moreeee tox cards Flashcards
(29 cards)
Types of toxidromes
anticholinergic
cholinergic
antidopaminergic
serotonergic
sympathomimetic
methaemoglobinaemia.
Key features of anticholingergic toxidrome
Peripheral and CNS effects- delirium, mumbling, picking at bed sheets or imaginary objects, mydriasis, tachycardia
List some pure anticholinergic drugs
Atropine
Benzatropine
Oxybutynin
Hyoscine N buty;bromide
Drugs with anticholinergic effects
TCAs
Antihistamines
Antipsychotics
Plants with anticholingeric effects
Brugmansia species (angel’s trumpet)
Datura stramonium (jimsonweed or thorn apple)
Atropa belladonna (belladonna or deadly nightshade)
Duboisia species (corkwood).
Clin f of anticholingergic toxidrome
peripheral anticholinergic effects—dry skin, dry mouth, mydriasis, tachycardia, urinary retention, gastrointestinal ileus (reduced bowel sounds, abdominal distension), raised temperature (especially in children)
CNS anticholinergic effects—confusion, hallucinations (mainly visual), repetitive gesturing such as picking movements, incoherent speech, agitation, aggression, delirium, sedation, occasionally seizures.
Mng of anticholingeric toxidrome
Severe: physostigmine–> if not available: sedation with droperidol for behavioural disturb
Depending on level of agitation, can also give a PO benzo or observe
Delirium: low stimulus enviro and close observation
Acute urinary retention: catheter
Indications and contraindications for Physostigmine
I: Mng of severe pure anticholingergic toxidrome
CI: Bradycardia, bronchospasm
Key features of cholingeric toxidrome
A patient with cholinergic toxidrome characteristically has altered conscious state, weakness, bradycardia and is ‘wet’ (ie has symptoms of lacrimation, salivation, bronchorrhoea and sweating).
Cholingergic drugs/toxins
Cholinergic drugs or toxins increase acetylcholine activity in the body, and include acetylcholinesterase inhibitors that prevent the breakdown of acetylcholine, and acetylcholine receptor agonists.
Acetylcholinesterase inhibitors cause both muscarinic and nicotinic systemic effects, and include:
organophosphate and carbamate pesticides
chemical warfare nerve agents
donepezil and rivastigmine
neostigmine and pyridostigmine.
Acetylcholine receptor agonists include:
nicotinic receptor agonists such as:
nicotine in tobacco products, patches, gum, lozenges and e-cigarette liquid
nicotine in plants
varenicline
neonicotinoid insecticides
muscarinic receptor agonists—Amanita muscaria mushrooms, and Clitocybe and Inocybe mushroom species.
Clin f of cholinergic toxidrome
central nervous system effects—agitation, delirium, coma, seizures
neuromuscular effects due to nicotinic receptor stimulation—muscle fasciculations, weakness and paralysis
autonomic effects due to muscarinic receptor stimulation—salivation, lacrimation, sweating, flushing, miosis
respiratory effects due to muscarinic receptor stimulation—bronchorrhoea (increased pulmonary secretions), bronchoconstriction
cardiovascular effects
bradycardia or tachycardia, arrhythmias
hypertension or, with severe toxidrome, hypotension
metabolic effects—hypokalaemia, hyperglycaemia, metabolic acidosis
gastrointestinal effects—abdominal pain, vomiting, diarrhoea.
Mng of cholinergic toxidrome
If having bradycardia and increased pulmonary secretions: atropine
Agitation and seizures: IV benzos
Antidotes where relevant
key features of methaemoglobinaemia
Methaemoglobinaemia occurs when the ferrous iron in red blood cells is oxidised to the ferric form. This causes a left-shift of the oxygen–haemoglobin dissociation curve that results in reduced oxygen-carrying capacity of haemoglobin, functional anaemia and impaired delivery of oxygen to the tissues.
Drugs that cause methaemoglobinemia
nitrites and nitrates
nitrites and nitrates found in well water
sodium nitrite (eg in preserved foods, some liniments and laxatives)
sodium nitroprusside, glyceryl trinitrate
amyl nitrite (a recreational drug commonly known as a ‘popper’ or ‘rush’)
local anaesthetics—commonly prilocaine, benzocaine; occasionally lidocaine, articaine, tetracaine (amethocaine)
antibiotics—sulfonamides, dapsone
antimalarials—commonly chloroquine, primaquine
pesticides
herbicides—paraquat, propanil
aniline dyes, nitrobenzene
naphthalene
potassium permanganate
fertilisers.
Clin f of methaemoglobinaemia
Related to the metaemoglobin fraction in the blood
<10%- none
10-20% = slate grey skin discolouration, cyanosis
20-30%= HA, anxiety, tachycardia
30-50%- drowsiness, fatigue, confusion, tachypnea
50-70% = increasing CNS depression, coma, seizures, arrhythmias, metabolic acidosis
>70%= lethal
Tx of methaemoglobinemia
Mng airway
Stop causative and start oxygen therapy
If cyanosis but no other clinical effects + methaemoglobin fraction of <25% = admit and observe
Give methylene blue if: symptomatic and methaemoglobin fraction of >20% OR asx but fraction of >25%
Key features of neuroleptic malignant syndrome
Neuroleptic malignant syndrome is a rare, idiosyncratic complication of antipsychotic drugs (and rarely other drugs that affect dopaminergic neural transmission). It is potentially life threatening if not diagnosed and treated early. Extrapyramidal effects are always present, but other features (hyperthermia, autonomic and cognitive change) are also required to make the diagnosis.
