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Katom Toxicity
Cardiovascular Presentations
Abdominal aortic aneurysm
Acute coronary syndrome (NSTEMI)
Acute coronary syndrome (STEMI)
Acute decompensated heart failure
Acute limb ischemia
Acute mesenteric ischemia
Aortic dissection
Aortic stenosis
Atrial fibrillation and flutter
Bradyarrhythmia and heart block
Cardiac arrest
Deep vein thrombosis
Myocarditis
Pericarditis
Pulmonary embolism
Stable angina
Superficial thrombophlebitis
Superior vena cava syndrome
Supraventricular tachycardia
Syncope (cardiogenic)
Unstable angina
Ventricular tachycardia
Respiratory Presentations
Acute bronchitis
Acute respiratory failure
Aspiration pneumonia
Asthma exacerbation
Bronchiolitis
Community-acquired pneumonia
COVID-19 pneumonia
COPD exacerbation
Croup
Croup (laryngotracheobronchitis)
Epiglottitis
Hemothorax
Hospital-acquired pneumonia
Pleural effusion
Pneumothorax (traumatic)
Pulmonary contusion
Spontaneous pneumothorax
Neurological Presentations
Bell's palsy
Benign paroxysmal positional vertigo
Brain abscess
Cauda equina syndrome
Cervical radiculopathy
Concussion (mild traumatic brain injury)
Encephalitis
Guillain-Barré syndrome
Hemorrhagic stroke (intracerebral)
Ischemic stroke
Lumbar radiculopathy
Malignant spinal cord compression
Migraine
Peripheral neuropathy (acute)
Retropharyngeal abscess
Schizophrenia (acute exacerbation)
Seizure (breakthrough:known epilepsy)
Seizure (first-time)
Spinal cord injury
Status epilepticus
Subarachnoid hemorrhage
Tension headache
Transient ischemic attack
Traumatic brain injury (moderate-severe)
Vestibular neuritis
Viral meningitis
Gastrointestinal Presentations
Acute appendicitis
Acute cholecystitis
Acute diverticulitis
Acute pancreatitis
Anal fissure
Choledocholithiasis and cholangitis
Clostridioides difficile colitis
Gastritis
Gastroenteritis (viral and bacterial)
Gastroesophageal reflux disease
Incarcerated or strangulated hernia
Inflammatory bowel disease flare
Large bowel obstruction
Lower GI hemorrhage
Peptic ulcer disease
Perforated viscus
Small bowel obstruction
Upper GI hemorrhage
Genitourinary and Reproductive Presentations
Acute prostatitis
Acute urinary retention
Ectopic pregnancy
Epididymitis
Orchitis
Ovarian torsion
Paraphimosis
Pelvic inflammatory disease
Priapism
Pyelonephritis
Renal laceration
Ruptured ovarian cyst
Testicular torsion
Tubo-ovarian abscess
Urinary tract infection (uncomplicated)
Urolithiasis (renal colic)
Vaginal bleeding (non-pregnant)
Infectious Disease Presentations
Acute sinusitis
Acute tonsillitis
Acute upper respiratory infection
Animal bite
Bacterial meningitis
Cellulitis
Conjunctivitis (bacterial)
Dental abscess
Endocarditis
Febrile neutropenia
Fournier gangrene
Hand-foot-mouth disease
Hepatitis (acute)
Herpes zoster
HIV-related illness
Human bite
Impetigo
Infected diabetic foot ulcer
Infectious mononucleosis
Influenza
Necrotizing fasciitis
Osteomyelitis
Otitis externa
Parasitic infection
Periorbital cellulitis
Peritonsillar abscess
Scabies
Sepsis
Septic arthritis
Spontaneous bacterial peritonitis
Tick-borne illness (Lyme disease)
Tinea infection
Tuberculosis
Viral exanthem
Wound infection
Trauma Presentations
Achilles tendon rupture
ACL and mceniscus tear
Ankle fracture
Ankle sprain
Burn
Calcaneus fracture
Cervical spine fracture
Clavicle fracture
Dental avulsion
Distal radius fracture
Drowning
Elbow fracture and dislocation
Electrical injury
Facial bone fracture
Facial laceration
Femur fracture
Fingertip amputation
Forearm fracture (radius and ulna)
Frostbite
Hand:finger laceration
Heat exhaustion
Heat stroke
Hip fracture
Humeral shaft fracture
Knee dislocation
Knee sprain
Lightning injury
Mandible fracture
Metacarpal fracture
Metatarsal fracture
Muscle strain
Nasal fracture
Non-accidental trauma
Orbital fracture
Patella fracture
Phalanx fracture (finger)
Proximal humerus fracture
Pulmonary contusion
Rib fracture
Rotator cuff tear (acute traumatic)
Scalp laceration
Scaphoid fracture
Shoulder dislocation
Skull fracture
Splenic laceration
Sternal fracture
Supracondylar pediatric fracture
Tendon laceration (hand:wrist)
Thoracic and lumbar spine fracture
Tibia:fibula fracture
Tibial plateau fracture
Toe fracture
Traumatic epistaxis
Traumatic hyphema
Toxicologic Presentations
Acetaminophen toxicity
Alcohol intoxication
Alcohol withdrawal
Anticholinergic toxicity
Anticoagulant overdose
Benzodiazepine overdose
Benzodiazepine:sedative overdose
Beta-blocker and calcium channel blocker toxicity
Carbon monoxide poisoning
Caustic ingestion
Digoxin toxicity
Drug eruption
Foreign body ingestion
Opioid intoxication
Opioid overdose
Opioid withdrawal
Organophosphate
Salicylate toxicity
Serotonin syndrome
Stimulant intoxication (cocaine, methamphetamine)
Tricyclic antidepressant overdose
Psychiatric Presentations
Acute anxiety
Acute psychosis
Agitation:behavioral emergency
Bipolar disorder
Conversion disorder
Major depressive episode
Neuroleptic malignant syndrome
Suicidal ideation and attempt
Musculoskeletal and Rheumatologic Presentations
