Methamphetamine Toxicity

Updated: Jan 30, 2023
Author: John R Richards, MD, FAAEM; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD 


Practice Essentials

Methamphetamine is a highly addictive psychostimulant drug that is chemically related to amphetamine. Methamphetamine can produce euphoria and stimulant effects like those from other stimulants such as cocaine. In addition, methamphetamine is easily synthesized from inexpensive and readily obtainable chemicals. Those qualities have led to the widespread and rampant abuse of this dangerous drug.[1]

Use of methamphetamine and amphetamine has increased rapidly throughout the world, with more than 34 million users worldwide. East and Southeast Asia and North America remain the two main subregions for methamphetamine trafficking worldwide. The quantities of methamphetamine seized worldwide grew fivefold over 2010-2020. Methamphetamine seizures were 72% of all amphetamine-type substances seized over the period 2016–2020.[2]

In 2021, the National Institute on Drug Abuse reported that lifetime methamphetamine use by those 12 years of age and older in the US had increased to 6% of the population; use in the past year increased from 0.5% to 0.9% of the population between 2016 and 2021.[3]  

Methamphetamine is available in powder and crystalline forms. It may be taken orally or intravenously, or be snorted or smoked. The smokable form of methamphetamine (“ice”) produces an immediate euphoria similar to that of crack cocaine, but the effects may last much longer.[4, 5]

Inadvertent absorption of methamphetamine may occur in “body packers”, who swallow packages of the drug for transportation purposes, or “body stuffers”, who insert bags of methamphetamine rectally or vaginally in an attempt to elude drug enforcement. There are also users who indulge in "parachuting", in which the drug is loosely wrapped to delay absorption and prolong effect. These persons, and body stuffers, are at high risk for toxicity as the drug wrapping may be compromised and allow complete drug absorption.[6]

North American methamphetamine abusers are predominantly white men in their 30s and 40s.[7, 8] However, epidemic abuse has been described in adolescents; they cite availability, low cost, and a longer duration of action than cocaine as reasons for their drug preference.[9]

Most cases of methamphetamine toxicity can be managed supportively. In severe overdoses, termination of methamphetamine-induced seizure activity and arrhythmias are of immediate importance. Correction of hypertension, hypotension, hyperthermia, metabolic and electrolyte abnormalities, and control of severe psychiatric agitation are indicated. See Treatment and Medication.

For patient education information, see What is Methamphetamine? and Addiction Treatment & Recovery - Methamphetamine.


The medical history of amphetamine-like compounds extends back over a century, beginning with the identification of ephedrine as the active ingredient in extracts from the Ephedra sinica shrub, which had long been used in traditional Chinese and Indian medicine.[4, 5, 10] A Japanese pharmacologist first synthesized methamphetamine from ephedrine in 1919.

A more detailed analysis of the pharmacology of amphetamine derived from the basic phenylethylamine structure was reported in 1930. In the 1930s, amphetamine was introduced in the form of inhalers for rhinitis and asthma treatment. The stimulant, euphoric, and anorectic effects of amphetamine were quickly recognized, leading to its abuse.

In 1937, a report that amphetamine enhanced intellectual performance and wakefulness further contributed to its popularity. Amphetamines were used extensively by Allied and Axis armed forces during World War II and during the recent Iraq and Afghanistan conflicts to increase wakefulness and attention.[4, 11]

In the late 1950s, initial federal controls were enacted; however, in spite of additional regulation and increased enforcement, amphetamines continued to be used by students, athletes, shift workers, long haul drivers, and for weight loss.[4, 5] The Controlled Substance Act of 1970 stringently regulated the manufacture of amphetamine.


Methamphetamine is structurally similar to amphetamine and to the neurotransmitter dopamine. Amphetamines stimulate the central nervous system (CNS), which results in clinical effects that include the following[4, 12] :

  • Inducing euphoria
  • Intensifying emotions
  • Altering self-esteem
  • Increasing alertness, aggression, and sexual appetite.

