Resource TOXBASE access

[uncat_]

hey! could you look up trazodone OD doses? it's pretty much my only option for CBT right now, i'd probably mix with alcohol.

 

[sserafim]

Could you do Dexedrine (dextroamphetamine), Desoxyn (meth) and cocaine (if it's included)? I just want to know lol

 

[WoNkEy_DoNkEy]

@uncat_
@sserafim

She's in hospital at the moment and probably won't be out for a week. When she hopefully pulls through I'm sure she'll check this thread again.

 

[alltoomuch2]

Hey all,

I still have access to the TOXBASE app (only medical professionals can access this app) if anyone wants any information from a particular drug I will reply with the TOXBASE answer! I know researching different types of drugs is a pain in the arse but TOXBASE has all the correct symptoms and ingestion dosages + outcomes of real case study's.

Could I have info on pentobarbitone injectable liquid please? The one vets use for euthanasing animals

 

[uncat_]

@uncat_
@sserafim

She's in hospital at the moment and probably won't be out for a week. When she hopefully pulls through I'm sure she'll check this thread again.

oh wow, i hope shes doing okay /:

 

[CocoToxBase]

Thanks.

Thiopental/pentothal?

Type of Product

Short-acting substituted barbiturate. Used as a general anaesthetic, to reduce intracranial pressure and in the treatment of status epilepticus.

Synonyms

Thiopentone sodium

Ingredients

Thiopental sodium
Injection 500 mg vial
Powder for solution for injection 500 mg vial

Toxicity

The main toxic features are coma and respiratory depression.

A neonate born at 33 weeks was given 3 mg/kg of thiopental, a 10-fold overdose. The patient developed temporary hypotension and oxygen desaturation, remaining unconscious for longer than expected with a suppressed electroencephalography for 48 hours. The patient made a full recovery with normal psychomotor development at 2 years (Norman et al, 2009).
Solutions of thiopental sodium injection are strongly alkaline (pH of 10-11) and may cause corneal injury.
Accidental intra-arterial injection of thiopentone can cause intense pain around the injection site and arterial spasm.
Following intravenous administration, unconsciousness occurs within 30 seconds and will be continued for 20 to 30 minutes after a single dose. Rapid uptake occurs to most vascular areas of the brain followed by redistribution into other tissues (Thiopentone injection SPC, 2019).
Thiopental is highly plasma protein bound and is more lipid soluble than other barbiturates. After being slowly released from lipid stores, it undergoes hepatic metabolism to form inactive metabolites. The terminal elimination half-life is 10-12 hours in adults and about 6 hours in children but may be prolonged up to 26-28 hours in obese patients and pregnant patients (Martindale, 2011).
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.

hey! could you look up trazodone OD doses? it's pretty much my only option for CBT right now, i'd probably mix with alcohol.

Type of Product

Antidepressant acting as a serotonin modulator.

Ingredients

Trazodone hydrochloride
Capsules - 50 mg, 100 mg
Tablets - 150 mg
Liquid - 10 mg/mL, 20 mg/mL (available in a 120 mL bottle)

