3.Oct.2022-Expires: 7 days - Do not archive

Charge (BZP)

Charge (BZP)
3.Oct.2022-Expires: 7 days - Do not archive



Benzylpiperazine (BZP)


Psychoactive Central Stimulant

Piperazine-Based Hallucinogenic Stimulant


Charge Capsule
105 mg Benzylpiperazine (BZP)
Recommended dose is 1 to 2 capsules, then another 1 to 2 after 2 hours. Maximum dose 3 capsules. Available in packets of 6 or 18.
Warning: Tablets claim to contain "500 mg". However, this refers to total mg of all ingredients, not active ingredients, and is effectively a meaningless statement.


While piperazine-based hallucinogenics or stimulants are not currently used therapeutically, they are misused. It is believed to have a similar action as the hallucinogenic-amphetamines, explaining the reason for its abuse. It is less potent than methamphetamine or MDMA, but is being sold in continuously increasing doses, making the effects more consistent with these more potent drugs.[1]


Intervention Level

The correct identification of the substance is important. If the symptoms are inconsistent with those described in the literature, or the history is considered unreliable, other substances may need to be considered.



Appropriate medical assessment and observation is recommended for:
- Any exposure to a piperazine based hallucinogenic stimulant


Appropriate medical assessment and observation is recommended:
- If > 400 mg of a piperazine-based hallucinogenic stimulant is ingested
- Symptomatic patients (other than mild)
- Exposures with intent to self-harm

Observation Period

Observation at Home

If the patient does not require medical observation they can be observed at home for 4 hours in the care of a reliable observer.
Medical attention should be sought if ANY symptoms occur, including:
Increased heart rate
Chest pain
Gastrointestinal upset

Medical Observation

If medical observation is required, the patient must be observed for 4 hours following exposure for onset or worsening of symptoms.
Those with mild signs and symptoms (e.g. euphoria, increased alertness, altered mental status, tachycardia) should be closely observed.
If the patient is clinically well except for slight tachycardia at the end of the observation period (there is no agitation or serotonergic signs, and temperature is normal), and provided that appropriate assessment and investigations have been carried out, they may be:
Discharged into the care of a reliable observer, or
Referred for psychological assessment (if the overdose or exposure was intentional)



Heart rate
Blood pressure
Body temperature
12 lead ECG
Blood glucose
Serum sodium


Serum concentrations are not readily available and do not aid management.

Admission Criteria

Admission to a closely monitored environment is recommended for:
Severe hypertension
Hyperthermia > 41 degrees C or > 39 degrees C that is not rapidly resolving with initial intervention
Cardiac ischemia as demonstrated by ECG evidence of ischemia or infarction or a rise in troponin concentration
Significant non-resolving cardiac dysrhythmias, including supraventricular tachycardias
Cerebral hemorrhage
Intractable seizures
Agitated delirium
Multisystem organ failure



Piperazine based hallucinogenic stimulants are considered to possess an hallucinogenic-amphetamine-like effect.
in the majority of cases gastrointestinal decontamination is unlikely to be beneficial. There is no antidote for intoxication and no methods for enhancing elimination can be recommended.
The majority of presentations will recover with a period of observation, calming environment and, if required, appropriate titrated doses of a benzodiazepine. Patients may become dehydrated and require significant volume replacement, however, it is imperative to recognize those suffering hyponatremia as administration of fluids may prove fatal. Serum sodium must be measured, and CT brain scan undertaken to exclude cerebral edema in those with CNS signs.
The severely toxic may suffer seizure or cardiovascular abnormality. Persistent seizures require treatment with a benzodiazepine or if refractory, a barbiturate. Chest pain may indicate an acute coronary syndrome (arteriospasm) which will likely settle if the patient is calmed with a benzodiazepine, nitrate, or in severe cases a vasodilator such as phentolamine. Hyperthermia should be immediately and actively managed, and the patient carefully monitored for further complications including rhabdomyolysis, DIC, and renal failure. Serotonin syndrome should be considered, especially in those using other serotonergic compounds either therapeutically or recreationally.[2]
Stimulant abuse may be via intravenous injection of ground tablets. Pulmonary granuloma formation in chronic abusers predisposes to reduced pulmonary function,[3] vascular obliteration, pulmonary hypertension, and cor pulmonale.[4][5]
Emergency Stabilization
Enhanced Elimination
Supportive Care
Fluid and electrolytes


Ensure Adequate Cardiopulmonary Function


Ensure the airway is protected if compromised (intubation may be necessary).


