{"id":5374,"date":"2011-09-06T15:55:33","date_gmt":"2011-09-06T15:55:33","guid":{"rendered":"http:\/\/crashtext.org\/misc\/5374.htm\/"},"modified":"2021-08-07T14:44:20","modified_gmt":"2021-08-07T18:44:20","slug":"general-toxicology-random-drugs","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/toxicology\/general-toxicology-random-drugs.htm\/","title":{"rendered":"*General Principles and Random Drugs"},"content":{"rendered":"

“All things are poison and nothing is without poison.\u00a0 Solely the dose determines that a thing is without poison.”<\/p>\n

–Paracelsus<\/p>\n

 <\/p>\n

<\/span>Tox Links<\/span><\/h2>\n

Vaults of Erowid<\/a><\/p>\n

www.lycaeum.org<\/a><\/p>\n

www.householdproducts.nlm.nih.gov<\/a><\/p>\n

www.ansci.cornell.edu\/plants<\/a><\/p>\n

www.dartmouth.edu\/~toxmetal<\/a><\/p>\n

www.toxed.com<\/a><\/p>\n

www.microdex.com\/products\/poisondex<\/a><\/p>\n

www.clinicalpharmacology-ip.com<\/a><\/p>\n

 <\/p>\n

 <\/p>\n

<\/span>Mnemonics<\/span><\/h2>\n

Do not adsorb to charcoal<\/h4>\n

PHAILS<\/p>\n

P<\/strong>esticides;<\/p>\n

H<\/strong>ydrocarbons;<\/p>\n

A<\/strong>cids and a<\/strong>lkali;<\/p>\n

I<\/strong>ron;<\/p>\n

L<\/strong>ithium; and<\/p>\n

S<\/strong>olvents<\/p>\n

 <\/p>\n

Repeat Dose Charcoal<\/h4>\n

ABCD<\/p>\n

A<\/strong>ntimalarials (quinine) and a<\/strong>minophylline (theophylline);<\/p>\n

B<\/strong>arbiturates (Phenobarbital) and b<\/strong>eta-blockers (nadolol);<\/p>\n

C<\/strong>arbamazepine<\/p>\n

D<\/strong>apsone<\/p>\n

and D<\/strong>ilantin (Phenytoin)<\/p>\n

Valproate<\/p>\n

Theophylline<\/p>\n

 <\/p>\n

Toxins Accessible To Hemodialysis<\/h4>\n

Small Molecule, Low Protein Binding, Water Soluble<\/p>\n

I STUMBLE<\/strong><\/p>\n

I<\/strong>sopropyl Alcohol<\/p>\n

S<\/strong>alicylates<\/p>\n

T<\/strong>heophylline (caffeine)<\/p>\n

U<\/strong>remia<\/p>\n

M<\/strong>ethanol<\/p>\n

B<\/strong>arbiturates, beta-blockers (water soluble, such as atenolol)<\/p>\n

L<\/strong>ithium<\/p>\n

E<\/strong>thylene glycol<\/p>\n

 <\/p>\n

<\/span>Vital Sign\/PE Mnemonic<\/span><\/h3>\n

s<\/p>\n

Bradycardia (PACED)<\/h4>\n

P<\/strong>ropranolol or other beta-blockers, poppies (opiates), propafenone, phenylpropanolamine<\/p>\n