Toxicity

Trazodone is an antagonist at 5-HT2 and alpha1 adrenergic receptors, and a serotonin reuptake inhibitor. In overdose, it has been associated with cardiotoxicity, SIADH and severe hyponatraemia.
Although associated with serotonin syndrome in multi-drug overdoses in the literature, it's role as 5-HT2 antagonist suggests it is unlikely to be causative.
Death associated with coma, bradycardia, prolonged QT and cardiac arrest was reported following ingestion of 4.5 g (Augenstein et al, 1987) but survival has also been reported more recently after ingestion of 4.5 g (Warnant et al, 2020).
Doses of 1.5-3 g have caused significant cardiovascular toxicity. A 54-year-old man with a history of cardiac disease overdosed on 2 g trazadone and developed hypokalaemia and QT prolongation, followed by cardiac arrest due to torsade de pointes. He recovered with treatment including magnesium sulphate, sodium bicarbonate and intralipid. His blood trazodone concentration was 4838 mg/dL (Taylor et al, 2020).
A 77-year-old female was found unconscious after an assumed overdose of 4.5 g trazodone 10-hours previously. She had a prolonged QT and bradycardia (39 bpm). Her GCS improved to 10/15 and her heart rate increased to 54 bpm following treatment with intravenous lipid emulsion (bolus 1.5 mL/kg followed by a 30 min infusion at 0.25 mL/kg/min). Her heart rate improved to 75 bpm after treatment with isoproterenol. Admission trazodone concentration was 1,172 mg/dL (Warnant et al, 2020).
A 55-year-old woman overdosed on 2-4.5 g of trazodone and developed ataxia followed by coma, hypertension and rigidity in proximal muscle groups. She was treated with potassium replacement, levetiracetam for suspected seizures and with hydralazine for hypertension. At 12-24-hours post ingestion, the patient developed QT prolongation that evolved into ventricular tachycardia, and varying types of atrial, nodal and ventricular conduction abnormalities, which resolved gradually with supportive treatments, including ventilation (Soe & Lee, 2019).
An 18-year-old patient ingested 2.5 g trazodone and developed QT prolongation and severe hypotension, which was resistant to adequate fluid resuscitation, but resolved after treatment with a peripheral infusion of noradrenaline (Camacho et al, 2019).
A review of 283 cases of accidental trazodone-only ingestions in children below 6 years of age reported that serious toxicity is unlikely at doses below 12 mg/kg. (Herrington et al, 2016). Of 84 patients for whom doses and outcomes were known, 52 (61.9%) had no clinical effects; 29 (34.5%) had minor effects (vomiting, dizziness, headache); and three (3.6%) had moderate effects (ataxia, slurred speech, priapism). No major effects or deaths were observed. Moderate effects were manifested at doses ≥6.9 mg/kg. Of those patients referred to a healthcare facility, 27 (39.7%) had ingested <6 mg/kg and none of them manifested symptoms beyond minor effects (Zahran et al, 2019).
Peak plasma levels are reached 1 hour after ingestion in a fasting state, and after 2 hours with food (Martindale, 2010). Terminal elimination half-life is 5-13 hours (Trazodone SPC, 2021).

Trazodone - features and managementUpdated 3/2022

Features

Dizziness, drowsiness, ataxia, nausea and vomiting are the most common features. In more serious cases coma, tachycardia, hypotension, hyponatraemia, SIADH, hypokalemia, convulsions and respiratory failure have been reported. Cardiac features may include bradycardia, PR and QT prolongation, torsades de pointes, heart block and acute myocardial infarction due to coronary vasospasm.
Serotonin syndrome is a possibility click here for management.

Could you do Dexedrine (dextroamphetamine), Desoxyn (meth) and cocaine (if it's included)? I just want to know lol

Dexedrine

Type of Product

D-enantiomer of amfetamine, metabolite of lisdexamfetamine. Used in management of narcolepsy and attention deficit/hyperactivity disorder (ADHD). Also used as a drug of abuse.

Synonyms

Dexamphetamine; Dextroamphetamine; D-Amphetamine; Dexedrine; Dex; Dexies; Dexys
NB also used as slang terms for amfetamines in general.

Ingredients

Dexamfetamine sulphate
Tablets - 5 mg, 10 mg, 20 mg
Oral Solution - 1 mg/mL
Street amfetamine - usually contains up to 5% amfetamine along with inert fillers or other stimulants.

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 toxicity 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 dexamfetamine.
Snorting, smoking or injecting amfetamines intravenously gives faster and more intense effects than ingestion.
The elimination half-life of amfetamine varies between 7-34 hours (Anggard et al, 1973), being faster in acidic urine. The average plasma half-life of dexamphetamine is 10.2 hours (Amfexa SPC, 2016).

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.

Desoxyn

Type of Product

A drug of abuse.
Substituted phenethylamine; used to treat ADHD and as an appetite suppressant in the United States (Desoxyn).
NOTE: Not to be confused with 4-methylamphetamine (1-(4-methylphenyl)propan-2-amine) where the methyl group is on the aromatic ring rather than the nitrogen.

Synonyms

Methamphetamine; methamfetamine; metamphetamine; metamfetamine; N-methylamphetamine; MA; Desoxyn; speed; meth; ice; glass; yaba; crank; splash; crystal; crystal meth; base; CAS 537-46-2
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

N-methyl-1-phenylpropan-2-amine
Street amphetamine usually contains up to 5% amphetamine along with inert fillers or other stimulants but purity may vary. Crystal methamphetamine (metamphetamine) typically has a higher purity level, often over 80% (ACMD, 2005).

