Tox and blood gas stations Flashcards
Teaching toxidromes
High and Fast DDx (all mydriatic)
- Sympathomimetic
- Anticholinergic
- Serotonin syndrome
- Neuroleptic malignant syndrome
- Hallucinogenics
- Sedative withdrawal
High and fast skin differentiation
- white and wet = sympathomimetic
- Red and wet = Serotonin syndrome
- Red and dry = Anticholinergic
Low and slow DDx (all miotic)
- Sedative hypnotic and opioids
- Sympatholytic (BB, CCB’s, clonidine)
- Digoxin and Amiodarone
- Cholinergic
Low and Slow skin differentiation
- Diaphoretic = Cholinergic
- Dry = Opioid and sedative hypnotic
- Sympatholytic, Dig and Amiodarone can be either
Na+ channel blocker overdose SCBD
Most common Na+ Blockers
Tricyclics
- QRS wide and tall R’ AVR
- Anticholinergic syndrome
- Antihistamine (CNS depression)
- Alpha blockers (hypotension)
Local Anaesthetic
- Cardiac depression and seizures
- Intralipid
Propranolol
- Low and slow toxidrome
- Wide QRS, tall R’ AV
Quinine
- More common in Geriatrics
- Cinchonism (tinnitus/hearing loss)
Hydroxychloroquine
- Mild Na+ blocking effects
- Drowsiness and hypokalaemia
Carbamezepine
- Mild Anticholinergic syndrome
- Greater degree of CNS depression
- Ataxia and slurred speech
Cocaine
- Sympathomimetic toxidrome
- coronary vasospasm
Bupropion
-anti smoking, anxiety disorders
- Sympathomimetic toxidrome
- High risk seizures, one of the most common causes of toxicological seizures
- Direct cardiac toxicity causing systolic heart failure and QTc prolongation
- Can have latent phase due to MR formulations (toxin time bomb)
- Agitated delerium from anticholinergic effects
Sodium Bicarbonate
- 1-2mls/kg (mmols/kg) of 8.4% Sodium bicarbonate bolus, can be repeated
- Aiming for pH 7.50-7.55
- If ECG normalises then continue infusion
- 150mmols added to 1L Dextrose (150mls removed), given at 250mls/hr
- In children this is given at twice the full maintenance dose
- Works by alkalinizing the serum which favours the non-ionized form of the drug, less available to receptor
- Also sodium load favours sodium over TCA at the Na+ channel
Consultant points
- Physostigmine is contraindicated in anticholinergic delerium from TCA’s due to risk of arrest
- Lidocaine 1mg/kg IV and Lipid emulsion 1.5ml/kg 20% are used for refractory treatment
- Consider ECMO in refractory cases
Volatile Substance use SCBD?
Main Hydrocarbons
- Toluene
- Terpentine
- Carbon tetra chloride
- Chloral hydrate (medication)
Sudden Sniffers Death
- Hydrocarbon (usually Toluene) causes sensitization of the myocardium to catecholamines
- Sudden catecholamine surge (ie when running from police) can induce arrhythmias such as VT/VF
- Chloral hydrate has similar issue and this is the mechanism responsible for overdose arrhythmias
Other Hydrocarbon side effects
- Chemical Pneumonitis (chronic or large doses)
- Liver failure AKA hydrocarbon induced hepatitis
- hyperchloraemic NAGMA and hypokalaemia due to nephrotoxicity and RTA 1 (distal)
- Hydrocarbon induced encephalopathy (coma, seizures, ataxia)
- Asphyxiation
Deviation of Resuscitation
- Due to the hydrocarbon induced cardiac catecholamine sensitization, adrenaline is contraindicated
- If strong suspicion of hydrocarbon use causing arrest, dont give adrenaline as part of ALS algorithm
- Consideration for beta blockers and Fentanyl as sympatholytics (ie Esmolol 50mcg/kg/min)
Deviation to Intubation
- Ketamine could potentiate VT, consider opioid induction (ie fent)
- Be careful with blood pressure, usinng Norad/Adrenaline to prevent induction hypotension may cause VT
- Can consider Phenylephrine or Metaraminol as vasopressors
Beta Blocker and Calcium channel blocker overdose SCBD
Mechanism CCB’s
- CCB’s block L-type calcium channels in cardiac and smooth muscle
- Prevents intracellular entry of Ca+
- Negative chronotrope, inotrope and vasodilatation
- CCB’s difficult to treat as most therapies require normal intracellular calcium to work
Differences
- CCB hyperglycaemia, BB hypo
- BB hyperkalaemia
- BB can get QT prolonging and Na+ effects (Sotalol, propranolol)