In the CNS, amphetamines block presynaptic reuptake of catecholamines (ie, dopamine, norepinephrine), causing hyperstimulation at selected postsynaptic neuron receptors. Indirect sympathomimetic effects result from blockade of presynaptic vesicular storage and by reduction in cytoplasmic destruction of catecholamines by inhibition of mitochondrial monoamine oxidase.[13, 14]

Indirectly, these hyperstimulated neurons can stimulate various other noncatecholaminergic central and peripheral nervous pathways. Changes in mood, excitation, motor movements, sensory perception, and appetite appear to be mediated more directly by CNS dopaminergic alterations. It has been postulated that serotonin alterations also contribute to mood changes, psychotic behavior, and aggressiveness.[15]

Long-term exposure to methamphetamine results in significant down-regulation of both presynaptic and postsynaptic aspects of the dopamine system in the striatum. Dysregulation of the dopamine system has been proposed as a mechanism of addiction.[16]  Oxidative stress and neuroinflammation appear to play a role in the psychosis and cognitive deficits induced by repeated low doses of methamphetamine.[17]

In humans, the half-life of methamphetamine ranges from 10-20 hours, depending on the urine pH, history of recent use, and dosage.[13] Metabolism occurs faster in acidic urine. Methamphetamine has greater CNS effects compared with D-amphetamine of equal milligram quantity. The majority of methamphetamine is metabolized to amphetamine, which provides further CNS stimulation.

Methamphetamine is absorbed readily from the gut, airway, nasopharynx, muscle, placenta, and vagina.[18, 19] Peak plasma levels are observed approximately 30 minutes after intravenous or intramuscular routes and 2-3 hours after ingestion.[14] Rapid tissue redistribution occurs with steady-state cerebrospinal fluid levels at 80% of plasma levels. Hepatic conjugation pathways with glucuronide and glycine addition result in inactivation and urinary excretion of metabolites.

When methamphetamine is used with ethanol, increased psychological and cardiac effects are observed.[20] This is presumed to be the result of pharmacodynamic rather than pharmacokinetic interactions. Similarly, the increased toxicity of concomitant opioids and amphetamines ("speedballing"), appear to result from pharmacodynamic interactions.

The euphoric effects produced by methamphetamine, cocaine, and various designer amphetamines are similar and may be difficult to clinically differentiate.[5] A distinguishing clinical feature is the longer pharmacokinetic and pharmacodynamic half-life of methamphetamine, which may be as much as 10 times longer than that of cocaine. Because of the variability in quality and concentration of illicitly purchased methamphetamines, the clinical observation of toxic effects is more relevant than estimated total ingested dose.[21]


Most of the methamphetamine abused in the United States is produced in so-called superlabs, many of which are located in Mexico.[22]  However, methamphetamine is relatively easy and inexpensive to synthesize, and small-scale illicit production occurs in home kitchens, workshops, recreational vehicles, and rural cabins.[5, 23] Instructions for synthesis can be found on the Internet and the precursors are not difficult to obtain.

A common method of synthesis begins with ephedrine, which is reduced to methamphetamine using hydriodic acid and red phosphorus. Alternative approaches include using a different acid, a different catalyst, or a substituted ephedrine (eg, chloroephedrine, methylephedrine). The federal government and some states have enacted laws decreasing the availability of necessary precursor chemicals such as ephedrine, but many of these agents can still be obtained in other countries.

The methamphetamine produced by ephedrine reduction is a lipid-soluble pure base form, which is fairly volatile and can evaporate if left exposed to room air temperature. This product is converted to the water-soluble form, methamphetamine hydrochloride (HCl) salt. The manufacture of "ice", the smokable form of methamphetamine, from standard quality methamphetamine HCl is essentially a purification process.

Illicitly synthesized methamphetamine is frequently contaminated by nonstimulant organic or inorganic impurities. Poisoning from heavy metals, such as lead and mercury, or from carcinogenic solvents used in the synthesis process, has been reported.[24, 25]  Street methamphetamine may be mixed with other drugs, including cocaine and phencyclidine.



United States

According to the 2021 National Survey on Drug Use and Health (NSDUH), approximately 2.5 million people had used methamphetamine in the past year. Approximate numbers of users by age group and percentages of that age group were as follows[3] :

  • 12-17 years: 37,000 (0.1%)
  • 18-25 years: 166,000 (0.5%)
  • 26 years or older: 2.3 million (1.1%)

The 2021 Annual Report of the American Association of Poison Control Centers' National Poison Data System reported 3721 single case exposures with 1252 moderate and 302 major outcomes and 217 fatalities.[26]


The United Nations Office on Drugs and Crime estimates that worldwide in 2018 there were 27 million past-year users of amphetamine-type stimulants, which includes methamphetamine. Past-year use was particularly high in North America, Australia, and New Zealand. Methamphetamine is a feature of amphetamine-type stimulant markets worldwide, but is particularly dominant in East and Southeast Asian Oceania, and North America  In East and Southeast Asia, the market for both tablet and crystalline methamphetamine is large and growing.[2]

