Toxicology Flashcards
What are the 3 primary causes of poisoning?
- Intentional - [deliberate self poisoning, malicious/3rd party]
- Accidental [occupational, domestic, error/misunderstanding, prescribed medications]
- Recreational
How are poison’s introduced into the body/4 entry routes?
- Ingested
- Inhaled
- Injected
- Absorbed
What is the primary approach to the poisoned patient?
Priority is to circulation, airway, breathing. Adults CAB, paeds ABC
What are possible concerns regarding a poisoned patient?
- Pt contamination, and toxic environment.
- Aggressive/agitated Pt
- Dysrhythmias
- Loss of airway reflexes/burns to airway
- Seizures
- Hypoglycaemia
- Hyperthermia
- Consider resuscitation antidotes and other management.
Why would you require CCP back up for a poisoned patient?
- Pacing
- Dysrhythmia management
- Inotropic/chronotropic support
- Atropine in organophosphate poisoning
- Sodium bicarbonate in tricyclic overdose
- Calcium in CCB overdose
- Glucagon in beta blocker OD
- Management and/or sedation of agitated Pt’s
What is the risk assessment for the poisoned patient?
- Hx
- Agent(s)
- Dose(s)
- Time since ingestion
- Clinical features and progress
- Patient factors (weight & co-morbidities)
What did you take? When did you take it? What did you take with it? Have you vomited?
What is the role of poison’s information centre?
It’s a handy source of information and guidance. On call toxicologists available in specific cases.
What is a toxidrome?
Is a group of examination findings [S&S & Hx], it may suggest the pharmacology behind a person’s clinical presentation.
What are common toxidrome’s?
- Cholinergic
- Anticholinergic
- Sympathomimetic
- Opioid
- Serotonin
Go through the muscarinic effect acronym SLUDGEM-BBB
S = salivation L = lacrimation U = urination D = defecation G = GI upset E = emesis M = miosis
B = bradycardia B = bronchorrhea B = bronchospasm
Go through the muscarinic effect acronym DUMBELS
D = diarrhoea & Diaphoresis U = urination M = miosis [pinpoint pupils] B = bronchorrhea, Bradycardia & Bronchospasm E = emesis L = Lacrimation S = salivation
What are the 4 primary causative agents of cholinergic toxidrome - muscarinic effecs
- Organophosphates & carbamate insecticides
- Chemical warfare nerve agents
- Agents used in alzheimers dementia [donepezil, galantamine, rivastigmine, tacrine]
- Agents used in myasthenia gravis [neostigmine, physostigmine, pyridostigmine, endrophonium]
What is the nicotinic effects? [Cholinergic toxidrome] - (MATCH)
M = muscle weakness/fasciculation A = adrenal medulla activity T = tachycardia C = cramping H = hypertension
What are some signs & symptoms of anticholinergic toxidrome? [Catch phrase]
“Red as a beet, dry as a bone, blind as a bat, mad as a hatter and hot as a hare”
- Dry skin
- Hyperthermia
- Thirst
- Dry mouth
- Dilated pupils
- Tachycardia
- Urinary retention
- Slowed gastric emptying
- Decreased bowel sounds
- Delirium
- Hallucinations
What are (up to) 10 examples of causative agents for anticholinergic toxidrome? [drugs/agents]
- Antiparkinsonian drugs [benxtropine, amantadine]
- Antitussives [dextromethorphan]
- Antihistamines [promethazine, doxylamine]
- Motion sickness agents [mecilizine, hyoscine-scopolamine]
- Bronchodilators [ipratropium]
- Antimuscarinic agents [atropine, hyoscyamine]
- Antidepressants [Tricyclic]
- Anticonvulsants
- Atypical antipsychotic agents
- Antipsychotic agents
What are the examples of sympathomimetic toxidrome?
- CNS excitation
- Seizures
- Tremor
- Hyperreflexia
- Hyper/hypotension
- Tachycardia
- Low potassium, raised blood glucose, acidosis
What are some causative agents for sympathomimetic toxidrome?
- Amphetamines
- Cocaine
- LSD
- Caffeine
- Theophylline [related to caffeine]
- Phencyclidine [amphetamine derivative]
- Methylphenidate [ritalin]
What is serotonin toxidrome [syndrome] ? (Factors related to it)
- Mental status [agitation/restlessness/ confusion/hypomania]
- Fever
- Motor system [clonus/myoclonus, tremor/shivering, hyperreflexia/rigidity]
- Autonomic nervous system [diaphoresis/tachycardia/flushing]
What are some causative agents for serotonin syndrome?