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

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 (Kuczenski et al, 1995; Rothman et al, 2001).
Individual response varies greatly and toxicity correlates poorly with the amount taken. Snorting, smoking or injecting amphetamine intravenously gives faster and more intense effects than ingestion. The crystalline form of methamphetamine (often called 'Ice' or 'Crystal Meth') can be smoked easily, leading rapidly to high blood levels (Cook et al, 1993).
A dose of greater than 150mg is expected to cause sympathomimetic toxicity in an infrequent adult user (Cho, 1990). There have been deaths reported following methamphetamine ingestion as low as 1.5 mg/kg (Zalis & Parmley, 1963).
Schep et al (2010) recorded the full range of reported toxicity following methamphetamine use and this is consistent with other amphetamines and may be severe or fatal.
Methamphetamine is rapidly absorbed with peak concentrations post exposure depending on route – intravenously 2 or 3 minutes, inhaling vapour or smoking at around 2.5 hours, intranasal at 3 hours and orally at 3.5 hours (Cruikshank et al, 2009; Schep et al, 2010). Distribution is wide due to high lipid solubility that facilitates CNS penetration, feto-maternal transfer and transfer into breast milk (reviewed in Schep, 2010). Metabolism is primarily hepatic via CYP 2D6 to amphetamine and up to 55% of the dose can be eliminated unchanged in urine. The mean terminal elimination half-life of methamphetamine is around 10 hours (Schepers et al, 2003).

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

Stimulants including amfetamines - features and managementUpdated 6/2022

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.

Cocaine

Type of Product

A stimulant drug of abuse formerly used as a local anaesthetic.

Synonyms

Bazooka, Bazucos, Bernice, Big C, Blow, Cadillac of Drugs, Cain, Candy, Cake, Champagne of Drugs, Charlie, Climax (also used for butyl nitrite and heroin), Coke, Crack, Dama blanca, Dose, Dust, Dynamite, Flake, Gold Dust, Happy Dust, Happy Trails, Heaven Dust, Hit, Ice (also used for amfetamines), Koks, Lady, Leaf, Line, Marching Powder, Mister Coffee, Nose Candy, Nuggets, Nuttendiesel, Paradise, Pearl Flake, Pimps, Pimp's Drug, Pink Peruvian Flake, Rock (also used for heroin), Smack (also used for heroin), Snort, Snow, The Lady, Thing, Toot, White.
Caution: using a slang term to try and identify a drug of abuse is potentially dangerous since there are many regional variations and the terms change over time.

Ingredients

Cocaine which may be cut (diluted) with numerous other powders including; lidocaine (lignocaine), benzocaine, phenytoin and levamisole.
Contamination of cocaine with levamisole has resulted in agranulocytosis in cocaine users; this is a recognised adverse effect of chronic levamisole use. Clinicians should consider the possibility of exposure to levamisole-adulterated cocaine in patients with otherwise unexplained fever and agranulocytosis (Zhu et al, 2009). Levamisole is also associated with leukoencephalopathy and cutaneous vasculitis (Gross et al, 2011, Buchanan et al, 2011).
Cocaine adulterants, such as local anaesthetics and phenacetin, may lead to methaemoglobinaemia (Hunter et al, 2011).

Formulations and routes of administration:
Cocaine hydrochloride ('street' cocaine, 'coke') is a water-soluble powder or granule that can be taken orally, intravenously or intranasally.
'Freebase' or 'crack' cocaine comprises crystals of relatively pure cocaine without the hydrochloride moiety. May be sniffed, smoked, ingested or injected.

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

Toxicity

May be due to sympathomimetic effects of cocaine or due to the effects of cutting agents.
Cocaine increases the levels of several neurotransmitters in the brain, exerts sodium and potassium channel blocking effects, causes vasoconstriction and increases sympathetic activity. It increases risk of thrombotic and non-thrombotic acute coronary syndrome, stroke and arterial dissection.
Concentrations in the blood peak very soon after IV administration or smoking but may not peak for an hour after intranasal use (Jatlow, 1988). Buccal absorption also occurs.
Cocaine is rapidly eliminated from the body with a biological half-life of about one hour (Jatlow, 1988). Cocaethylene is produced in the liver when cocaine is metabolised in the presence of ethanol. It may be more cardiotoxic and has a longer half-life allowing later detection of use (Wilson et al, 2001; Occupati et al, 2017).
Toxicity may result from cocaine adulterants, such as bupivacaine-induced methaemoglobinaemia and levamisole-induced agranulocytosis and vasculitis.
Patients who are thought to have swallowed a "wrap" or packages of cocaine (body packers and body stuffers) are a particularly high risk group - see body packers/stuffers entry.
Cocaine - features and managementUpdated 9/2022

