Emergency Medicine Flashcards
shockable side of the algorithm - initial energy value for shock
4J per kg
shockable side of the algorithm - after how many shocks do u give drugs
3 shocks
drugs given on shockable side of algorithm - doses and timing interval
ADRENALINE
10 mcg per kg
give after 3rd shock and every alternate cycle thereafter
AMIODARONE
5 mg per kg
give after 3rd shock and after 5th shock and that’s it!
max single dose of adrenaline during cpr
1 mg
max single dose of amiodarone during cpr
300 mg
non-shockable side of the rhythm, when do you give drugs and what are they
ADRENALINE
give as soon as possible
10 mcg per kg
and then give every 3-5 mins
4 H’s and 4 T’s
hypothermia
hypovolaemia
hypoxia
hyperkalaemia / electrolyte abnormalities
tension penumothorax
tamponade
thrombosis
toxic agents
classification of bradycardia
< 80 if < 1 year
< 60 if > 1 year
dose of atropine for bradycardia
up to 11y:
20 mcg / kg
12-17y:
300 - 600 mcg
if atropine doesn’t work for bradycardia, what should you consider giving
adrenaline
10 mcg/kg and repeat if necessary
shocks for synchronised cardioversion for SVT
1st shock 1J / kg
2nd shock 2J/kg, consider up to 4 J/kg
Rx torsades de pointes VT
magnesium
dose of IM adrenaline for <6m
100 - 150 micrograms (0.1 - 0.15mL)
of 1: 1000
dose of IM adrenaline for 6m - 6 years
150 micrograms (0.15mL)
of 1: 1000
dose of IM adrenaline for 6 - 12 years
300 micrograms (0.3mL)
of 1 :1000
dose of IM adrenaline for 12 years and above
500 micrograms (0.5mL)
of 1: 1000
why does the HR not increase appropriately in neurogenic shock
there is loss of sympathetic tone
Rx for choking in infant
5 back blows then 5 chest thrusts
Rx for choking in child
5 back blows then 5 abdominal thrusts
skin layers involved in 1st degree burn
epidermis only
blistering in 1st degree burns - Y or N
No
skin layers involved in 2nd degree burn
epidermis + papillary and reticular layers of dermis
blistering in 2nd degree burns - Y or N
Yes
skin layers involved in 3rd degree burns
entire epidermis and dermis (ie full thickness)
why are 3rd degree burns not painful
loss of nerve endings
what areas should nto be included in total % area calculation of burns
areas of erythema
Ix for burns
laser doppler to measure depth of the burns
carboxyhaemoglobin level
reflectance confocal microscopy + OCT to visualise tissue subcellularly
what do the colours in laser doppler mean
yellow = 2nd degree
blue = 3 rd degree
timings of when laser doppler is valid after burns
48h - 5d
how to calculate fluid resuscitaiton in burns
% burn x weight x 3
timings of giving fluid resus in burns
give 1/2 in the first 8h from time of onset of injury and then the next 1/2 given over the next 16h
fluid replacement on day 2 of burns
50% of the volume from day 1 due to reabsorption of oedema
what are infantile spasms also known as
west syndrome
what is the most prevalent epilepsy syndrome in infancy
west syndrome aka infantile spasms
pathophysiology of west syndrome
an insult to the brain during a critical period of dendritic spine formation, which causes a structural or functional disturbance in subcortical neurotransmitter pathways
presentation of infantile spasms
4-8mths
bilateral symmetrical brief contractions
repetitive head bobbing or nodding
occur in clusters with 5-30s between spells
what conditions are infantile spasms associated with
tuberose sclerosis
neurofibromatosis
EEG in infantile spasms
hypsarrhythmia -
no discernable pattern with disorganised electrical activity
what phase of sleep do infantile spasms NOT occur in
REM sleep
Rx for infantile spasms if cause unknown
- ACTH
- High dose pred
Rx for infantile spasms if cause is tuberose sclerosis
Vigabatrin
how does a febrile seizure normally present
generalised tonic clonic seizure followed by post ictal drowsiness
1st line agents in seizure Rx
buccal midazolam 0.3-0.5mg/kg
OR
IV/IO lorazepam 0.1mg/kg
timing of when to give 1st line seizure agent
after 5 min if seizure hasn’t self resolved
what to give if seizure hasn’t terminated with buccal midaz or lorazepam
2nd dose of lorazepam 0.1mg/kg
timing of when to give 2nd line agents in seizure
15-35 min
2nd line seizure agents
Levetiracetam
OR
Phenytoin
OR
Phenobarbital
what does the treatment algorithm recommend if 2nd line seizure agents havent worked and timing of doing this
20-40 min
can either give another alternative 2nd line drug, or if prepping to intubate and ventilate at this point then mvoe to 3rd line agents
3rd line seizure agents
thiopental
or
propofol
equation for cpp
CPP = MAP - ICP
what does the CPP need to be maintained above to prevent brain ischaemia
> 400 mmHg
Rx cushings triad
head up at 20 degrees in midline to aid venous drainage
mannitol 20%
- osmotic diuretic
changes to resus protocol when temp <30C
limit defibrillation to 3 shocks
dont give antiarrhytmic and inotropic drugs
changes to resus protocol when temp 30-35 C
double the dose interval for drugs
pathophysiology of carbon monoxide poisoning
