Resource TOXBASE access

[KarmaBus]

Thank you for sharing this in depth information with us.

Do you have any information on:
Flubrotizolam & Flubromazepam?

 

[CocoToxBase]

Thank you for sharing this info with us! Would you mind doing clonidine, gabapentin, and oxycodone please?

Type of Product
Selective central presynaptic alpha-2 adrenergic receptor agonist and imidazoline receptor agonist. In high concentrations non-selective activation of peripheral alpha-1 adrenoceptors is thought to occur.
Used in the management of hypertension, migraine, vascular headache, menopausal symptoms, sedation and for analgesia. Also used in the treatment of children with attention deficit hyperactivity disorder, and Tourette syndrome.

Ingredients
Clonidine hydrochloride
Tablets - 0.025 mg, 0.1 mg
Injection (1 mL amp) - 0.15 mg/mL
Oral - 0.05 mg/5mL solution

Toxicity
Toxicity results primarily from the central sympathetic depressant effects of the drug (Catapres SPC, 2017).
Children are particularly at risk and and 1 or 2 tablets may cause symptoms (Eddy & Howell, 2003).
In a review of 27,825 paediatric clonidine exposures 45% of cases presented with CNS depression, 10% bradycardia, 9% hypotension, 3% had respiratory features and 7 (0.025%) patients suffered a cardiac arrest (Wang et al, 2014).
In a series of 11 toddlers who ingested 0.01-0.57 mg/kg clonidine, all developed an altered level of consciousness; 5 developed miosis, hypotension and hypothermia; 6 developed both apnoea and respiratory depression; and 8 developed bradycardia. Mild features were present in patients who have ingested less than 0.01 mg/kg. Patients who had ingested more than 0.02 mg/kg are at significant risk of respiratory depression (Fiser et al, 1990).
In a retrospective study of 40 adults ingesting clonidine at doses between 400-15,000 micrograms; 68% developed bradycardia which persisted for a median of 20 hours, 55% of patients developed a decreased level of consciousness, 25% became hypotensive, and 5% were comatose (Isbister et al, 2017).
Click here for further case reports of clonidine exposure.
Clonidine is well absorbed via ingestion and dermally, with peak plasma concentrations and maximal hypotensive effect occurring 1 to 5 hours after an oral therapeutic dose and 1 hour after topical application (Bassani & Banov, 2016). Steady state features usually manifest rapidly within 30 to 90 minutes and rarely develop if symptom-free more than 4 hours after ingestion. The elimination half-life of clonidine ranges between 5 and 24 hours but can be prolonged up to 41 hours in patients with severely impaired renal function (Catapres SPC, 2013).

Gabapentin
Type of Product
An anticonvulsant and analgesic used for neuropathic pain. Also used off-license for migraine prophylaxis.
A potential drug of abuse as notified by the European Monitoring Centre for Drugs and Drug Addiction (EMCDDA) in 2013.

Ingredients
Gabapentin
Capsules - 100 mg, 300 mg, 400 mg
Tablets - 600 mg, 800 mg
Oral solution (150 mL bottle) - 50 mg/mL

Toxicity
Exact mechanism of action and toxicity unknown. It is a structural analogue of GABA but does not appear to act on GABA receptors (Rose & Kam, 2002).
A 62-year-old woman was found dead with high plasma levels of gabapentin. While the total dose ingested was unknown, a prescription of 150 capsules of 300 mg gabapentin was dispensed one day prior. Post-mortem findings showed a blood concentration 88 micrograms/mL (therapeutic concentration: 2.6 micrograms/mL). Gabapentin was the only drug found in excess (Middleton, 2011). However, a 59-year-old woman is reported to have had symptoms of only mild sedation and nausea after ingesting approximately 90 g (serum concentration 72.8 micrograms/mL) (Schauer & Varney, 2013).
A case series of 20 gabapentin overdoses in adults and children (doses 50 mg to 35 g) reported symptoms of drowsiness, dizziness/ataxia, nausea/vomiting, tachycardia and hypotension (Klein-Schwartz et al, 2003).
Peak plasma concentrations are reached 2-3 hours after an oral dose. Bioavailability of a 300 mg capsule is approximately 60% but decreases with increasing dose. The therapeutic half-life is 5-7 hours (Gabapentin SPC, 2018).

Features
The most significant effect in overdose is CNS depression, which may occasionally be profound. Ataxia, nystagmus, agitation, slurred speech and myoclonus are reported. Very rarely convulsions may occur.
GI upset, hypotension, tachycardia, syncope, ECG abnormalities such as AV block and cardiac failure may also occur.
Rhabdomyolysis and acute kidney injury have been reported.
When co-ingested with alcohol, opiates and other central nervous system depressants, the effects of gabapentinoids are potentially more severe.
Hypersensitivity reactions have been reported shortly after starting pregabalin therapy.


Oxycodone

Type of Product
Semisynthetic opioid analgesic.

Ingredients
Oxycodone
Modified release tablets - 5 mg, 10 mg, 15 mg, 20 mg, 30 mg, 40 mg, 60 mg, 80 mg, 120 mg
Capsules - 5 mg, 10 mg, 20 mg
Tablets - 5 mg, 10 mg, 20 mg
Oral solution - 1 mg/mL, 10 mg/mL
Injection - 10 mg/mL, 50 mg/mL
Orodispersible tablets - 5 mg, 10 mg, 20 mg (available in Ireland)

Toxicity
The most serious toxic features are respiratory depression, hypercapnoea, reduced consciousness/coma and airway obstruction, mediated by mu and kappa opioid receptor agonism. The toxic dose is very variable according to individual tolerance. These effects will be potentiated by simultaneous ingestion of other sedatives including alcohol.
Tablets may be crushed and snorted or injected for recreational use.
A 45-year-old woman who ingested up to 4 g of sustained release oxycodone received a total of 188 mg intravenous naloxone over 11 hours. Following this she required mechanical ventilation for 2 days; the patient recovered (Schneir et al, 2002).
Nasal insufflation of oxycodone can cause nasal abscess and nasopharyngeal necrosis (Pulia & Reiff 2014; Rosenbaum et al, 2012).
A retrospective review of a clinical database reported that oxycodone was associated with bradycardia and QT prolongation in around 20% of 137 overdoses (Berling et al, 2013). However, this may be confounded by the effects of other co-ingested cardiotoxic drugs.
In comparison with morphine, oxycodone has a high absolute bioavailability of 87% after oral administration. Peak plasma concentrations are reached within 1-1.5 hours after ingestion of normal release preparations, and 3 hours after ingestion of sustained release preparations. Oxycodone has an elimination half-life of approximately 3.5 hours in normal release preparations and 4.5 hours in sustained release preparations (Lynlor capsules SPC, 2021; Oxycontin SPC, 2021).

Features
Severe opioid toxicity produces depression of the respiratory and central nervous systems and pin-point pupils. If untreated the depression of the level of consciousness can lead to deep coma, convulsions and respiratory arrest.

• Effects in overdose will be potentiated by co-ingestion of alcohol and other centrally acting drugs.
• Effects will appear very rapidly after exposure to high-potency opioid drugs (e.g. veterinary sedating agents like etorphine).
• Severe and recurrent respiratory depression can occur after ingestion of transdermal patches.

Milder opioid toxicity may produce nausea, vomiting, nightmares, anxiety, agitation, euphoria, dysphoria, depression, paranoia and hallucinations. While pin-point pupils are often present, this is not a reliable clinical sign and their absence does not exclude opioid toxicity. Sedation may be associated with hypotension, bradycardia and hypothermia.
Toxic leukoencephalopathy has been reported following recreational use of heroin, methadone, oxycodone and buprenorphine. Malignant cerebellar oedema and raised intracranial pressure has been reported in one child following unintentional dihydrocodeine ingestion.
For certain opioids (such as morphine, diamorphine, codeine and pethidine), the risk of toxicity is significantly increased if kidney function is impaired due to reduced elimination of the parent opioid or active metabolite.
Opioids, in particular codeine, can cause histamine release, causing urticaria and pruritis. Non-cardiac pulmonary oedema and rhabdomyolysis may occur after intravenous injection of opioid analgesics.
Some opioids may cause cardiotoxicity e.g. methadone, which causes potassium channel blockade and QT prolongation or dextropropoxyphene, which causes sodium channel blockade and QRS prolongation.
Co-administration of opioids with serotonergic agents such as SSRIs, SNRIs, MAOIs etc. may increase the risk of serotonin syndrome. For more information click here. For the management of serotonin syndrome click here.
The route of opioid administration may produce important clinical features such as soft-tissue infections and abscesses at the sites of intravenous heroin injection. The presence of infections distant to the injection site should also be specifically determined (for example, endocarditis, lung abscesses). Inadvertent intra-arterial injection can cause severe limb ischaemia.
The possibility of viral hepatitis and HIV infection should be considered in all intravenous drug users and testing should be routinely offered or recommended.
Rarely, sudden sensorineural hearing loss (SSHL) has been reported following opioid overdose. Recovery of hearing has been reported in some cases.

Thank you for sharing this in depth information with us.

Do you have any information on:
Flubrotizolam & Flubromazepam?

Flubromazepam HIGHLY TOXIC SUBSTANCE

Type of Product
A drug of abuse. A benzodiazepine.