Acute low back pain (mechanical)
Bursitis
Cervical radiculopathy
Costochondritis
Gout (acute)
Lumbar radiculopathy
Pseudogout
Tendinitis
Dermatology Presentations
Acute eczema (Eczema acute flare)
Allergic contact dermatitis
Erythema multiforme
Henoch-Schönlein purpura
Pressure injury
Psoriasis (acute flare)
Stevens-Johnson syndrome
Toxic epidermal necrolysis
Urticaria (acute)
Environmental and Exposure Presentations
Envenomation (snake, spider, insect)
High-altitude illness
Hypothermia
Hematologic and Oncologic Presentations
Acute chest syndrome
Coagulopathy
Hyperviscosity syndrome
Sickle cell crisis (vaso-occlusive)
Symptomatic anemia
Thrombocytopenia (severe)
Tumor lysis syndrome
Pediatric-Specific Presentations
Bronchiolitis
Croup
Emergency delivery
Febrile seizure
Kawasaki disease
Neonatal jaundice
Neonatal sepsis
Nursemaid's elbow
Pediatric fever 0 to 28 days
Pediatric fever 29 to 60 days
Pediatric fever 61 to 90 days
Pyloric stenosis
Slipped capital femoral epiphysis
Intussusception
Endocrine and Metabolic Presentations
Adrenal crisis
Diabetic ketoacidosis
Hypercalcemia
Hyperosmolar hyperglycemic state
Hypertensive emergency
Hypertensive urgency
Hypoglycemia
Myasthenia gravis crisis
Myxedema coma
Severe hyperkalemia
Severe hyponatremia
Thyroid storm
ENT and Maxillofacial Presentations
Acute laryngitis
Acute otitis media
Acute pharyngitis
Cerumen impaction
Epistaxis (anterior)
Nasal foreign body
Otitis externa
Tympanic membrane perforation
Ophthalmologic Presentations
Acute angle-closure glaucoma
Central retinal artery occlusion
Chemical eye injury
Corneal abrasion
Corneal ulcer
Globe rupture
Ocular foreign body
Orbital cellulitis
Retinal detachment
Obstetric Presentations
Hyperemesis gravidarum
Painful vaginal bleeding in pregnancy
Placenta previa
Placental abruption
Preeclampsia:eclampsia
Preterm labor
Threatened:inevitable:incomplete abortion
Systemic and Miscellaneous Presentations
Anaphylaxis
Angioedema
Cannabis-induced hyperemesis
Katom Toxicity
POCUS
Procedures
Calculators
Resuscitation
ECG Guide
Back
Clinical Assessment Checklist
Browse categories and answer follow-up questions to refine your symptom profile.
Approach to the Critical Patient
Immediate priorities
Airway and breathing threats
▶
Respiratory depression — most critical life threat
▶
SpO2 < 94% or rising EtCO2
GCS < 8 or inability to protect airway
Rate < 10 per minute
If respiratory depression with opioid-like features, trial naloxone before intubation
▶
Naloxone 0.4–2 mg IV/IM/IN; repeat q2–3 min as needed
Response variable — kratom is partial mu-opioid agonist
If refractory to naloxone or airway unprotected, proceed to RSI
▶
Class I recommendation for definitive airway
Circulation and arrhythmia threats
▶
Sinus tachycardia most common (OR 8.61 vs controls)
▶
Differentiate from hemodynamic instability
IV fluids for volume depletion with tachycardia
QTc prolongation with ventricular arrhythmia risk
▶
Avoid QTc-prolonging agents in management
Continuous cardiac monitoring if QTc > 500 ms
Hemodynamic instability: hypotension or hypertension
▶
SBP < 90 mmHg — IV fluid resuscitation, vasopressors if refractory
Hypertension with agitation — benzodiazepines first-line
Neurological threats
▶
Seizures (6.1% of exposures)
▶
Benzodiazepines first-line
Lorazepam 4 mg IV or diazepam 5–10 mg IV
Altered mental status (altered in ~90% of poisoning cases)
▶
Glucose bedside immediately
Toxidrome identification: opioid vs sympathomimetic vs mixed
Monitoring and targets
Monitoring bundle
▶
Continuous pulse oximetry — SpO2 target > 94%
▶
Waveform capnography if respiratory concern
Repositioning if SpO2 trending down
Continuous cardiac monitoring
▶
Serial ECGs for QTc assessment
QTc > 500 ms or delta > 60 ms from baseline warrants intervention
Neurological reassessment every 15–30 minutes
▶
GCS trend
Pupillary size and reactivity
Escalation triggers
▶
Recurrent respiratory depression after naloxone
▶
Naloxone infusion: 2/3 of effective bolus per hour
ICU-level monitoring
Refractory seizures after two benzodiazepine doses
▶
Phenobarbital or propofol for refractory status
Hepatic failure signs: coagulopathy, encephalopathy
▶
Hepatology urgent consultation
Consider NAC empirically
Immediate consults
Consultation triggers
▶
Poison Control Center — all significant exposures
▶
1-800-222-1222 (US)
Management guidance for atypical presentations
Toxicology for complex polysubstance presentations
▶
Serotonin syndrome features
Refractory cardiac arrhythmia
Hepatology for acute liver injury
▶
Jaundice with elevated bilirubin
Coagulopathy or encephalopathy
Addiction medicine or psychiatry
▶
Kratom use disorder or withdrawal management
Suicidal ideation with ingestion
History
Presentation pattern
Toxidrome characterization
▶
Low-dose stimulant effects
▶
Increased energy, alertness, reduced fatigue
Tachycardia, hypertension
High-dose opioid-like effects
▶
CNS depression, sedation
Miosis, respiratory depression
Mixed or serotonergic features
▶
Agitation, diaphoresis, clonus
Hyperthermia
Exposure history
Product formulation consumed