- BB bronchospasm
- CCB profound vasodilatation and lactic acidosis
Decontamination
- Activated charcoal 1gm/kg
- MDAC for SR (unproven)
- WBI for SR CCB’s
Treatment
- There is NO single predictable antidote for BB and CCB overdose
- Fluids and inotropes (guided by echo findings)
- Atropine for bradycardia
- Pacing although may not work
- Glucagon (5mg IV)
- HIET
- Calcium (aiming Ca+ 1.5-2.0mmol)
- Others (Intra-aortic balloon pump, methlyene blue, intralipid)
- Consideration for ECMO
HIET
- 50mls/50% glucose as bolus (if BSL <15mmols)
- Infusion 100mls (3-5ml/kg)/hr 10% Dextrose
- 1U/kg bolus then 1U/kg/hr infusion actrapid, titrate up to max 10U/kg/hr
- Side effects include low BSL, hypo K and vasodilation
Differentials for Tox Bradycardia
- BB’s
- CCB’s
- Digoxin
- Amiodarone
- Clonidine
- GHB
- Organophosphates
Acute Digoxin Overdose CBD
Mechanism
- Na/K+ ATPase inhibition
- Leads to increased cardiac intracellular calcium (increased automaticity and inotropy) and extracellular potassium
- Digoxin also enhances vagal tone leading to SA/AV node suppression
- Non-digoxin glycosides include Bufotoxin (cane toad) and oleander
ECG changes
- Accelerated (>40) junctional escape rhythm (specific and most common)
- Paroxysmal atrial tachycardia with AV block (specific)
- Slow AF/Aflutter
- Regularised AF (specific)
- High grade AV block
- Ventricular arrhythmias and bigeminy
- Bidirectional VT (specific, see image)
- SVT with aberrancy
- Salvador dali sign (down sloping ST depression)
Treatment
- Digibind 2-5 ampoules for toxicity
- 5-20 ampoules for arrest
Consultant points
- K+ higher than expected for acidosis, consider Digoxin
- In cardiac arrest Electricity and adrenaline are unlikely to help, Amiodarone is contraindicated
- Consider Lignocaine 100mg and or MgSo4 for tachydysrhythmias
- Give Digibind 5-20 ampules ASAP for arrest and consider ECMO
One Pill Kills SCBD
Mnemonic ABC GET MOM N’ PA
A - Amphetamines (including MDMA)
B - Beta blockers
C - CCB’s, Clonidine, Corrosives, Camphor
G - Gliclazide (sulfonylureas)
E - Ethylene glycol, Eucalyptus oil
T - Theophylline, TCA’s
M - Methanol (ie nail polish remover), Moth balls (Napthalene)
O - Opiates, Organophospates
M - Methyl salicylates (oil of wintergreen)
N’ - Nicotine (vapes, cigarettes, insecticides)
P- Paraquat, Parkinsons (Selegiline)
A- Antidepressants (Temazepam and Diazepam, Venlafaxine, Bupropion) and Antimalarials
Resuscitation
- Always check temparture
- Always check and correct sugar
Corrosive Ingestions SCBD
Alkali
- Liquefactive necrosis
- Minimal pain so easier to drink larger volumes
- Strongly penetrates through mucosa, often minimal makes it to stomach but significant damage to oesophagus/oropharynx
- High chance Mediastinitis
Acid
- Coagulative necrosis
- Very painful so often spit it out, difficult to drink large amounts
- More makes it to the stomach, tend to have less damage to oesophagus
- Acid causes pylorospasm leading to it sitting in stomach, more likely to cause gastric perforation and peritonitis
- However higher likelihood of upper airway damage, unclear but thought to be due to choking/gagging
- Lower chance mediastinitis
Signs/Symptoms
- Oropharyngeal, epigastric and retrosternal pain
- Odyno/dysphagia
- Hypersalivation
- Vomiting/haematemesis
- Larynx/epiglottic injury has hoarseness, aphonia and stridor
Glyphosate
- A very common pesticide/Acid
- A mild corrosive although in hgih doses can cause transmural burns
- HAGMA with high lactate
- Myocardial depression
- Hyperkalaemia
Button Batteries
- Contain strongly concentrated alkali substance
- Injury from alkali burns, electrical current discharge and pressure necrosis
Toxic Alcohols SCBD
Ethylene Glycol
- Flank pain and haematuria
- Oliguria
- HAGMA, Osmolar gap
- Calcium oxalate crystals
- Hypocalcaemia
Methanol
- Visual blurring/scotoma leading to blindness
- HAGMA and osmolar gap
Isopropyl Alcohol
- Resembles ethanol toxicity
- Osmolar gap but no HAGMA
- fruity breath and CNS depression
Ethylene Glycol Mx