Synonyms
Flubromazepam
Caution: using a slang term/abbreviation to try and identify a drug of abuse is potentially dangerous since there are many regional variations and the terms change over time.

Ingredients
7-bromo-5-(2-fluorophenyl)-1,3-dihydro-2H-1,4-benzodiazepin-2-one

Caution: exact ingredients may vary. Different products will have different compositions. The label may not accurately reflect the contents.


Caution: the purity of the ingredients in recreational drugs may vary greatly.

Toxicity
At the time of writing, there was limited information on the toxicity of this drug. It is anticipated that it will be like other benzodiazepines in its toxicity.
Benzodiazepines cause CNS depression through their agonist action at the (GABAA) receptor. Features of severe toxicity include coma, hypotension, bradycardia, respiratory depression, rhabdomyolysis and hypothermia. Effects are likely to be more severe when co-ingested with alcohol and other CNS depressants.

A half-life of 100 hours has been reported for this flubromazepam, however this was in a single individual (following an oral dose of 4 mg; Moosmann et al, 2013).
Flubromazepam was detected in 0.65% of samples from 766 patients presenting to participating Emergency Departments in the UK with severe toxicity related to suspected NPS use since 2015 (IONA study, 2020, unpublished data).

Features
Benzodiazepines commonly cause drowsiness, ataxia, dysarthria and nystagmus. Coma, hypotension, bradycardia and respiratory depression occasionally occur but are seldom serious if these drugs are taken alone. Coma usually lasts only a few hours but may be prolonged in elderly patients.
Benzodiazepine respiratory depressant effects are more serious in patients with chronic obstructive airways disease. Severe effects in overdose also include rhabdomyolysis and hypothermia.
ECG abnormalities include transient first degree and second degree block and QT prolongation. Abnormal LFTs may also occur.
Microembolisation can result from intravenous injection of crushed tablets. Accidental intra-arterial injection of benzodiazepines can cause severe limb ischaemia and gangrene necessitating limb amputation.
Co-ingestion of alcohol and other central nervous system depressants potentiates the effects of benzodiazepines and can increase toxicity.


Flubromazolam

Type of Product
A drug of abuse. A benzodiazepine.

Synonyms
Flubromazolam
Caution: using a slang term/abbreviation to try and identify a drug of abuse is potentially dangerous since there are many regional variations and the terms change over time.

Ingredients
8-bromo-6-(2-fluorophenyl)-1-methyl-4H-[1,2,4]triazolo-[4,3a][1,4]benzodiazepine

Caution: exact ingredients may vary. Different products will have different compositions. The label may not accurately reflect the contents.

Caution: the purity of the ingredients in recreational drugs may vary greatly.

Toxicity

At the time of writing, there was limited information on the toxicity of this drug. It is anticipated that it will be like other benzodiazepines in its toxicity.
Benzodiazepines cause CNS depression through their agonist action at the (GABAA) receptor. Features of severe toxicity include coma, hypotension, bradycardia, respiratory depression, rhabdomyolysis and hypothermia. Effects are likely to be more severe when co-ingested with alcohol and other CNS depressants.

Flubromazolam is reported to be highly potent, causing strong sedation and amnesia following oral doses as low as 0.5 mg (Moosmann et al, 2015).
A 27-year-old male who reportedly ingested 3 mg of flubromazolam developed severe, prolonged depression of the central nervous system with cardio-respiratory failure (Lukasik-Glębocka et al, 2016).

Features
Benzodiazepines commonly cause drowsiness, ataxia, dysarthria and nystagmus. Coma, hypotension, bradycardia and respiratory depression occasionally occur but are seldom serious if these drugs are taken alone. Coma usually lasts only a few hours but may be prolonged in elderly patients.
Benzodiazepine respiratory depressant effects are more serious in patients with chronic obstructive airways disease. Severe effects in overdose also include rhabdomyolysis and hypothermia.
ECG abnormalities include transient first degree and second degree block and QT prolongation. Abnormal LFTs may also occur.
Microembolisation can result from intravenous injection of crushed tablets. Accidental intra-arterial injection of benzodiazepines can cause severe limb ischaemia and gangrene necessitating limb amputation.
Co-ingestion of alcohol and other central nervous system depressants potentiates the effects of benzodiazepines and can increase toxicity.

 

[nofunclub]

Type of Product
Selective central presynaptic alpha-2 adrenergic receptor agonist and imidazoline receptor agonist. In high concentrations non-selective activation of peripheral alpha-1 adrenoceptors is thought to occur.
Used in the management of hypertension, migraine, vascular headache, menopausal symptoms, sedation and for analgesia. Also used in the treatment of children with attention deficit hyperactivity disorder, and Tourette syndrome.

Ingredients
Clonidine hydrochloride
Tablets - 0.025 mg, 0.1 mg
Injection (1 mL amp) - 0.15 mg/mL
Oral - 0.05 mg/5mL solution

Toxicity
Toxicity results primarily from the central sympathetic depressant effects of the drug (Catapres SPC, 2017).
Children are particularly at risk and and 1 or 2 tablets may cause symptoms (Eddy & Howell, 2003).
In a review of 27,825 paediatric clonidine exposures 45% of cases presented with CNS depression, 10% bradycardia, 9% hypotension, 3% had respiratory features and 7 (0.025%) patients suffered a cardiac arrest (Wang et al, 2014).
In a series of 11 toddlers who ingested 0.01-0.57 mg/kg clonidine, all developed an altered level of consciousness; 5 developed miosis, hypotension and hypothermia; 6 developed both apnoea and respiratory depression; and 8 developed bradycardia. Mild features were present in patients who have ingested less than 0.01 mg/kg. Patients who had ingested more than 0.02 mg/kg are at significant risk of respiratory depression (Fiser et al, 1990).
In a retrospective study of 40 adults ingesting clonidine at doses between 400-15,000 micrograms; 68% developed bradycardia which persisted for a median of 20 hours, 55% of patients developed a decreased level of consciousness, 25% became hypotensive, and 5% were comatose (Isbister et al, 2017).
Click here for further case reports of clonidine exposure.
Clonidine is well absorbed via ingestion and dermally, with peak plasma concentrations and maximal hypotensive effect occurring 1 to 5 hours after an oral therapeutic dose and 1 hour after topical application (Bassani & Banov, 2016). Steady state features usually manifest rapidly within 30 to 90 minutes and rarely develop if symptom-free more than 4 hours after ingestion. The elimination half-life of clonidine ranges between 5 and 24 hours but can be prolonged up to 41 hours in patients with severely impaired renal function (Catapres SPC, 2013).

Gabapentin
Type of Product
An anticonvulsant and analgesic used for neuropathic pain. Also used off-license for migraine prophylaxis.
A potential drug of abuse as notified by the European Monitoring Centre for Drugs and Drug Addiction (EMCDDA) in 2013.

Ingredients
Gabapentin
Capsules - 100 mg, 300 mg, 400 mg
Tablets - 600 mg, 800 mg
Oral solution (150 mL bottle) - 50 mg/mL

Toxicity
Exact mechanism of action and toxicity unknown. It is a structural analogue of GABA but does not appear to act on GABA receptors (Rose & Kam, 2002).
A 62-year-old woman was found dead with high plasma levels of gabapentin. While the total dose ingested was unknown, a prescription of 150 capsules of 300 mg gabapentin was dispensed one day prior. Post-mortem findings showed a blood concentration 88 micrograms/mL (therapeutic concentration: 2.6 micrograms/mL). Gabapentin was the only drug found in excess (Middleton, 2011). However, a 59-year-old woman is reported to have had symptoms of only mild sedation and nausea after ingesting approximately 90 g (serum concentration 72.8 micrograms/mL) (Schauer & Varney, 2013).
A case series of 20 gabapentin overdoses in adults and children (doses 50 mg to 35 g) reported symptoms of drowsiness, dizziness/ataxia, nausea/vomiting, tachycardia and hypotension (Klein-Schwartz et al, 2003).
Peak plasma concentrations are reached 2-3 hours after an oral dose. Bioavailability of a 300 mg capsule is approximately 60% but decreases with increasing dose. The therapeutic half-life is 5-7 hours (Gabapentin SPC, 2018).

Features
The most significant effect in overdose is CNS depression, which may occasionally be profound. Ataxia, nystagmus, agitation, slurred speech and myoclonus are reported. Very rarely convulsions may occur.
GI upset, hypotension, tachycardia, syncope, ECG abnormalities such as AV block and cardiac failure may also occur.
Rhabdomyolysis and acute kidney injury have been reported.
When co-ingested with alcohol, opiates and other central nervous system depressants, the effects of gabapentinoids are potentially more severe.
Hypersensitivity reactions have been reported shortly after starting pregabalin therapy.


Oxycodone

Type of Product
Semisynthetic opioid analgesic.