Features

Tachycardia, hypertension, chest pain and myocardial infarction may occur. Cardiac dysrhythmias (including ventricular fibrillation, monomorphic and polymorphic ventricular tachycardia and supraventricular tachyarrhythmias), aortic or coronary artery dissection are possible.
Euphoria, agitation, delirium and hallucinations, convulsions, headache, subarachnoid and intracerebral haemorrhage and cerebral infarction have been reported.
Tachypnoea, sweating, ataxia, dilated pupils, nausea, vomiting, gastrointestinal haemorrhage and gut ischaemia may occur. There may also be hyperpyrexia, rhabdomyolysis and renal failure, electrolyte disturbance and metabolic acidosis.
Serotonin syndrome may occur. Click here for the features and management of serotonin syndrome.
Complications:
Fever, agranulocytosis, vasculitis (including purpuric lesions of face [especially of the ear lobes], and unusually extensive destruction of nasal and sinus bony walls), methaemoglobinaemia, acute or chronic kidney injury, haematuria, and bladder cancer may occur due to cutting agents following chronic use. Granulomatosis with polyangiitis (GPA, previously known as Wegener's granulomatosis) may occur.
Complications of the methods of abuse:
These include perforation of the nasal septum, rhinitis, lung granulomas, pulmonary oedema, pneumothorax and pneumomediastinum.

Could I have info on pentobarbitone injectable liquid please? The one vets use for euthanasing animals

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.

 

[Alexei_Kirillov]

I'm not sure exactly what name it would be under in the database, but could you please check NPK fertilizer? NPK being nitrogen-phosphorus-potassium.

 

[CocoToxBase]

I'm not sure exactly what name it would be under in the database, but could you please check NPK fertilizer? NPK being nitrogen-phosphorus-potassium.

Can't find it on search if you could reply with what it could be I'll search again

 

[Alexei_Kirillov]

Can't find it on search if you could reply with what it could be I'll search again

Hmm maybe just try potassium oxide (K2O).

 

[sanitystruggle]

Hmm maybe just try potassium oxide (K2O).

NPK doesn't denote a particular fertilizer formulation, it's a labeling/rating system used to compare the nutrient content of different fertilizer blends and compounds:

Labeling of fertilizer - Wikipedia

en.m.wikipedia.org

Actual fertilizers don't contain K2O - it's a highly reactive compound that reacts violently with water to form potassium hydroxide. The K in NPK is expressed as potassium as an equivalent amount of K2O but the actual compound is usually a potash derivative like potassium chloride or potassium sulphate.

 

[Alexei_Kirillov]

NPK doesn't denote a particular fertilizer formulation, it's a labeling/rating system used to compare the nutrient content of different fertilizer blends and compounds:

Labeling of fertilizer - Wikipedia

en.m.wikipedia.org

Actual fertilizers don't contain K2O - it's a highly reactive compound that reacts violently with water to form potassium hydroxide. The K in NPK is expressed as potassium as an equivalent amount of K2O but the actual compound is usually a potash derivative like potassium chloride or potassium sulphate.

Thanks for the extra info. So if I wanted to calculate how much potassium (K) there is in a 100g container of 20-20-20 fertilizer, I'd have to do 0.83 (the percentage of K in K2O) * 20 = 17% = 17g of potassium in the container. Is this correct?

 

[sanitystruggle]

Thanks for the extra info. So if I wanted to calculate how much potassium (K) there is in a 100g container of 20-20-20 fertilizer, I'd have to do 0.83 (the percentage of K in K2O) * 20 = 17% = 17g of potassium in the container. Is this correct?

Yes, that sounds right.

 

[WoNkEy_DoNkEy]

@CocoToxBase has now fallen unconscious following SN consumption. I'm glad I persuaded her to change her username to that as she will be known by many for it and hopefully this thread will be a useful resource. R.I.P....may all your suffering be at an end beautiful lady.

 

[WoNkEy_DoNkEy]

Just so people know, @CocoToxBase is NOT dead at the time of writing this and will probably be back at some point in the future to help with any remaining entries from the TOXBase that people have. For those who didn't know please see her GBT below;

Goodbye Thread <3

Hey all I'm going to keep this gbt short and simple. I will be posting updates on this thread of my pulse and oxygen if anyone is interested. I am currently admitted in hospital (physical health) following a Pulmonary Embolism which needed surgery but they have allowed me to go home get a shower...

sanctioned-suicide.net