- Selective serotonin re-uptake
- SNRIs
- Antidepressants
- Monoamine oxidase inhibitors
- Lithium
- Antiemetics
- Analgesic agents and antitussives
- Anticonvulsants
- Drugs of abuse
- Ginseng
- St Johns Wort
How would you manage serotonin syndrome?
Manage ABC’s, hyperthermia, dehydration, hyperreflexia/rigidity (CCP’s)
What are some conditions that result from opioid toxidrome?
- CNS depression
- Hypoventilation
- Hypotension
- Miosis
- Rapid response to naloxone
What are 3 other opioids/medications that have special cases for risk assessment?
- Destropropoxyphene
- Tramadol
- Pethidine
What are some clinical features of opioids?
- Opioid toxidrome [CNS depression, hypoventilation, hypotension]
- Tachycardia
- Bradycardia
- Pulmonary oedema
- N & V
- Prolonged non-lethal intoxication can lead to hypothermia, compartment syndrome, skin necrosis, hypoxic brain injury.
What are some opioid management principles? (4)
- Dangers [drug paraphernalia]
- Maintenance of airway and breathing
- Use of naloxone
- Manage other presentations [seizures, pulmonary oedema, hypothermia]
What occurs after benzodiazepines consumption/overdose?
- They are sedative-hypnotics
- Involved in up to 1/3 of deliberate self-poisonings
- Potential for airway obstruction and aspiration
- Patient may present with hypothermia, hypotension and bradycardia.
- Increased risk of complications if co-ingestion of CNS depressants [alcohol, opioids, antidepressants]
What are some clinical features of benzodiazepines?
- Onset usually within 1-2hrs [more rapid if IV]
- Lethargy
- Ataxia
- Slurred speech
- Drowsiness
- Reduced responsiveness
- Profound coma is rare [more common in elderly]
How would you manage benzodiazepine overdose?
- Manage ABC’s [positioning, respiratory support]
- May need more aggressive treatment if co-ingestion occurred
What are some concerns with corrosive ingestion?
- Can cause injury to upper airway & GI tract
- Upper airway injury is potentially life threatening
- Significant GI tract injury is indicated by stridor, drooling & vomiting
- The absence of lip or oral burns does exclude GI injury
What is your corrosive management?
- DRABC’s
- mouth may be washed
- small amount of water may be administered orally [1/2 cup] but avoid copious amounts of oral fluids.
- Transport without delay
- Do not induce vomiting*
What is paraquat poisoning?
- It is a widely used herbicide
- Potentially lethal following ingestion as little as a mouthful
- Usually results in fulminating multi-organ failure - death
- May present with signs of oral burns and/or GI S&S
How do you treat paraquat poisoning?
- Do NOT induce vomiting
- Consider giving foods or other solids
- Withhold oxygen
- Urgent transport
What is glyphosate and what can it cause?
A common herbicide.
- GI corrosive symptoms
- Upper airway complications from oropharyngeal corrosive injury
- Aspiration pneumonitis and non-cardiogenic pulmonary oedema
- Myocardial depression and hypotension
- Can lead to multi-organ failure and metabolic acidosis
What does hydrocarbons include?
- Petroleum distillates
- Kerosene
- Turpentine
- Essential oils
- Beneze
- Toluene
- Xylene
[deliberate misuse of the above]
What are some clinical features of hydrocarbon poisoning?
- Immediate coughing or gagging [aspiration]
- Wheeze, tachypnoea, hypoxia, haemoptysis and pulmonary oedema
- Dysrhythmias
- Profound CNS depression & coma
- Seizures
- Ataxia
- N & V
What is your management plan for hydrocarbon poisoning?
- Remove Pt from source
- De-escalation strategy if agitated
- Do NOT induce vomiting [if ingested]
- Provide oxygen and bronchodilators, if bronchospasm presents
- Manage seizures as per guidelines
- CCP backup for dysrhythmia management.
What is carbon monoxide poisoning?
CO is a common cause of fatal and disabling poisoning in most developed countries.
Haemoglobin - carboxyhaemoglobin
[innacurate pulse oximetry]
What are the effects of carbon monoxide poisoning?