Ingredients
Oxycodone
Modified release tablets - 5 mg, 10 mg, 15 mg, 20 mg, 30 mg, 40 mg, 60 mg, 80 mg, 120 mg
Capsules - 5 mg, 10 mg, 20 mg
Tablets - 5 mg, 10 mg, 20 mg
Oral solution - 1 mg/mL, 10 mg/mL
Injection - 10 mg/mL, 50 mg/mL
Orodispersible tablets - 5 mg, 10 mg, 20 mg (available in Ireland)

Toxicity
The most serious toxic features are respiratory depression, hypercapnoea, reduced consciousness/coma and airway obstruction, mediated by mu and kappa opioid receptor agonism. The toxic dose is very variable according to individual tolerance. These effects will be potentiated by simultaneous ingestion of other sedatives including alcohol.
Tablets may be crushed and snorted or injected for recreational use.
A 45-year-old woman who ingested up to 4 g of sustained release oxycodone received a total of 188 mg intravenous naloxone over 11 hours. Following this she required mechanical ventilation for 2 days; the patient recovered (Schneir et al, 2002).
Nasal insufflation of oxycodone can cause nasal abscess and nasopharyngeal necrosis (Pulia & Reiff 2014; Rosenbaum et al, 2012).
A retrospective review of a clinical database reported that oxycodone was associated with bradycardia and QT prolongation in around 20% of 137 overdoses (Berling et al, 2013). However, this may be confounded by the effects of other co-ingested cardiotoxic drugs.
In comparison with morphine, oxycodone has a high absolute bioavailability of 87% after oral administration. Peak plasma concentrations are reached within 1-1.5 hours after ingestion of normal release preparations, and 3 hours after ingestion of sustained release preparations. Oxycodone has an elimination half-life of approximately 3.5 hours in normal release preparations and 4.5 hours in sustained release preparations (Lynlor capsules SPC, 2021; Oxycontin SPC, 2021).

Features
Severe opioid toxicity produces depression of the respiratory and central nervous systems and pin-point pupils. If untreated the depression of the level of consciousness can lead to deep coma, convulsions and respiratory arrest.

• Effects in overdose will be potentiated by co-ingestion of alcohol and other centrally acting drugs.
• Effects will appear very rapidly after exposure to high-potency opioid drugs (e.g. veterinary sedating agents like etorphine).
• Severe and recurrent respiratory depression can occur after ingestion of transdermal patches.

Milder opioid toxicity may produce nausea, vomiting, nightmares, anxiety, agitation, euphoria, dysphoria, depression, paranoia and hallucinations. While pin-point pupils are often present, this is not a reliable clinical sign and their absence does not exclude opioid toxicity. Sedation may be associated with hypotension, bradycardia and hypothermia.
Toxic leukoencephalopathy has been reported following recreational use of heroin, methadone, oxycodone and buprenorphine. Malignant cerebellar oedema and raised intracranial pressure has been reported in one child following unintentional dihydrocodeine ingestion.
For certain opioids (such as morphine, diamorphine, codeine and pethidine), the risk of toxicity is significantly increased if kidney function is impaired due to reduced elimination of the parent opioid or active metabolite.
Opioids, in particular codeine, can cause histamine release, causing urticaria and pruritis. Non-cardiac pulmonary oedema and rhabdomyolysis may occur after intravenous injection of opioid analgesics.
Some opioids may cause cardiotoxicity e.g. methadone, which causes potassium channel blockade and QT prolongation or dextropropoxyphene, which causes sodium channel blockade and QRS prolongation.
Co-administration of opioids with serotonergic agents such as SSRIs, SNRIs, MAOIs etc. may increase the risk of serotonin syndrome. For more information click here. For the management of serotonin syndrome click here.
The route of opioid administration may produce important clinical features such as soft-tissue infections and abscesses at the sites of intravenous heroin injection. The presence of infections distant to the injection site should also be specifically determined (for example, endocarditis, lung abscesses). Inadvertent intra-arterial injection can cause severe limb ischaemia.
The possibility of viral hepatitis and HIV infection should be considered in all intravenous drug users and testing should be routinely offered or recommended.
Rarely, sudden sensorineural hearing loss (SSHL) has been reported following opioid overdose. Recovery of hearing has been reported in some cases.

Flubromazepam HIGHLY TOXIC SUBSTANCE

Type of Product
A drug of abuse. A benzodiazepine.

Synonyms
Flubromazepam
Caution: using a slang term/abbreviation to try and identify a drug of abuse is potentially dangerous since there are many regional variations and the terms change over time.

Ingredients
7-bromo-5-(2-fluorophenyl)-1,3-dihydro-2H-1,4-benzodiazepin-2-one

Caution: exact ingredients may vary. Different products will have different compositions. The label may not accurately reflect the contents.


Caution: the purity of the ingredients in recreational drugs may vary greatly.

Toxicity
At the time of writing, there was limited information on the toxicity of this drug. It is anticipated that it will be like other benzodiazepines in its toxicity.
Benzodiazepines cause CNS depression through their agonist action at the (GABAA) receptor. Features of severe toxicity include coma, hypotension, bradycardia, respiratory depression, rhabdomyolysis and hypothermia. Effects are likely to be more severe when co-ingested with alcohol and other CNS depressants.

A half-life of 100 hours has been reported for this flubromazepam, however this was in a single individual (following an oral dose of 4 mg; Moosmann et al, 2013).
Flubromazepam was detected in 0.65% of samples from 766 patients presenting to participating Emergency Departments in the UK with severe toxicity related to suspected NPS use since 2015 (IONA study, 2020, unpublished data).

Features
Benzodiazepines commonly cause drowsiness, ataxia, dysarthria and nystagmus. Coma, hypotension, bradycardia and respiratory depression occasionally occur but are seldom serious if these drugs are taken alone. Coma usually lasts only a few hours but may be prolonged in elderly patients.
Benzodiazepine respiratory depressant effects are more serious in patients with chronic obstructive airways disease. Severe effects in overdose also include rhabdomyolysis and hypothermia.
ECG abnormalities include transient first degree and second degree block and QT prolongation. Abnormal LFTs may also occur.
Microembolisation can result from intravenous injection of crushed tablets. Accidental intra-arterial injection of benzodiazepines can cause severe limb ischaemia and gangrene necessitating limb amputation.
Co-ingestion of alcohol and other central nervous system depressants potentiates the effects of benzodiazepines and can increase toxicity.


Flubromazolam

Type of Product
A drug of abuse. A benzodiazepine.

Synonyms
Flubromazolam
Caution: using a slang term/abbreviation to try and identify a drug of abuse is potentially dangerous since there are many regional variations and the terms change over time.

Ingredients
8-bromo-6-(2-fluorophenyl)-1-methyl-4H-[1,2,4]triazolo-[4,3a][1,4]benzodiazepine

Caution: exact ingredients may vary. Different products will have different compositions. The label may not accurately reflect the contents.

Caution: the purity of the ingredients in recreational drugs may vary greatly.

Toxicity

At the time of writing, there was limited information on the toxicity of this drug. It is anticipated that it will be like other benzodiazepines in its toxicity.
Benzodiazepines cause CNS depression through their agonist action at the (GABAA) receptor. Features of severe toxicity include coma, hypotension, bradycardia, respiratory depression, rhabdomyolysis and hypothermia. Effects are likely to be more severe when co-ingested with alcohol and other CNS depressants.

Flubromazolam is reported to be highly potent, causing strong sedation and amnesia following oral doses as low as 0.5 mg (Moosmann et al, 2015).
A 27-year-old male who reportedly ingested 3 mg of flubromazolam developed severe, prolonged depression of the central nervous system with cardio-respiratory failure (Lukasik-Glębocka et al, 2016).

Features
Benzodiazepines commonly cause drowsiness, ataxia, dysarthria and nystagmus. Coma, hypotension, bradycardia and respiratory depression occasionally occur but are seldom serious if these drugs are taken alone. Coma usually lasts only a few hours but may be prolonged in elderly patients.
Benzodiazepine respiratory depressant effects are more serious in patients with chronic obstructive airways disease. Severe effects in overdose also include rhabdomyolysis and hypothermia.
ECG abnormalities include transient first degree and second degree block and QT prolongation. Abnormal LFTs may also occur.
Microembolisation can result from intravenous injection of crushed tablets. Accidental intra-arterial injection of benzodiazepines can cause severe limb ischaemia and gangrene necessitating limb amputation.
Co-ingestion of alcohol and other central nervous system depressants potentiates the effects of benzodiazepines and can increase toxicity.

Thank you for this!

 

[suicode2024]

Do you have any information about:
Vinylbital?

 

[suicode2024]

Mustn't be any info on vinylbital I guess?

 

[Relic]

Mustn't be any info on vinylbital I guess?

Interesting, if there's not. Because it is in this list:

List of most commonly encountered drugs currently controlled under the misuse of drugs legislation

www.gov.uk

 

[sserafim]

Do you have any information about Ritalin (methylphenidate) or Adderall (amphetamine)? These are my ADHD meds lol. My sister takes Vyvanse (lisdexamfetamine) for it. Could you get the info about it as well? I'm curious…

 

[leavingthesoultrap]

Pregabalin pls?

 

[Relic]

Do you have any information about Ritalin (methylphenidate) or Adderall (amphetamine)? These are my ADHD meds lol. My sister takes Vyvanse (lisdexamfetamine) for it. Could you get the info about it as well? I'm curious…

While you wait:

 

[suicode2024]

Coco03 hasn't been here since I posted about vinylbital, so I presume we won't see them until maybe during the week. Surely they would have access to the information about this particular drug. It's a barbiturate, so maybe they didn't bother answering as everyone knows how barbiturates kill...but seriously, it would be interesting because this is a rare barbiturate to my knowledge, and I often wonder if it is slightly different to other barbs.

 

[CocoToxBase]

Do you have any information about:
Vinylbital?

