Emergency Medicine Flashcards
3 Cs of TCA poisoning
Convulsions
Coma
Cardiac (widened QRS –>VT)
**as TCA is a sodium channel blocker–> channelopathy –> wide QRS
**essentially leads to anticholinergic/seritonergic syndrome
Treat with 2C’s: BI -Carbonate if QRS widened or ventricular arrythmia
Can give activted charcoal if severe but need to intubate first
after intubation, hyperventilate to optimise pH to 7.5 (alkalise)
Anticholinergic antidote
Normally just supportive - treat symptoms
Physostigmine- contravertial
Sodium bicarbonate if TCA
Anticholinergic syndrome - triggering agents
Antihistamines
Anti tussives
Dextromethopha, diphenhydramine
Antipsychotics
Anti convulsants- carbamazepine
Anti emetics - hyoscine
Other: benztropine glycopyrrolate, oxybutynin
“travelcalm” - antihistamine + hysocine bromide
Anticholinergic syndrome presentation
fever
delirium
confusion
dilated pupils/mydriasis
dry flushed skin and mouth
constipation, reduced bowel sounds
urinary reterntion
hypertension
picking
Severe:
coma
HTN
QRS widening and increased QT
rhabdomyolysis
seizures
B blocker antidote
glucagon
or
high dose insulin with glucose infusion
benzodiazapine antidote
flumazenil (if iatrogenic, as can cause seizures in withdrawal)
usually only need supportive care
beta blocker overdose presentation
bradycardia
altered mental state - coma
hypotension
ventricular arrythmias –> VT
hypoglycemia
brain imaging when CNS tumor suspected
Persistent headache in the following settings: wakes a child from sleep; occurs upon waking; in any child less than four years of age; associated with disorientation or confusion.
Persistent vomiting upon waking.
Visual findings including papilloedema, optic atrophy, new onset nystagmus, reduced acuity not due to refractive error, visual field reduction, proptosis, and new onset paralytic (non-comitant) squint.
Motor findings including regression in motor skills, focal motor weakness, abnormal gait and/or coordination, bell’s palsy with no improvement over four weeks, and swallowing difficulties without an identifiable local cause
how do you maximise urinary excretion of aspirin
urinary alkalinisaiton with sodium bicarbonate
Organophosphate ingestion
= cholinergic syndrome
KILLER Bs
Bronchospasm
Bronchorroas
Bradycardia
Pinpoint pupils
SLUDGE
Salivation
Lacrimation, lethargy
Urination
Diarrhoea + abdo cramping
Emesis
think WATER FROM EVERYWHERE
+ agitation, anxiety, seiixures, coma, flaccid paralysis
Pinpoint pupils
Rx: atropine
which toxidromes have pinpoint pupils
cholinergic syndrome
opioids- morphine, fentanyl
alcohol
BZDs
which toxidromes have hyperthermia
anticholinergic (hot as a hare)
sympathomimetic
seritonin syndrome
main features serotonin syndrome
Cognitive effects: delirium, headache, agitation, hypomania, mental confusion, hallucinations, coma
Autonomic effects: shivering, sweating, hyperthermia, hypertension, tachycardia, nausea, diarrhoea.
Somatic effects: myoclonus (muscle twitching), hyperreflexia (manifested by clonus), tremor.
DILATED PUPILS
which are the “single pill can kill” drugs
Emphetamines (ecstacy)
Ca channel blockers
Beta blockers
Opioids
Sulfonylureas
Theophylline
TCA
Chloroquine
when can activated charcoal be used for ingestions?
<120 mins since ingestion
Chloroquine
Ca channel blocker
carbamazepine
cochicine
beta blockers
flecanide
salicilates
Contraindications for activated charcoal
Alt mental status- high risk of aspiration (would need to intubate first)
Acid/alkali
GI perforation
Ethanol
Hydrocarbons
Any metals, potassium , iron, lead etc
>1 hour post ingestion
when is whole bowel irrigation used
only for slow release enteric coated tablets
can be used for iron when desferroxamine has not been effective
organophosphate antidote
atropine (anticholintergic)
iron antidote
desferoxamine
lead antidote
EDTA
methonol or ethylene glycol antidote
ethanol
BZD antidote
flumazenil
MoA anticholinergic syndrome
Anticholinergic syndrome results from competitive antagonism of acetylcholine at central and peripheral muscarinic receptors. Central inhibition leads to an agitated (hyperactive) delirium - typically including confusion, restlessness and picking at imaginary objects - which characterises this toxidrome.