▶
Leaves, tea, powder, capsules, concentrated extracts
▶
Extracts carry higher alkaloid loads and toxicity risk
Alkaloid content unregulated and highly variable
Dose, frequency, and duration of use
▶
Frequency correlates more strongly with dependence than dose amount
Timing of last use and quantity ingested
▶
Route and preparation method (brewed vs raw powder)
Intent and context of use
▶
Self-treatment of pain or opioid withdrawal
▶
History of opioid use disorder
Chronic pain conditions
Mood enhancement or recreational "legal high"
▶
Psychiatric comorbidities: depression, anxiety, PTSD
Prior kratom use, tolerance, and previous toxicity episodes
Co-ingestants — critical
Polysubstance use history
▶
79% of kratom-associated deaths involved multiple substances
▶
Opioids, benzodiazepines, alcohol specifically
Gabapentinoids, stimulants
Polysubstance exposure: hospitalization rate 44–56% vs 24–29% single-substance
▶
Serious outcomes 57–66% vs 41–49%
Current medications for CYP interaction risk
▶
CYP3A4 substrates: midazolam AUC increased ~1.4-fold even at 2 g kratom dose
CYP2D6 substrates: methadone, certain antidepressants, antipsychotics
Alarm features in history
High-risk symptoms requiring urgent evaluation
▶
Respiratory depression (2.8% of single-substance exposures)
▶
Dyspnea, slowed breathing
Seizures (6.1% of exposures)
▶
Loss of consciousness, convulsions
Cardiac symptoms
▶
Palpitations, chest pain, syncope
Jaundice or dark urine
▶
Hepatotoxicity median latency 14–21 days from use onset
Cholestatic pattern: pruritus, pale stools
Suicidal intent with ingestion
Risk factors
Demographic and use pattern risk
▶
Male sex (70.8% of exposures)
▶
Age 20–39 years most common demographic
Age 40–59 rapidly increasing
High-dose and high-frequency use
▶
Use of concentrated extract products vs whole-leaf
Source reliability
▶
Online purchase, smoke shops, gas stations
Contamination with heavy metals (lead) reported
Medical risk factors for severe outcomes
▶
Pre-existing liver disease — increased hepatotoxicity susceptibility
Cardiac history: arrhythmias, QTc-prolonging conditions
History of opioid use disorder
Withdrawal features
Kratom withdrawal syndrome if cessation suspected
▶
Myalgia, anxiety, irritability
▶
Lacrimation, rhinorrhea
Insomnia, diarrhea, tremors
Duration: days to weeks after cessation
▶
Onset typically 12–24 hours after last use
Up to 20% of regular users meet DSM-5 criteria for kratom use disorder
Physical Exam
Vitals and general
Vital sign assessment
▶
Temperature
▶
Hyperthermia: serotonin syndrome or sympathomimetic toxidrome
Hypothermia: severe opioid CNS depression
Heart rate
▶
Tachycardia in 16.9–21.4% of exposures
Bradycardia: severe opioid toxidrome
Blood pressure
▶
Hypertension with stimulant-predominant presentation
Hypotension: severe opioid toxidrome or dehydration
Respiratory rate
▶
Rate < 12 as opioid toxicity marker
Rate > 20 with hyperthermia as serotonin syndrome marker
Oxygen saturation room air
Neurological exam
Level of consciousness (altered in ~90% of poisoning cases)
▶
GCS: eye, verbal, motor components
▶
GCS < 8: airway management threshold
Orientation and mentation
▶
Confusion, disorientation
Hallucinations (4.8% of exposures)
Agitation assessment (18.6% of exposures)
▶
Severity scale for sedation planning
Pupillary and reflex exam
▶
Pupil size and reactivity
▶
Miosis: opioid-predominant effect
Mydriasis: sympathomimetic or mixed
Deep tendon reflexes
▶
Hyperreflexia and clonus: serotonin syndrome
Hyporeflexia: opioid toxidrome
Cardiovascular exam
Cardiac assessment
▶
Rate and rhythm
▶
Sinus tachycardia most common
Irregular rhythm: concern for arrhythmia
Blood pressure bilaterally
▶
Significant asymmetry: vascular complication consideration
Peripheral perfusion
▶
Capillary refill, skin color
Diaphoresis: sympathomimetic or withdrawal
Respiratory exam
Breathing adequacy assessment
▶
Rate and depth
▶
Shallow breathing with opioid toxidrome
Accessory muscle use
Auscultation
▶
Aspiration findings if vomiting occurred
Clear vs abnormal breath sounds
Oxygen saturation trend
Abdominal and skin exam
Hepatotoxicity signs
▶
Jaundice and scleral icterus
▶
Predominantly cholestatic pattern
RUQ tenderness, hepatomegaly
Signs of dehydration
▶
Dry mucosa, reduced skin turgor
Vomiting in 11.2% of exposures
Skin findings
▶
Diaphoresis pattern
▶
Diffuse: serotonin syndrome or sympathomimetic
Track marks or injection sites
▶
Co-substance use indicator
PITFALLS
Exam pitfalls
▶
Normal vital signs do not exclude significant toxicity
▶
Opioid depression can develop hours after ingestion
Hepatotoxicity absent on acute presentation
Variable pupil size misleads toxidrome identification
▶
Mixed toxidrome with competing pharmacology
Do not rely on pupils alone for diagnosis
Agitation may mask concurrent respiratory depression
▶
Reassess after sedation
Differential Diagnosis
Opioid and CNS depressant toxidromes
Opioid overdose (traditional opioids, fentanyl)
▶
ICD-10: T40.1–T40.4 (opioid poisoning)
▶
Classic miosis, respiratory depression, CNS depression