That's the first drug that's not on TOXBASE I wonder what the doctors would do they'd have no clue

Pregabalin pls?

Type of Product
GABA analogue for the treatment of central and peripheral neuropathic pain in adults and as an adjunct in adults with focal seizures with or without secondary generalisation. Also used in the treatment of generalised anxiety disorder (GAD).
Pregabalin may be used as a drug of abuse, usually together with opiates, to potentiate their effects on the user.

Ingredients
Pregabalin
Capsules - 25 mg, 50 mg, 75 mg, 100 mg, 150 mg, 200 mg, 225 mg, 300 mg
Oral solution - 20 mg/mL (473 mL bottle)

Toxicity
Pregabalin binds to an auxiliary subunit (a2d) of voltage-gated calcium channels in the central nervous system.
Clinical features in toxicity may include CNS depression and myoclonus.
A case series of 23 patients presenting following pregabalin overdose reported CNS effects in 8 patients (headache, altered mental status, confusion, agitation, delirium, lethargy, or coma); cardiac effects in 5 patients (tachycardia, bradycardia); neuromuscular effects in 4 patients (tremors, fasciculations, ataxia, asterixis, dystonia, myoclonus) and GI symptoms in 3 patients (Wills et al, 2014).
Click here for further cases.
Peak plasma concentration occurs within 1 hour of ingestion following single or multiple doses. The mean elimination half-life is 6.3 hours but may be prolonged in renal failure (Lyrica SPC, 2019).

Features
The most significant effect in overdose is CNS depression, which may occasionally be profound. Ataxia, nystagmus, agitation, slurred speech and myoclonus are reported. Very rarely convulsions may occur.
GI upset, hypotension, tachycardia, syncope, ECG abnormalities such as AV block and cardiac failure may also occur.
Rhabdomyolysis and acute kidney injury have been reported.
When co-ingested with alcohol, opiates and other central nervous system depressants, the effects of gabapentinoids are potentially more severe.
Hypersensitivity reactions have been reported shortly after starting pregabalin therapy.

Do you have any information about Ritalin (methylphenidate) or Adderall (amphetamine)? These are my ADHD meds lol. My sister takes Vyvanse (lisdexamfetamine) for it. Could you get the info about it as well? I'm curious…

Ritalin

Type of Product
Central nervous system stimulant and indirect-acting sympathomimetic used in the treatment of attention-deficit hyperactivity disorder and narcolepsy (unlicensed indication).

Ingredients
Methylphenidate hydrochloride
Tablets - 10 mg

Toxicity
Toxicity is due to enhanced dopamine and norepinephrine neurotransmission due to pre-synaptic reuptake inhibition (Hannestad et al, 2010). Methylphenidate is a more potent inhibitor of dopamine and noradrenaline reuptake than serotonin reuptake (Luethi et al, 2017).
A 28-year-old woman died after injection of 40 mg methylphenidate (Levine, 1986). Methylphenidate tablets may be crushed up and snorted; death has occurred following this method of abuse (Massello & Carpenter, 1999).
Survival has been reported after ingestion of 1134 mg by a 14-year-old female; the patient suffered tachycardia, hypertension, agitation and hallucinations (Klampfl et al, 2010).
An 8-year-old male accidentally ingested 36 mg modified-release methylphenidate instead of his therapeutic lisdexamfetamine and developed psychosis causing secondary polydipsia and hyponatremia (due to excess water intake) (Patel et al, 2017).
Injection of crushed tablets can cause thrombosis, ischaemia and necrosis resulting in limb amputation (Bruggisser et al, 2011).
A study using poisons centre data found that symptoms, most commonly tachycardia, agitation, lethargy, insomnia and rash, occurred in 23% of patients accidentally ingesting immediate-release methylphenidate, of whom 96% were children (White & Yadao, 2000). Another study reported that children who had ingested less than 1 mg/kg did not suffer adverse events, although 10/35 (29%) developed symptoms (drowsiness and hyperactivity) (Foley et al, 2000).
Peak plasma concentrations occur about 2 hours after ingestion of standard-release preparations (Medikinet SPC, 2017). With modified-release preparations, there is a rapid increase in concentration for 1-2 hours, followed by a slow increase to peak plasma concentrations at 6-8 hours after ingestion (Concerta XL SPC, 2018). The plasma elimination half-lives of standard-release and modified-release preparations are 1-2 hours and 3.5 hours respectively (Concerta XL SPC, 2018).

If taken with other serotonergic agents there is a greater risk of serotonin toxicity (serotonin syndrome).

Features
Clinical features vary according to the individual substance and reflect variation in the amount and type of monoamines released; some are more dopaminergic, others more serotoninergic. Amfetamines and cathinones generally cause psychostimulation with euphoria, increased alertness, intensified emotions and enhanced self-esteem.
Other effects include tremor, sweating, dilated pupils, agitation, confusion, headache, anxiety, vomiting, abdominal pain, convulsions, anxiety, hallucinations or delusions. Chest pain, palpitations, dyspnoea, systemic hypotension or hypertension may occur. Hypoglycaemia, metabolic acidosis and rarely ischaemic colitis has been reported.
Severe features may include hyperthermia, stroke, myocardial infarction, marked hyponatraemia, rhabdomyolysis, DIC, pulmonary oedema, hepatic and renal failure. Narrow-complex tachycardias are common. Ventricular tachycardia or ventricular fibrillation may also occur. Intravenous amphetamine abuse may be complicated by acute cardiomyopathy.
Poor prognostic signs include persistent convulsions, hyperthermia above 39°C, coma, or focal neurological signs.
Serotonin Toxicity
Serotonin toxicity may occur, especially in those exposed to multiple drugs affecting the serotonin system. Features include CNS effects (including agitation or coma), autonomic instability (including hyperpyrexia), and neuromuscular excitability (including clonus and raised CK).
Death of patients with serotonin toxicity may be due to hyperpyrexia with associated multi organ failure.
For further information click here.

Adderall

HIGHLY TOXIC SUBSTANCE​

All patients who have been exposed to this product as a result of self-harm should be referred for assessment. All children should be referred for medical assessment. Symptomatic adults should be referred for medical assessment. Consider discussion with NPIS: In the UK NPIS 0344 892 0111 / in Ireland NPIC (01) 809 2566.​

Type of Product
For treatment of narcolepsy and ADHD. Available in the USA and Canada.

Ingredients
Amfetamine
Dexamfetamine
Sustained release (XR) capsules - 5 mg,10 mg, 15 mg, 20 mg, 25 mg, 30 mg
Tablets - 5 mg, 7.5 mg,10 mg, 12.5 mg, 15 mg, 20 mg, 30 mg

Toxicity
Many deaths and episodes of severe toxicity are reported following stimulant-type clinical presentations.

Toxicity is due to enhanced dopamine, norepinephrine and to a lesser extent serotonin (5-HT) neurotransmission primarily by increased pre-synaptic monoamine release and, to a lesser extent, pre-synaptic reuptake inhibition (Berridge & Stalnaker, 2002; Kuczenski et al, 1995; Rothman et al, 2001). This results in sympathomimetic toxicity, with the main toxic features being psychosis, severe agitation, hypertension, convulsions and cardiac tachyarrhythmias (including VT).

The acute lethal dose of amfetamine in adults has been reported to be 20-25 mg/kg (Zalis & Parmley, 1963) but individual response varies greatly due to tolerance, and toxicity correlates poorly with the amount taken.
Snorting, smoking or injecting amphetamine intravenously gives faster and more intense effects than ingestion.
The elimination half-life of amphetamine varies between 7-34 hours (Anggard et al, 1973), being faster in acidic urine (Huang et al, 2020; Beckett et al, 1969).

If taken with other serotonergic agents there is a greater risk of serotonin toxicity.

Features
Clinical features vary according to the individual substance and reflect variation in the amount and type of monoamines released; some are more dopaminergic, others more serotoninergic. Amfetamines and cathinones generally cause psychostimulation with euphoria, increased alertness, intensified emotions and enhanced self-esteem.
Other effects include tremor, sweating, dilated pupils, agitation, confusion, headache, anxiety, vomiting, abdominal pain, convulsions, anxiety, hallucinations or delusions. Chest pain, palpitations, dyspnoea, systemic hypotension or hypertension may occur. Hypoglycaemia, metabolic acidosis and rarely ischaemic colitis has been reported.
Severe features may include hyperthermia, stroke, myocardial infarction, marked hyponatraemia, rhabdomyolysis, DIC, pulmonary oedema, hepatic and renal failure. Narrow-complex tachycardias are common. Ventricular tachycardia or ventricular fibrillation may also occur. Intravenous amphetamine abuse may be complicated by acute cardiomyopathy.
Poor prognostic signs include persistent convulsions, hyperthermia above 39°C, coma, or focal neurological signs.
Serotonin Toxicity
Serotonin toxicity may occur, especially in those exposed to multiple drugs affecting the serotonin system. Features include CNS effects (including agitation or coma), autonomic instability (including hyperpyrexia), and neuromuscular excitability (including clonus and raised CK).
Death of patients with serotonin toxicity may be due to hyperpyrexia with associated multi organ failure.
For further information click here.

 

[Alexei_Kirillov]

Could you please check 1,1-Difluoroethane?

 

[sserafim]

Ritalin

Type of Product
Central nervous system stimulant and indirect-acting sympathomimetic used in the treatment of attention-deficit hyperactivity disorder and narcolepsy (unlicensed indication).

