Emergency/surgical conditions Flashcards
Causes of arrest - requiring CPR
- Hypoxaemia
- Hypovolaemia
- Hyper/hypokalaemia or metabolic disturbances
- Hypo/hyperthermia
- Tension pneumothorax
- Tamponade/cardiac
- Toxins
- Thrombosis - PE or coronary (incl spontaneous intracranial bleed)
- Trauma
How long to do CPR for?
30 minutes
What are shockable rhythms?
How many joules to give per shock?
VF
Pulsesless VT
4J/kg
Indications for giving three stacked shocks at the onset of a shockable rhythm
- in cardiac cath lab
- in ICU or cardiac ward post cardiac surgery
- in other circumstances when defibrillator is already attached
in all other cases the standard s to give one shock then bak to CPR
how many joules to give in SVT?
0.5-1J/kg - if haemodynamically unstable
Adrenaline in resus - MOA
Alpha adrenergic receptors: vasoconstriction and increase blood flow to cerebral and coronary artery circulation
Beta adrenergic receptors: inotropic and chronotrophic
Indications for amiodarone in resus
Shock resistant VF and atrial tachycardia
SE: hypotension, CHD, bradycardia
Cx of fluid boluses for hypovolaemia/shock
hyperchloraemic acidosis
oedema
hyponatraemia
Vasopressor vs inotrope
Vasopressor - causes vasoconstriction and incr MAP
Inotrope - cardiac and vascular effects -> incr contractility and CO
Noradrenaline
- effect
- receptor
- use
vasopressor
alpha 1
septic, cardiogenic and hypovolaemic shock
Adrenaline
- effect
- receptor
- use
vasopressor and chronotrope
alpha 1 and mod beta 1 and 2 effects and low dose
anaphylactic shock
add on for septic shock
Dopamine
- effect
- receptor
- use
dose dependent effects
- alpha 1 at high dose
- beta 1 med dose
- D1 and low dose
2nd lnie for septic shock
Incr SV -> incr CO
Incr splanchnic blood flow
Dobutamine
- effect
- receptor
- use
inotrope - incr cardiac contractility
beta 1 R
Use: low output cariogenic shock
2nd line for septic shock
Used post cardiac surgery
Milrinone
- effect
- receptor
- use
- inotrope
- beta 1 receptor
- use for refractory cariogenic shock
- cardiac contractility and incr HR
- Decr BP
Indications for CTB in head injury
PECARN/NICE guidelines
Impaired mental status
LOC >5 sec
Vomiting >2yo
Severe injury mechanism
Signs of basilar skull #
Severe headache
Abnormal behaviour if <2yo
Palpable skull # if <2yo
Palpable scalp haematoma (unless frontal)
Risks of CT scan
Risk of malignancy - 24% more likely in those who did not have CTB <19yo
extradural vs subdural haematoma (which metabolic disease is SDH seen in?)
EDH
- doesn’t cross suture lines
- can appear as a big egg on the head, convex/lense shaped and contained/limited in scope
SDH
- crosses suturelines
- crescent shaped
- can be extensive as not contained
- seen in SHAKEN infants (NAI)
- seen in metabolic disease glutaric aciduria type I
- can be chronic w progressive enlargement w hx of irritability, poor feeding, lethargy
Subarachnoid haemmhorage
Sx/presentation
- Intracranial bleed within cisterns and sulci
- ‘Worst headache of my life’ +/- LOC
- Meningism 6-12 hrs post beed
- SZ
- N&V
- CT sensitivities best within first 8-12 hrs, decr day 6-7
- LP: isolated RBC in CSF, non-clearing
Treatment of status epilepticus
Benzo (midaz) at 5 min, then another 5 minutes.
ConSEPT trial: re choice of 2nd line antiepileptic.
