Trauma Flashcards
What’s the approach to assessment (& simultaneous management) of a trauma patient?
Ax:
Airway & C-spine stabilisation
Breathing & ventilation assessment + oxygenation (target SpO2 >92% & PaO2 >65mmHg): utilise lung-protective ventilation
Circulation (>=2x lg-bore PIVC, art line +/- CVC (shouldn’t delay urgent surgical intervention), control haemorrhage (including limit coagulopathy, electrolyte & acid-base derangements) & maintain end-organ perfusion, FAST scan, damage control resus principles until haemorrhage arrested, consider cell salvage for OT)
Disability (neurological examination, analgesia/sedation/anaesthesia)
Exposure (hypothermia, smoke inhalation, intoxicants- undress to search for possible injury while preventing hypothermia- aim temp >=35.5degc
What’s the PaO2 & SpO2 target for trauma pts? why?
PaO2 >65mmHg
SpO2 >92% & <98%
hyperoxaemia associated with increased mortality in acutely ill patients with TBI, recent cardiac arrest or stroke
No evidence supporting high FiO2 in trauma patients
How does IO work?
there are veins draining medullary sinuses of long bones which don’t collapse in shock or hypovolemia
What are the sites & venous drainage of the various IO sites?
proximal tibia (popliteal vein)
femur (branches of femoral vein)
distal tibia/medial malleolus (great saphenous vein)
proximal humerus (axillary vein)
manubrium/upper sternum (internal mammary & azygous vein)
Which IV drugs or routine resus fluids can be administered safely via IO route? How to give a drug?
All, with same dosing as for IV administration, but the IO route may not be as effective as UL peripheral IV access for adenosine in Rx of SVT in young infants
for rapid fluid administration & viscous solutions, administer under pressure (infusion pump, pressure bag). monitor site frequently for infiltration. Infusion rates similar to a 21g PIVC are generally achieved (approx 160mL/min)
Onset of action & serum drug [] after IO infusion during CPR are comparable to IV
Flush the IO cannula before U& after each medication
what are absolute & relative contraindications to IO?
absolute:
fracture or previously penetrated bone
extremity with vascular interruption
ideally avoid if: cellulitis burns osteomyelitis osteogenesis imperfecta or osteoporosis R)- to L)- intracardiac shunts as they may be @ higher risk of cerebral fat or bone-marrow emboli
Where should be the first attempt site (unless a contraindication) for IO placement?
proximal tibial
where is IO inserted in infants/children? adults?
1-2cm (1 finger) below tibial tuberosity & up to 1cm medial on the tibial plateau
adults 3cm below inferior tip of patella & 2cm medially
prep skin
angle 10-15 degrees caudal from vertical
drill until get give (no further)
What labs are not accurate from an IO? how much waste before sample
blood oxygenation, WCC, plt, potassium, AST, ALT & ionised calcium
plt likely to be lower
bcc higher
waste of 1mL
Can marrow aspirates be used for a group & screen?
yes
can also be used for glucose, Hb, pH, pCO2, serum bicarb, Na+, Cl-, BUN, Cr, serum drug levels & cultures
What elements are assessed on the FAST scan?
pericardium (looking for hemoperricardium & tamponade)
R) & L) flank, pelvis to look for intraperitoneal free fluid
pneumothorax (in extended FAST (E-FAST))
What are the damage control resus BP goals? and after haemostasis achieved?
SBP approx 90mmHg & <=110mmHg for older adults
once haemostasis, >=90mmHg & MAP >=65mmHg
What are some dynamic parameters for guiding intraoperative fluid therapy?
systolic pressure variations- easy to manually calculate but depends on diastolic pressure & on changes in pleural pressure & hasn’t been studied in prone
pulse pressure variations- directly related to stroke volume variations. not easy to manually calculate & needs a specific device for continuous display
stroke volume variations- accurate analysis despite multiple extrasystoles, needs specific device (on transgastric LV short-axis view with TEE, hypovolaemia vs normovolaemia shows decreased LV end-diastolic area and diameter.