Ingredients
Methylphenidate hydrochloride
Tablets - 10 mg

Toxicity
Toxicity is due to enhanced dopamine and norepinephrine neurotransmission due to pre-synaptic reuptake inhibition (Hannestad et al, 2010). Methylphenidate is a more potent inhibitor of dopamine and noradrenaline reuptake than serotonin reuptake (Luethi et al, 2017).
A 28-year-old woman died after injection of 40 mg methylphenidate (Levine, 1986). Methylphenidate tablets may be crushed up and snorted; death has occurred following this method of abuse (Massello & Carpenter, 1999).
Survival has been reported after ingestion of 1134 mg by a 14-year-old female; the patient suffered tachycardia, hypertension, agitation and hallucinations (Klampfl et al, 2010).
An 8-year-old male accidentally ingested 36 mg modified-release methylphenidate instead of his therapeutic lisdexamfetamine and developed psychosis causing secondary polydipsia and hyponatremia (due to excess water intake) (Patel et al, 2017).
Injection of crushed tablets can cause thrombosis, ischaemia and necrosis resulting in limb amputation (Bruggisser et al, 2011).
A study using poisons centre data found that symptoms, most commonly tachycardia, agitation, lethargy, insomnia and rash, occurred in 23% of patients accidentally ingesting immediate-release methylphenidate, of whom 96% were children (White & Yadao, 2000). Another study reported that children who had ingested less than 1 mg/kg did not suffer adverse events, although 10/35 (29%) developed symptoms (drowsiness and hyperactivity) (Foley et al, 2000).
Peak plasma concentrations occur about 2 hours after ingestion of standard-release preparations (Medikinet SPC, 2017). With modified-release preparations, there is a rapid increase in concentration for 1-2 hours, followed by a slow increase to peak plasma concentrations at 6-8 hours after ingestion (Concerta XL SPC, 2018). The plasma elimination half-lives of standard-release and modified-release preparations are 1-2 hours and 3.5 hours respectively (Concerta XL SPC, 2018).

If taken with other serotonergic agents there is a greater risk of serotonin toxicity (serotonin syndrome).

Features
Clinical features vary according to the individual substance and reflect variation in the amount and type of monoamines released; some are more dopaminergic, others more serotoninergic. Amfetamines and cathinones generally cause psychostimulation with euphoria, increased alertness, intensified emotions and enhanced self-esteem.
Other effects include tremor, sweating, dilated pupils, agitation, confusion, headache, anxiety, vomiting, abdominal pain, convulsions, anxiety, hallucinations or delusions. Chest pain, palpitations, dyspnoea, systemic hypotension or hypertension may occur. Hypoglycaemia, metabolic acidosis and rarely ischaemic colitis has been reported.
Severe features may include hyperthermia, stroke, myocardial infarction, marked hyponatraemia, rhabdomyolysis, DIC, pulmonary oedema, hepatic and renal failure. Narrow-complex tachycardias are common. Ventricular tachycardia or ventricular fibrillation may also occur. Intravenous amphetamine abuse may be complicated by acute cardiomyopathy.
Poor prognostic signs include persistent convulsions, hyperthermia above 39°C, coma, or focal neurological signs.
Serotonin Toxicity
Serotonin toxicity may occur, especially in those exposed to multiple drugs affecting the serotonin system. Features include CNS effects (including agitation or coma), autonomic instability (including hyperpyrexia), and neuromuscular excitability (including clonus and raised CK).
Death of patients with serotonin toxicity may be due to hyperpyrexia with associated multi organ failure.
For further information click here.

Adderall

HIGHLY TOXIC SUBSTANCE​

All patients who have been exposed to this product as a result of self-harm should be referred for assessment. All children should be referred for medical assessment. Symptomatic adults should be referred for medical assessment. Consider discussion with NPIS: In the UK NPIS 0344 892 0111 / in Ireland NPIC (01) 809 2566.​

Type of Product
For treatment of narcolepsy and ADHD. Available in the USA and Canada.

Ingredients
Amfetamine
Dexamfetamine
Sustained release (XR) capsules - 5 mg,10 mg, 15 mg, 20 mg, 25 mg, 30 mg
Tablets - 5 mg, 7.5 mg,10 mg, 12.5 mg, 15 mg, 20 mg, 30 mg

Toxicity
Many deaths and episodes of severe toxicity are reported following stimulant-type clinical presentations.

Toxicity is due to enhanced dopamine, norepinephrine and to a lesser extent serotonin (5-HT) neurotransmission primarily by increased pre-synaptic monoamine release and, to a lesser extent, pre-synaptic reuptake inhibition (Berridge & Stalnaker, 2002; Kuczenski et al, 1995; Rothman et al, 2001). This results in sympathomimetic toxicity, with the main toxic features being psychosis, severe agitation, hypertension, convulsions and cardiac tachyarrhythmias (including VT).

The acute lethal dose of amfetamine in adults has been reported to be 20-25 mg/kg (Zalis & Parmley, 1963) but individual response varies greatly due to tolerance, and toxicity correlates poorly with the amount taken.
Snorting, smoking or injecting amphetamine intravenously gives faster and more intense effects than ingestion.
The elimination half-life of amphetamine varies between 7-34 hours (Anggard et al, 1973), being faster in acidic urine (Huang et al, 2020; Beckett et al, 1969).

If taken with other serotonergic agents there is a greater risk of serotonin toxicity.

Features
Clinical features vary according to the individual substance and reflect variation in the amount and type of monoamines released; some are more dopaminergic, others more serotoninergic. Amfetamines and cathinones generally cause psychostimulation with euphoria, increased alertness, intensified emotions and enhanced self-esteem.
Other effects include tremor, sweating, dilated pupils, agitation, confusion, headache, anxiety, vomiting, abdominal pain, convulsions, anxiety, hallucinations or delusions. Chest pain, palpitations, dyspnoea, systemic hypotension or hypertension may occur. Hypoglycaemia, metabolic acidosis and rarely ischaemic colitis has been reported.
Severe features may include hyperthermia, stroke, myocardial infarction, marked hyponatraemia, rhabdomyolysis, DIC, pulmonary oedema, hepatic and renal failure. Narrow-complex tachycardias are common. Ventricular tachycardia or ventricular fibrillation may also occur. Intravenous amphetamine abuse may be complicated by acute cardiomyopathy.
Poor prognostic signs include persistent convulsions, hyperthermia above 39°C, coma, or focal neurological signs.
Serotonin Toxicity
Serotonin toxicity may occur, especially in those exposed to multiple drugs affecting the serotonin system. Features include CNS effects (including agitation or coma), autonomic instability (including hyperpyrexia), and neuromuscular excitability (including clonus and raised CK).
Death of patients with serotonin toxicity may be due to hyperpyrexia with associated multi organ failure.
For further information click here.

Thanks, that was interesting. Could you please check lisdexamfetamine as well? Thanks

 

[CocoToxBase]

Thanks, that was interesting. Could you please check lisdexamfetamine as well? Thanks

Lisdexamfetamine
Type of Product
Prodrug of dexamphetamine used in the management of attention deficit hyperactivity disorder (ADHD).

Synonyms
L-lysine-dextroamphetamine; LDX

Ingredients
Lisdexamfetamine dimesylate
Capsules - 20 mg, 30 mg, 40 mg, 50 mg, 60 mg, 70 mg

Toxicity
Toxicity is due to enhanced dopamine, norepinephrine and to a lesser extent serotonin (5-HT) neurotransmission primarily by increased pre-synaptic monoamine release and, to a lesser extent, pre-synaptic reuptake inhibition (Berridge & Stalnaker, 2002; Kuczenski et al, 1995; Rothman et al, 2001). This results in sympathomimetic toxicity, with the main toxic features being psychosis, severe agitation, hypertension, convulsions and cardiac tachyarrhythmias (including VT).

Symptoms of serotonin syndrome have been reported in a 6-year-old patient who accidentally ingested an unknown amount of lisdexamfetamine (Akingbola & Singh, 2012).
A 10-month-old female developed tachycardia, hypertension, dyskinesia and altered mental status (responsive to pain not voice) after ingesting an unknown amount of lisdexamfetamine (Wood & Krasowski, 2016).
The acute lethal dose of amfetamine in adults has been reported to be 20-25 mg/kg (Zalis & Parmley, 1963) but individual response varies greatly due to tolerance, and toxicity correlates poorly with the amount taken. No specific information is available for lisdexamfetamine.
Snorting, smoking or injecting amfetamines intravenously gives faster and more intense effects than ingestion.
Lisdexamfetamine is metabolised to dexamfetamine. The mean time to peak plasma concentration of dexamfetamine is 3.8 hours after fasting, and 4.7 hours following ingestion of a high fat meal. The elimination half-life of dexamfetamine is approximately 11 hours (Elvanse SPC, 2017).
If taken with other serotonergic agents there is a greater risk of serotonin toxicity.