Typically more consistent and complete naloxone response than kratom
Differentiating clue: kratom response to naloxone variable and partial
Benzodiazepine toxicity
▶
ICD-10: T42.4
▶
CNS and respiratory depression without miosis
Flumazenil response in pure benzodiazepine toxicity
Often present as co-ingestant in kratom exposures
Sympathomimetic and serotonergic syndromes
Sympathomimetic toxidrome (amphetamines, cocaine)
▶
ICD-10: T43.6, T40.5
▶
Tachycardia, hypertension, agitation, mydriasis
Hyperthermia, diaphoresis
Differentiating clue: no CNS depression component
Serotonin syndrome
▶
ICD-10: T43.9
▶
Clonus, hyperreflexia, hyperthermia, agitation
Kratom itself can contribute via serotonergic activity
Hunter criteria: clonus is key differentiating feature
Anticholinergic toxidrome
▶
ICD-10: T44.3
▶
Mydriasis, dry flushed skin, urinary retention, delirium
Tachycardia without diaphoresis distinguishes from serotonin syndrome
Mixed and polysubstance presentations
Mixed polysubstance overdose
▶
Most common real-world scenario for serious kratom toxicity
▶
79% of kratom-associated deaths involved multiple substances
Competing pharmacological effects obscure clinical pattern
Approach: treat dominant life threat regardless of specific agent
Withdrawal syndromes
▶
Opioid, alcohol, benzodiazepine withdrawal
▶
Tachycardia, hypertension, diaphoresis, tremors
Kratom withdrawal mimics opioid withdrawal
Hepatotoxicity differentials
Viral hepatitis (A, B, C)
▶
ICD-10: B15–B19
▶
Serology distinguishes; kratom injury is drug-induced
Kratom hepatotoxicity predominantly cholestatic — R ratio median 3.4
Acetaminophen hepatotoxicity
▶
ICD-10: T39.1
▶
Hepatocellular pattern; APAP level rules out
Must co-measure in all kratom presentations
Primary biliary cholangitis
▶
Kratom liver injury can histologically mimic PBC
▶
Timeline (drug exposure vs chronic autoimmune) differentiates
AMA serology and liver biopsy distinguish
Alcoholic hepatitis
▶
ICD-10: K70.1
▶
Ethanol level, AST:ALT ratio > 2:1
Laboratory Tests
Core toxicology panel
Urine drug screen limitations
▶
Standard immunoassays do NOT detect mitragynine
▶
False negative common on routine UDS
Specialized LC-MS/MS required for confirmation
Comprehensive toxicology panel including synthetic opioids and fentanyl
▶
Fentanyl not always detected on standard UDS panels
Serum toxicology
▶
Acetaminophen level — rule out co-ingestion in all presentations
▶
Hepatotoxicity overlap if APAP elevated
Salicylate level
▶
Concurrent ingestion alters management
Ethanol level
▶
CNS depression synergy quantification
Mitragynine blood levels (specialized)
▶
LC-MS/MS required — not widely available or rapid
▶
Living patients: levels 5–340 ng/mL reported
Deceased patients: levels 3.5–7,500 ng/mL reported
Not needed for acute management decisions
Metabolic and hepatic panel
Comprehensive metabolic panel
▶
Liver function tests for hepatotoxicity assessment
▶
AST, ALT, ALP, GGT, total and direct bilirubin
Kratom hepatotoxicity predominantly cholestatic: elevated ALP and bilirubin
Mixed biochemical pattern; median R ratio 3.4
Creatinine and BUN
▶
Renal injury reported in some cases
Glucose — bedside first, serum confirmation
▶
Altered mental status workup
Coagulation studies
▶
INR/PT if hepatotoxicity suspected
▶
Elevated INR indicates acute liver failure trajectory
Albumin for synthetic function assessment
Hematologic and metabolic
Complete blood count
▶
Leukocytosis with infection co-complication
▶
Eosinophilia: immune-mediated hepatotoxicity pattern
Thrombocytopenia in severe hepatic dysfunction
Lactate
▶
Hemodynamic instability or respiratory compromise
▶
Lactate >= 2 mmol/l indicates tissue hypoperfusion
Serial lactate for resuscitation targets
Creatine kinase
▶
Prolonged immobilization or seizures
▶
Rhabdomyolysis risk
Myalgia in withdrawal or seizure context
Blood gas and cardiac
Arterial or venous blood gas
▶
Respiratory depression assessment
▶
PaCO2 rising: ventilatory failure indicator
pH < 7.35 with metabolic acidosis: shock or seizure sequela
Bedside lactate from VBG acceptable for initial screen
Troponin
▶
Chest pain, hemodynamic instability, or arrhythmia
▶
Cardiac injury with severe toxicity
BNP if pulmonary edema concern
Diagnostic Tests
Scoring Systems
RUCAM score (Roussel Uclaf Causality Assessment Method)
▶
Indicated for suspected kratom-induced liver injury
▶
Assesses likelihood of drug-induced liver injury causality
Score > 8: highly probable DILI
Score 6–8: probable DILI
Key RUCAM domains for kratom
▶
Time to onset from drug exposure (typically 14–21 days)
Course after cessation
Alternative cause exclusion
Clinical Opiate Withdrawal Scale (COWS)
▶
Assessment of kratom withdrawal severity
▶
Score 5–12: mild withdrawal
Score 13–24: moderate withdrawal
Score > 25: severe withdrawal
Guides buprenorphine induction timing
▶
COWS score >= 8–12 before buprenorphine initiation
DSM-5 Substance Use Disorder criteria
▶
Assessment for kratom use disorder
▶
Up to 20% of regular users may meet DSM-5 SUD criteria