A<\/strong>nticholinesterase drugs<\/p>\n

C<\/strong>lonidine, calcium-channel blockers<\/p>\n

E<\/strong>thanol or other alcohols<\/p>\n

D<\/strong>igoxin<\/p>\n

 <\/p>\n

Tachycardia (FAST)<\/h4>\n

F<\/strong>ree base or other forms of cocaine<\/p>\n

A<\/strong>nticholinergics, antihistamines, amphetamines<\/p>\n

S<\/strong>ympathomimetics (cocaine, amphetamines), solvent abuse<\/p>\n

T<\/strong>heophylline<\/p>\n

\u00a0<\/strong><\/p>\n

Hypothermia (COOLS)<\/h4>\n

C<\/strong>arbon monoxide<\/p>\n

O<\/strong>piates<\/p>\n

O<\/strong>ral hypoglycemics, insulin<\/p>\n

L<\/strong>iquor<\/p>\n

S<\/strong>edative-hypnotics<\/p>\n

\u00a0<\/strong><\/p>\n

Hyperthermia (NASA)<\/h4>\n

N<\/strong>euroleptic malignant syndrome, nicotine<\/p>\n

A<\/strong>ntihistamines<\/p>\n

S<\/strong>alicylates, sympathomimetics<\/p>\n

A<\/strong>nticholinergics, antidepressants<\/p>\n

\u00a0<\/strong><\/p>\n

Hypotension (CRASH)<\/h4>\n

C<\/strong>lonidine, calcium-channel blockers<\/p>\n

R<\/strong>eserpine or other antihypertensive agents<\/p>\n

A<\/strong>ntidepressants, aminophylline<\/p>\n

S<\/strong>edative-hypnotics<\/p>\n

H<\/strong>eroin or other opiates<\/p>\n

\u00a0<\/strong><\/p>\n

Hypertension (CT SCAN)<\/h4>\n

C<\/strong>ocaine<\/p>\n

T<\/strong>hyroid supplements<\/p>\n

S<\/strong>ympathomimetics<\/p>\n

C<\/strong>affeine<\/p>\n

A<\/strong>nticholinergics, amphetamines<\/p>\n

N<\/strong>icotine<\/p>\n

\u00a0<\/strong><\/p>\n

Rapid respiration (PANT)<\/h4>\n

P<\/strong>CP, paraquat, pneumonitis (chemical)<\/p>\n

A<\/strong>SA and other salicylates<\/p>\n

N<\/strong>on-cardiogenic pulmonary edema<\/p>\n

T<\/strong>oxin-induced metabolic acidosis<\/p>\n

\u00a0<\/strong><\/p>\n

Slow respiration (SLOW)<\/h4>\n

S<\/strong>edative-hypnotics (including GHB)<\/p>\n

L<\/strong>iquor<\/p>\n

O<\/strong>piates, sedative-hypnotics<\/p>\n

W<\/strong>eed (marijuana)<\/p>\n

 <\/p>\n

Miosis (COPS)<\/h4>\n

C<\/strong>holinergics, clonidine<\/p>\n

O<\/strong>piates, organophosphates<\/p>\n

P<\/strong>henothiazines, pilocarpine<\/p>\n

S<\/strong>edative-hypnotics<\/p>\n

\u00a0<\/strong><\/p>\n

Mydriasis (AAAS)<\/h4>\n

A<\/strong>ntihistamines<\/p>\n

A<\/strong>ntidepressants<\/p>\n

A<\/strong>tropine and other anticholinergics<\/p>\n

S<\/strong>ympathomimetics<\/p>\n

 <\/p>\n

Drugs Causing Pneumonitis Or Pulmonary Edema<\/h4>\n

(MOPS)<\/strong><\/p>\n

M<\/strong>eprobamate, methadone<\/p>\n

O<\/strong>piates, organophosphates<\/p>\n

P<\/strong>henobarbital, propoxyphene, phenothiazines<\/p>\n

S<\/strong>alicylates, smoke inhalation (including cocaine smoke), solvents<\/p>\n