- Hypoxia
- Endovascular oxidative injury and inflammation
What are some guiding principles to organophosphorous agents?
- Protection of self and others from contamination
- Remove Pt from contamination
- If Pt contaminated will need to be decontaminated
- Maintenance of ABC’s
- Management of hypotension
- CCP backup & prenotify
What happens in paracetamol poisoning?
Paracetamol overdose leads to a depletion of glutathione stores → body then unable to convert intermediate toxic metabolites into non-toxic metabolites .
Easy to access in bulk.
What are the clinical features of iron overdose?
- N & V, may be haematemesis
- Diarrhoea
- Abdominal pain
- Can be potentially fatal
What are some things to consider with iron overdose; regarding treatment plan?
Manage hypovolaemia and transport to hospital.
What are 3 examples of hypoglycaemic agents?
- Insulin
- Sulphonylureas
- Biguanides
How will you manage hypoglycaemic patients?
Manage ABC’s, and per the QAS guideline.
What are 3 examples of cardiovascular drugs?
- Beta blockers
- Calcium channel blockers
- Digitalis [digoxin]
Why are beta blockers potentially fatal?
Due to their cardiovascular effects. [Sotalol and propranalol are considered more toxic]
What are the clinical features of beta blockers?
- PR prolongation
- Bradycardia
- Hypotension
- Delirium
- Coma
- Seizures
- Bronchospasm
- Hyperkalaemia
- Hypo/hyperglycaemia
Why do verapamil and diltiazem cause cardiovascular collapse?
Due to the central cardiac effects and peripheral vasodilation.
What are some clinical features of calcium channel blockers?
- Bradycardia [1st deg heart block]
- Hypotension
- CNS depression
- Seizures
- Sinus of myocardial ischaemia and stroke may occur
- N & V
- Hyperglycaemia
What is your management plan for calcium channel blockers?
- Manage ABC’s
- Manage hypotension
- Urgent transport to hospital
- Call CCP’s for: calcium, pacing, chronotropic support and arrhythmia management.
What are the clinical features of Digoxin overdose?
- N & V
- Hypotension
- Abdominal pain
- Bradycardia
- Increasing automaticity
- Lethargy
- Delirium
- Confusion
- Visual disturbances
What drugs are included in the Selective Serotonin Reuptake Inhibitors (SSRI) group?
- Fluoxetine
- Sertraline
- Paroxetine
- Fluvoxamine
- Citalopram
*Seizure management
What is the major brand encountered in the Serotonin Noradrenaline Reuptake Inhibitors (SNRI) class?
Venlafaxine [effexor].
*14% or Pt’s have seizures but is dose related
TCA overdose is the leading cause of morbidity & mortality, and the ingestion of 10-20mg/kg is potentially life threatening. T/F
True
What is the 3 major effects of TCA overdose?
- CNS [sedation & coma]
- Anticholinergic effects [agitation, delirium & restlessness, mydriasis, dry/warm/flushed skin, tachycardia, myoclonic jerks]
- CVS [initially sinus tach, hypotension, broad complex tachy/bradyarythmias]
Fantasy is a street name for Gamma Hydroxybutyrate [GHB] and is a colourless & odourless liquid. T/F
T
What are the clinical features for GHB?
- Miosis
- Myoclonic movements
- Possible airway obstruction
- Cheyne-Stokes breathing
- Vomiting
- Sometimes mimicking generalised seizures
- Agitation and delirium
- Coma
- Respiratory depression
- Bradycardia
- Sweating
What are the clinical features for psychostimulant toxicity?
- Dilated pupils that react sluggishly to light
- Clenched jaw
- Restlessness, agitation,
repetitive movements - Rapid speech
- Motor agitation or pacing
- Hypertension
- Tachycardia
- Sweaty palms, flushed diaphoretic facial skin
- Hypervigilance, • Paranoia
- Hyperthermia
What will you need to manage in regards to psychostimulant toxicity?
- Manage CABs/ABCs.
- Verbal de-escalation strategy if agitated
- May need restraint
- Manage hyperthermia
- Manage seizures as per guidelines
- Manage poor perfusion/dehydration
- Manage chest pain
[Aspirin is not recommended for chest pain if the patient is hypertensive due to increased risk of cerebral haemorrhage.]