Dependence correlates more with frequency than dose
MRI
MRI brain indications in kratom toxicity
▶
Not routinely indicated for uncomplicated kratom toxicity
▶
Reserve for focal neurological deficits unexplained by toxidrome
Post-seizure with prolonged altered mental status
MRI liver
▶
Hepatotoxicity with unclear etiology
Bile duct characterization if biliary obstruction concern
CT
CT head indications
▶
Altered mental status with unclear or atypical etiology
▶
Seizures with head trauma
Focal neurological deficits
Not indicated for classic kratom opioid-like toxidrome
▶
Reserve for when diagnosis uncertain
CT abdomen indications
▶
Hepatotoxicity with complication concern
▶
Acute abdomen features co-occurring
Portal hypertension assessment
Not first-line for kratom hepatotoxicity evaluation
Chest imaging
▶
Chest X-ray for respiratory depression or aspiration concern
▶
Pulmonary aspiration if vomiting occurred
CT chest if pulmonary embolism or pneumonia concern
Ultrasound
RUQ ultrasound
▶
Hepatotoxicity suspected based on LFTs or clinical findings
▶
Hepatomegaly evaluation
Biliary obstruction exclusion (bile duct diameter)
Gallstones as alternative cholestasis cause
Not routinely needed in acute intoxication without liver injury
POCUS cardiac
▶
Hemodynamic instability
▶
Cardiac function and volume status assessment
IVC collapsibility for fluid responsiveness
Wall motion abnormalities with troponin elevation
ECG — not ultrasound but essential cardiac diagnostic
▶
All symptomatic kratom exposures
▶
QTc measurement: dose-dependent prolongation risk
hERG channel inhibition raises concern for torsades de pointes
Sinus tachycardia most common finding (OR 8.61 vs controls)
Ventricular arrhythmias: reported especially with polysubstance use
Disposition
Admit to ICU
ICU admission criteria
▶
Refractory respiratory depression requiring naloxone infusion
▶
Intubated patients
Recurrent desaturation despite naloxone
Seizures requiring ongoing benzodiazepine or second-line therapy
▶
Status epilepticus or recurrent seizures
Hemodynamic instability or significant arrhythmia
▶
QTc > 500 ms with symptoms
Ventricular arrhythmia
Altered mental status not clearing with treatment
▶
GCS < 13 not improving
Admit to ward
General admission criteria
▶
Evidence of hepatotoxicity (elevated LFTs, jaundice)
▶
Hepatology consultation and monitoring
INR trending for synthetic function
Significant polysubstance ingestion with prolonged observation need
▶
Coingestion of opioids, benzodiazepines
Suicidal intent with ingestion
▶
Psychiatry consultation and safety planning
Withdrawal management requiring IV medications
▶
Clonidine IV inpatient detoxification
Observation (4–6 hours minimum)
Observation criteria
▶
Mild-moderate symptoms with improving trajectory
▶
Single-substance exposure
Stable vitals
Initial ECG abnormality requiring serial monitoring
▶
QTc prolongation — trending every 2 hours
Uncertainty regarding co-ingestants or dose
Discharge criteria
Copy
Safe discharge requirements
▶
Asymptomatic or symptoms fully resolved after observation
▶
Normal vital signs, mental status, and ECG
Reliable follow-up arranged
▶
Safe home environment confirmed
No concern for hepatotoxicity acutely
▶
Counsel: hepatotoxicity may manifest 14–21 days after use onset
Naloxone prescription provided if co-using CNS depressants
▶
APA recommends naloxone for kratom users co-using CNS depressants
Transfer criteria
Transfer to higher-level care
▶
Acute liver failure beyond local hepatology capacity
▶
Liver transplant center evaluation
Refractory ventricular arrhythmia
▶
Cardiology center with electrophysiology
Treatment
Immediate stabilization
Airway management
▶
Naloxone trial before intubation for opioid-like features
▶
0.4–2 mg IV/IM/IN; repeat every 2–3 minutes
Response in 2/3 of cases in single-substance exposures
Titrate to adequate respiration — avoid precipitating acute withdrawal
If naloxone fails or airway unprotected, proceed to RSI
▶
Ketamine 1.5 mg/kg IV induction (avoid propofol if hypotensive)
Succinylcholine 1.5 mg/kg IV or rocuronium 1.2 mg/kg IV
Naloxone infusion for recurrent respiratory depression
▶
Calculate: 2/3 of effective reversal bolus per hour
▶
Example: 2 mg effective bolus → 1.3 mg/hour infusion
Titrate to adequate respiratory rate and SpO2
Continue for at least 4–6 hours after last rescue dose
Reason: kratom alkaloids have longer half-life than naloxone
Decontamination
▶
Activated charcoal: within 1–2 hours of ingestion only if airway protected
▶
50 g adult dose via nasogastric tube if obtunded
Contraindicated if aspiration risk
Seizure management
First-line benzodiazepines
▶
Lorazepam 4 mg IV; repeat once if no response in 5 minutes
▶
Alternative: diazepam 5–10 mg IV
Alternative IM: midazolam 10 mg IM if no IV access
Seizures from kratom respond to benzodiazepines as for other toxin-induced seizures
Refractory seizures
▶
Phenobarbital 20 mg/kg IV at 50–100 mg/min
▶
Monitor for respiratory depression — have intubation ready
Propofol infusion if intubated
▶
1–4 mg/kg/hour; titrate to seizure suppression on EEG monitoring