 <\/p>\n

Causes of high Osmal Gap<\/h4>\n

ME DIE<\/strong><\/p>\n

M<\/strong>ethanol<\/p>\n

E<\/strong>thylene glycol<\/p>\n

D<\/strong>iuretics (osmotic diuretics like mannitol)<\/p>\n

I<\/strong>sopropyl alcohol<\/p>\n

E<\/strong>thanol<\/p>\n

Also acetone<\/strong><\/p>\n

 <\/p>\n

Drugs that cause Seizures<\/h4>\n

Aspirin<\/p>\n

Tramadol (Ultram\u00ae, Ultracet\u0099)<\/p>\n

Tricyclic antidepressants<\/p>\n

Bupropion (Wellbutrin\u00ae, Zyban\u00ae)<\/p>\n

Diphenhydramine (Benadryl\u00ae)<\/p>\n

Amphetamines\/Cocaine<\/p>\n

Venlafaxine (Effexor\u00ae)<\/p>\n

Leon from the Poison Review has this mnemonic:<\/strong><\/p>\n

O \u2013 <\/strong>organophosphates
\nT<\/strong> \u2013 tricyclic antidepressants
\nI<\/strong> \u2013 isoniazid, insulin (hypoglycemia)
\nS<\/strong> \u2013 sympathomimetics, synthetic cannabinoids (Spice)<\/p>\n

C \u2013 <\/strong>cocaine, camphor
\nA \u2013 <\/strong>amphetamines, anticholinergics, atypical antipsychotics
\nM<\/strong> \u2013 methylxanthines (theophylline, caffeine)
\nP<\/strong> \u2013 phencyclidine (PCP)
\nB<\/strong> \u2013 botanicals (e.g., water hemlock), bath salts, benzo withdrawal,\u00a0bupropion
\nE<\/strong> \u2013 ethanol withdrawal
\nL<\/strong> \u2013 lead, lindane
\nL \u2013 <\/strong>lithium, lidocaine<\/p>\n

 <\/p>\n

 <\/p>\n

Smells of Toxicology (River’s)<\/strong><\/h4>\n

Nitrites, Isopropyl alcohol:\u00a0 fruit like<\/strong><\/p>\n

Phenols:\u00a0 disinfectant<\/strong><\/p>\n

Cyanide:\u00a0 bitter almonds<\/strong><\/p>\n

Chloral Hydrate:\u00a0 pear-like<\/strong><\/p>\n

Arsine, phosphorous, tellerium, organophosphates:\u00a0 garlic<\/strong><\/p>\n

Turpentine:\u00a0 violets<\/strong><\/p>\n

Hydrogen Sulfide:\u00a0 rotten eggs<\/strong><\/p>\n

Camphor, naphthalene:\u00a0 mothballs<\/strong><\/p>\n

Phosgene:\u00a0 hay<\/strong><\/p>\n

Methylsalicylate:\u00a0 wintergreen<\/strong><\/p>\n

<\/span>Presentations<\/span><\/h2>\n

Brady+Vomiting=Digoxin<\/p>\n

Also av or nodal block with atrial or ventricular irritability<\/p>\n

Tachy+Vomiting=think theo<\/p>\n

Extrapyramidal Toxidrome<\/h4>\n

TROD seen with zines, haldol, reglan<\/p>\n

T<\/strong>remor, torticollis, trismus<\/p>\n

R<\/strong>igidity<\/p>\n

O<\/strong>pisthotonos, Oculogyric Crisis<\/p>\n

D<\/strong>ysphonia, dysphagia<\/p>\n

<\/span>Activated Charcoal<\/span><\/h2>\n

AC only helps in tylenol overdose if given within 1 hour of ingestion (J Toxicol Clin Toxicol 2001;39(6):601)<\/p>\n

Position Statement Am Acad Toxicol, no AC after 1 hour can be supported by evidence, only give in patients with intact or protected airway<\/p>\n

A different opinion on charcoal<\/a><\/p>\n

Doesn’t adsorb charged ions (potassium, sodium, etc.)<\/p>\n

<\/span>Malignant Hyperthermia<\/span><\/h2>\n

Rare inherited disorder: autosomal dominant with variable expression and incomplete penetrance<\/p>\n

May occur up to 24 hours after the use of succinylcholine or inhaled anesthetics<\/p>\n