Immediately establish secure intravenous access.
A range of acute cardiovascular emergencies may occur due to vasospasm or vascular rupture. Such events include hemorrhagic or ischemic stroke, cardiac dysrhythmia/arrest, and dissection of large vessels including the aorta.
A range of acute cardiovascular emergencies may occur due to vasospasm or vascular rupture. Such events include hemorrhagic or ischemic stroke, cardiac dysrhythmia/arrest, dissection of large vessels including the aorta.

Cardiac Arrest

Prolonged cardiac resuscitation following standard protocols may be appropriate in selected cases as recovery with a good neurological outcome is reported in some severely poisoned patients receiving CPR for hours.[6] Artificial circulatory support interventions including veno-arterial or veno-venous extracorporeal membrane oxygenation (VA- or VV-ECMO), where available, can be considered for selected cases of severe refractory shock or severe respiratory failure due to acute respiratory distress syndrome.[6][7] There is growing experience treating poisoned patients at many ECMO-capable centers.[8][9]


Administer a benzodiazepine as first-line treatment to patients with seizure activity.[10]
Blood glucose concentration should be promptly determined. If the result indicates hypoglycemia, or is unobtainable, supplemental dextrose should be administered IV.

Emergency Monitoring

Heart rate
Blood pressure
12 lead ECG
Body temperature
Respiratory rate
State of hydration
Serum electrolytes - especially sodium
Blood glucose
Neurological status



Decontamination Not Recommended

Efficacy of gastrointestinal decontamination is questionable as these compounds are rapidly absorbed and the patient is likely a late presenter and less than co-operative. As the risks likely outweigh benefit, activated charcoal is not recommended.


There Are No Antidotes For This Substance

There is no specific antidote for the treatment of this poisoning. Treatment is based on symptomatic and supportive care.


The correct identification of the substance is important. If the symptoms are inconsistent with those described in the literature, or the history is considered unreliable, other substances may need to be considered.
Piperazines have a stimulant effect resulting from increased monoamine (dopamine, serotonin, norepinephrine (noradrenaline)) availability.[11]
Piperazine toxicity commonly causes tachycardia, hypertension, palpitations, gastrointestinal upset (nausea, abdominal pain, vomiting), dehydration, headache, anxiety, fever, and agitation.[12][13][14][2] Mydriasis, blurred vision, sweating, tremor, and confusion are relatively common. Trismus and paresthesia may uncommonly occur,[12] while hallucinations, hyperventilation, shortness of breath, and flushed skin are rare.[2]
In more severe cases, seizures, collapse, myoclonic jerking, and extrapyramidal features (choreoathetoid movements, dystonic reactions) may occur.[12] Serotonin syndrome has also been reported.[15] Hypertension can be severe.[12] If prolonged or severe, fever and excessive motor activity may lead to hyperthermia, metabolic acidosis, disseminated intravascular coagulation, and acute kidney injury.[16] Psychosis has been reported.[17] Given piperazine's mechanism of action, theoretical concerns are cardiac dysrhythmia, acute hepatitis/liver failure, and death.[18]
Hypersensitivity reactions, such as bronchospasm, Stevens-Johnson syndrome, acute hepatitis, thrombocytopenia, hemolytic anemia and angioedema have occurred in individuals taking piperazine therapeutically.