Features
Clinical features vary according to the individual substance and reflect variation in the amount and type of monoamines released; some are more dopaminergic, others more serotoninergic. Amfetamines and cathinones generally cause psychostimulation with euphoria, increased alertness, intensified emotions and enhanced self-esteem.
Other effects include tremor, sweating, dilated pupils, agitation, confusion, headache, anxiety, vomiting, abdominal pain, convulsions, anxiety, hallucinations or delusions. Chest pain, palpitations, dyspnoea, systemic hypotension or hypertension may occur. Hypoglycaemia, metabolic acidosis and rarely ischaemic colitis has been reported.
Severe features may include hyperthermia, stroke, myocardial infarction, marked hyponatraemia, rhabdomyolysis, DIC, pulmonary oedema, hepatic and renal failure. Narrow-complex tachycardias are common. Ventricular tachycardia or ventricular fibrillation may also occur. Intravenous amphetamine abuse may be complicated by acute cardiomyopathy.
Poor prognostic signs include persistent convulsions, hyperthermia above 39°C, coma, or focal neurological signs.
Serotonin Toxicity
Serotonin toxicity may occur, especially in those exposed to multiple drugs affecting the serotonin system. Features include CNS effects (including agitation or coma), autonomic instability (including hyperpyrexia), and neuromuscular excitability (including clonus and raised CK).
Death of patients with serotonin toxicity may be due to hyperpyrexia with associated multi organ failure.
For further information click here.

Could you please check 1,1-Difluoroethane?

1,1-Difluoroethane
Type of Product
Used as a refrigerant and propellant for aerosols.

Synonyms
Freon 152a, ethylidene difluoride, HFC-152a, R-152a
CAS 75-37-6

Toxicity
Toxicity is generally considered to be low but few data are available regarding acute exposure. Inhalation of high concentrations of related compounds can cause acute lung injury, reduced conscious level and cardiac sensitisation (causing arrhythmias e.g. VF).
Ingestion of toxic quantities from aerosols is highly unlikely unless it is first sprayed into another container.
Contact with flames or very hot surfaces can produce degradation products that may include phosgene, hydrogen bromide, hydrogen chloride, hydrogen fluoride, carbon monoxide and carbonyl fluoride. However, the concentrations produced are likely to be too low to cause clinical features.
Where stored under pressure cold burns may occur after dermal contact.

A 25-year-old woman with a history of halogenated hydrocarbon abuse presented to a healthcare facility after being found unresponsive surrounded by several cans of compressed air duster (containing 1,1-difluoroethane). Upon paramedic arrival, she was asymptomatic. She developed ventricular tachycardia followed by ventricular fibrillation from which she was successfully resuscitated while undergoing a left ventriculogram. She then developed stress-induced cardiomyopathy and delayed fatal dysrhythmia at 32 hours post-presentation (Yanta et al, 2015).
A 28-year-old-man who chronically inhaled a computer cleaner containing 1,1-difluoroethane developed skeletal fluorosis. He developed difficulty walking and an abnormal gait, left hip pain, loss of mobility in his right wrist and forearm, and progressive deformities including enlargement of the digits of both hands (Tucci et al, 2017).

Features
Inhalation
Dyspnoea with airway irritation, bronchial constriction, cough, chest tightness and chronic reactive airways disease have been reported after inhalation. Pulmonary oedema has been observed after inhalation of a mixture of hydrofluorocarbons.
Headache, dizziness, lethargy, hypoxia, coma, hypertension or hypotension, tachycardia, oliguria, pulmonary oedema, liver injury and increased CK have also been reported.
Halogenated hydrocarbons have been reported to cause sudden death due to cardiac arrhythmias (in particular ventricular fibrillation), which may be due to sensitisation of the myocardium to the effects of endogenous catecholamines. However, there are several other potential explanations including a direct effect on the cardiac conduction system.
Exposure to a compressed propellant may result in cold burns.
Ingestion
Cold injury of the mouth and upper GI tract due to the freezing effect is likely. Gastric perforation and acute liver injury has been reported.
Skin
Cold burns may occur. Haemorrhagic bullae, swelling, pain, necrosis and third-degree burns have been described after dermal exposure.
Eye
It is possible that irritation or cold damage could result from topical exposure.
Corneal oedema has been reported when perfluorodecalin was left in the eye after retinal detachment.

 

[sserafim]

Lisdexamfetamine
Type of Product
Prodrug of dexamphetamine used in the management of attention deficit hyperactivity disorder (ADHD).

Synonyms
L-lysine-dextroamphetamine; LDX

Ingredients
Lisdexamfetamine dimesylate
Capsules - 20 mg, 30 mg, 40 mg, 50 mg, 60 mg, 70 mg

Toxicity
Toxicity is due to enhanced dopamine, norepinephrine and to a lesser extent serotonin (5-HT) neurotransmission primarily by increased pre-synaptic monoamine release and, to a lesser extent, pre-synaptic reuptake inhibition (Berridge & Stalnaker, 2002; Kuczenski et al, 1995; Rothman et al, 2001). This results in sympathomimetic toxicity, with the main toxic features being psychosis, severe agitation, hypertension, convulsions and cardiac tachyarrhythmias (including VT).

Symptoms of serotonin syndrome have been reported in a 6-year-old patient who accidentally ingested an unknown amount of lisdexamfetamine (Akingbola & Singh, 2012).
A 10-month-old female developed tachycardia, hypertension, dyskinesia and altered mental status (responsive to pain not voice) after ingesting an unknown amount of lisdexamfetamine (Wood & Krasowski, 2016).
The acute lethal dose of amfetamine in adults has been reported to be 20-25 mg/kg (Zalis & Parmley, 1963) but individual response varies greatly due to tolerance, and toxicity correlates poorly with the amount taken. No specific information is available for lisdexamfetamine.
Snorting, smoking or injecting amfetamines intravenously gives faster and more intense effects than ingestion.
Lisdexamfetamine is metabolised to dexamfetamine. The mean time to peak plasma concentration of dexamfetamine is 3.8 hours after fasting, and 4.7 hours following ingestion of a high fat meal. The elimination half-life of dexamfetamine is approximately 11 hours (Elvanse SPC, 2017).
If taken with other serotonergic agents there is a greater risk of serotonin toxicity.

Features
Clinical features vary according to the individual substance and reflect variation in the amount and type of monoamines released; some are more dopaminergic, others more serotoninergic. Amfetamines and cathinones generally cause psychostimulation with euphoria, increased alertness, intensified emotions and enhanced self-esteem.
Other effects include tremor, sweating, dilated pupils, agitation, confusion, headache, anxiety, vomiting, abdominal pain, convulsions, anxiety, hallucinations or delusions. Chest pain, palpitations, dyspnoea, systemic hypotension or hypertension may occur. Hypoglycaemia, metabolic acidosis and rarely ischaemic colitis has been reported.
Severe features may include hyperthermia, stroke, myocardial infarction, marked hyponatraemia, rhabdomyolysis, DIC, pulmonary oedema, hepatic and renal failure. Narrow-complex tachycardias are common. Ventricular tachycardia or ventricular fibrillation may also occur. Intravenous amphetamine abuse may be complicated by acute cardiomyopathy.
Poor prognostic signs include persistent convulsions, hyperthermia above 39°C, coma, or focal neurological signs.
Serotonin Toxicity
Serotonin toxicity may occur, especially in those exposed to multiple drugs affecting the serotonin system. Features include CNS effects (including agitation or coma), autonomic instability (including hyperpyrexia), and neuromuscular excitability (including clonus and raised CK).
Death of patients with serotonin toxicity may be due to hyperpyrexia with associated multi organ failure.
For further information click here.

1,1-Difluoroethane
Type of Product
Used as a refrigerant and propellant for aerosols.

Synonyms
Freon 152a, ethylidene difluoride, HFC-152a, R-152a
CAS 75-37-6

Toxicity
Toxicity is generally considered to be low but few data are available regarding acute exposure. Inhalation of high concentrations of related compounds can cause acute lung injury, reduced conscious level and cardiac sensitisation (causing arrhythmias e.g. VF).
Ingestion of toxic quantities from aerosols is highly unlikely unless it is first sprayed into another container.
Contact with flames or very hot surfaces can produce degradation products that may include phosgene, hydrogen bromide, hydrogen chloride, hydrogen fluoride, carbon monoxide and carbonyl fluoride. However, the concentrations produced are likely to be too low to cause clinical features.
Where stored under pressure cold burns may occur after dermal contact.

A 25-year-old woman with a history of halogenated hydrocarbon abuse presented to a healthcare facility after being found unresponsive surrounded by several cans of compressed air duster (containing 1,1-difluoroethane). Upon paramedic arrival, she was asymptomatic. She developed ventricular tachycardia followed by ventricular fibrillation from which she was successfully resuscitated while undergoing a left ventriculogram. She then developed stress-induced cardiomyopathy and delayed fatal dysrhythmia at 32 hours post-presentation (Yanta et al, 2015).
A 28-year-old-man who chronically inhaled a computer cleaner containing 1,1-difluoroethane developed skeletal fluorosis. He developed difficulty walking and an abnormal gait, left hip pain, loss of mobility in his right wrist and forearm, and progressive deformities including enlargement of the digits of both hands (Tucci et al, 2017).