- May need intubation, will need hyperventilation and apnoeic BVM to prevent worsening of acidosis
- Support BP
- Treat concomitant hyperkalaemia
- Treat hypocalcaemia if refractory seizures or long QT
- Antidote is Ethanol and Fomepizole
- Haemodialysis is ultimate treatment
Fomepizole
- 15mg/kg loading dose then 10mg/kg IV infusions
- Expensive but minimal side effects
- Doesnt need titration to blood level
Ethanol Antidote
- 1.8ml/kg 43% ethanol loading dose (usually via NG)
- Equivalent is 3x 40ml shots of vodka in a 70kg adult
- 0.4ml/kg/hr 43% ethanol maintenance (40mls shot/hr)
- Needs titration to ethanol level of 100-150mg/dl (BAC 0.1-0.15)
Serotonin Syndrome vs NMS vs anticholinergic delerium SCBD
SS vs NMS
- SS hyperreflexic and clonus
- SS more acute, NMS more chronic
- NMS rigidity, autonomic instability
SS Triad
- Autonomic dysfunction (hyperthermia and tachycardia)
- Delerium (agitation, seizures)
- Neuromuscular (Hyperreflexia, clonus, mild rigidity, tremor)
NMS Tetrad
- Hyperthermia
- Muscular (cogwheel) rigidity
- Delerium (mutism, catatonia)
- Autonomic instability
Anticholinergic delerium
- Hyperthermia
- Delerium (mumbling speech, picking behaviour)
NMS diagnostic criteria
- Exposure to dopamin antagonist or withdrawal of dopamine agonist
- Hyperthermia
- Muscular rigidity
- Delerium
- Evidence of rhabdomyolysis (CK >4 times normal)
- Significant autonomic instability affecting 2 or more areas (ie BP and HR, or RR and Diaphoresis)
- Negative workup for all else
Treatment
- Benzos and Cyproheptadine (12m or or NG) for SS
- Supportive care
- Active cooling
- Temp >41.1C is suggestive of severe disease and will likely need early intubation
Big Black Spider Bites SCBD
Funnel Web Basics
- Any big black spider QLD/NSW
- Atrax robustus
- Severely painful bite with obvious fang marks
- Systemic envenomation within 30mins
Toxin effects
- Potent neurotoxin that block Na+ channels and produces cholinergic + adrenergic stimulation
- Increase autonomic activity and neuromuscular excitation
CVS - Tachycardia, HTN, but also brady and hypo (cholinergic)
Neuro Oral paraesthesias, fasciculation, paralysis, coma
General Pain, agitation, GI upset, lacrimation, sweating, salivation
MX
- PIB indicated
- 4 ampules antivenom cardiac arrest, 2 ampules for symptoms
- Supportive care including intubation
- Atropine for cholinergic effects
Red Back basics
- Temperate areas, not northern Aus or tasmania
- Pain comes on 5-10mins later, at bite site that radiates proximally
- PBI not indicated
Latrodectosus
- Pain radiates from origin to regional and then general
- Severe back, abdomen, neck, head pain etc
- N/V, diaphoresis, piloerection
- Sweating may be localised to limb or generalised
- Children may get penile erection
Snake bite SCBD
Organophosphate SCBD and Weakness critical DDx
Toxic Weakness DDx
- Organophosphates
- Funnel web spider
- Snake bite (descending)
- Blue ringed octopus (descending)
- Botulism (honey, wounds, canned foods) descending
- Tick paralysis (ascending)
- Mushroom Ingestion (Clitocybe and Inocybe species)
- Rhabdomyolysis secondary to toxin
- Non-Tox (GBS, transverse myelitis, CVA, spinal cord compression, myaesthenia gravis)
Other Differentials
- AMI with cardiogenic shock
- SAH
- Trauma
- Metabolic issues ie hypoglycaemia
Muscarinic effects
- DUMBELLS (see pic)
- CNS depression/delerium
Nicotinic effects
- Fasciulations/tremor
- Weakness
- Paralysis
- Tachycardia, hypertension
Basics of Management
Initial
- Universal precautions and well ventilated room, remove all clothes and decontaminate skin
Atropinisation
- 1.2mg boluses every 2-5mins aiming for Hr >80, SBP >100, mydriasis and dried secretions
Airway
- Progressive weakness and vomiting, almost always intubated, prepare for soiled airway
Seizures
- Direct toxic effect and hypoglycaemia
- Benzo’s are mainstay, discuss with tox
- Seek and treat hypoglycaemia and other electrolyte disturbances
Pralidoxime
- Controversial, 2gm IV load, discuss with tox
Disposition
- ICU vs retrieval when stable
- NGT and IDC, assess for ileus
