01Approach to the Critical Patient/attcp52

Immediate stabilization

›Airway and breathing threats

›Inability to protect airway from severe agitation or obtundation

›Prepare for rapid sequence intubation

›Ketamine preferred induction agent in hemodynamically unstable patient

›Respiratory failure from prolonged seizure or hyperthermia

›SpO2 target 94% to 98%

›Supplemental oxygen via non-rebreather mask initially

›Aspiration risk from altered mental status or vomiting

›Suction at bedside

›NPO until mental status clears

›Hemodynamic threats

›Severe hypertension

›SBP >180 mmHg with end-organ signs is hypertensive emergency

›Titrate short-acting agents; avoid long-acting antihypertensives

›Tachycardia with hemodynamic compromise

›HR >150 bpm with hypotension requires urgent intervention

›Avoid pure beta-blockers due to unopposed alpha stimulation risk

›Cardiogenic shock from takotsubo or dysrhythmia

›VA-ECMO or IABP consideration for refractory cases

›Cardiology consult immediately

›Hyperthermia response

›Core temperature >40°C is the single most dangerous finding

›Active cooling must begin immediately

›Ice water immersion is fastest and preferred method

›Evaporative cooling as alternative

›Hyperthermia drives rhabdomyolysis, DIC, and multi-organ failure

›Target temperature normalisation within 30 minutes

02History/hx41

Substance use history

›Specific substance identification

›Street names: bath salts, flakka, cloud nine, vanilla sky, ivory wave, plant food

›Common agents: MDPV, mephedrone, methylone, alpha-PVP

›Route of administration

›Insufflation (snorting) most common

›Oral, IV, smoking, rectal routes described

›Amount and pattern of use

›Single versus repeated dosing

›Intoxication typically lasts 6 to 8 hours but can be prolonged

›Purchase source

›Gas stations, head shops, internet

›Often labeled "not for human consumption"

Symptom history

›Onset and progression

›Euphoria followed by agitation, paranoia, psychosis, combativeness

›Hallucinations: visual and auditory

›Suicidal ideation or self-harm attempts

›Chest pain or palpitations

›Dark urine suggesting myoglobinuria

›Muscle pain or rigidity

›Coingestions

›Alcohol — extremely common; alters clinical picture

›Cannabis

›Amphetamines or cocaine

›Opioids

›Ethanol and amphetamine co-use may increase cathinone toxicity

03Physical Exam/exam39

Vital signs

›Sympathomimetic vital sign pattern

›Tachycardia — HR often 110 to 170 bpm

›Hypertension — SBP commonly 160 to 220 mmHg

›Hyperthermia — core temperature measurement critical

›>40°C indicates life-threatening toxicity

›Rectal thermometry required for accuracy

›Tachypnea from agitation, hyperthermia, or metabolic acidosis

Neurological and psychiatric exam

›Neurological findings

›GCS assessment

›Mydriasis — pupil size and reactivity

›Hyperreflexia and tremor

›Clonus — distinguishes from anticholinergic toxidrome where clonus absent

›Seizure activity or postictal state

›Psychiatric and behavioral findings

›Agitation severity assessment

›Paranoia and persecutory ideation

›Hallucinations: content and modality

›Combativeness and risk to staff

›Disorganized thought pattern

Skin and general exam

›Skin findings

›Diaphoresis — key distinguishing feature from anticholinergic toxidrome

›Skin excoriations from scratching or self-harm

›Track marks or injection sites if IV use

›Cardiovascular exam

›Tachycardia rhythm quality

04Differential Diagnosis/ddx46

Life-threatening mimics

›Stimulant intoxications

›Amphetamine or methamphetamine intoxication

›ICD-10 F15.929

›Clinically indistinguishable; only differentiated by specific confirmatory testing

›Cocaine toxicity

›ICD-10 F14.929

›Shorter duration; positive urine immunoassay common

›MDMA (ecstasy) toxicity

›ICD-10 F15.929

›Serotonergic features more prominent; hyponatremia risk

›Psychedelic and dissociative intoxications

›PCP intoxication

›ICD-10 F16.929

›Similar agitation and psychosis; nystagmus and analgesia may be present

›Synthetic cannabinoid toxicity

›ICD-10 F12.929

›Bradycardia possible; less sympathomimetic pattern

›Toxidrome mimics

›Serotonin syndrome

›ICD-10 T43.206A

›Clonus, hyperreflexia, and diarrhea; medication history key

›Neuroleptic malignant syndrome

›ICD-10 G21.0

›Lead-pipe rigidity; antipsychotic exposure history

›Anticholinergic toxidrome

›Dry skin versus diaphoresis; urinary retention; absent bowel sounds

05Laboratory Tests/lt48

Core metabolic panel

›Basic metabolic panel

›Serum electrolytes

›Hyponatraemia if severe agitation and hyperthermia

›Hyperkalaemia from rhabdomyolysis or acidosis

›Renal function (creatinine and urea)