The European Monitoring Centre for Drugs and Drug Addiction reports that methamphetamine use has generally been low and was historically concentrated in the Czech Republic and Slovakia. In 2020, treatment program entrants reporting primary methamphetamine use were concentrated in Czechia, Germany, Slovakia, and Turkey.[27]  

An Australian study that used liquid chromatography–mass spectrometry to analyze wastewater (an increasingly popular method for monitoring trends of illicit drug use) reported that from 2009-2015, methamphetamine consumption increased fivefold. In the study, which involved wastewater from wastewater treatment plants in South East Queensland, methamphetamine residues were consistently detected in both urban and rural catchments.[28]

Race-, Sex-, and Age-related Demographics

Demographic variations include the following[7, 8] :

  • In North America, methamphetamine use is predominantly by whites
  • Males are more likely to abuse methamphetamine than females
  • Peak methamphetamine use is observed in the 20- to 40-year-old range


Acute methamphetamine overdose may result in sympathetic overdrive, intracranial hemorrhage,[29]  cardiovascular collapse, rhabdomyolysis, ventricular tachyarrhythmia, and death. Incidental injuries from blunt and penetrating trauma are common.[4, 12, 30, 31]

Long-term methamphetamine use may result in the following[32] :

In a study of 590 patients between 18 and 50 years old with cardiomyopathy or heart failure who were seen at a single medical center from 2008-2012, the 223 patients with a history of methamphetamine use were more likely to have a moderately or severely reduced left ventricular ejection fraction (≤40%). Male methamphetamine users were more likely to have worse left ventricular systolic dysfunction.[33]

Methamphetamine abuse has severe adverse effects on oral health, colloquially termed "meth mouth". As a result of its sympathomimetic effects, methamphetamine results in significantly reduced saliva production and pH, and increased bruxism. Consequently, long-term abusers are at increased risk for caries, dental erosion, periodontal lesions, and temporomandibular joint pain.[34]

Use of methamphetamine during pregnancy has been associated with intrauterine growth restriction and preterm birth. Neonates have an increased incidence of poor cardiorespiratory adaptation, cardiac defects, and floppy muscle tone.[35]  Prenatal exposure may have a long-term impact on cognitive skills that becomes more pronounced with age.[36]

Complications of methamphetamine use include the following:




Cardiovascular signs and symptoms of methamphetamine use are as follows[37, 38, 39, 40, 41, 42] :

  • Chest pain, aortic dissection, myocardial ischemia/infarction
  • Palpitations, tachyarrhythmia
  • Dyspnea and edema
  • Hypertension

Central nervous system manifestations of methamphetamine use are as follows[43, 44, 45, 46] :

  • Agitation, violent behavior, self-harm
  • Coma
  • New-onset seizure, movement disorders
  • Emotional lability, confusion, psychosis, paranoia, hypersexuality, and hallucinations
  • Headache

Respiratory manifestations of methamphetamine use are as follows[47, 48, 49] :

  • Dyspnea
  • Wheezing
  • Pneumothorax

Skin manifestations of methamphetamine use are as follows[50] :

  • Delusional parasitosis
  • Abscess, cellulitis

Gastrointestinal manifestations of methamphetamine use are as follows[18, 51] :

  • Abdominal pain
  • Obstruction

Dental manifestations of methamphetamine use are as follows[52, 53] :

  • Caries
  • Peridental abscesses

Physical Examination

Acute and long-term methamphetamine use may lead to abnormal findings on examination of the following organ systems:

  • Cardiovascular
  • Central nervous system
  • Gastrointestinal
  • Renal
  • Skin
  • Dental

Cardiovascular findings are as follows:

  • Tachycardia and hypertension is frequently observed[54]

  • Atrial and ventricular arrhythmias may occur[54]

  • Chest pain from cardiac ischemia and infarction following methamphetamine use has been reported; patients are at risk because of accelerated atherosclerosis from chronic use; acute aortic dissection or aneurysm has been associated with methamphetamine abuse[41, 38]

  • Hypotension may be observed with methamphetamine overdose with profound depletion of catecholamines[55]