Avoid phenytoin — ineffective for toxin-induced seizures
Cardiac management
QTc prolongation management
▶
Discontinue all QTc-prolonging co-medications
▶
Avoid methadone, haloperidol, certain antibiotics
Magnesium sulfate for QTc > 500 ms or torsades risk
▶
2 g IV over 10–15 minutes
Repeat if torsades develops
If torsades de pointes develops
▶
Overdrive pacing or isoproterenol to increase heart rate
Cardiology consultation
Hypertension and tachycardia management
▶
Benzodiazepines first-line for sympathomimetic-pattern hypertension
▶
Lorazepam 1–2 mg IV titrated
Avoid beta-blockers alone (unopposed alpha)
IV fluids for tachycardia from dehydration
▶
Normal saline 1–2 L over 1–2 hours initially
Serotonin syndrome management
Serotonin syndrome treatment
▶
Cyproheptadine: serotonin antagonist for mild-moderate cases
▶
12 mg oral/NG loading dose, then 2 mg every 2 hours
Maximum 32 mg/day
Benzodiazepines for agitation and muscle rigidity
▶
Lorazepam 1–2 mg IV; titrate to effect
Hyperthermia management if temperature > 41 C
▶
Active cooling measures
Paralysis and intubation for refractory hyperthermia
Hepatotoxicity management
Kratom-induced liver injury treatment
▶
Cessation of kratom — cornerstone of management
▶
Most cases resolve spontaneously after cessation
Median time to recovery: weeks to months
N-acetylcysteine (NAC)
▶
Consider empirically if acetaminophen co-ingestion cannot be excluded
150 mg/kg IV over 1 hour, then 50 mg/kg over 4 hours, then 100 mg/kg over 16 hours
Supportive care
▶
Hydration, electrolyte management
Avoid hepatotoxic medications and alcohol
Hepatology consultation for acute liver failure
▶
Liver transplant evaluation if INR rising despite cessation
Withdrawal and dependence management
Kratom withdrawal management
▶
Buprenorphine-naloxone (Suboxone) — first-line for kratom use disorder
▶
Home induction successfully reported via telehealth
Initiate when COWS score >= 8–12
Start 2–4 mg sublingual; titrate to 8–24 mg/day
Evidence level: multiple case series and observational studies
Clonidine — alternative for inpatient detoxification
▶
0.1 mg orally every 6–8 hours; titrate to autonomic symptoms
Maximum 0.3 mg per dose; monitor for hypotension
Supportive pharmacotherapy for withdrawal symptoms
▶
NSAIDs or acetaminophen (caution with liver injury) for myalgia
Antiemetics for nausea and vomiting
Loperamide for diarrhea
Drug interaction precautions
CYP450 interaction management
▶
Kratom inhibits CYP3A4 (time-dependent) and CYP2D6
▶
Midazolam AUC increased ~1.4-fold even at 2 g kratom dose
Methadone, certain antidepressants, antipsychotics at increased levels
Avoid additional opioids, sedatives in acute setting
▶
Synergistic CNS and respiratory depression
Avoid QTc-prolonging agents
▶
Haloperidol, certain antipsychotics, fluoroquinolones
Harm reduction
Naloxone prescription
▶
Provide to all patients continuing kratom use
▶
APA 2024 harm reduction guidelines
Especially those co-using CNS depressants
Nasal naloxone 4 mg/0.1 mL: educate patient and household contacts
Addiction medicine referral
▶
All patients with identified kratom use disorder
▶
Buprenorphine-naloxone treatment program
Co-occurring substance use disorder management
Special Populations
Pregnancy
Kratom use in pregnancy
▶
No FDA-approved use; classified as not safe in pregnancy
▶
Mitragynine crosses placenta — fetal opioid receptor exposure
Case reports of neonatal abstinence syndrome
Obstetric consultation for any kratom exposure in pregnancy
▶
Fetal monitoring if acute intoxication
Serial ultrasound for growth restriction with chronic use
Pharmacological considerations in pregnancy
▶
Naloxone: safe in pregnancy for opioid-like respiratory depression
▶
Monitor fetal heart rate after administration
May precipitate withdrawal and preterm labor with chronic use
Buprenorphine: preferred agent for kratom use disorder in pregnancy
▶
Buprenorphine monoproduct preferred over buprenorphine-naloxone
Reduces neonatal abstinence syndrome severity vs untreated use
Benzodiazepines: use with caution; neonatal withdrawal risk
▶
Short duration only for acute seizure or agitation management
Hepatotoxicity in pregnancy
▶
Maternal hepatotoxicity: risk of acute fatty liver of pregnancy overlap
▶
Urgent maternal-fetal medicine consultation
INR and liver function critical safety parameters
Geriatric
Age-related pharmacokinetic changes
▶
Reduced hepatic and renal clearance of alkaloids
▶
Prolonged and enhanced effects vs younger adults
Lower dose thresholds for toxicity
Increased CNS sensitivity
▶
Falls and fracture risk with sedation
Delirium more common presentation
Comorbidity and polypharmacy interactions
▶
Higher prevalence of CYP3A4/2D6 substrate medications
▶
Statins, antihypertensives, anticoagulants at risk
Baseline cardiac arrhythmia and QTc prolongation risk
▶
More vulnerable to kratom-induced QTc prolongation
Baseline hepatic dysfunction increases hepatotoxicity risk
▶
Lower threshold for LFT monitoring
Dosing modifications in geriatric patients
▶