Routes of Exposure

Benzylpiperazine (BZP) liquid and dust is known to be corrosive. This may cause burns to the gastrointestinal tract if swallowed or to the eye or skin if these areas are contaminated. Piperazine based hallucinogenic stimulants are also smoked by some individuals and there is also the potential for effects similar to inhalation of a corrosive (or acid) gas to manifest.
Tablets are often dissolved and directly injected. Due to the bulk of these tablets being composed of non-water soluble agents such as talc there is a high rate of complications following granuloma formation and vascular obliteration.[5][4] While the lung is a particular target with resultant pulmonary hypertension/cor pulmonale, other organs can be affected. Infection following such abuse is also a concern.[3]

Onset/Duration of Symptoms

Onset of affect is usually delayed about 2 hours post-ingestion.[1][19] Effects generally persist for about 12 to 24 hours, but may occur for up to 72 hours following use.[12] There may be a role for monoamine depletion/withdrawal in prolonged toxicity.

Severity of Poisoning

Mild Piperazine ToxicityModerate Piperazine ToxicitySevere Piperazine Toxicity
Increased alertness
Bruxism (grinding of teeth)
Altered mental status
Abdominal pain
Chest pain
Metabolic acidosis
DIC (disseminated intravascular coagulation)
Acute renal failure


Hypersensitivity reactions, such as bronchospasm, Stevens-Johnson syndrome, acute hepatitis, thrombocytopenia, hemolytic anemia and angioedema have occurred in individuals taking piperazine therapeutically.[20]
Given their mechanism of action, theoretical concerns following chronic us/abuse of piperazines would be similar to hallucinogenic amphetamines.


Chronic oral amphetamine abuse has been associated with:[21][22]
Cardiomyopathy (non-ischemic)
Vascular spasm
Aortic dissection
Congestive heart failure[5][23]
Pulmonary hypertension[5]
Chronic intravenous abuse with:[24]
Widespread necrotising angiitis
Segmental stenosis
Vascular rupture
Pulmonary edema
Renal failure


If large amounts of amphetamine or amphetamine-like compounds are consumed over a long period of time, amphetamine psychosis can develop, which is similar to paranoid schizophrenia. The psychosis is manifested by hallucinations, delusions and paranoia. Symptoms usually disappear within a few weeks after drug use stops.
A range of sequelae have been noted following chronic human abuse including:
Choreoathetoid movements[25]
Auditory (less common)
A lasting paranoid psychotic reaction may develop,[27] and behavior can become destructive and violent. While the majority of patients recover within 10 days, effects persist for more than 6 months in 10% of cases.[28][29][30] Single re-exposures may produce acute exacerbations even after long periods of abstinence.


Ischemic colitis can occur following long-term use of amphetamines.[31]


Diffuse hair loss has been associated with long-term amphetamine use.[32][33]
Amphetamine and amphetamine-like compounds have rarely produced aplastic anemia and a fatal pancytopenia after prolonged use.[34]
Infections such as hepatitis B and C and HIV are possible complications of intravenous use of amphetamine and amphetamine-like compounds.[34]


Tolerance can develop to the anorectic and various autonomic effects including body temperature, blood pressure, heart rate and respirations.[35]

Withdrawal Syndrome

Acute withdrawal may precipitate severe depression and suicidal thoughts. Symptoms usually peak after 2 to 3 days and are seldom directly life-threatening.
Physical symptoms associated with withdrawal are:[36][37][38]
Abdominal cramps
Moderate to severe depression
Increased appetite
Mental confusion
Psychotic reaction

Washout Syndrome

A washout syndrome has been reported following cocaine use[39][40][41] and it is thought a similar syndrome with may occur with amphetamines or other stimulants. Most commonly observed after extended binges, the mechanism is thought to be depletion of adrenergic neurotransmitters due to prolonged and persistent CNS stimulation.[39][40][41]
Effects associated with washout are:[39][40]
Decreased level of consciousness
Psychomotor retardation
Dysconjugate gaze