  • Acute and chronic cardiomyopathy results directly from methamphetamine cardiac toxicity and indirectly from chronic hypertension and ischemia; intravenous use may result in endocarditis; patients may present with dyspnea, edema, and other signs of acute congestive heart failure (CHF) exacerbation[56, 39]

Central nervous system findings are as follows:

  • New-onset seizures may occur from direct CNS methamphetamine toxicity[45]

  • Acute and chronic methamphetamine exposure has been associated with a jerking, choreoathetoid movement disorder; these repetitive movements, hyperactivity, and inability to focus thought have been referred to as "tweaking"[44, 46]

  • Headache and cerebrovascular accidents with focal neurologic deficits may be caused by hemorrhage or vasospasm, cerebral edema, and cerebral vasculitis[42]

  • Acute psychosis, agitation, violence, and paranoia frequently results from alteration in CNS dopamine, serotonin, and glutamate pathways[57, 15]

  • Coma may result from depletion of catecholamine stores and/or concomitant ingestion of sedatives such as ethanol or narcotics[55]

Respiratory findings are as follows:

  • Barotrauma, including pneumomediastinum, pneumothorax, and pneumopericardium may result from forceful inhalation[47]

  • Acute noncardiogenic pulmonary edema and pulmonary hypertension may result from acute and chronic use, as well as from adulterants introduced during intravenous use such as talc or cornstarch[47, 48, 49]

  • Wheezing from reactive airway disease may be induced by methamphetamine[47]

Gastrointestinal findings are as follows:

  • Hepatocellular damage has been reported with methamphetamine after acute and chronic abuse; direct effects such as hypotension, hepatotoxic contaminants, hepatic vasoconstriction, lipid peroxidation, occult viral causes, and necrotizing angiitis have been postulated[58]

  • Severe abdominal pain may result from acute mesenteric vasoconstriction; methamphetamine has also been associated with the formation of ulcers and ischemic colitis.[51]

  • Necrotizing angiitis with arterial aneurysms and sacculations have been observed in the liver, pancreas, and small bowel of methamphetamine drug abusers[42]

Renal failure associated with amphetamines has been related to the following[59] :

  • Hypoxemia
  • Rhabdomyolysis
  • Necrotizing angiitis
  • Acute interstitial nephritis
  • Cardiovascular shock with subsequent  acute tubular necrosis

Skin findings include the following:

  • Delusions of parasitosis and chronic skin-picking may result in neurotic excoriations and prurigo nodularis ("speed bumps")[5]

  • Methamphetamine injectors frequently present with abscess and cellulitis, which they often blame on a "spider bite"[50]

  • Production workers in illicit methamphetamine laboratories may present with extensive thermal and/or chemical burns.[23]

On dental examination, severe caries, especially of the maxillary teeth, is commonly seen in chronic methamphetamine users ("meth mouth"). This results from maxillary artery vasoconstriction, xerostomia, and poor hygiene.[52, 53]

Pregnancy and lactation

Methamphetamine use during pregnancy can be fatal to the mother and fetus.[60, 61]  Methamphetamine has been shown to cause placental vasoconstriction and interfere with placental monoamine transporters resulting in spontaneous abortion.[62]

Methamphetamine is secreted in breast milk.[63] Cases of infant death from ingestion of methamphetamine-toxic breast milk have been reported.[64]





Laboratory Studies

Laboratory studies should be selected on the basis of the patient's symptoms. Although hair and saliva analysis may be obtained, most toxicological monitoring or testing is performed with urine and blood samples. Studies to obtain may include the following:

  • Complete blood count (CBC) and chemistry panel - To assess renal and electrolyte function

  • Creatine kinase (CK) and/or myoglobin levels - To exclude rhabdomyolysis

  • Serial troponin levels - If there is concern for myocardial ischemia

  • B-type natriuretic peptide (BNP) level - If acute heart failure is suspected

  • Pregnancy test - In women of childbearing age

  • Toxicology screens - Useful for patients who cannot or will not disclose drug use history and for pediatric patients with new-onset seizure

Imaging Studies

Order a chest radiograph for patients with pulmonary symptoms or chest trauma.

In patients with altered mental status, perform a head CT scan to exclude intracranial bleeding. Such bleeding may be the result of either methamphetamine-induced hypertension or associated head trauma.

Patients who are suspected body-packers, body-stuffers, or "parachuters" should undergo abdominal imaging; low-dose CT is considered state-of-the-art for this purpose[65]

Other Tests

Obtain an electrocardiogram for patients with chest pain, altered mental status, and tachycardia.