how do you achieve cooling in overdose such as ecstasy where there is hyperthermia
Removal of clothing
Ice packs to nape of neck, armpits
Fans
Gastric lavage
Cooled IV fluids
ethylene glycol
Found in Anti-Freeze/Carpet fabric cleaners
Toxic levels: 100mls - Adults, 20mls - Child
3 stages - CNS depression—> CVS/Resp depression —> Renal failure
High anion gap metabolic Acidosis —> Renal Failure
24-36hrs - to be fatal
Levels able to be measured
Neuroleptic Malignant syndrome
life threatening neorological emerency associated with use of antipsychotic agents
Increased body temperature >38°C
Confusion, delirium or altered consciousness
Fever
Rigidity
Dysautonomia
–> rhabdo, hyperkalemia, AKI, seizures
both typical and atypical antipsychotics
Carbon monoxide poisoning
CO preferentially binds to haemoglobin (200x higher affinity for Hb compared to O2) reducing its oxygen-binding capacity, it shifts the oxygen dissociation curve to the left thus inhibiting the release of bound oxygen in the periphery and it acts as a direct cellular toxin by impairing aerobic metabolism.
myalgia, headache, weakness, clumsiness, blurry vision, flu like illness-> seizure, coma, cardiac arrest
COhb >10-40%
Rx:100% high flow O2 or hyperbaric O2 to replace carboxyHb and supersaturate blood with O2
D: may cause Parkinsonism
**Displaces O2 from haemoglobin as CO has much higher affinity for Hb than O2
Methaemoglobinaemia
Methaemoglobinaemia is the state of excessive methaemoglobin in the blood
methaemoglobin is an altered state of Hb where ferrous ions (Fe2+) of haem are oxidised to the ferric state (Fe3+) and rendered unable to bind O2
normal level is < 1.5%
Can occur with ingestion of cold packs or nitrites in meat
can also be congenital
Rx: high flow 100% O2. methylene blue.
Lead poisoning
non specific signs from chronic ingesiton
Fanconi syndrome, microcytic anemia, reduced bone and muscle growth, behavior problems, lower IQ
Lead lines on Xray
calcium channel blocker antidote
calcium gluconate
Insulin/glucose
intralipid
calcium channel blocker o/d presentation
bradycardia
hypotension
shock
complications amphetamine overdose
DILATED PUPILS
Severe hyperthermia- requiring cooling
Rhabdo
Seizures
Intracranial haemorrhage
Hyponatremia
Cerebral oedema
cholinergic overdose
WET- secretions everywhere
Confusion, coma
Pinpoint pupils
Wet- salivation, lacrimation,urination, diarrhoea, vomiting
Killer Bs- bronchorroea, bradycardia, bronchospasm
Hypotension –> cardiovascular collapse
Examples- organophosphates, nerve agents, physostigmine, poisonous mushrooms
Antidote: ATROPINE
Pralidoxime binds organophosphate
cyanide antidote
hydroxocobalamin
dicobalt edetate
sodium thiosulphate
difference between serotonin syndrome and neuroleptic malignant syndrome
Serotonin- abrupt onset, resolves quickly, increased reflexes, myoclonus and tremor, dilated pupils
neuroleptic malignant - gradual onset, prolonged course, muscle rigidity, hyporeflexic, normal pupils
digoxin antidote
digoxin immune Fab- Digibind
EBV symptoms
fever
malaise
cervical lymphadenopathy (posterior)
headache
pharyngitis/tonsilitis with exudate
herpangina
nausea/vomiting/anorexia
splenomegaly (hepatomegaly uncommon)
Ix: lymphocytosis, deranged LFTs
ethylene glycol antidote
ethanol
pyridoxine
eucalyptus oil poisoning
Onset: Within 30 mins to 4 hours post ingestion
Duration of symptoms: usually resolve within 24 hours
Dose related toxicity
Small ingestions of pure oil can lead to severe symptoms. A dose of 2-3 mL can induce mild CNS depression with drowsiness and/or dizziness and ataxia. A dose of ≥5 mL can induce significant CNS depression with coma
miosis/mydriasis
myoclonuc
CNS depression- drowsiness, dizziness, ataxia, seizures
tachycardia
hypotension
respoiratory depression, bronchospasm, apnoea, aspiration pneumonitis
nausea/vominting, epigastric pain, diarrhoea
Rx: supportive care
Hallucinagen O/D (eg LSD)
Hyperthermia
Tachycardia
Hypertension
Hallucinations
Agitation
Dilated pupils
Nystamus
Iron overdose
<20 mg/kg: asymptomatic
20-40 mg/kg: GI symptoms only. Symptoms usually last <6hrs
40-60 mg/kg: GI symptoms, systemic toxicity not expected. Symptoms usually last <8hrs
60-120 mg/kg: potential for systemic toxicity
>120 mg/kg potentially lethal
Presentation
Initial GI symptoms
Quiescent/latent period 6-24 hrs with improvement in GIT symptoms
Cardiogenic shock and acidosis - multi system organ failure, coma
Hepatic necrosis –> acute liver failure
Bowel obstriction after 2-8 weeks
Ix:
AXR if tablet ingestion
FBE: leukocytosis
UEC,LFT
VBG- high anion gap metabolic acidosis, hypoglycemia
Serum iron immediately and at 4 hours
Coags- coagulopathy secondary to liver
injury
Management
Antidote- desferrioxamine
WBI if desferrioxamine doesnt work
isoniazid antidote
pyridoxine
local anaesthetic antidote
intralipid
local anaesthetic o/d management
sodium bicarbonate if ventricular dysrythmias 2’ sodium channel blockade
intralipid 20% - severe cardiovascular toxicity
methylene blue for methaemoglobinaemia
brown snake bite effects
Coagulopathy
DIC
Neurotoxicity- rare, nil myotoxicity
abnormal INR, high aPTT, fibrinogen very low, D-dimer high
most common effect tiger snake bite
Consumptive coagulopathy
Neurotoxicity - 30%
Myotoxicity- 20%
most common effect of ethanol in young child
ypoglycemia
Alcohol poisoning – drowsiness, dysarthria, ataxic and hypoglycemia.