CO binds to Hb to form carboxyhaemoglobin (250x higher affinity for Hb than O2)
This reduces the oxygen carrying capacity of the blood
how does CO poisoning affect the oxygen dissociation curve
shifts it to the left
how does the % of carboxyhaemoglobin concentration in the blood affect symps
10% - rarely associated with symps
10-60% - headache and dyspnoea
60% - coma, convulsions, death
Ix for CO poisoning
exhaled breath test
- converts carbon monoxide concentrations into carboxyhaemoglobin levels
Rx CO poisoning
100% O2
what factors are associated with a worse prognosis in CO poisoning
exposure during pregnancy
coexisting CVS disease
pre-existing anaemia
acidotic on blood gas
which solitary features necessitate a CT within 1h
NAI suspicion
GCS <14 (or <15 if <1y) on initial ED assessment
GCS <15 2h post injury
any sign of BOS
focal neurological deficit
bruising or laceration <5cm on the head (for children <1y)
which features if > 1 present necessitate a CT within 1h
LOC > 5 mins
Abnormal drowsiness
3 or more discrete eps of vomiting
dangerous mechanism of injury
amnesia > 5min
N.B. if only has one of the above then observe for min 4h. If goes on to develop any in addition get CT within 1h
timing of CT for head injury in a child on anticoagulant
8h
criteria for CT C spine
GCS <13 on initial assessment
inutbated
focal peripheral neurological signs
paraesthesia in upper or lower limbs
definitive diagnosis of c-spine injury needed urgently
strong clinical suspicion despite normal xrays
plain xray suggests bony injury
what is decorticate posturing and what causes it
bent arms, clenched fists, utstretched legs
caused by brain lesions above the red nucleus, affecting the corticospinal tracts
what causes decerebrate posturing
a brain lesion below the red nucelus
what is opisthotonus posturing
rigid and arching back and head thrown backwards
cause of opisthotonus posturing
extrapyramidal effect from spamming of the axial muscles along the spinal column
CT finding of epidural haematoma
lentilucar hyperlucency
CT finding of subdural haematoma
biconcave hyperlucency
blood film appareance in lead poisoning
basophilic stippling
xray appearance in lead poisoning
increased metaphyseal density
what blood lead level necessitates Rx
45 and above
thresholds for different lead poisoning Rx
45-70 single agent
> 70 dual agent
oral agents for Rx of lead poisoning
DMSA
penicillamine
parenteral agents for Rx of lead poisoning
versenate
dimercaprol
what doses of paracetamol cause serious toxciity
> 150mg/kg if < 6 years
> 75mg/kg if > 6 years
two normal metabolites of pcm
glucuronide & sulphate
pathophysiology of pcm overdose
in overdose there is overwhelming of the normal pcm metabolism procress, so it is metabolised by an alternative pathway
this produces NAPQI
this is normally inactivated by glutathione, but if the glutathione stores are overwhelmed then NAPQI induces necrosis of the liver and kidney
acute vs staggered overdose of pcm
acute - ingestion over 1h or less
staggered - ingestion over >1h
timing of pcm level testing
acute - do at 4h
if staggered ingestion or ingestion >4h before presentation then take level at time of presentation
blood gas in pcm overdose
metabolic acidosis
how does n-acetylcysteine work
replaces glutathione stores
dose regimen of n-acetylcysteine
standard 21h regimen
total 300mg/kg
150mg/kg over 1h
50mg/kg over next 4h
100mg/kg over next 16h
pathophysiology of salicylate OD
high doses of salicylate > stimualte respiratory centre in medulla > hyperventilation > respiratory alkalosis
disruption of kreb’s cycle > accumulation of lactate & pyruvic acid > metabolic acidosis
hyperpyrexia due to uncoupling of oxidase phosphorylase
presentation salicylate poisoning
mild (125mg/kg)
- n&v/deafness/tinnitus/dizziness/lethargy
moderate (250mg/kg)
- sweaty/restless/bounding pulses/warm extremities/tachypnoea
severe (500mg/kg)
- pulm oedema/cerebral oedema/hyperpyrexia/seizures
when to measure salicylate concentrations in OD
at 2h if symptomatic
at 4h if asymptomatic
blood gas n salicylate OD
mixed metabolic acidosis and respiratory alkalosis
Rx salicylate OD
Urinary alkalinisation
- sodabic
- need to correct hypokalaemia prior to this
activated charcoal if taken <1h previous and ingestion is >125mg/kg
Gastric lavage within 1h if ingestion is >500mg/kg
Rx iron overdose
desferrioxamine
complication of iron overdose
pyloric stenosis - iron causes scarring of the gut mucosa
ECG changes in digoxin overdose
T wave flattening, short QT interval, prominent U waves
blood gas in ethylene gylcol OD
severe metabolic acidosis with significant base deficit
Rx ethylene glycol OD
IV fomepizole
Then sodabic to correct the acidosis
Rx TCA OD
activated charcoal every 2-4 aiming to prevent reabsorption
which substance causes unpleasant smell of rotting eggs in OD
hydrogen sulphide
which substance causes unpleasant smell of garlic in OD
arsenic
selenium
which substance causes unpleasant smell of bitter almonds in OD
cyanide