From abnormal calcium channels<\/p>\n

AMS, rigidity, hyperthermia, autonomic instability, acidosis<\/p>\n

Active Cooling<\/p>\n

Benzos<\/p>\n

Dantrolene-1 mg\/kg IV may repeat to dose of 10 mg\/kg.\u00a0 2 mg\/kg PO QID for 2 days after.<\/p>\n

 <\/p>\n

Malignant HYperthermia Review<\/a><\/p>\n

<\/span>Date Rape Drugs<\/span><\/h2>\n

GHB and flunitrazepam<\/p>\n

Barbs, benzos, ambien, carisoprodol, chloral hydrate, GHB, THC, Cocaine, methamphetamines, XTC, PCP and Ketamine, Scopolamine<\/p>\n

<\/span>Statins<\/span><\/h2>\n

Cholesterol membrane instability, muscle affected most<\/p>\n

Rhabdomyolysis b\/c of coenzyme Q inhibition in mitochondria.\u00a0 Myopathy and hepatotoxicity<\/p>\n

.<\/p>\n

<\/span>TB Meds<\/span><\/h2>\n

<\/span>Isoniazid (INH)<\/span><\/h3>\n

>20 mg\/kg needs evaluation<\/p>\n

>79 mg\/kg can lead to seizures<\/p>\n

May be asymptomatic for up to 2 hours post ingestion<\/p>\n

N\/V, photophobia, hallucinations, dizziness, ataxia, slurred speech, lethargy progressing to grand mal seizures, coma, and death<\/p>\n

Blocks GABA formation (active b6 catalyzes glutamate to GABA, INH makes you pee out B6 and decreases enzymatic formation of active B6), also inhibits conversion of lactate to pyruvate, so lactic acidosis<\/p>\n

 <\/p>\n

Benzos<\/p>\n

Pyridoxine (B6) should be administered to match gram for gram dose of INH up to 5 grams.\u00a0 If dose unknown, give 5 grams empirically<\/p>\n

Effects diminish rapidly, so 6 hours observation, then D\/C<\/p>\n

Side effect is hepatitis:\u00a0 10% have elevated enzymes, 10% of those get hepatitis, 10% of those die from it.<\/p>\n

Can also cause niacin deficiency:\u00a0 pellagra=diarrhea, dementia, dermatitis<\/p>\n

<\/span>Rifampin<\/span><\/h3>\n

Causes all fluids to turn red<\/p>\n

<\/span>Ethambutol<\/span><\/h3>\n

Optic Neuritis<\/p>\n

<\/span>Pyrazinamide<\/span><\/h3>\n

Hepatic dysfunction<\/p>\n

<\/span>Antimalarial Meds<\/span><\/h2>\n

Mefloquine<\/h4>\n

gives vivid dreams<\/p>\n

Quinine<\/h4>\n

C<\/strong>inchoism<\/strong>=n\/v, hearing loss, tinnitus, HA.<\/p>\n

Also blocks Na and K channels in heart causing QRS\/QT prolongation, requiring Bicarb.\u00a0 TDP as well.\u00a0 Give MdAC.\u00a0 Can get blindness from direct retinal toxicity.<\/p>\n

Chloroquine<\/h4>\n

GI Symptoms, Hypokalemia, QRS\/QT prolongation, severe hypotension.\u00a0 Give 2 mg\/kg diazepam over 30 min then 1-2 mg\/kg\/day.\u00a0 EPI .25 ug\/kg\/min until systolic > 100.\u00a0 Validated in France where this used to be a popular suicide med.<\/p>\n

May want to supplement K\/Mg before giving bicarb to avoid exacerbating K-channel blockade<\/p>\n

 <\/p>\n

Dapsone<\/h4>\n

MetHb<\/p>\n

<\/span>Paraphenylenediamine (Para, PPD)<\/span><\/h2>\n

In hair dyes<\/p>\n

Respiratory failure, myoglobinuria, vomiting, tongue swelling.\u00a0 Causes cancer.<\/p>\n