Lumbar puncture may be indicated in patients with altered mental status to rule out meningitis or subarachnoid hemorrhage.



Prehospital Care

Patients with acute methamphetamine intoxication may be highly agitated and present a serious safety risk to themselves and prehospital personnel. Seek additional help from police or other emergency medical services (EMS) providers before the patient is transported, if possible.

Patients' mental function may be sufficiently impaired that they are unable to make an informed decision to refuse treatment and transport. Prehospital intravenous access is warranted with or without patient consent, allowing for treatment of seizures and agitation using intravenous sedatives according to medical direction or protocol.

Emergency Department Care

Most cases of methamphetamine toxicity can be managed supportively. In the case of a severe overdose, immediate supportive care, including airway control, oxygenation and ventilation support, and appropriate monitoring is required. Specific treatments for heavy metal toxicity caused by contaminants in some methamphetamine preparations may be needed.

For suspected toxic oral ingestions, polyethylene glycol (PEG) solution should be initiated if possible. Animal studies suggest that orally ingested amphetamine-like compounds can be decontaminated with oral activated charcoal.[66]  In body packers, whole-bowel irrigation can be considered for removal of the ingested packets, although controlled data documenting improvement in clinical outcome with this technique are lacking.[67]

In severe overdoses, termination of methamphetamine-induced seizure activity and arrhythmias are of immediate importance. Correction of hypertension, hypotension, hyperthermia, metabolic and electrolyte abnormalities, and control of severe psychiatric agitation are indicated. Consider health maintenance activities, such as testing for viral hepatitis and HIV disease and rehabilitation follow-up.

Treatment of agitation

Because of the ability of methamphetamine to cause significant central nervous system (CNS) and psychiatric activation, patients who present to emergency departments (EDs) for acute intoxication often require physical restraint and pharmacologic intervention.

Treat hyperactive or agitated patients with droperidol or haloperidol, which are butyrophenones that antagonize CNS dopamine receptors and mitigate the excess dopamine produced from methamphetamine toxicity.[68] These medications should be administered intravenously (IV), with doses titrated to the symptoms (see Medication). However, obtaining IV access may be dangerous or impossible in violently agitated patients; in such cases, intramuscular administration of droperidol has been used, at doses as high as 10 mg.[69]

Multiple human and animal studies attest to the efficacy of droperidol and haloperidol in acute methamphetamine toxicity.[70, 71, 57] However, droperidol has been subject to a Black Box warning by the US Food and Drug Administration (FDA), based on concerns of QT prolongation and the potential for torsade de pointes. As a result, some institutions restrict its use. Nevertheless, a position statement by the American Academy of Emergency Medicine concluded that droperidol is effective and safe in the treatment of nausea, headache, and agitation, and that intramuscular doses of up to 10 mg appear to be as safe and as effective as other medications used for sedation of agitated patients; that the QT-prolonging effects have been shown to be transient, and that the risk of torsade de pointes is rare at the doses administered in the ED.[69]

The FDA advises that if the potential benefit of droperidol therapy is thought to outweigh the risk of arrhythmia, the patient should undergo a 12-lead electrocardiogram (ECG) prior to initiation of treatment, to assess for a prolonged QT interval (corrected QT > 440 msec for males or 450 msec for females), and if the QT inverval is normal and droperidol is used, ECG monitoring should be continued for 2 to 3 hours after completing treatment. The American Academy of Emergency Medicine position statement agrees that a pretreatment ECG should be obtained in patients at high risk for  prolonged QT, but found that a literature search did not support mandating ECG or telemetry monitoring for droperidol doses < 2.5 mg.[69, 72]  

Benzodiazepines diminish methamphetamine-induced behavioral and psychiatric intoxication.[68] This class of drug is also used to terminate methamphetamine-induced seizures.[70, 73] However, benzodiazepines may cause respiratory depression and often require repeated dosing to achieve adequate sedation.