Features
Inhalation
Dyspnoea with airway irritation, bronchial constriction, cough, chest tightness and chronic reactive airways disease have been reported after inhalation. Pulmonary oedema has been observed after inhalation of a mixture of hydrofluorocarbons.
Headache, dizziness, lethargy, hypoxia, coma, hypertension or hypotension, tachycardia, oliguria, pulmonary oedema, liver injury and increased CK have also been reported.
Halogenated hydrocarbons have been reported to cause sudden death due to cardiac arrhythmias (in particular ventricular fibrillation), which may be due to sensitisation of the myocardium to the effects of endogenous catecholamines. However, there are several other potential explanations including a direct effect on the cardiac conduction system.
Exposure to a compressed propellant may result in cold burns.
Ingestion
Cold injury of the mouth and upper GI tract due to the freezing effect is likely. Gastric perforation and acute liver injury has been reported.
Skin
Cold burns may occur. Haemorrhagic bullae, swelling, pain, necrosis and third-degree burns have been described after dermal exposure.
Eye
It is possible that irritation or cold damage could result from topical exposure.
Corneal oedema has been reported when perfluorodecalin was left in the eye after retinal detachment.

Can Ritalin, Adderall, or Vyvanse itself (maybe even combined with caffeine) give you serotonin syndrome?

 

[sauan]

Hello.
Do you have any info about 1,4-Butanediol ?

 

[deadinsidex2]

Heey Oh yess please,4 butanediol that would be really great very much appreciated. @sauan @Coco03

 

[CocoToxBase]

You need to change your username (when you can @Coco03 ) to- CocoToXBaSE03

I actually will ahahah

Hello.
Do you have any info about 1,4-Butanediol ?

Heey Oh yess please,4 butanediol that would be really great very much appreciated.

HIGHLY TOXIC SUBSTANCE​

All those who have been exposed as a result of self-harm should be referred for assessment. All children and symptomatic adults should be referred for medical assessment. Consider discussion with NPIS: In the UK NPIS 0344 892 0111 / in Ireland NPIC (01) 809 2566.​ If there are concerns about unknown drugs of abuse click here for further advice.​

Type of Product
GHB and its analogues (GBL, 1,4-BD, GVL and GHV) are sedative drugs of abuse, which are also used as body-building agents.
Sodium oxybate is a liquid preparation of the GHB sodium salt, used in the treatment of narcolepsy. It is available as a 500 mg/mL oral solution, under the brand name Xyrem.
GBL and 1,4-BD are metabolised to GHB. They are organic industrial solvents found in products such as acetone-free nail polish removers, paint strippers, cleaning products, and glue debonders.
Gamma-hydroxyvaleric (GHV) is a 4-methyl-substituted analogue of GHB, reported to be a direct GABA receptor agonist. Gamma-valerolactone (GVL) is a precursor of GHV.

Synonyms
Click here for a list of synonyms

Ingredients
GHB sodium salt is a white solid. It dissolves in water to form a clear, colourless and often tasteless liquid. It is presented as either a liquid or a powder (loose, or as tablets/capsules).
GBL and 1,4-BD are colourless liquids. They can be obtained from commercially available solvents.

Caution: the purity of the ingredients in recreational drugs may vary greatly.

Toxicity
GHB occurs endogenously in the brain at low concentrations. It is an agonist at GABA-B and GHB receptors (Busardò & Jones, 2015).
GBL and 1,4-BD are precursors for GHB. The latter may cause delayed toxicity when co-ingested with alcohol due to enzyme inhibition and delayed conversion of 1,4-BD to GHB (Schneidereit, 2000). High anion gap metabolic acidosis with raised anion gap has been reported following overdose of 1,4-butanediol (Stefani & Roberts, 2020).
GHB is rapidly absorbed from the gut with peak effects occurring 30-60 minutes post-ingestion. GHB is metabolised to carbon dioxide and water. The elimination half-life is between 20-60 minutes and prolonged in patients with hepatic impairment (Schep et al, 2012).
Severe clinical features may occur due to:
• Acute toxicity
• Severe withdrawal reactions after dose-reduction or abstinence following prolonged use
Click here for information on cases.
Features of acute toxicity include CNS and respiratory depression, hypersalivation, bradycardia and hypotension. Clinical effects are potentiated by ethanol, benzodiazepines, antipsychotics and other CNS depressants, including some co-ingested recreational drugs.

Click here for further details on clinical features and management of toxicity due to GHB and analogues.
Features of withdrawal include severe agitation, hallucinations, insomnia, tachycardia and hypertension.

 

[Sinikrath]

Sodium azide?

 

[CocoToxBase]

Sodium azide?

HIGHLY TOXIC SUBSTANCE​

All patients exposed to this chemical should be referred to an Emergency Department. Treating clinicians should discuss all cases with their local poisons information service: in the UK NPIS 0344 892 0111, in Ireland NPIC (01) 809 2566.​ If this exposure has occurred at work or in a public space, consider the implications for others exposed. Primary responders and secondary carers must consider wearing personal protective equipment (PPE). Click here for more information.​

Type of Product
A colourless, odourless, and water-soluble solid or powder used in automobile air bags, and as a chemical reagent in organic synthesis, preservatives and biocides. Forms hydrazoic acid explosively after contact with water.

Synonyms
Hydrazoic acid sodium salt, smite
CAS 26628-22-8
UN 1687
EC 247-852-1

Ingredients
Sodium azide
Solutions for laboratory reagents include:
0.1-10% w/v in water

Toxicity
The mechanism of sodium azide toxicity is not fully understood. While causing cytochrome C oxidase inhibition and cell death similar to cyanide, the main mechanism of lethality is proposed to be convulsions and severe vasodilation (Smith et al, 1991), possibly due to conversion of the azide to nitric oxide (Swafford et al, 2004; Schwarz et al, 2014).
Highly toxic. Ingestion is the most likely route of exposure to sodium azide salt.
When combined with aqueous acidic solutions, sodium azide forms highly soluble, more explosive hydrazoic acid. The gaseous phase has a pungent odour and high acute toxicity. Formation of hydrazoic acid may cause combined traumatic and toxicological injury. Heated dissolutions of sodium azide in water may culminate in a vigorous or explosive reaction.
Inhalation and dermal exposure to hydrazoic acid vapour or gas after mixing sodium azide with acidic or heated solutions is also possible. The onset of effects tends to be rapid with recovery occurring within a few hours in mild to moderate exposures.
Survival has occurred in patients ingesting up to 150 mg (Chang & Lamm, 2003). Deaths have occurred following ingestions of 700 mg to 55 g, and following skin exposure (Chang & Lamm, 2003). Accidental and intentional fatalities from sodium azide exposure are usually seen within laboratory environments, or in those who have access to buffer solutions of sodium azide.
In reports of fatal azide ingestions, death occurred within 2-84 hours after consumption of more than 700 mg of sodium azide salt (Howard et al, 1990; Chang & Lamm, 2003). Deaths were caused by rapidly progressive hypotension often refractory to fluids and/or inotropes, profound metabolic acidosis and non-cardiac pulmonary oedema (Judge & Ward,1989).
Information on incidents/cases involving deliberate/accidental release
Toxicokinetics
Sodium azide is rapidly absorbed from the GI tract, skin, respiratory tract and injection sites and rapidly distributed across the body where it is metabolised in liver and CNS. It is also converted to cyanides and nitrogen oxide in erythrocytes (Rojek, 2015). It is renally excreted with a half-life of 2.5 hours (Senda, 2001).
Workplace exposure limits
Long-term UK workplace exposure limit (8 hours) for skin exposure: 0.1 mg/m3
Short-term UK workplace exposure limit (15 mins) for skin exposure: 0.3 mg/m3
Sodium azide - features and managementUpdated 10/2019

Alert for hospital doctors​

This agent is potentially very toxic and clinicians managing patients are encouraged to discuss allcases with your poisons information service: in the UK NPIS 0344 892 0111, in Ireland NPIC (01) 809 2566. Click here for details you may be required to give when telephoning NPIS.​

Features
Ingestion/Systemic Toxicity
The key feature of sodium azide poisoning is severe hypotension.
Ingestion causes headache, GI upset, pallor, blurred vision, dilated pupils, restlessness, syncope, muscle weakness, dyspnoea, sweating, palpitations, tachycardia, hypothermia, hyporeflexia or areflexia, and hypotension (occasionally preceded by hypertension).
In severe cases there may be profound hypotension which may develop late, bradycardia, ventricular tachycardia and fibrillation, coma, convulsions and respiratory failure. Acute lung injury and cerebral oedema may occur. Cardiomyopathy has been reported.
Metabolic acidosis with wide anion gap (due to lactate accumulation), hyperglycaemia and leucocytosis may occur.
Inhalation
Inhalation causes headache, dizziness, nausea, coughing, nasal irritation and bronchospasm. Palpitations and dyspnoea have also been reported. Systemic features may occur.
Dermal Exposure
Skin contact typically causes local irritation. Severe exposure can cause dermal burns and systemic features including hypotension, metabolic acidosis and bradycardia.
Eye Exposure
Eye contact results in irritation and conjunctivitis.
Chronic Exposure
Chronic exposure may cause nausea, vomiting, headache, hypotension and palpitations.

 

[h.s.p.]

Could you please look up for Metopimazine? Brand name is Vogalib. Thank you

 

[CocoToxBase]

Could you please look up for Metopimazine? Brand name is Vogalib. Thank you

Not on TOXBASE surprisingly sorry

 

[losi]

chloroquine please.

 

[CocoToxBase]

chloroquine please.

Type of Product
Antimalarial.