<\/span>Hydrazine<\/span><\/h2>\n

can cause stat epilepticus, contained in jet fuel<\/p>\n

<\/span>Baclofen<\/span><\/h2>\n

<\/span>Withdrawal<\/span><\/h3>\n

Fever, AMS, rebound spasticity, rhabdo, organ failure<\/p>\n

Can be caused by catheter malfunction, empty reservoir, dead batteries<\/p>\n

RX:\u00a0 restart the pump, oral baclofen, benzos<\/p>\n

<\/span>Poisonings in Lab workers<\/span><\/h2>\n

CO, Cyanide, Azides, MetHb inducing chemicals<\/p>\n

Fatal inhalations-CO, Hydrogen Sulfide, Asphyxiants, NOs, Smoke, Halogens<\/p>\n

Blood Screening-Na Azide, cyanide, CO, sulfide<\/p>\n

<\/span>Sodium Azide (NaN3)<\/span><\/h3>\n

Highly toxic and highly explosive<\/p>\n

Used in detonators and as preservative in lab reactions<\/p>\n

In vapor form, colorless, pungent.<\/p>\n

Sx arise suddenly and dissipate in a few hours<\/p>\n

ABD cramps, chest pain, dysphoria, faintness, flushing, headache, incontinence, n\/v, palpitations, weakness, agitation, diarrhea, hyperventilation, hypo or hypertension, leukocytosis, pallor, syncope, sweats, tachycardia, and vomiting.\u00a0 Larger doses can give blindness, dilated pupils, NCPE, myocardial dysfunction, myocarditis, shock, seizures and coma.\u00a0 Uncouples oxidative phosphorylation.<\/p>\n

GI Decon and supportive care<\/p>\n

Review Article<\/a><\/p>\n

<\/span>Mitochondrial Toxins<\/span><\/h2>\n

propofol<\/p>\n

b. cereus toxin<\/p>\n

valproate<\/p>\n

hiv meds<\/p>\n

can see ketoacidosis, lactic acidosis, myopathy<\/p>\n

<\/span>Propofol Infusion Syndrome<\/span><\/h2>\n

Inten Care Med 2003;29:1417<\/p>\n

cardiac depressant<\/p>\n

infusion syndrome is associated with catecholamine and steroid tretament simultaneous with propofol<\/p>\n

consider after >48 hours of infusion<\/p>\n

catechols-increased CO causes increased clearance requiring higher doses<\/p>\n

Causes cardiac failure and rhabdomyolysis<\/p>\n

>5 mg\/kg\/hr is considered high dose and puts pts at risk<\/p>\n

 <\/p>\n

Often seen in kiddies, but reported in adults (Burow BK – Anesthesiology – 01-JUL-2004; 101(1): 239-41 followed by editorial comment)<\/p>\n

Green Urine is Seen<\/p>\n

 <\/p>\n

Phase 1. Fast distribution from blood to tissue; half-life, 2 to 3 minutes<\/p>\n

 <\/p>\n

The desired clinical response can be titrated by either bolus injections of 0.5 mg\/kg every 10 seconds to a total dose of 2 to 2.5 mg\/kg or by continuous infusion.<\/p>\n

 <\/p>\n

Although hypotension is the most commonly reported adverse event, volume loading with 12 mg\/kg of Ringer\u0092s lactate solution is effective in maintaining hemodynamic stability.18 Interestingly, propofol in high doses has also been rarely reported to cause seizures, but the mechanism is unknown.19,20<\/p>\n

Annals EM Dec 2003 42:6; 793.\u00a0 propofol recovery time is 5-15 minutes with a 30 second onset<\/p>\n

strong anti-emetic properties<\/p>\n

can cause hypotension, apnea, and pain on injection<\/p>\n

Bassett Peds Study-hypoxia in 5%, airway repositioning in 2% and apnea needing BVM in .8%<\/p>\n