Naloxone: same initial doses but monitor for overshooting
▶
Titrate carefully to avoid abrupt opioid withdrawal complications
Benzodiazepines: lowest effective dose
▶
Paradoxical agitation and respiratory depression risk increased
Discharge planning includes caregiver education and fall precautions
Pediatrics
Pediatric exposure considerations
▶
Unintentional ingestions in young children
▶
Higher alkaloid dose per kg body weight
Rapidly progressive CNS and respiratory depression
Adolescent intentional use
▶
Often with other substances
Social and psychiatric context important
Pediatric clinical differences
▶
More rapid progression to severe toxicity in young children
▶
Small ingestion (single capsule or small amount of tea) may cause significant toxicity
Seizure threshold lower in children
▶
Higher seizure rate relative to adults
Hepatotoxicity: pediatric cases reported but less frequent
Weight-based dosing for pediatric treatment
▶
Naloxone: 0.01 mg/kg IV/IM/IN (max 0.1 mg); titrate q2–3 min
▶
If no IV access: intranasal preferred
Infusion: same proportional calculation as adults
Lorazepam for seizures: 0.1 mg/kg IV (max 4 mg per dose)
▶
Diazepam rectal 0.5 mg/kg as alternative without IV access
Activated charcoal: 1 g/kg (max 50 g) if within 1–2 hours and airway protected
Pediatric disposition
▶
Lower threshold for admission vs adults
▶
Any altered mental status or respiratory depression: admit
Poison Control consultation mandatory for all pediatric exposures
▶
Child protective services involvement if neglect or intentional exposure concern
Background
Epidemiology
Prevalence and incidence trends
▶
Kratom-related poison center reports increased approximately 1,200% from 2015 to 2025
▶
National Poison Data System (NPDS) surveillance data
Towers et al., MMWR 2026
Estimated 10–15 million kratom users in the United States
▶
Legal and available as dietary supplement in most US states
Male sex: 70.8% of exposures
▶
Age 20–39 years most common demographic
Age 40–59 rapidly increasing proportion
Mortality and morbidity
▶
Single-substance exposures: serious outcomes 41–49%
▶
Death rate 0.6% for single-substance exposures
Polysubstance exposures: serious outcomes 57–66%
▶
79% of kratom-associated deaths involved multiple substances
Hepatotoxicity: predominantly reversible
▶
Acute liver failure rare but reported
Regulatory context
▶
Not FDA-approved for any indication
▶
Classified as dietary supplement — unregulated product quality
DEA temporarily classified as Schedule I in 2016; decision reversed after public opposition
Available online, smoke shops, gas stations with variable alkaloid content
Pathophysiology
Primary active alkaloids
▶
Mitragynine and 7-hydroxymitragynine
▶
Partial mu-opioid receptor agonists
7-hydroxymitragynine: more potent, higher intrinsic efficacy at mu receptor
Additional receptor activity
▶
Adrenergic: alpha-2 agonism contributes to analgesia and sedation
Serotonergic: contributes to mood effects and serotonin syndrome risk
Dopaminergic: reinforcement and addiction potential
Dose-dependent toxidrome mechanism
▶
Low dose (1–5 g): stimulant predominance
▶
Adrenergic and dopaminergic activity dominant
Tachycardia, increased alertness, appetite suppression
High dose (>5 g): opioid-like predominance
▶
Mu-receptor agonism: CNS depression, analgesia, respiratory depression
Miosis, sedation, nausea
Cardiovascular mechanism
▶
QTc prolongation via hERG potassium channel inhibition
▶
Dose-dependent in vitro and clinical findings
Sodium channel blockade also hypothesized (similar to propoxyphene)
Sinus tachycardia: most common cardiac finding
▶
OR 8.61 vs unexposed controls (Leong Abdullah et al., 2021)
Hepatotoxicity mechanism
▶
Predominantly cholestatic injury pattern
▶
Direct bile duct toxicity and immune-mediated mechanisms proposed
Median R ratio 3.4 (cholestatic predominance)
Median latency 14–21 days from exposure onset
▶
Histology can mimic primary biliary cholangitis
Generally reversible with cessation
CYP450 drug interaction mechanism
▶
Time-dependent inhibition of CYP3A4
▶
Midazolam AUC increased ~1.4-fold at 2 g dose
Inhibition of CYP2D6
▶
Affects metabolism of methadone, some antidepressants, antipsychotics
Therapeutic Considerations
Naloxone response rationale
▶
Partial mu-opioid agonism explains variable naloxone response
▶
Response in approximately 2/3 of cases
Higher doses may be needed vs traditional opioid overdose
Half-life of kratom alkaloids exceeds naloxone
▶
Naloxone infusion necessary for sustained respiratory depression
Buprenorphine rationale for dependence
▶
Partial mu-opioid agonist with ceiling effect on respiratory depression
▶
Cross-tolerance with kratom alkaloids supports efficacy
Home induction via telehealth reported successfully
Reduces craving and withdrawal without full opioid reinforcement
Hepatotoxicity treatment evidence
▶
Most cases resolve with kratom cessation alone
▶
NAC role not established for kratom DILI specifically
Empiric NAC reasonable if acetaminophen cannot be excluded
Liver biopsy reserved for uncertain diagnosis