Drugs that cause neuroleptic malignant syndrome
opamine antagonist drugs include all antipsychotic drugs:
first-generation antipsychotic drugs—chlorpromazine, droperidol, flupentixol, haloperidol, periciazine, zuclopenthixol
second-generation antipsychotic drugs—amisulpride, aripiprazole, asenapine, brexpiprazole, clozapine, lurasidone, olanzapine, paliperidone, quetiapine, risperidone, ziprasidone.
Although almost all antipsychotics have been associated with neuroleptic malignant syndrome, it is more common with high-potency drugs (eg haloperidol) and depot preparations.
Dopaminergic drugs, which on withdrawal can cause neuroleptic malignant syndrome, include:
levodopa plus benserazide
levodopa plus carbidopa
bromocriptine.
Clin F of neuroleptic malignant syndrome
The classic tetrad of clinical features in neuroleptic malignant syndrome is:
extrapyramidal effects—‘lead-pipe’ rigidity, bradykinesia or akinesia, dystonia, abnormal movement and posture, dysphagia, tremor
temperature dysregulation, including hyperthermia with a temperature of more than 39ºC
autonomic effects—tachycardia, hypertension, labile blood pressure, sweating, tachypnoea
central nervous system effects—drowsiness, confusion, coma, mutism, incontinence.
Abnormal investigation findings common (though not specific) in neuroleptic malignant syndrome include:
serum creatine kinase concentration more than 3 times the upper limit of normal
leucocytosis
low serum iron concentration
diffuse slowing on an electroencephalogram, consistent with a metabolic encephalopathy
cerebrospinal fluid examination (lumbar puncture) may be normal, or have a slightly raised protein concentration.
Diagnostic criteria for neuroleptic malignant syndrome
major criteria—must have all three
exposure to a dopamine antagonist drug
severe muscle rigidity
hyperthermia
other criteria—at least two of
tachycardia, hypertension, labile blood pressure, sweating
raised serum creatine kinase, leucocytosis
dysphagia, tremor
altered conscious state, mutism, incontinence.
Mng of neuroleptic malignant sydnroem
stopping the causative drug and any drugs that potentiate neuroleptic malignant syndrome (eg anticholinergic drugs, lithium)
supportive care- mng hyperthermia
prevention of complications (eg thromboembolism, rhabdomyolysis, aspiration pneumonitis)
exclusion of other medical, toxicological or psychiatric differential diagnoses.
If severe/prolonged= bromocriptine
Key features of serotonergic toxidomre
Serotonergic toxidrome (also known as serotonin toxicity) develops within hours of:
commencing or increasing the dose of a serotonergic drug
poisoning with a serotonergic drug
interaction between serotonergic drugs.
Serotonergic toxidrome is best described as a spectrum of severity (ie not serotonin syndrome). It is characterised by a triad of clinical effects:
neuromuscular excitation—hyperreflexia, clonus (inducible or spontaneous), ocular clonus, myoclonus, shivering, tremor, hypertonia, rigidity
autonomic effects—hyperthermia (temperature more than 39ºC or rapidly rising), sweating, flushing, mydriasis, tachycardia
central nervous system (CNS) effects—agitation, anxiety, confusion, altered conscious state. Delirium is not prominent.
Management of serotonergic toxidrome focuses on supportive care, gentle sedation, cooling, and sometimes antidotal therapy.
Serotonergic drugs
SSRIS
SNRIS
Some TCAS- clomipramine, imipramine
Some opiods - dextromethorphan, tramadol, pethidine, methadone, tapentadol
St john’s wort
MOAIS
Stimulants- amfetamines, phentermine, metamfetamine, MDMA, cocaine
Lithium
Clin F of serotonin syndrome
Effects of mild serotonergic toxidrome include tremor, mild tachycardia, inducible clonus, and lower limb hyperreflexia. It is unlikely to trouble the patient and often occurs at therapeutic doses of serotonergic drugs.
Effects of moderate serotonergic toxidrome include agitation, sustained clonus, tachycardia and hyperthermia less than 39ºC. It causes the patient distress and requires symptomatic relief.
Severe serotonergic toxidrome (serotonergic crisis) is a medical emergency and progresses to life-threatening multiorgan failure if not treated within hours. Effects of severe serotonergic toxidrome include rapidly progressive hyperthermia, muscle rigidity with sustained clonus, and seizures. It most commonly occurs with co-ingestion of serotonergic drugs that cause serotonin excess through different pharmacological actions. A monoamine oxidase inhibitor or stimulant drug is often involved in the most severe cases.