 <\/p>\n

Great review of lit<\/h4>\n

Propofol (2,6 di-isopropylphenol) is a very short acting non-opioid sedative\u0096hypnotic agent. It is thought to work by potentiating the binding of -amino butyric acid to receptor sites in the central nervous system (CNS).6 It has no analgesic properties and must be used in conjunction with adequate pain relief. Studies vary regarding the extent of amnesic properties compared to benzodiazepines.6,7 but it has recognised antiemetic and euphoric effects. Onset of action is <60 seconds (one arm\u0096brain circulation). Despite a half life of 13\u009644 hours, duration of action is approximately 10 minutes, owing to rapid redistribution from CNS tissue to muscle and fat. Metabolic clearance equals or exceeds hepatic blood flow, suggesting extrahepatic clearance, possibly pulmonary.6 Pharmacokinetics are unaffected by renal or hepatic disease but dose reduction is required in the elderly,6 as volume of distribution falls with age.<\/p>\n

 <\/p>\n

Bassett et al19 (table 1) is a further study in the same institution following almost the same protocol. Patients were fasted for 3 hours and 10 litres of oxygen was administered routinely. At least three deviations from protocol were noted when patients were not given oxygen, and all of these patients became hypoxic.<\/p>\n

 <\/p>\n

(EMJ 2006;23(2):89)<\/p>\n

Screening with CPK (<5000 for discontinuation) may be an effective prevention strategy (Injury, Int. J. Care Injured 45 (2014) 245\u2013249)<\/p>\n

 <\/p>\n

<\/span>Nail Polish Removers<\/span><\/h2>\n

most contain acetonitrile which is converted to cyanide in vivo.<\/p>\n

<\/span>Dystonic Reactions<\/span><\/h2>\n

buccolingual-protruding or pulling sensation of tongue<\/p>\n

Torticollic-neck or facial spasm<\/p>\n

Oculogyric-roving or deviated gaze<\/p>\n

Tortipelvic-abd rigidity and pain<\/p>\n

Opisthotonic-spasm of entire body<\/p>\n

 <\/p>\n

Give 50 mg of benadryl IV<\/p>\n

 <\/p>\n

<\/span>Strychnine<\/span><\/h2>\n

seizure while awake, lift back off bed<\/p>\n

muscle spasms<\/p>\n

Strychnine poisoning is an unusual but dramatic poisoning in which convulsions are the major threat to life. Convulsions are predominantly at the spinal level, and the key to recognition of this poisoning is observation of convulsive activity in the awake patient without a postictal phase. Successful treatment requires aggressive airway control and treatment of seizures with benzodiazepines or barbiturates. Neuromuscular blockade may be required. Gastrointestinal decontamination is usually indicated in recent acute ingestions but may precipitate convulsions. Recovery from strychnine poisoning is usually complete and rapid if treatment is aggressive. In the absence of trauma, compartment syndrome, rhabdomyolysis, or anoxic central nervous system injury, no neurologic or musculoskeletal sequelae are expected. Confirmation of strychnine poisoning is best obtained by submitting urine or gastric aspirate for analysis utilizing a qualitative test such as thin layer chromatography (TLC).<\/p>\n

 <\/p>\n

<\/span>Malignant Hyperthermia<\/span><\/h2>\n

\"\"<\/a><\/p>\n

 <\/p>\n

 <\/p>\n

<\/span>Dextromethorphan<\/span><\/h2>\n

DXM<\/p>\n

skittles, red hots, triple cs<\/p>\n

presents with new-onset and otherwise unexplained psychosis. Although the authors don\u2019t mention it, one clue to the diagnosis might be the presence of nystagmus. One other take-home lesson is that DXM will not itself show up on a urine drug screen, but in large amounts can produce a false-positive urine screen for PCP.<\/p>\n