- no difference between phenytoin and keppra
- using BOTH may delay or prevent further seizures and thus need for intubation/need for PICU beds
C spine clearance
- If unconcious:
Spinally immobilise
Needs CT - IF conscious, able to communicate:
POsterior midline spinal tenderness
Painful distracting injury
Focal neurological defects
Opiod medications masking ability to communicate
–> needs plain imaging (X-rays); look for soft tissue swelling
–> re-examined if imaging looks good
–> if improved, can remove collar and clear spine
Examining C spine X-ray for ?fracture
Above C2: Normal soft tissue is <1/3 of vertebral body width
C3-C7: Normal is <1 vertebral body width, progressively narrowing towards C7
Any soft tissue swelling larger than this is abnormal , ?fracture
what does seat belt sign indicate?
significant risk of intra abdominal trauma
why are kids more prone to intraabdominal injury relative to adults?
small size so multiple system involved
thin abdo
ribs pliable, less protective
liver nad spleen relatively take up more space in abdo relative to adults
diaphragm is horizontal
seat belts ill fitting <8yo or <140cm
Potential injuries in intraabdominal trauma
Injury to liver/spleen/pancreas
-> LFTs, lipase
Intestinal rupture
GU - bladder rupture/kidney/urethral
–> need urine MCS
Management of abdominal truama
IV access x2
Bloods including lipase, LFT, UEC, FBE and crossmatch
Urine MCS
Fluid boluses +/- blood (if hypotensive, suspect intraabdominal bleed so replace like with like)
Tranexamic acid is suspect intra abdominal bleed
FAST scan - look for free fluid
-> needs CTAP as gold standard to detect haemoperitoneum
Surgery only if haemodyanamic instability (otherwise conservative mx)
Greenstick fracture
Distal radius fracture
Break of one cortical surface
requires below elbow plaster
Buckle fracture
Distal radius fracture
hairline fracture not breaching cortical surfaces
Manage with splint (same outcome as below elbow pOP)
Indications for reduction of distal radial #
Age dependent due to remodelling potential
<5yo: <20 degrees angulation
5-10yo: <15 deg angulation
10-15yo: <10deg angulation
Indications for referral to orthopaedic with fractures
Salter harris 3-4 fractures (ankle)
Open fractures
NV compromise
Monteggia fracture vs galeazzi
Moteggia (mountain - ‘top of the mountain’ and ‘ggiA’ -UlnA): Prox Rad-ulnar joint dislocation with associated fracture of ULNA
Galeazzi (ground): DISTAL Rad-ula joint dislocation with assoc fracture of RADIUS
Facial lacerations - mx
glue
- aponeurosis on view of <3cm
sutures
periosteum on view or >3cm
Intussusception
Surgical emergency <2yo
Intermittent colicky abdo pain
legs drawn up
pallor
lethargy
Pain
palpable sausage shaped abdo mass
red currant jelly stool
dx - abdo uss (target sign)
mx - air emema or surgical reduction +/- resection if air enema unsuccessful
often occurs at ileocolic junction
post viral aetiology (adenovirus)
or think of pathological lead points for recurrent episodes (lymphoma, meckel’s diverticulum, intestinal polyps)
Indications for removal of foreign body
- HIGH risk objects: all require imaging and referral for removal
- Sharp and remaining in oesophageal and stomach (ok if below diaphragm)
- Long/large (>5cm long or >2.5cm wide)
- Magnet x2 or 1xmagnet + metal object
- Disk or button batteries
- toxic objects (ex containing lead) - LOCATION
- In oesophagus (stomach and below ok as long as low-risk)
- -> upper oesophageal obstruction worse
- -> lower oesophageal obstruction can be obersved 24 hrs as long as asymptomatic to see if it resolves - Concern for clinical compromise:
- signs of airway compromise
- near or complete oesophageal obstruction
- signs or sx suggesting inflammation or intestinal obstruction
Points of obstruction for FB
thoracic inlet
aortic arch
gasto oesopageal junction
MDMA overdose
= 3,4-Methylenedioxymethamphetamine,
= Ecstacy
= Molly
Sympathomimetic and serotonin syndrome toxidrome:
anxiety
tachycardia
HTN
Diaphoresis
Dry mouth
dilated pupils
jaw clenching
dehydration
rhabdomyolysis
hyperthermia
arrhythmias (VF, astystole; infarct possible)
Supportive care
Fluids
Agitation - benzos, olanzapine, haloperidol or droperidol
GHB overdose (gammahydroybutyrate)
Commonly used as date rape drug (liquid, can be slipped into drinks)
Euphoria in first hour, rapidly