Risk to Staff
- Very low risk, take universal precautions
- Symptoms in staff often related to solvent exposure
- Any staff affected should have appropriate risk assessment, treatment and documentation
- Consider counselling and debrief
Hallucinogenics
Cannabis
- inhaled 15-30mins onset
- Ingested 30-120mins
- Low dose reduced attention, executive function and short term memory
- high dose get delerium, panic attacks/anxiety, N/V, myoclonic jerks and psychosis
Other symptoms
- Sympathomimetic (hypertension, and tachcycardia
- Anticholinergic (dilated pupils, dry mouth, red eyes, hunger)
- ETOH-like (nystagmus, ataxia and slurred speech)
Paediatric ingestions
- Ataxia
- Behaviour changes
- Hyperkineses (excessive purposeless movements limbs)
- Coma and resp depression
Cannabinoid Hyperemesis syndrome
- Diagnosis Rome IV criteria (cyclical vomiting, prolonged heavy cannabis use, relief with cannabis cessation)
- Cyclical vomiting and abdominal pain relieved by hot showers/baths
- Droperidol and Capsaicin have the most evidence
Acid base disturbance differentials
HAGMA = SULK
S- Salicylates
U- Uraemia
L- Lactate
K- ketones
NAGMA = BAND
B- Bicarb loss (excessive diarrhoea, RTA, pancreaticoduodenal fisula)
A- Adrenal (adrenal crisis, mineral or glucocorticoid deficiency)
N- NaCl in excess (iattrogenic)
D- Drugs (Spironolactone, acetazolamide)
Metabolic Alkalosis = CHED
C- Compensation/COPD
H- HCL loss (vomiting)
E- endocrine (adrenal excess, barters syndrome, gluco/mineral corticoid excess)
D- Drugs (DIURETICS, NaHC03, milk alkali, laxative abuse)
Respiratory Alkalosis
hypoxia vs non-hypoxia mediated
Hypoxia
- PE, ARDS, APO, asthma etc
Non-Hypoxia
- Stimulants (sympathomimetics, MDMA etc)
- Salicylates
- Head injury/bleed, central stimulation
- Anxiety, pain
Respiratory Acidosis LOAF
L- Lung insult (contusions, haemo pneumothorax, ARDS, PE, APO etc)
O- Obtundation
A- Acute airway disorders ie airway obstruction, Asthma, acute on chronic COPD
F- Fatigue (toxins, myopathies, GBS)
Lactate rise causes
Type A
- Ischaemia or hypoxia
Type B
B1- Disease related (liver failure, leukaemia, sepsis, catecholamines etc)
B2- most toxins, beta agonists
B3- Inborn errors of metabolism
Key Toxicological Parameters
Charcoal Use
- SSRI’s
Dialysable drugs
- Aspirin
- Lithium
- Ehylene glycol/toxic alcohols
- valproate/Carbamezepine
- Postassium
- Metformin
Key doses
- Citalopram >600mg
Key serum levels
Valproate
-
Iron
- >90umol
Key antidotes
Na+/LAST
- Intralipid 1.5ml/kg
Methaemglobinaemia
- Methylene blue 1mg/kg
Digoxin
- Digibind 5-20 vials for arrest, 2-5 for non-arrested
Organophsophates
- Atropine 1200mcg Q5mins
- Pralidoxime
Dabigatran
- Idarucizumab 5gm
Flumazenil
- 100mcg or 5mcg/kg
Toxic Alcohols
- Fomepizole 15mg/kg load, 10mg/kg
- Ethanol 96% solution 8ml/kg load then 2ml/kg/hr, aim BAC 0.1-0.15
Iron
- Desferrioxamine 5mg/kg
Paracetamol
- NAC 200mg/kg 4hrs, then 100mg/kg over 16hrs
Paracetamol overdose
Acute IR Preparation
- >10gm or >200mg/kg
- Abdo pain, N/V
- Liver failure (coagulopathy and encephalopathy)
- NAC if APAP level elevated at 4 or more hours post ingestion
- If presenting after 8hrs then start empiric NAC, continue if APAP high or ALT >50
- If presenting >24hrs them start NAC, continue NAC if ALT >50 or detectable APAP
NAC Mechanism
- Increases glutathione production
- Direct binding of NAPQI
- Provision of inorganic sulfates (ie thiol) that bind NAPQI
- Can reduce NAPQI back to paracetamol
NAC issues
- Relative contraindication is previous anaphylactoid reaction
- Anaphylactioid reactions occur 10-40% of cases, if it occurs then cease infusion, treat the reaction then slowly restart the infusion
- Pregnancy is not a contraindication
NAC can be ceased at 20hrs if
- Measure 2hrs prior to end of NAC
- Conc <10mg/L or 66umol/L
- ALT <50
- INR <2.0
- Patient clinically stable
NAC dosing
- 200mg/kg over 4hrs, then 100mg/kg over 16hrs
- If in an acute ingestion paracetamol level is more than double the nomogram, > 30gm or >500mg/kg then double the 2nd bag to 200mg/kg