▶
Predominantly cholestatic histology; can mimic PBC
ICD-10 coding
▶
T65.891 — Toxic effects of other specified substances (kratom/mitragynine)
▶
Classify as: A (accidental), S (self-harm), X (undetermined intent)
F19.10 — Other psychoactive substance use disorder, mild (kratom use disorder)
K71.6 — Toxic liver disease with cholestasis (kratom hepatotoxicity)
Patient Discharge Instructions
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Copy
Discharge instructions for kratom toxicity
▶
You were seen today for symptoms related to kratom (Mitragyna speciosa) use
▶
Kratom is not FDA-approved and is an unregulated supplement
Product quality and alkaloid content vary widely between products
Your symptoms should continue to improve over the next 24–48 hours
▶
If you were treated for withdrawal, symptoms may persist for days to weeks
Medications prescribed
▶
Take all prescribed medications as directed
▶
If prescribed buprenorphine-naloxone (Suboxone), follow induction instructions carefully
If prescribed naloxone (Narcan), carry it with you and teach household contacts to use it
Liver monitoring instructions
▶
Kratom can cause liver damage that may appear 2 to 7 weeks after use
▶
Follow up with your doctor in 1–2 weeks for repeat blood tests (liver enzymes)
Earlier follow-up if you develop jaundice, dark urine, pale stools, or abdominal pain
Avoid alcohol and all other potential liver stressors during recovery
Return to emergency department immediately for
▶
Difficulty breathing, very slow or shallow breathing
▶
Use your Narcan if prescribed and call 911
Chest pain or irregular heartbeat
Seizures or unresponsiveness
Confusion, extreme drowsiness, or inability to wake
Yellowing of skin or eyes (jaundice)
Dark urine or very pale stools
Severe abdominal pain
Worsening symptoms after leaving the hospital
Kratom safety information
▶
Using kratom with opioids, benzodiazepines, alcohol, or other depressants dramatically increases your risk of death
▶
This combination accounts for 79% of kratom-related deaths
Kratom products are not regulated — contamination and variable potency are real risks
Resources for help with kratom or substance use are available:
▶
SAMHSA National Helpline: 1-800-662-4357 (free, confidential, 24/7)
Poison Control: 1-800-222-1222
References
Guidelines and key sources
Towers EB, Thomas YT, Holstege CP, Farah R.
▶
Increases in Kratom-Related Reports to Poison Centers — National Poison Data System, United States, 2015–2025
▶
MMWR Morb Mortal Wkly Rep. 2026
PMID 41886310
Hartley C, Bulloch M, Penzak SR.
▶
Clinical Pharmacology of the Dietary Supplement Kratom (Mitragyna speciosa)
▶
Journal of Clinical Pharmacology. 2022
PMID 34775626
Heywood J, Smallets S, Paustenbach D.
▶
Beneficial and Adverse Health Effects of Kratom (Mitragyna speciosa): A Critical Review
▶
Food and Chemical Toxicology. 2024
PMID 39134135
Schimmel J, Dart RC.
▶
Kratom (Mitragyna speciosa) Liver Injury: A Comprehensive Review
▶
Drugs. 2020
PMID 31919755
Ahmad J, Odin JA, Hayashi PH, et al.
▶
Liver Injury Associated With Kratom: Experience From the U.S. Drug Induced Liver Injury Network
▶
Drug and Alcohol Dependence. 2021
PMID 33257199
Toxicology and pharmacology references
Rogers JM, Weiss ST, Epstein DH, et al.
▶
Kratom Addiction Per DSM-5 SUD Criteria, and Kratom Physical Dependence
▶
Drug and Alcohol Dependence. 2024
PMID 38788532
Tanna RS, Nguyen JT, Hadi DL, et al.
▶
Clinical Assessment of the Drug Interaction Potential of Kratom
▶
Clinical Pharmacology and Therapeutics. 2023
PMID 36924284
Eggleston W, Stoppacher R, Suen K, Marraffa JM, Nelson LS.
▶
Kratom Use and Toxicities in the United States
▶
Pharmacotherapy. 2019
PMID 31099038
Chichagi F, Alikhani R, Beigi Harchegani A.
▶
Cardiovascular Health in Kratom Users: A Narrative Review
▶
Journal of Addictive Diseases. 2024
PMID 37982301
Leong Bin Abdullah MFI, Singh D.
▶
The Adverse Cardiovascular Effects and Cardiotoxicity of Kratom: A Comprehensive Review
▶
Frontiers in Pharmacology. 2021
PMID 34646135
Gorelick DA.
▶
Kratom: Substance of Abuse or Therapeutic Plant?
▶
Psychiatric Clinics of North America. 2022
PMID 36055730
Kiyokawa M, Kwon AK, Cape MC, Streltzer JM.
▶
Kratom Use Disorder: Successful Treatment With Home Induction of Buprenorphine-Naloxone
▶
Family Practice. 2023
PMID 37499179
Fenno L, Shenoi N, Ashley K, et al.
▶
APA Resource Document on Harm Reduction
▶
American Psychiatric Association. 2024
psychiatry.org
Post S, Spiller HA, Chounthirath T, Smith GA.
▶
Kratom Exposures Reported to United States Poison Control Centers: 2011–2017
▶
Clinical Toxicology. 2019
PMID 30786220
Gandhi D, Ahuja K, Quade A, Batts KP, Patel L.
▶
Kratom Induced Severe Cholestatic Liver Injury Histologically Mimicking Primary Biliary Cholangitis
▶
World Journal of Hepatology. 2020
PMID 33200023
SymptomDx is an educational tool for medical professionals. It does not replace clinical judgment. Verify all clinical data and drug dosages with authoritative sources.
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