lorazepam 2–4 mg IV; diazepam 5–10 mg IV

›Repeat every 5 minutes if seizure continues

›Phenobarbital 20 mg/kg IV if benzodiazepines fail

›Second-line for toxin-induced seizures

›Drugs to avoid

›Phenytoin/fosphenytoin — ineffective for toxin-induced seizures; may worsen cardiac arrhythmia

›Refractory status epilepticus

›Propofol infusion 1–2 mg/kg IV bolus, then 20 mcg/kg/min infusion

›Intubation for airway protection and EEG monitoring

Rhabdomyolysis management

›Fluid resuscitation

›0.9% NaCl 1–2 L/hr initial rate

›Target urine output 1–3 mL/kg/hr

›Titrate fluids to UOP and CK trend

›Urine alkalinization (controversial)

›Sodium bicarbonate added to D5W if urine pH <6.5 and CK >5,000 U/L

›No definitive evidence of benefit; not universally recommended

›Electrolyte monitoring

›Hyperkalemia — CK release liberates intracellular potassium

›Hypocalcemia — calcium deposition in damaged muscle

›Serial BMP every 4–6 hours

›Renal replacement therapy

›Dialysis if AKI with fluid overload, refractory hyperkalemia, or uremia

Chest pain and ACS management

›Standard ACS workup

›Aspirin 325 mg PO (if not contraindicated)

›Nitroglycerin for ongoing ischemic pain

›Serial ECGs and high-sensitivity troponin

›Cardiology consultation for STEMI or hemodynamic instability

›Percutaneous coronary intervention preferred over thrombolytics if STEMI

›Avoid pure beta-blockers if cocaine co-ingestion suspected

›Benzodiazepines reduce sympathomimetic-driven demand ischemia

Cardiac arrest management

›Standard ACLS algorithm

›CPR, defibrillation for shockable rhythms, epinephrine 1 mg IV every 3–5 minutes

›Reversible causes emphasis

›Hypoxia, hyperkalemia (rhabdomyolysis), acidosis

›VA-ECMO consideration

›Refractory cardiogenic shock from takotsubo cardiomyopathy or direct cardiac toxicity

›AHA 2025 guidelines support consideration of ECMO in refractory arrest from poisoning

09Special Populations/sp52

Pregnancy

›Maternal risks

›Severe hypertension — risk of placental abruption and eclampsia

›Hyperthermia — fetal neural tube injury and preterm labor risk

›Placental vasoconstriction — fetal growth restriction and stillbirth

›Methamphetamine use in pregnancy associated with preterm delivery and low birth weight

›Fetal monitoring

›Continuous fetal heart rate monitoring in viable pregnancies (>24 weeks)

›Obstetrics consultation urgently for maternal instability

›Drug safety in pregnancy

›Benzodiazepines — preferred for acute agitation despite teratogenic classification

›Risk of acute maternal harm outweighs fetal risk in acute emergency

›Antipsychotics — olanzapine and quetiapine relatively safer; avoid haloperidol in first trimester

›Avoid sodium nitroprusside — cyanide toxicity risk to fetus

›Hydralazine 5–10 mg IV or labetalol 20 mg IV for hypertensive emergency in pregnancy

›Neonatal considerations

›Neonatal abstinence syndrome if chronic maternal use

›Notify neonatology for delivery anticipation

Geriatric

›Physiologic vulnerability

›Reduced cardiac reserve — hypertensive surges cause greater end-organ damage

›Reduced renal function — AKI from rhabdomyolysis more common and severe

›Higher fall risk during agitation — head injury from ground-level fall

›Drug dosing modifications

›Benzodiazepines — reduce initial dose by 50% to avoid over-sedation and respiratory depression

›Lorazepam 1–2 mg IV initial dose

›Midazolam 2.5 mg IM initial dose

›Antipsychotics — increased sensitivity to QTc prolongation

10Background/b70

Epidemiology

›Global and national burden

›Methamphetamine is the second most used illicit drug globally after cannabis

›Use disorder affects an estimated 2 million Americans

›Rising prevalence across all demographic groups in the United States

›Mortality and morbidity

›Most deaths result from long-term cumulative exposure rather than acute "overdose"