[1] Bye C, Munro-Faure AD, Peck AW, Young PA. A comparison of the effects of 1-benzylpiperazine and dexamphetamine on human performance tests. Eur J Clin Pharmacol 1973 Oct; 6 (3): 163-9.
[2] Schep LJ, Slaughter RJ, Vale JA, Beasley DM, Gee P. The clinical toxicology of the designer "party pills" benzylpiperazine and trifluoromethylphenylpiperazine. Clin Toxicol (Phila) 2011 Mar; 49 (3): 131-41.
[3] Parran TV Jr, Jasinski DR. Intravenous methylphenidate abuse. Prototype for prescription drug abuse. Arch Intern Med 1991 Apr; 151 (4): 781-3.
[4] Hahn HH, Schweid AI, Beaty HN. Complications of injecting dissolved methylphenidate tablets. Arch Intern Med 1969 Jun; 123 (6): 656-9.
[5] Lewman LV. Fatal pulmonary hypertension from intravenous injection of methylphenidate (Ritalin) tablets. Hum Pathol 1972 Mar; 3 (1): 67-70.
[6] Gunja N, Graudins A. Management of cardiac arrest following poisoning. Emerg Med Australas 2011 Feb; 23 (1): 16-22.
[7] de Lange DW, Sikma MA, Meulenbelt J. Extracorporeal membrane oxygenation in the treatment of poisoned patients. Clin Toxicol (Phila) 2013 Jun; 51 (5): 385-93.
[8] Weiner L, Mazzeffi MA, Hines EQ, Gordon D, Herr DL, Kim HK. Clinical utility of venoarterial-extracorporeal membrane oxygenation (VA-ECMO) in patients with drug-induced cardiogenic shock: a retrospective study of the Extracorporeal Life Support Organizations' ECMO case registry. Clin Toxicol (Phila) 2020; 58 (7): 705-10.
[9] Ramanathan K, Tan CS, Rycus P, MacLaren G. Extracorporeal membrane oxygenation for poisoning in adult patients: outcomes and predictors of mortality. Intensive Care Med 2017 Oct; 43 (10): 1538-39.
[10] Chen HY, Albertson TE, Olson KR. Treatment of drug-induced seizures. Br J Clin Pharmacol 2016 Mar; 81 (3): 412-9.
[11] Baumann MH, Clark RD, Budzynski AG, Partilla JS, Blough BE, Rothman RB. N-substituted piperazines abused by humans mimic the molecular mechanism of 3,4-methylenedioxymethamphetamine (MDMA, or 'Ecstasy'). Neuropsychopharmacology 2005 Mar; 30 (3): 550-60.
[12] Gee P, Richardson S, Woltersdorf W, Moore G. Toxic effects of BZP-based herbal party pills in humans: a prospective study in Christchurch, New Zealand. N Z Med J 2005 Dec 16; 118 (1227): U1784.
[13] Theron L, Jansen K, Miles J. Benzylpiperizine-based party pills' impact on the Auckland City Hospital Emergency Department Overdose Database (2002-2004) compared with ecstasy (MDMA or methylene dioxymethamphetamine), gamma hydroxybutyrate (GHB), amphetamines, cocaine, and alcohol. N Z Med J 2007 Feb 16; 120 (1249): U2416.
[14] Gee P, Gilbert M, Richardson S, Moore G, Paterson S, Graham P. Toxicity from the recreational use of 1-benzylpiperazine. Clin Toxicol (Phila) 2008 Nov; 46 (9): 802-7.
[15] Klaassen T, Ho Pian KL, Westenberg HG, den Boer JA, van Praag HM. Serotonin syndrome after challenge with the 5-HT agonist meta-chlorophenylpiperazine. Psychiatry Res 1998 Jul 13; 79 (3): 207-12.
[16] Gee P, Jerram T, Bowie D. Multiorgan failure from 1-benzylpiperazine ingestion--legal high or lethal high? Clin Toxicol (Phila) 2010 Mar; 48 (3): 230-3.
[17] Austin H, Monasterio E. Acute psychosis following ingestion of 'Rapture'. Australas Psychiatry 2004 Dec; 12 (4): 406-8.
[18] Greene SL, Dargan PI, O'connor N, Jones AL, Kerins M. Multiple toxicity from 3,4-methylenedioxymethamphetamine ("ecstasy"). Am J Emerg Med 2003 Mar; 21 (2): 121-4.