followed by a period of profoundly depressed level of consciousness-> can progress to coma
Coma/stupor alternates with extreme agitation/combativeness
Resp depression/apnoea
potential seizures
Seizure-like movements and myoclonus are common
Bradycardia
Hypotension
Need to be tubed, ventilated and sent to ICU for monitoring
Mx
- No reversible agents
- Supportive tx
- Gastric lavage/charcoal NOT indicated
Cannabis/THC overdose
Tachycardia
Paranoia, fear
Hallucination and disorientation
Dilated pupils
Fluctuations in BP
Synthetic cannabinoids/Marley - significant bradycardia and SEVERE paranoia/hallucinations etc
Repeated supra therapeutic ingestion of paracetamol
Paracetamol level and Alt
- if normal ALT and paracetamol <120, no risk of hepatotoxicity -> DC
- if abnormal -> NAC etc
It is safe to wait for the paracetamol concentration to decide on the need for NAC in all cases that present within 8 hours of ingestion AND where a paracetamol concentration result will be available for interpretation within 8 hours of ingestion
Single supra therapeutic ingestion of paracetamol
If paracetamol level >200mg/kg or unknown quantity ingested
It is safe to wait for the paracetamol concentration to decide on the need for NAC in all cases that present within 8 hours of ingestion AND where a paracetamol concentration result will be available for interpretation within 8 hours of ingestion
<8 hrs post ingestion- paracetamol level and plot on nomogram, commence tx if indicated
>8 hrs
- commence NAC immedicately
- get paracetamol and ALT level - can stop NAC if level is below tx threshold
MASSIVE quantities (30g) - seek advise from toxicologist
Iron toxicity
- Tablets can be seen on X-ray if not yet absorbed -> tx w whole bowel irrigation
- If absorbed (N xray) -> desferrioxamine which is an iron chelator
Mitochondrial Toxin to GI mucosa; also to liver, lungs, heart
Phase 1: first 6 hrs post ingestion, effects due to local corrosive effects
- haematemesis
- diarrhoea
- abdo pain
- early hypovolaemia from bleed +/- diarrhoea and third spacing due to inflammation
- -> tissue hypo perfusion and metabolic acidosis
- -> convulsions, shock and coma if decr circulating blood vol
Phase 2: 4-12 hrs post ingestion
- improvement in sx with absorption of Fe by various tissues
- Systemic acidosis
- End organ dysfunction begins (liver enzyme derangement etc)
Phase 3: 12-24 hrs post ingestion -> multi organ failure
- Fe2+ -> Fe3+ and is concentrated within mitochondria -> free radical formation and lipid peroxidation
- Worsening metabolic acidosis, cell death, tissue injury
- Hypovolaemic shock and cariogenic shock
- Coagulopathy (liver failure)
TCA overdose ECG changes
Due to Na channel blockade
ECG changes
- QRS prolongation >100ms (>100ms is predictive of seizures and >160ms is predictive of ventricular tachycardia)
- R axis deviation
- Tall R wave in AVR
- QTc prolongation
Pathophys and sx of TCA overdose
- Na channel blockage in His-purkinje bundle system
- > Incr duration of repolarisation and refractory period
- > ventricular dysrhythmias, tachycardia, hypotension - ACh receptor antagonist
- > anticholingeric syndrome (dilated pupils, dry mouth/eyes, constipation/ileus, urinary retension)
- > confusion, delirium, myoclonic jerks, seizures - alpha adrenergic blockage
- > hypotension
Mgmt of TCA overdose
ABCs (can be very sick)
Intubate and HYPERventilate (aim for pH 7.5-7.55 because systemic acidosis worsens the TCA poisoning)
IV access -> Sodium bicarb (if hypotensive, arrhythmias or QRS >100ms)
NGT and charcoal within 2 hrs of ingestion
Treat other things as they come up
- Midaz for seizures (phenytoin CI)
- Fluid bolus for hypotension (the Norad 2nd line)
- If further arrhythmias, repeat sodium bicarb, then lignocaine
CO poisoning
Presentation
Treatment
When is hyperbaric o2 indicated?
When to suspect: house fires, poor ventilation, heaters, cars etc
Binds 240x more efficiently to haem than O2 (displaces O2 so lower O2 concentration in blood and harder to offload O2 to tissues)
Confusion, headache, irritability, nausea, seizures, coma
Myocardial dysfunction
ABCs and supportive care
ABG/VBG
Give 100% O2 to washout CO
Hyperbaric oxygen indicated only if HbCO 25% on gas OR signs of end organ dysfunction (ie seizure)
What is most common cause of fatal snake bike
What is its hallmark/cause of death?