›AKI from rhabdomyolysis-induced tubular injury

›Serial monitoring every 4 to 6 hours in moderate to severe cases

›Blood glucose

›Point-of-care glucose immediately to exclude hypoglycaemia

›Hyperglycaemia from catecholamine surge

›Serum bicarbonate

›Metabolic acidosis from hyperthermia and tissue hypoperfusion

Rhabdomyolysis and muscle injury markers

›Creatine kinase (CK)

›Often markedly elevated; values >10,000 U/L indicate severe rhabdomyolysis

›Serial CK every 6 to 8 hours to track trend

›CK >5,000 U/L associated with increased AKI risk

›Urine dipstick positive for blood without RBCs suggests myoglobinuria

›Urinalysis

›Myoglobinuria: tea-coloured or brown urine

›Positive haem on dipstick without RBCs on microscopy

›Urine output monitoring target >1 to 2 mL/kg/hr with rhabdomyolysis

Cardiac and coagulation markers

›Troponin

›Rule out myocardial infarction from coronary vasospasm

›Serial troponin at 0 and 3 to 6 hours if chest pain or ECG changes

›Elevated troponin with normal coronaries possible (vasospasm, stress cardiomyopathy)

06Diagnostic Tests/dt72

Scoring Systems

›Agitation severity assessment

›Richmond Agitation-Sedation Scale (RASS)

›Guides sedation titration in ED and ICU

›Target RASS 0 to -1 for cooperative patient

›RASS -5 indicates unarousable state requiring ventilation reassessment

›Altered Mental Status Scale

›GCS less than 13 triggers urgent CT head evaluation

›Serial GCS to track trajectory

›Toxicology severity scoring

›Poisoning Severity Score (PSS)