Alcohol inhibits gluconeogenesis but plasma glucose can usually be maintained from glycogen breakdown
neuroleptic malignant syndrome antidotes
dantrolene
bromocriptine
in mild cases - starts with benzos (loraz or diaz)
neuroleptic malignant syndrome presentation
fever
tachycardia
labile BP
tachypnoea
confusion agitated delirium
dilated pupils
muscle rigidity
rhabdomyolysis
hyperkalaemia
renal and liver failure
Ix: increased WCC, CK, LFTs, hypocalcemia and hypomagnesemia, hyperkalemia, metabolic acidosis
high mortality, 10-20%
caused by antipsychotics and antiemetics (eg domperidone, droperidol, metoclopramide, promethazine)
central dopamine receptor blockade
usually first 2 weeks of antipsychotic therapy
higher risk with rapid dose escalation, switch from one agent to another, IM administration
opioid toxicity
Constricted pupils
CNS depression
Low temp, HR, BP, RR
Hyporeflexia
Eg heroin, morphine, methadone, oxycodne, codeine
oral hypoglycemic antidote
octreotide
paraphymosis
when foreskin is retracted past the coronal sulcus and the prepuce cannot be pulled back over the glans, resulting in venous stasis and severe oedema
phimosis
inability to retrace prepuce
usally physiological
becomes retractable by age of 3 years in 90%
pre pubertal hymen appearance
Annular – most common in newborns/infants.
Cresenteric- most commmon early childhod
Fimbriated – i.e. redundant hymen. More common in newborns (or pubertal adolescents) due to effect of oestrogen (maternal oestrogen in the case of newborns).
Septated – normal variant in about 5% of cases only.
sedative overdose
eg BZD, barbiturate, alcohol
everything goes down
Hypothermia
Bradycardia
Bradypnoea
Hypotension
CNS depression/confusion/coma
Constricted pupils
Hyporeflexia
Causes serotoninc syndrome
introduction or increase of single seritonergic drug
drug interaction between 2 seritonergic drugs- most common
SSRIs/SNRIs
MAOIs
TCAs
Lithium
Tramadol
Pethidine
Fentanyl
MDMA
LSD
Amphetamines
Cocaine
Ondansatron
Metoclopramide
Sumatriptan
St Johns wart
Serotonin syndrome management
IV benzodiazepine
Serotonin antagonist if symptoms refractory
Cyproheptadine
Chlorpromazine
sulphonylurea antidote
octreotide- somatostatin analogue. suppresses insulin release from pancreatic cells
but first give IV glucose bolus –>10% glucose infusion if hypoglycemic
Sympathomimetic toxicity
eg cocaine, amphetamine, methamphetamine, ritalin, LSD, MDMA
Fever
Tachycardia
Hypertension
Mydriasis - but briskly reactive
Diaphoresis
Psychomotor agitation, paranoia, psychosis
Increased energy
Hyperactive bowel sounds
Reduced pain response
***can only differentiate from sedative/ETOH withdrawal with history
Sympathomimetics
Treatment
Supportive
IV Benzodiazepines
Cooling for hyperthemia
TCA o/d
one pill can kill
signs usually within an hour of ingestion
Anticholinergic syndrome
CVS- reduced cardiac contractility and hypotension, widened QRS —> VT/VF, prolonged QT
CNS depression/coma, seizures
tachycardia
vomiting
blurred vision
ataxia
delirium
urinary retention
ileus
Ix: VGG (acidosis), TCA levels, ECG,
Rx: Doses >10-15mg/kg need to be intubated, ventilated and given charcoal
If QRS widened–> sodium bicarbonate bolus
warfarin antidote
vit k
FFP
prothrombinex
ETT tube size equation (uncuffed)
(age /4 ) +4
Carboxyhaemoglobin
- Product of the reaction between carbon
Monoxide and haemaglobin- Affinity of CO for Hb is 200 x greater than for O2
- Causes Hb dissociation curve to shift to left
- –> hypoxia
- Also binds to intracellular cytochromes, impairing aerobic metabolism
in carbon monoxide poisoning, carboxyhaemoglobin levels provide an approximate guide to status.