 <\/p>\n

<\/span>Reglan<\/span><\/h2>\n

Metoclopramide<\/p>\n

Rate of Akasthisia is directly related to rate of infusion. Over 10 minute infusion sig. less side effects than 2 minute IV Bolus (EMJ 2005;22(9):621)<\/p>\n

 <\/p>\n

<\/span>Toxin Induced Hyperthermia<\/span><\/h2>\n

Crit Care 2007; 11:236<\/p>\n

 <\/p>\n

<\/span>Colchicine<\/span><\/h2>\n

review of toxicity<\/a><\/p>\n

<\/span>Methotrexate<\/span><\/h2>\n

Methotrexate (MTX) is a chemotherapeutic drug that is structurally similar to folic acid. MTX inhibits dihydrofolate<\/p>\n

reductase, an enzyme that reduces folic acid to tetrahydrofolic acid. This inhibition interferes with DNA<\/p>\n

synthesis and cell reproduction. MTX is used in the treatment of a variety of illnesses including cancer, rheumatoid<\/p>\n

arthritis, systemic lupus erythematosus, and psoriasis. It is given intravenously, intramuscularly, orally<\/p>\n

and intrathecally.<\/p>\n

Methotrexate toxicity develops due to increased patient susceptibility during treatment, excessive parenteral<\/p>\n

or intrathecal administration, therapeutic errors by patients (e.g. taking MTX orally daily instead of weekly),<\/p>\n

self-administration to induce abortion, or intentional oral overdoses. Clinical manifestations of toxicity include<\/p>\n

nausea, vomiting, diarrhea, mucositis, stomatitis, esophagitis, elevated hepatic enzymes, renal failure, rash,<\/p>\n

myelosuppression (leukopenia, pancytopenia, thrombocytopenia), acute lung injury, tachycardia, hypotension,<\/p>\n

and neurologic dysfunction (depression, headache, seizures, motor dysfunction, stroke-like symptoms, encephalopathy,<\/p>\n

coma). Toxic effects may occur hours to days to weeks after MTX administration or overdose.<\/p>\n

Treatment of MTX toxicity includes the administration of activated charcoal in the event of a recent, oral overdose.<\/p>\n

Renal failure may be prevented by adequate hydration and urinary alkalinization with sodium bicarbonate.<\/p>\n

There are three antidotes that have been used for MTX toxicity: leucovorin, thymidine and glucarpidase.<\/p>\n

Leucovorin (folinic acid) is the reduced and active form of folic acid. It selectively \u0093rescues\u0094 normal cells from<\/p>\n

the toxic effects caused by MTX\u0092s inhibition of the production of reduced folates. The recommended dosage in<\/p>\n

most cases is 100 mg\/m<\/p>\n

2 intravenously every 3 to 6 hours until the plasma MTX level is less than 0.01<\/p>\n

mcmol\/L or for 3 days or longer if levels are not available. Thymidine rescues cells from the cytotoxic effects of<\/p>\n

MTX. Its use is investigational and is only given along with other therapies. Glucarpidase (carboxypeptidase) is<\/p>\n

an antidote that has been used recently for MTX toxicity in combination with leucovorin. It converts MTX to an<\/p>\n

inactive form and rapidly lowers MTX blood levels. It is given as a single bolus of 50 units\/kg intravenously<\/p>\n

over 5 minutes. Leucovorin should be continued for 48 hours after glucarpidase administration. Hemodialysis<\/p>\n

and hemoperfusion have been used to lower MTX levels. Intrathecal overdoses require special measures including<\/p>\n

cerebrospinal fluid drainage and exchange, steroids, and antidotes. (Maryland ToxTidbits)<\/strong><\/p>\n

 <\/p>\n

<\/span>Dinitrophenol (DNP)<\/span><\/h2>\n

Fatal 2,4-dinitrophenol poisoning . . . coming to a hospital near you. Siegmueller C, Narasimhaish R. Emerg Med J<\/em> 2010 May 29 [Epub ahead of print]<\/strong><\/p>\n