›Grade 0: No symptoms

›Grade 1: Mild, transient, spontaneously resolving

›Grade 2: Moderate, prolonged, requiring treatment

›Grade 3: Severe, life-threatening

›Grade 4: Fatal

›Clinical application

›PSS grade 2 or higher warrants ICU-level monitoring

›No ACEP-specific validated scoring tool exists for synthetic cathinone toxicity

MRI

›MRI brain

›Not indicated for acute bath salts toxicity management

›Agitation precludes MRI in most cases

›CT is faster and more accessible

›Deferred indications after stabilisation

›Persistent unexplained focal neurological deficits after clearing

›Suspected ischaemic stroke not seen on CT

›Subacute cerebral edema characterisation

07Disposition/dispo44

ICU admission criteria

›Indications for ICU admission

›Hyperthermia >40°C

›Ongoing cooling required

›Multi-organ failure risk

›Intubation and mechanical ventilation

›Airway protection failure

›Refractory seizures requiring deep sedation

›Rhabdomyolysis with AKI

›CK >10,000 U/L with rising creatinine

›Oliguria despite aggressive IV hydration

›Cardiac ischaemia or haemodynamic instability

›ST-elevation MI pattern

›Refractory tachyarrhythmia or shock

›Refractory agitation requiring continuous sedation

›Large-dose benzodiazepine requirement

›Dexmedetomidine infusion initiated

Observation and telemetry criteria

›Moderate-severity monitoring indications

›Moderate agitation responding to intermittent benzodiazepines

›RASS improvement to -1 or better

›No further escalation required

›Mild tachycardia and hypertension with trend improvement

›HR <120 bpm trending down

›SBP <160 mmHg on monitoring

›Elevated CK without renal impairment

›Creatinine stable or improving

›Urine output adequate with IV fluids

08Treatment/t117

Agitation management

›Benzodiazepines — first-line for all bath salts toxicity

›Lorazepam IV

›2 to 4 mg IV every 5 to 10 minutes

›Titrate to sedation effect; large doses often required

›Maximum limited by respiratory monitoring

›Midazolam IV or IM

›5 mg IV or 5 to 10 mg IM for rapid onset

›Onset 2 to 5 minutes IV; 5 to 10 minutes IM

›Preferred for IM route when IV access not yet established

›Diazepam IV

›5 to 10 mg IV every 5 to 10 minutes

›Longer duration; reduces redosing frequency

›Clinical goals

›Controls agitation and prevents seizures

›Reduces hyperthermia by decreasing muscle activity

›Reduces rhabdomyolysis progression

›Class I evidence for benzodiazepines in stimulant toxicity

Refractory agitation

›Second-line antipsychotics

›Haloperidol

›5 to 10 mg IM or IV

›QTc prolongation risk; obtain ECG before if possible

›Lowers seizure threshold — use only after adequate benzodiazepine dosing

›Droperidol

›2.5 to 5 mg IM or IV

›Rapid onset; QTc prolongation monitoring required

›Cautions with antipsychotics

›Increased hyperthermia risk at high doses

›May worsen NMS if co-existing

›Ketamine

›4 mg/kg IM for acute refractory agitation

›1 to 2 mg/kg IV slow push for controlled sedation

›Preferred over antipsychotics for severe undifferentiated agitation

›Preserves airway reflexes at lower doses

›ICU-level sedation

›Dexmedetomidine infusion

›0.2 to 1.5 mcg/kg/hr IV continuous infusion

›Titrate to RASS target -1 to -2

›Alpha-2 agonism reduces sympathetic hyperactivity

›ASAM/AAAP guideline endorsed for severe stimulant toxicity

›Propofol infusion

›5 to 50 mcg/kg/min continuous infusion for intubated patients

›Monitor for propofol infusion syndrome in prolonged high-dose use

Hyperthermia management

›Active cooling — initiate immediately for temperature >40°C

›Ice water immersion

›Most effective cooling method

›Target temperature <39°C within 30 minutes

›Continuous rectal temperature monitoring during cooling

›Evaporative cooling

›Tepid water mist plus fan

›Less effective but more feasible in ED

›Cold IV fluids

›1 to 2 L crystalloid at 4°C as adjunct

›Does not replace surface cooling

›Stop cooling at 38.5°C to prevent overshoot hypothermia

›Pharmacologic adjuncts for hyperthermia

›Benzodiazepines reduce muscle-generated heat

›Avoid antipyretics (acetaminophen, NSAIDs) — not effective for toxidrome hyperthermia

›Dantrolene only if NMS or malignant hyperthermia is the diagnosis

Cardiovascular management

›Hypertensive emergency

›Phentolamine

›1 to 5 mg IV bolus; repeat every 5 minutes

›Alpha-blocker preferred for catecholamine-driven hypertension

›Sodium nitroprusside

›0.3 to 10 mcg/kg/min IV infusion

›Titrate to SBP target 140 to 160 mmHg initially

›Cyanide toxicity risk with prolonged high-dose infusion

›Dihydropyridine calcium channel blockers

›Nicardipine 5 to 15 mg/hr IV infusion

›Amlodipine if oral route feasible

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

›Coronary vasospasm and myocardial ischaemia

›Nitroglycerin

›0.4 mg sublingual every 5 minutes for chest pain

›5 to 200 mcg/min IV infusion for refractory vasospasm

›Calcium channel blockers

›Diltiazem 0.25 mg/kg IV bolus then infusion

›First-line for coronary vasospasm with preserved LV function

›Aspirin 325 mg PO if ischaemia suspected

›Beta-blocker contraindication

›Pure beta-blockers contraindicated

›Propranolol, metoprolol, atenolol contraindicated

›Unopposed alpha stimulation worsens hypertension and vasospasm

›If beta-blockade needed, use labetalol or carvedilol

›Labetalol 10 to 20 mg IV every 10 minutes

›Combined alpha and beta blockade avoids unopposed alpha effect

›Dysrhythmia management

›Sinus tachycardia — treat underlying cause (agitation, hyperthermia)

›VT or VF — standard ACLS; amiodarone 300 mg IV bolus

›QTc prolongation — discontinue antipsychotics; magnesium 2 g IV for torsades risk

›SVT — adenosine 6 mg IV rapid push if unstable

Rhabdomyolysis and renal protection

›IV fluid resuscitation

›Isotonic crystalloid (normal saline or lactated Ringer's)