›Cerebrovascular complications account for approximately 55% of methamphetamine-related deaths

›Methamphetamine present in 63% of opioid-related deaths — polysubstance use driving mortality

›Increasing cardiac mortality from methamphetamine-associated cardiomyopathy

›Population patterns

›Increasingly used across rural, suburban, and urban settings

›Strong association with STIs including HIV and hepatitis C (IV users)

›Methamphetamine strongly associated with sex work and transmission networks

›Disproportionate burden in LGBTQ+ communities — "chemsex" patterns

Pathophysiology

›Mechanism of action

›Catecholamine releasing agent — stimulates release of dopamine, norepinephrine, serotonin

›Inhibits reuptake transporters (DAT, NET, SERT) — prolongs neurotransmitter effect

›Reverses VMAT2 — forces cytoplasmic catecholamine release from vesicles

›Net effect: massive surge in synaptic catecholamines (10x greater than cocaine)

›Cardiovascular pathophysiology

›Hypertension from peripheral alpha-1 adrenergic vasoconstriction

›Tachycardia from beta-1 adrenergic cardiac stimulation

›Coronary vasospasm causing demand and supply ischemia

›Takotsubo (stress) cardiomyopathy from catecholamine surge

›Methamphetamine-associated cardiomyopathy from chronic direct cardiotoxicity

›Mitochondrial dysfunction, oxidative stress, myocyte apoptosis

›Neurologic pathophysiology

›Intracranial hemorrhage from acute hypertensive surges

›Ischemic stroke from vasospasm, embolism (endocarditis), or cardioembolism

›Dopaminergic neurotoxicity in basal ganglia with chronic use

›Methamphetamine psychosis — dopamine receptor dysregulation in mesolimbic pathway

›Hyperthermia mechanism

›Increased psychomotor activity generates heat (muscle thermogenesis)

›Peripheral vasoconstriction impairs heat dissipation

›Hypothalamic set-point not elevated — differentiates from fever

›Rhabdomyolysis mechanism

›Excessive muscular activity and psychomotor agitation

›Hyperthermia-induced myocyte injury

›Direct methamphetamine myotoxicity

›Physical restraint contributing

Therapeutic Considerations

›Pharmacotherapy rationale

›Benzodiazepines work via GABA-A potentiation — counteract catecholamine excess

›Address agitation, seizures, hypertension, and hyperthermia simultaneously

›First-line for all manifestations of sympathomimetic toxicity

›Antipsychotics — D2 antagonism for psychosis; sedation for agitation

›Adjunct role; not first-line monotherapy

›QTc monitoring required for haloperidol and droperidol

›Ketamine — NMDA antagonist producing dissociative sedation

›Allows safe approach to severely agitated patient

›Intramuscular route valuable before IV access established

›Controversial areas

›Beta-blocker debate

›"Unopposed alpha stimulation" concern repeatedly debunked for methamphetamine

›Labetalol (combined alpha/beta) and carvedilol are acceptable per ASAM/AAAP

›Pure beta-blockers remain controversial with cocaine co-ingestion

›Urinary alkalinization for rhabdomyolysis

›No RCT evidence; sometimes used empirically for urine pH <6.5 with high CK

›Antipsychotic selection

›Droperidol has stronger sedation evidence but requires QTc monitoring

›Olanzapine avoids IV route risk with benzodiazepines

›Long-term treatment evidence

›Contingency management — most evidence-based psychosocial intervention

›Cognitive behavioral therapy (CBT) — established efficacy

›Pharmacotherapy (off-label): mirtazapine (reduces use), bupropion, naltrexone

›No FDA-approved medication for methamphetamine use disorder as of 2025

›Harm reduction principles

›Naloxone provision for all patients — high opioid co-use rate

›Needle exchange programs for IV users

›HIV pre-exposure prophylaxis (PrEP) referral for high-risk patients

›Screen and treat hepatitis C (highly curable with direct-acting antivirals)