Between 10-20%: headache and dyspnoea on exertion;
above 20%: confusion and irritability;
above 50%: unconsciousness, with death likely if exposure is prolonged;
above 70%: death is rapid.
NOT cyanotic
RX: high low O2 via non rebreather, or hyperbaric O2
methaemoglobin
- methaemoglobin is an altered state of Hb where ferrous ions (Fe2+) of haem are oxidised to the ferric state (Fe3+) and rendered unable to bind O2
Main inherited cause: cytochrome B5 reductase deficiency - normal level is < 1.5%
- S/S: cyanosis, chest pain, altered mental state
- Blood has chocolate brown hue
- Ix: high metHb
- Rx: high flow O2 via non rebreather
- Methylene blue
in a child presenting with opiate toxicity, what do you need to do prior to giving naloxone
O2 and increase ventilation to normalise CO2 level
NSAID overdose
risk of mutliorgan dysfunction when >400mg/kg taken (normal dose is 10mg/kg so 40 x normal dose)
Should observe all kids ingesting >200 mg/kg for mild GI and CNS side effects
Aspirin overdose
Initial hyperventilation with respiratory alkalosis —> metabolic acidosis (High anion gap)
Only symptomatic >150mg/kg (needs monitoring). Severe symptoms >300mg/g
Can use activated charcoal if massive overdose within 1 hour of ingestion
Antidote: IV SODIUM BICARBONATE for urinary alkalisation ; need to correct metabolic acidosis to limit CNS penetration
Apnoea associated with intubation may worsen acidosis and lead to cardiac arrest. Consider pre-loading with sodium bicarbonate
Cardiac arrest - shockable rhythm
Shock 4J/kg immediately
Recommence CPR 15:2 for 2 minutes
Assess rhythm
Shock if shockable
Adrenaline 10mcg/kg (1:10,000) after 2nd shock, then every 2nd loop (ie after 2nd, 4th, 6th)
Amiodorone 5mg/kg after 3rd shock
Adrenaline 10mcg/kg = 0.01 mg/kg = 0.1ml/kg
Cardiac arrest- non shockable
Recommence CPR
Adrenaline 10mcg/kg (1:10000) immediately then every 2nd loop (1st, 3rd, 5th cycle)
Recommence CPR 2 minutes
Then assess rhythm
Anaphylaxis
Cardiac arrest -> cardiac arrest algorithm
No cardiac arrest:
Position flat (or slightly tilted if resp distress worse when lying)
IM adrenaline 10mcg/kg (1:1000) or 0.01ml/kg (max 0.5ml)
Bradycardia APLS
Adrenaline 10mcg/kg
Atropine if vagal overactivity
Status epilepticus
Airway
High flow O2
BSL (if <2.6, give glucose 10% 2ml/kg)
At 5 mins:
Midaz 0.15mg/kg IV/IM
OR
Midaz 0.3 mg/kg buccal/intranasal
At 10 mins: 2nd dose as above
At 15 mins: Levetiracetam 40-60mg/kg (over 5 min) or phentoin 20 mg/kg (over 20 min)
5 mins after infusion finished if still fitting: give whatever not given prior
5 mins later: rapid sequence induction and intubation
phenytoin contraindicated in Dravet syndrome (sodium channel blocker)
SVT algorithm
If shock:
Oxygen via NRB
Vagal manouvre if not delaying other steps
If has vascular access–> IV adenosine 100mcg/kg
If no vascular access –> synchronous DC shock 1J/kg –> 2J/kg
Consider amiodrone
adenosine via rapid push into large vein
If no shock of IV access faster than obtaining defib
Adenosine 100mcg/kg, 200, 300, 400 mcg/kg (max 300mg/kg in neonate)
Consider synchronous DC shock or amiodorone
MOA MDMA
stimulates release and inhibiting reuptake of serotonin
increases release of nerepinepthine and dopamine and blocks their reuptake to a lesser extent
ie indirect stimulation of serotonin and dopamine receptor