›Initial bolus 1 to 2 L IV

›Maintain urine output 1 to 2 mL/kg/hr

›Target 200 to 300 mL/hr urine output with severe rhabdomyolysis

›Urine alkalinisation

›Sodium bicarbonate 1 to 2 mEq/kg IV then infusion

›Target urine pH >6.5 to prevent myoglobin crystallisation

›Controversial; expert consensus supports use with CK >5,000 U/L

›Monitor for fluid overload

›Pulmonary oedema risk in cardiac dysfunction

›Adjust rate based on urine output and POCUS findings

Seizure management

›Benzodiazepines first-line

›Lorazepam 2 to 4 mg IV

›Repeat every 5 minutes for status epilepticus

›Refractory seizures

›Phenobarbital 20 mg/kg IV at 50 to 100 mg/min

›Preferred for toxicologic seizures

›Propofol infusion for intubated patient

›Phenytoin and fosphenytoin should be avoided

›Ineffective for toxicologic seizures

›May worsen cardiac conduction abnormalities

Physical restraint protocol

›Restraints as temporary bridge only

›Chemical sedation must accompany or immediately follow physical restraint

›Sustained restraint without adequate sedation is associated with death

›Positional asphyxia risk — avoid prone restraint

›Reassess need for restraints every 15 minutes

09Special Populations/sp60

Pregnancy

›Pregnancy-specific considerations

›Physiologic changes affecting toxicity

›Increased blood volume may dilute catecholamine effect

›Uteroplacental circulation at risk from vasospasm

›Preterm labour triggered by hyperthermia and catecholamine surge

›Fetal monitoring

›Continuous fetal heart rate monitoring for viable gestation (>24 weeks)

›Obstetrics consult immediately for any pregnancy with bath salts toxicity

›Treatment modifications

›Benzodiazepines remain first-line for agitation and seizures despite fetal CNS depression risk

›Neonatal monitoring required if benzodiazepines used near delivery

›Antipsychotics (haloperidol) — limited data; use only if benzodiazepines inadequate

›Temperature management

›Maternal hyperthermia causes fetal neural tube injury and increased miscarriage risk

›Aggressive cooling equally urgent in pregnant patient

›Imaging

›CXR with abdominal shielding when clinically indicated

›CT head if neurological indication present; fetal risk is low for single head CT

›Drug safety

›Sodium nitroprusside — avoid in pregnancy (fetal cyanide toxicity risk)

›Nicardipine or hydralazine preferred for hypertensive emergency in pregnancy

Geriatric

›Older adult considerations

›Altered pharmacokinetics

›Reduced renal clearance increases drug accumulation risk

›Reduced hepatic metabolism prolongs drug effects

›Lower volume of distribution changes peak concentrations

10Background/b66

Epidemiology

›Prevalence and trends

›Peak US emergency department visits from synthetic cathinones 2010 to 2012

›AAPCC data: >22,000 calls related to bath salts in 2012

›Decline after DEA emergency scheduling of MDPV, mephedrone, methylone in 2011

›Ongoing emergence of novel synthetic cathinones

›Alpha-PVP (flakka) major epidemic 2014 to 2015 particularly in Florida

›Novel agents continuously synthesised to evade scheduling

›Demographics

›Young adults 18 to 35 predominantly

›Male predominance

›Geographic clustering around areas of high drug availability

›Mortality and morbidity

›Death uncommon with early recognition and aggressive management

›Mortality from hyperthermia, rhabdomyolysis-induced renal failure, cardiac arrest, or restraint-related asphyxia