What are presenting features/complications that can arise?
- *Brown snak**e (Brown - colour of old BLOOD = coagulopathy)
- hallmark consumptive coagulopathy; prolonged INR >3, low/undetectable fibrinogen, elevated d-dimer
–> may present with bleeding gums or bleeding around the IV site, rarely this can manifest as an intracerebral haemorrhage or intraabdominal haemorrhage
–> can cause collapse and cardiac arrest (NO rhabdo and neurotoxicity is rare)
–> can cause TMA (Thrombotic microangiopathy): classic triad of thrombocytopenia, microangiopathic haemolytic anaemia and acute renal failure
Most common snakes causing paralysis and rhabdo
- Black snake (Eschar, dead tissue, is BLACK)
- N Australia and PNG
- characterised by lots of tissue necrosis at site
- coagulopathy rare - Tiger snake (tigers are black and brown -> has features of both black and brown snakes)
- Southern and eastern seaboard
- coagulopathy a big component
Sx/signs of snake bite
Sx
- headachce
- nausea/vomiting
- abdo pain
- collapse or confusion
Signs
- fang marks (single or paired) or scratch mark
- blurred vision, diplopia or ptosis (drooping eyelids)
- difficulty speaking, swallowing or breathing
- swollen tender glands in axilla or groin of BITTEN LIMB
- limb weakness/paralysis
- Rest weakness or arrest
Mx snake bike
Pressure immobilisation bandage
Indications for antivenin (give 1 vial brown and 1 vial tiger)
- significant coagulopathy (INR >3 or prolonged bleeding)
- evidence of neurotoxic paralysis
- hx of the 4 Cs: coma (LOC)/collapse/convulsions/cardiac arrest
No indication for use of venom detection kits
Mgmt of coaguloapthy secondary to snake bites
Give antivneom if significant INR derangement (>3) or prolonged bleeding time
- bleeding should cease within 20-30min of giving AV but coag profile can take 6 hours to normalise
- No role for giving MORE than 1 antivenom or for giving FFP (has not been shown to be beneficial to outcomes)
Red back side bite
Local intense pain 5-10min after bite
Sweating and piloreection within an hour
Mild erythma, puncture bites often NOT seen
Tender proximal lymph nodes
Pain ++++++
Tx simple analgesia -> opioids
Antivenom if severe pain and unwell, unrelieved by simple supportive tx (2 ampoules)
Box jelly fish
sx and mx
Deaths within 5 min of sting - direct cardiotoxicity
Severe pain and linear welts at site
Hypertension, Bradycardia or tachyardia, arrhythmia
Delayed reaction in 50%
Mx:
Liberal amounts of vinegar
No pressure/immob bandage
Antievenom if cardiac arrest
MgSO4 has not been validated
Irunkanji syndrome
Jellyfish bite
No welts or feel of sting
Envenomation causing massive catecholamine release -> toxic cardiomyopathy -> cariogenic shock, pulm oedema and sudden death
Mx - if not immediately fatal, tx w vinegar, IV fentanyl and GTB for mgmt of HTN
Use of ondans in head injury
Can mask Sx so frowned upon
- ie can have 2 vomits but any more than this, should have CTB
Ok to give for sx control in LOW RISK situation
oesophageal atresia +/- tracheo-oesophageal fistula
- presentation and diagnosis
Presentation
- maternal polyhydramnios (60%)
- recurrent aspiration pneumonia
- coughing episodes w cyanosis
- abdominal distension (air passing from lungs into gut via fistula)
- intermittent choking w feeds (H-type -> oesophagus to stomach, no atresia, with fistula between oesophagus and bronchus)
Diagnosis
- inability to pass NGT into stomach
- AXR - prominent gastric bubble +/- dilated distal oesophagus, NGT coiled in upper oesophagus
- CXR - areas of lung collapse
- contrast-study to define the lesion
Downs syndrome child p/w bilious vomiting - what do you suspect as ddx?
Duodenal atresia
Presentation of intestinal atresias
BILIOUS vomiting
Polyhydramnios antenatally
Abdo distension +/- visible peristalsis
Delayed or absent passage of mec