In a study of 146 patients presenting to the ED agitated, violent, or psychotic from methamphetamine, droperidol produced more rapid and profound sedation than lorazepam. Both droperidol and lorazepam produced clinically significant reductions in pulse, systolic blood pressure, respiration rate, and temperature over a 60-minute period.[57]

Newer antipsychotics such as olanzapine and risperidone have been used to treat amphetamine psychosis.[74, 75, 76] A study of 58 patients comparing haloperidol to olanzapine demonstrated that both were effective, but olanzapine had fewer adverse side effects such as extrapyramidal symptoms.[74] To date, no large studies in the ED setting have been performed.[77]

Dexmedetomidine, a sedative with analgesic, sympatholytic, and anxiolytic effects, has been used to control agitation in several case series involving amphetamine toxicity and may be useful if available in the ED. This drug has an added advantage of causing minimal respiratory depression.[78, 79, 68]

Lipid-soluble beta-blockers (eg, metoprolol), which cross the blood-brain barrier, may also mitigate agitation as well as sympathomimetic symptoms.[80, 68]

After chemical restraint has been successfully implemented, physical restraints should be loosened or removed altogether. If physical and chemical restraint is unsuccessful, rapid sequence induction, paralysis, and intubation may be required in extreme cases.

Treatment of hypertension and tachycardia

If sedation fails to reduce blood pressure, antihypertensive agents such as beta-blockers and vasodilators are effective in reversing methamphetamine-induced hypertension and tachycardia.

With regard to choice of beta-blockers, labetalol is preferred because of combined anti–alpha-adrenergic and anti–beta-adrenergic effects. Labetalol has been shown to safely lower mean arterial pressure in cocaine-positive patients.[81] Carvedilol, which like labetalol is a nonselective beta-blocker with alpha-blocking activity, may also be effective for this indication.[82, 83] Esmolol is advantageous because of its short half-life but must be administered via IV drip. Metoprolol has excellent CNS penetration characteristics and may also ameliorate agitation, as previously mentioned.

These drugs should be given IV in smaller than usual doses and titrated to effect. The concern for "unopposed alpha stimulation," with sudden rise in blood pressure or coronary artery vasoaspasm after beta-blocker therapy, is theoretical and has never been demonstrated in patients with methamphetamine toxicity.[68] An extensive evidence-based systematic review of this topic demonstrated the safety and efficacy of beta-blockers for this indication.[68] At our institution, we routinely use beta-blockers for methamphetamine-induced tachycardia and hypertension with good results.

In rare instances, afterload reduction with agents such as hydralazine, nitroprusside, or fenoldopam may be necessary.[68]

Treatment of acute coronary syndrome

The approach to the patient with methamphetamine-induced cardiac ischemia should be no different than standard of care treatment for acute coronary syndrome (ACS). Nitrates, beta-blockers, aspirin, heparin, and morphine should be administered if indicated.

Based on the latest American College of Cardiology Foundation/American Heart Association guidelines, methamphetamine- and cocaine-using patients with chest pain and suspected ACS should also receive sublingual nitroglycerin if labetalol is used to treat hypertension (systolic blood pressure >150 mm Hg) or sinus tachycardia (pulse >100 beats per min).[84]

Patients with ST-segment elevation should be triaged to thrombolytic treatment and/or catheterization with cardiology consultation.

Treatment of seizures

Treat methamphetamine-induced seizures like other seizures of unknown etiology, as follows:

  • Administer benzodiazepines IV (see Medication)

  • In patients who do not have IV access, an agent with intramuscular absorption can be used (eg, lorazepam, midazolam)

  • After control of the acute episode, longer-acting agents such as phenobarbital, may be necessary

  • Patients with methamphetamine-induced seizures are at high risk for intracranial hemorrhage and should undergo computed tomography (CT) imaging as soon as possible

Treatment of rhabdomyolysis

Suspect rhabdomyolysis and follow creatine kinase (CK) levels in patients who present to the ED with severe agitation from methamphetamine or have had prolonged periods of immobilization. Management of rhabdomyolysis is as follows:

  • Administer aggressive volume therapy with IV crystalloid

  • Admit the patient to the hospital after obtaining nephrology consultation

  • Closely monitor renal function, vital signs, and fluid input and output

  • Administration of sodium bicarbonate prevents precipitation of myoglobin in renal tubules by preventing acidic urine pH

  • Early and aggressive fluid and electrolyte treatment of potential rhabdomyolysis can improve the clinical outcome and decrease potential nephrotoxicity; however, hemodialysis may be necessary in certain severe cases


Critical care management may be needed for patients with any of the following:

  • Persistent hypertension
  • Severe rhabdomyolysis
  • Seizures
  • Stroke
  • Coma
  • Hyperthermia
  • Congestive heart failure
  • Acute coronary syndrome


For body-packers, body-stuffers, or "parachuters," consultation with surgery or gastroenterology specialists may be warranted. Consult with a regional poison control center or a local medical toxicologist (certified through the American Board of Medical Toxicology and/or the American Board of Emergency Medicine) to obtain additional information and patient care recommendations. Cardiology, nephrology, and psychiatry consultation may be indicated in certain cases.