›Psychiatric morbidity: psychosis may persist days to weeks after last use

Pathophysiology

›Mechanism of action

›Monoamine reuptake inhibition and release

›Blocks dopamine, norepinephrine, and serotonin transporters

›Net effect: massive increase in synaptic monoamine levels

›Potency comparison

›MDPV has 10-fold greater potency than cocaine at dopamine transporter

›Mephedrone acts similarly to MDMA with prominent serotonergic effects

›Methylone more balanced dopamine and serotonin effects

›Sympathomimetic toxidrome mechanism

›Excess catecholamines cause hypertension, tachycardia, and hyperthermia

›Peripheral vasoconstriction from alpha-adrenergic activation

›Coronary vasospasm from direct vascular effects

›Downstream complications

›Hyperthermia pathway

›Agitation and muscle hyperactivity generate heat

›Impaired heat dissipation from vasoconstriction and diaphoresis

›Core temperature >42°C causes protein denaturation

›Rhabdomyolysis cascade

›Muscle breakdown releases myoglobin

›Myoglobin precipitates in renal tubules causing AKI

›CK elevation correlates with muscle injury severity

›Cardiac injury mechanism

›Catecholamine-mediated direct myocardial toxicity

›Coronary vasospasm can cause STEMI with normal coronaries

›Takotsubo cardiomyopathy from catecholamine surge

Therapeutic Considerations

›Evidence basis for treatment

›No randomised controlled trials for bath salts toxicity treatment

›Benzodiazepines first-line based on class effect in sympathomimetic toxicity

›Extrapolated from cocaine and amphetamine toxicity literature

›Expert consensus and AHA 2025 guidelines endorse benzodiazepines

›ASAM/AAAP 2024 guideline on stimulant use disorder

›Supports dexmedetomidine for severe hyperadrenergic states

›Supports alpha-2 agonists (clonidine) for mild to moderate cases

›AHA 2023 focused update on cardiac arrest in toxicity

›Emphasises benzodiazepines for stimulant-induced dysrhythmias

›ECMO consideration for refractory cardiogenic shock

›Pharmacological strategy principles

›Treat the toxidrome, not the specific agent

›Exact cathinone rarely identified acutely

›Sympathomimetic toxidrome management applies regardless of agent

›Avoid drugs that worsen QTc or lower seizure threshold

›Phenothiazines, typical antipsychotics with caution

›Phenytoin not useful for toxicologic seizures

›Titrate to effect rather than fixed doses

›Benzodiazepine doses may be 10 to 20 times standard for severe agitation

›Intubation preferable to inadequate sedation

›Long-term considerations

›High addictive potential of synthetic cathinones

›Psychotic symptoms may persist days to weeks after abstinence

›Addiction medicine referral prior to discharge

›Synthetic cathinones can unmask underlying psychiatric illness

11Patient Discharge Instructions/pdi30

copy discharge instructions

›Bath salts toxicity discharge instructions

›You were treated in the emergency department for toxicity from synthetic stimulants called bath salts

›These drugs can cause severe side effects including agitation, high blood pressure, racing heart, high body temperature, muscle breakdown, and kidney damage

›Your lab work and heart monitoring were checked before discharge

›Activity and recovery instructions

›Rest at home for the next 24 to 48 hours

›Drink plenty of fluids to support your kidneys

›Do not use bath salts or other synthetic stimulants

›Do not drink alcohol for at least 72 hours

›Avoid strenuous exercise until cleared by a doctor

›Return to the emergency department immediately if you experience

›New or returning confusion or agitation

›Chest pain or irregular heartbeat

›Dark brown or tea-coloured urine

›Decreased urination despite drinking fluids

›Fever above 38.5°C

›Seizure

›Thoughts of harming yourself or others

›Muscle pain that is getting worse

›Follow-up appointments

›See your primary care provider within 3 to 5 days

›Psychiatry follow-up if you experienced hallucinations or paranoia that has not fully resolved

›Addiction medicine or substance use program referral is strongly recommended

›Repeat blood tests for kidney function and CK in 3 to 5 days if instructed

›Important safety information

›Synthetic cathinones are highly addictive with unpredictable potency

›These substances are often mislabelled and contaminated

12References/r26

Guidelines and key sources

›Primary guidelines

›AHA 2025 Guidelines Part 10: Adult and Pediatric Special Circumstances of Resuscitation (Cao D et al, Circulation 2025)

›Benzodiazepines endorsed as first-line for stimulant-induced cardiac and neurologic toxicity

›AHA 2023 Focused Update on Management of Cardiac Arrest or Life-Threatening Toxicity Due to Poisoning (Lavonas EJ et al, Circulation 2023)

›ECMO consideration for refractory cardiogenic shock from stimulant toxicity

›ASAM/AAAP Clinical Practice Guideline on Management of Stimulant Use Disorder (Journal of Addiction Medicine 2024)

›Dexmedetomidine for severe hyperadrenergic states

›Alpha-2 agonists for mild to moderate cases

›Landmark studies and case series

›Ross EA et al: Psychoactive Bath Salts Intoxication With MDPV (Am J Medicine 2012)

›Clinical characterisation of MDPV toxidrome

›Banks ML et al: Synthetic Cathinones (J Emergency Medicine 2014)

›Pharmacology, clinical presentation, and treatment review

›Imam SF et al: Bath Salts Intoxication Case Series (J Emergency Medicine 2013)

›Clinical characteristics and ED management outcomes

›Miotto K et al: Clinical and Pharmacological Aspects of Bath Salt Use (Drug Alcohol Dependence 2013)

›Psychiatric sequelae and addiction potential

›Pieprzyca E et al: Toxicological Analysis of Synthetic Cathinone Intoxications (J Analytical Toxicology 2022)

›Laboratory detection methods and confirmatory testing

›Coding references

›ICD-10 codes

›T43.641A synthetic cathinone poisoning, accidental, initial encounter

›T43.642A synthetic cathinone poisoning, intentional self-harm, initial encounter

›F15.929 other stimulant use disorder, unspecified

›SNOMED CT

›Synthetic cathinone toxicity disorder concept

Evidence & Review

Evidence & Review