How to interpret respiratory variations in the arterial waveform?
if high variation, on the steep part of the Frank-Starling curve. goal= to increase cardiac output until it reaches the plateau of the Frank-Starling relationship. Lower volume status= higher systolic pressure variation (reduction in VR & CO with mechanical ventilation)
According to ATLS, what’s the maximum amount of warm 0.9% saline that could be given before blood?
1L
What’s the incidence of haemolytic reaction in a pt w negative screen receiving type-specific blood? and for uncross-matched O-type blood?
1/50,000
1%
What’s the risk of mortality in haemorrhagic shock if Hb falls from 50-69 to 30-49%, and if the Hb falls to <30g/L
mortality increases by 13% & 28% respectively
What does 2:1:1 transfusion ratio mean?
rbc:plasma:plt
What are some aetiologies for acute coagulopathy after severe TBI?
acidosis, hypothermia (exposure & fluid administration), systemic anticoagulation with activation of protein C & S, hyperfibrinolysis from amplification of tPA, plt dysfunction following plt activation, hemodilution, consumption of clotting factors (DIC)
What is low fibrinogen or fibrinolysis generally treated with?
fib conc or cryoprecipitate
What are some causes of shock aside from haemorrhagic?
neurogenic/vasoplegic shock from SCI
severe myocardial ischemia causing cariogenic shock
tension PTx, pericardial tamponade or increased IAP causing obstructive shock
What’s the principle of vasopressor use in haemorrhagic shock?
avoid vasopressors in the early stages. early use vasopressors thought to be associated with worsening vasoconstriction & organ failure in the absence of adequate volume resuscitation
utilise if vasoplegia or insufficient vasoconstrictive response (eg. neurogenic shock, SIRS)
Low-dose NAdr (0.01-0.09 microg/kg/min) or vasopressin (0.3 units/min)
What are the principles of induction for a trauma pt?
minimal dosing to produce unconscious state while maintaining end-organ perfusion; decompensated or haemorrhagic shock= smaller VD for all anaesthetic agents
Have vasopressor infusion in-line for immediate administration (concurrently with the induction agent if the pt is haemodynamically unstable)
RSI indicated- typically ketamine, if haemodynamically stable a reduced-dose propofol (0.5mg/kg) can be used
adjuvants (opioids, lignocaine, midaz) are eliminated in heamodynamically unstable pts
Sux 1.5mg/kg
maintain w volatile- increase MAC to >=0.5 if SBP >=90mmHg achieved
if TBI, TIVA or volatile <=1MAC
utilise adjuvants during periods of light anaesthesia (eg. midaz 104mg)
What’s the shock index & what’s it useful for?
HR/SBP, >0.8->0.9 predicts induction hypoT
pre-Rx with fluid bolus & Rx BP w metaraminol & use lower-dose induction agents (ketamine)
Why avoid N2O in trauma patients?
- it expands all gas spaces & can worsen a traumatic pneumothorax or pneumocephalus
- may increase the CMRO2 & may increase ICP
- increases PVR & may worsen pulm HTN
- may cause apoptosis & altered immunologic responses to infection
What’s lung-protective ventilation for trauma pts?
TVs 6-8mL/kg
mild permissive hypercapnia PaCO2 40-45mmHg unless metabolic acidosis or suspected/known TBI (in which case aim PaCO2 30-35mmHg)
initial PEEP at 0cmH2O until haemodynamic stability & adequate resus then PEEP incr incrementally to 5-10cmH2O if tolerated without providing hypotension
Wean FiO2 to maintain SpO2 90%
(aim= balance between minimising lung injury & preventing haemodynamic instability (in haemorrhagic shock it’s particularly important to avoid high levels of PEEP & dynamic hyperinflation with development of auto-PEEP which increases pIT, decreases VR/CO/SBP) & avoiding hyperoxia)
In rare cases, for which trauma patients may ECMO be considered?
if trauma-related refractory respiratory distress syndrome, V-V ECMO may be employed
in trauma pt with cariogenic shock after cardiac arrest, V-A ECMO may be employed