Ingredients
Chloroquine sulphate
Syrup - 68 mg/5 mL (equivalent to 50 mg/5 mL base)

Chloroquine phosphate
Tablets - 250 mg (equivalent to 155 mg base)
Syrup - 80 mg/5 mL (equivalent to 50 mg/5 mL base)

Toxicity
Highly toxic in overdose.

Toxicity is mediated via sodium channel blockade in the CNS and cardiovascular system. The degree of toxicity is related to the ingested dose and to the degree of hypokalaemia on presentation to hospital (Clemessy et al, 1995; Angel et al, 1995).
A single dose of chloroquine of 20 mg/kg is considered toxic and doses of 30 mg/kg have resulted in fatalities (Taylor et al, 2004; McKenzie, 1996).
A 12-month-old child died following ingestion of one (300 mg) tablet (Kelly et al, 1990). Ventricular fibrillation occurred in a 13-year-old male patient 45 minutes after ingesting 750 mg of chloroquine base (Collee et al, 1992).
Psychosis has been described in a 7-year-old female after ingestion of approximately 100 mg/kg over a period of 12 hours (Zaki et al, 2009).
In adults, an ingested dose of 5 g or more is often associated with a fatal outcome (Riou et al, 1988; Jaeger, 2012) but recovery with supportive care has been reported following ingestions of 10g and 11.2g respectively (Messant et al, 2004; Payen et al, 2008).
A 25-year-old male patient developed methaemoglobinamia (54%) requiring treatment with methylene blue following ingestion of 600 mg of chloroquine base (Rizvi et al, 2012).
Peak plasma levels are expected between 1 and 3 hours in therapeutic use but may occur as long as 6 hours post ingestion (Avloclor SPC 2014, MHRA SPC 2014). A mean half-life of approximately 24 hours was reported in one case series (Jaeger et al, 1987), whilst another report described a terminal half-life of 60 days (Frisk-Holmberg et al, 1983).

Chloroquine - features and managementUpdated* 6/2020

Features
Absorption from the gastrointestinal tract is rapid and symptoms usually develop within 1-3 hours.
Severe toxicity is associated with cardiotoxicity and hypokalaemia.
Cardiac features which may present early include hypotension, prolongation of the QRS and QT intervals, ventricular tachycardia, pulmonary oedema and cardiovasular collapse
Hypokalaemia is due to altered intracellular distribution of potassium rather than true potassium depletion and therefore caution is required when correcting hypokalaemia.
Other clinical features include GI upset, metabolic acidosis, methaemoglobinaemia, headache, dizziness, drowsiness, diplopia, tinnitus and paraesthesia. Rarely hepatotoxicity, nephritis, gastric haemorrhage, haematological abnormalities, and psychiatric features may occur.

 

[CocoToxBase]

HIGHLY TOXIC SUBSTANCE​

All patients who have been exposed (including skin or eye exposure) to any volume of a highly potent veterinary sedative should be urgently assessed. These are concentrated solutions that can produce rapid CNS depression and cardiovascular collapse. The patient should not attempt to drive. Consider discussion with NPIS: In the UK NPIS 0344 892 0111 / in Ireland NPIC (01) 809 2566.​

Type of Product
Short acting barbiturate, not licensed for human use in the UK, used in veterinary medicine for euthanasia. Used in some countries as a sedative and in the short-term management of insomnia.

Synonyms
Mebubarbital, mebumal, pentobarbitone
CAS 57-33-0

Ingredients
Pentobarbital sodium B.P.
Veterinary solution 20% (200 mg/mL), 30% (300 mg/ml), 40% (200 mg/mL), 50% (500 mg/mL)
(Also available outwith the UK & Ireland as oral (tablet & capsule), IM & IV preparations for human use).

Toxicity
The main toxic features are coma and respiratory depression.

In a study of 61 fatal cases, the lethal dose of pentobarbital when ingested ranged between 2 g and 10 g. In combination with alcohol lower doses have been reported as fatal (Cravey et al, 1977).
A 45-year-old male ingested 20 g of pentobarbital powder and became unresponsive with PEA arrest occurring within 20 minutes. He responded to CPR and was admitted to ICU with GCS 3/15, fixed dilated pupils and absent brainstem reflexes. He remained comatose with absent brainstem reflexes and vasopressor requirement for 5 days. On day 5 there was return of gag reflex and he responded to painful stimuli. Serial serum pentobarbital concentrations showed a peak of 116 mg/mL at 29 hrs post-ingestion. He made a complete neurological recovery and was discharged 22 days post-overdose (Druda et al, 2019 ).
A young man reportedly ingested 13 g of pentobarbital and became unconscious. He required ventilation for respiratory arrest. He was initially also hypothermic and hypotensive, and treated with rewarming and inotropes. He was weaned off inotropes on day 3, and recovered consciousness on day 6, although he needed ventilation until day 13. He subsequently recovered without neurological sequelae (Singh, 2014).

A 17-year-old boy died following intravenous injection of pentobarbital. The serum pentobarbital concentration 4 hours post-injection was 30.7 mg/L (Cordell et al, 1986).

Pentobarbital is well absorbed after oral or rectal administration. The elimination half-life ranges between 15-50 hours and is dose–dependent (Martindale, 2009).

Barbiturates - features and managementUpdated 3/2022

Features
Oral or parenteral administration can produce rapid CNS depression and cardiovascular collapse.
CNS features include drowsiness, dysarthria, ataxia, nystagmus and disinhibition.
Additional CNS features may include coma, hypotonia, hyporeflexia, hypothermia, and respiratory depression. The duration of coma may be prolonged due to its slow elimination. Non-convulsive status epilepticus has been reported.
Cardiac features include hypotension, cardiovascular collapse and cardiac arrest.
Acute kidney injury may occur secondary to hypotension or rhabdomyolysis, particularly after a long lie. Blisters (erythematous or haemorrhagic) may occur, particularly at pressure points.
Paradoxical excitement and irritability can occur, particularly in elderly patients, children and patients in acute pain. Agitation may occur during recovery.
The effects in overdose will be potentiated by simultaneous ingestion of alcohol and other psychotropic drugs.
Barbiturates decrease gut motility, which may lead to a slow onset and worsening of symptoms, or cyclical improvement and worsening of symptoms.
Eye Contact - Veterinary solutions are alkaline in nature and corneal damage may occur. Click here for eye contact.

 

[CocoToxBase]

Bump

 

[rotciv]

Fentanyl was already mencioned?

 

[CocoToxBase]

Fentanyl was already mencioned?

HIGHLY TOXIC SUBSTANCE​

All patients exposed to this chemical should be referred to an Emergency Department. Treating clinicians should discuss all cases with their local poisons information service: in the UK NPIS 0344 892 0111, in Ireland NPIC (01) 809 2566.​ If this exposure has occurred at work or in a public space, consider the implications for others exposed. Primary responders and secondary carers must consider wearing personal protective equipment (PPE). Click here for more information.​

Type of Product
Highly potent opioid receptor agonists that can be disseminated to rapidly and simultaneously incapacitate multiple casualties.

Ingredients
Possible agents include:
Alfentanil
Carfentanyl
Etorphine
Fentanyl
Remifentanil
Sufentanil

Toxicity
Highly toxic; several people could be simultaneously exposed through inhalation if aerosol is released in a public space. Severe toxicity may also occur from exposure through injection, ingestion or skin contact. Unconsciousness may occur within minutes and could lead to death from respiratory depression.
The most serious toxic features are respiratory depression, hypercapnoea, reduced consciousness/coma and airway obstruction, mediated by mu and kappa opioid receptor agonism.
One instance of deliberate release occurred when a fentanyl-type drug (possibly in combination with an anaesthetic gas) was used to incapacitate Chechen rebels during the Moscow theatre siege in October 2002. The use of this aerosolised opioid was associated with the death of 127 (16%) of the 800 hostages in the theatre. 650 survivors required hospitalisation. Patients are reported to have had pinpoint pupils, unconsciousness, and depressed breathing, and are reported to have responded to naloxone (Wax et al, 2003). Subsequent studies have indicated that carfentanil and remifentanil were components of the aerosol used in this incident (Riches et al, 2012).

Opioids with potential for human incapacitation - features and managementUpdated 2/2023

Alert for hospital doctors​

This agent is potentially very toxic and clinicians managing patients are encouraged to discuss allcases with your poisons information service: in the UK NPIS 0344 892 0111, in Ireland NPIC (01) 809 2566. Click here for details you may be required to give when telephoning NPIS.​

Features
Severe opioid toxicity produces depression of the respiratory and central nervous systems and pin-point pupils. If untreated the depression of the level of consciousness can lead to deep coma, convulsions and respiratory arrest.
The effects will be potentiated by simultaneous ingestion of alcohol and other centrally acting drugs.
Milder opioid toxicity may produce nausea, vomiting, nightmares, anxiety, agitation, euphoria, dysphoria, depression, paranoia and hallucinations. While pin-point pupils are often present, this is not a reliable clinical sign and their absence does not exclude opioid toxicity. Sedation may be associated with hypotension, bradycardia and hypothermia.
The risk of toxicity may be significantly increased if kidney function is impaired due to reduced elimination of the parent opioid or active metabolite.
Opioids can cause histamine release, most commonly causing urticaria and pruritis.
Some opioids may cause cardiotoxicity.

 

[rotciv]

Thanks.

Thiopental/pentothal?

 

[Dayrain]

Thanks.

Thiopental/pentothal?