11Patient Discharge Instructions/pdi36

copy discharge instructions

›What happened and why you were treated

›You were treated for the effects of methamphetamine on your body

›Methamphetamine causes your heart to race, blood pressure to rise, and body temperature to increase

›These effects can be serious and even life-threatening

›Your tests showed specific findings that required treatment

›Lab values and any abnormalities were explained to you by your doctor

›Medications prescribed

›Take all prescribed medications as directed

›Do not combine with other drugs or alcohol — this is very dangerous

›If prescribed any new medications, fill the prescription today

›Return to the Emergency Department immediately if you experience

›Chest pain or pressure

›Severe headache unlike any you have had before

›Weakness, numbness, or drooping on one side of your face or body

›Seizure or loss of consciousness

›Dark brown or cola-colored urine

›Unable to urinate for more than 8 hours

›Return of severe agitation, paranoia, or hearing/seeing things

›Thoughts of harming yourself or others

›Very fast or irregular heartbeat

›Important safety information

›Do not drive or operate machinery for at least 24 hours

›Do not use methamphetamine again — repeated use increases your risk of heart failure, stroke, and death

›Effects of methamphetamine can last 12–24 hours; psychosis may persist for days to weeks in regular users

›Withdrawal symptoms (fatigue, increased sleep, low mood, increased appetite) are expected and not medically dangerous

›Follow-up appointments

›Primary care or addiction medicine within 1 week

12References/r25

Guidelines and key sources

›Coffin PO, Suen LW. Methamphetamine Toxicities and Clinical Management. NEJM Evidence. 2023

›Comprehensive review of clinical toxicology and management strategies

›Addresses beta-blocker controversy and evidence base

›Lavonas EJ, Akpunonu PD, Arens AM, et al. 2023 AHA Focused Update on Management of Cardiac Arrest or Life-Threatening Toxicity Due to Poisoning. Circulation. 2023

›Class I recommendation for benzodiazepines as first-line

›ECMO for refractory cardiogenic shock guidance

›Cao D, Arens AM, Chow SL, et al. Part 10: Adult and Pediatric Special Circumstances of Resuscitation: 2025 AHA Guidelines for CPR and Emergency Cardiovascular Care. Circulation. 2025

›Updated guidance on poisoning-related resuscitation

›The ASAM/AAAP Clinical Practice Guideline on the Management of Stimulant Use Disorder. Journal of Addiction Medicine. 2024

›Beta-blocker guidance: labetalol acceptable with persistent hyperadrenergic state after benzodiazepines

›Contingency management and CBT as evidence-based long-term treatments

›Leyde S, Tilhou AS, Tsui JI. Methamphetamine Use Disorder. JAMA. 2025

›Updated epidemiology and long-term treatment options

›Opioid co-use statistics and harm reduction guidance

›Schep LJ, Slaughter RJ, Beasley DM. The Clinical Toxicology of Metamfetamine. Clinical Toxicology. 2010

›Foundational pharmacology and mechanistic review

›Paulus MP, Stewart JL. Neurobiology, Clinical Presentation, and Treatment of Methamphetamine Use Disorder. JAMA Psychiatry. 2020

›Neurobiological basis of dopaminergic neurotoxicity and psychosis

›Gulati M, Levy PD, Mukherjee D, et al. 2021 AHA/ACC Guideline for the Evaluation and Diagnosis of Chest Pain. JACC. 2021

›ACS evaluation framework applicable to methamphetamine-associated chest pain

Toxicology resources

›American College of Medical Toxicology (ACMT) and American Academy of Clinical Toxicology (AACT) position statements

›Poison Control Center — 1-800-222-1222 (24/7 consultation)

›Toxicology consultation available by phone for all emergency providers

›National Institute on Drug Abuse (NIDA) — methamphetamine research updates

›Epidemiology and neuroscience of stimulant use disorder

Evidence & Review

Evidence & Review