Long-Term Monitoring

Referral to a drug treatment center and/or psychiatrist may be indicated. Methamphetamine addiction is notoriously difficult to treat successfully, as it is difficult to remove the patient from the subculture involved in the production, distribution, and abuse of the drug.

A study by McKetin et al attempted to evaluate the impact of community-based drug treatment on methamphetamine use. Participants were methamphetamine users entering community-based detoxification (n = 112) or residential rehabilitation (n = 248) services and a quasi-control group of methamphetamine users (n = 101) recruited from the community. Compared to the quasi-control group, detoxification did not reduce methamphetamine use at follow-up. Residential rehabilitation showed some efficacy in reducing methamphetamine use, but the decrease was time-limited.[85]

Studies of methamphetamine-dependent patients have found that methamphetamine withdrawal is marked by sleep disruption. Withdrawal symptoms typically resolve over 2 to 3 weeks, and particularly in the first week. Depression typically improves during that time, but anxiety may not.[86, 87]  

To date, phase II trials have yet to identify a pharmacologic agent that is strongly effective in helping patients achieve abstinence from methamphetamine. However, agents with novel therapeutic targets appear promising.[88]



Medication Summary

The goals of pharmacotherapy are to reduce the toxic effects of the drug, reduce morbidity, and prevent complications. Treatment measures may include gastrointestinal decontamination, sedation, seizure control, and control of catecholamine-induced hypertension and tachycardia.

GI decontaminant

Class Summary

Empirically used to minimize systemic absorption of the toxin.

Polyethylene glycol (PEG) solution

Laxative with strong electrolyte and osmotic effects. Cathartic actions in GI tract. May be indicated in treatment of methamphetamine ingestion in people who carry methamphetamine packages in their body. Must administer after activated charcoal. Liquid reconstituted per package instructions.

Activated charcoal (Liqui-Char)

A form of carbon processed to be riddled with small, low-volume pores that increase the surface area available for adsorption or chemical reactions. Due to its high degree of microporosity, one gram of activated charcoal has a surface area in excess of 500 square meters, and further chemical treatment often enhances adsorption properties.


Class Summary

Neuroleptic agents are CNS dopamine antagonists that are useful for control of agitated patients. By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, benzodiazepines depress all levels of CNS, including limbic and reticular formation. Haloperidol and droperidol are D2 receptor antagonists that interfere with dopaminergic neurotransmission in the limbic system and the cerebral cortex.

Lorazepam (Ativan)

Benzodiazepine. GABA receptor agonist.

Diazepam (Valium)

Benzodiazepine. GABA receptor agonist.

Midazolam (Versed)

Benzodiazepine. GABA receptor agonist.

Haloperidol (Haldol)

CNS dopamine D2 receptor antagonist.

Droperidol (Inapsine)

CNS dopamine D2 receptor antagonist.

Olanzapine (Zyprexa, Zydis)

The exact mechanism of action of olanzapine is not known. It binds to alpha-1, dopamine, histamine H-1, muscarinic, and serotonin type 2 (5-HT2) receptors.

Ziprasidone (Geodon)

Dopamine and serotonin receptor antagonist. It also inhibits the re-uptake of serotonin and norepinephrine in the CNS.

Cardiovascular Agents

Class Summary

Used to control catecholamine-induced hypertension and tachycardia.

Labetalol (Normodyne, Trandate)

Blocks beta1-, alpha-, and beta2-adrenergic receptor sites, decreasing blood pressure. When given IV, acts primarily as a beta-receptor antagonist.

Metoprolol (Lopressor, Toprol)

Blocks beta1-adrenergic receptor sites, decreasing heart rate.


Questions & Answers


What is methamphetamine toxicity?

Where can patient education information about methamphetamine toxicity be found?

What is the historical background of methamphetamine?

What is the pathophysiology of methamphetamine toxicity?

What cause methamphetamine toxicity?

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How is agitation managed in methamphetamine toxicity?

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How are hypertension and tachycardia managed in methamphetamine toxicity?

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Which medications in the drug class Cardiovascular Agents are used in the treatment of Methamphetamine Toxicity?

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