[19] Campbell H, Cline W, Evans M, Lloyd J, Peck AW. Comparison of the effects of dexamphetamine and 1-benzylpiperazine in former addicts. Eur J Clin Pharmacol 1973 Oct; 6 (3): 170-6.
[20] Sweetman SC, editor. Martindale. The complete drug reference. 33rd ed. London: Pharmaceutical Press; 2002. p. 105-6.
[21] Davis GG, Swalwell CI. Acute aortic dissections and ruptured berry aneurysms associated with methamphetamine abuse. J Forensic Sci 1994 Nov; 39 (6): 1481-5.
[22] Wijetunga M, Seto T, Lindsay J, Schatz I. Crystal methamphetamine-associated cardiomyopathy: tip of the iceberg? J Toxicol Clin Toxicol 2003; 41 (7): 981-6.
[23] Haning W, Goebert D. Electrocardiographic abnormalities in methamphetamine abusers. Addiction 2007 Apr; 102 Suppl 1 (): 70-5.
[24] Citron BP, Halpern M, McCarron M, Lundberg GD, McCormick R, Pincus IJ, Tatter D, Haverback BJ. Necrotizing angiitis associated with drug abuse. N Engl J Med 1970 Nov 5; 283 (19): 1003-11.
[25] Lundh H, Tunving K. An extrapyramidal choreiform syndrome caused by amphetamine addiction. J Neurol Neurosurg Psychiatry 1981 Aug; 44 (8): 728-30.
[26] Jackson JG. The hazards of smokable methamphetamine. [Letter] N Engl J Med 1989 Sep 28; 321 (13): 907.
[27] Sato M. A lasting vulnerability to psychosis in patients with previous methamphetamine psychosis. Ann N Y Acad Sci 1992 Jun 28; 654 (): 160-70.
[28] Schaffer CB, Pauli MW. Psychotic reaction caused by proprietary oral diet agents. Am J Psychiatry 1980 Oct; 137 (10): 1256-7.
[29] Ando K, Hironaka N, Yanagita T. Psychotic manifestations in amphetamine abuse--experimental study on the mechanism of psychotic recurrence. Psychopharmacol Bull 1986; 22 (3): 763-7.
[30] Iwanami A, Kato N, Nakatani Y. P300 in methamphetamine psychosis. Biol Psychiatry 1991 Oct 1; 30 (7): 726-30.
[31] Dirkx CA, Gerscovich EO. Sonographic findings in methamphetamine-induced ischemic colitis. J Clin Ultrasound 1998 Nov-Dec; 26 (9): 479-82.
[32] Eckert J, Church RE, Ebling FJ, Munro DS. Hair loss in women. Br J Dermatol 1967 Oct; 79 (10): 543-8.
[33] Alexander S. Diffuse alopecia in women. Trans St Johns Hosp Dermatol Soc 1965; 51 (1): 99-102.
[34] McEvoy GK, editor. AHFS drug information. Bethesda (MD): American Society of Health-System Pharmacists; 1997. p. 1764-6.
[35] Robinson TE, Becker JB. Enduring changes in brain and behavior produced by chronic amphetamine administration: a review and evaluation of animal models of amphetamine psychosis. Brain Res 1986 Jun; 396 (2): 157-98.
[36] Schep LJ, Slaughter RJ, Beasley DM. The clinical toxicology of metamfetamine. Clin Toxicol (Phila) 2010 Aug; 48 (7): 675-94.
[37] OSWALD I, THACORE VR. Amphetamine and phenmetrazine addiction. Physiological abnormalities in the abstinence syndrome. Br Med J 1963 Aug 17; 5354 (): 427-31.
[38] Meredith CW, Jaffe C, Ang-Lee K, Saxon AJ. Implications of chronic methamphetamine use: a literature review. Harv Rev Psychiatry 2005 May-Jun; 13 (3): 141-54.
[39] Roberts JR, Greenberg MI. Cocaine washout syndrome. [Letter] Ann Intern Med 2000 Apr 18; 132 (8): 679-80.
[40] Sporer KA, Lesser SH. Cocaine washed-out syndrome. [Letter] Ann Emerg Med 1992 Jan; 21 (1): 112.
[41] Trabulsy ME. Cocaine washed out syndrome in a patient with acute myocardial infarction. Am J Emerg Med 1995 Sep; 13 (5): 538-9.

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