Abstract<\/a><\/em><\/p>\n

Dinitrophenol (DNP) is an industrial chemical used in the manufacture of explosives, herbicides, dyes, and wood preservatives. \u00a0When ingested, DNP uncouples mitochondrial oxidative phosphorylation, interfering with the cells\u0092 ability to store energy as ATP. \u00a0Instead, the energy is dissipated as \u00a0heat, causing severe hyperthermia that in case reports has proven very difficult if not impossible to control. In addition, the ATP depletion causes release of calcium from the sarcoplasmic reticulum in muscles. \u00a0The resulting uncontrolled muscular contraction produces even more heat. Patients with DNP toxicity often die of hyperthermia, multi-organ failure, and cardiovascular collapse. Presenting signs and symptoms of acute DNP toxicity include hyperthermia, diaphoresis, nausea and vomiting, and diarrhea.<\/p>\n

In the 1930s, DNP was often used as a diet aid after a clinical pharmacologist found that \u0097 by increasing the metabolic weight \u0097 controlled doses of DNP could cause an average loss of 1.5 \u0096 2.0 pounds per week. \u00a0One laboratory brought out a product called Formula 281, that contained DNP 1.5 grains. \u00a0The promotional brochure gushed: \u0093Here, at last, is a reducing remedy that will bring you a figure men admire and women envy, without danger to your health or change in your regular mode of living.\u0094 Enthusiasm for these products waned when it became apparent that the gap between the \u0093therapeutic\u0094 and toxic doses was extremely narrow, and customers taking even the recommended dose started to go blind from \u0093dinitrophenol cataracts<\/a>\u0093.<\/p>\n

Unfortunately, DNP is being sold again \u0097 over the internet \u0097 as a weight-loss product. \u00a0This fascinating case report from \u00a0London describes\u00a0an adult male who suicidally ingested 14\u00d7200 mg DNP tablets purchased from a website. \u00a0On arrival at hospital 12 hours after ingestion, he had vomiting and diarrhea, diaphoresis, and dehydration. \u00a0His pulse was 150\/min, BP 104\/64, respiratory rate 28.min, and temperature 38.4\u00b0C. \u00a0The clinicians instituted \u00a0treatment recommended by the U.K. National Poison Information Service guidelines, including fluids, cooling, and sedation. However, the patient\u0092s condition deteriorated and he developed respiratory failure and an asystolic cardiac arrest from which he could not be resuscitated.<\/p>\n

The authors make the point that the U.K. NPIS guidelines recommend treating DNP toxicity with dantrolene if the patient\u0092s temperature is greater than 39-40\u00b0C. \u00a0Although this is based \u0097 as far as I can determine \u0097 on just a single abstract<\/a>, the pharmacology makes sense: dantrolene specifically inhibits calcium release from sarcoplasmic reticulum. \u00a0The authors argue that the NPIS threshold for administering dantrolene may be set too high, and that giving it earlier in significant DNP toxicity may be beneficial.<\/p>\n

 <\/p>\n

<\/span>Drug Stuffers and Body Packers<\/span><\/h2>\n

Mules<\/p>\n

The protocol from EMJ<\/a><\/p>\n

 <\/p>\n

<\/span>Review of Blood Purification<\/span><\/h2>\n

From Adv in Chronic Kidney Dis<\/a><\/p>\n

<\/span>Drug-Induced Hyperthermia<\/span><\/h2>\n

Best Review Article of Drug-Induced Hyperthermia<\/a><\/p>\n

<\/span>2,4 Dinotrophenol<\/span><\/h2>\n

https:\/\/criticalcarenorthampton.com\/2018\/10\/03\/too-hot-to-handle\/<\/p>\n

 <\/p>\n","protected":false},"excerpt":{"rendered":"

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