Trauma Flashcards
Goals of prehospital
- ensure patent airway
- adequate ventilation
- control ext. bleed (CABC)
first step in primary survey
Rapid assessment
physical exam
monitor
ultrasound/radiography (F.A.S.T)
FAST: primary survey
focused assessment sonography in Trauma
FAST: primary survey
early imaging to detect bleeding
within 6 minutes of arrival
2-4 step in primary survey
- Iv access
- Stat labs
- ABCDEs: airway, breathing, circulation, disability, exposure.
what is secondary survery goal?
if fast is negative !
Goal: to determine if any patient injuries may have been missed during the primary survey
complete head-to-toe assessment + neuro exam
primary goal of anesthesia team
facilitate rapid surgical management: get the patient to sleep
meds to intubate
ketamine 1
etomidate 0.2
succinylcholine 1
rocuronium 1.2
induction RSI
cricoid pressure 10-20 30-40 newtons
induction
OGT after ETT confirmed (not w basilar skull fracture)
contraindications to succinylcholine
burns
spinal cord injury
renal failure
hyperkalemia
pneumothorax s/s
hypotension
hypoxia
tachycardia
increased CVP
increased airway pressure
absence of breath sounds 1 side.
tension pneumothorax decompression
14-gauge into the 2nd or 3rd IC space anteriorly
OR
the 4th or 5th IC space laterally.
etiology of ARDS in trauma
consequence of high-volume resuscitation.
Pulmonary contusions can develop or “blossom” over a range of time and ultimately may develop into ARDS.
Pathology of ARDS
Protein-rich fluid leaks from the pulmonary capillaries.
Leakage is compounded by embolic events, which further increase intracapillary pressure and intensify interstitial leakage
culminates in hypoxia and decreased pulmonary compliance.
ARDS VENTILATION
low tidal volume/high RR
permissive hypercapnia
conservative fluid strategies
prone positioning
neuromuscular blockade
ECMO (extracorporeal membrane oxygenation) for those who do not respond to initial therapy
CIRCULATORY MANAGEMENT
-6 PRBC, 6 FFP, 1 PLT
2-3 large bore IVs
Arterial line
Hemodynamic support via vasopressors
Tranexamic Acid (TXA) dose
1 gram bolus followed by infusion (1g/8 hours)
Newtons first law
An object in motion stays in motion.
As the body decelerates abruptly, internal organs continue forward at the original velocity and are torn from their attachments by way of rotary and shearing forces.
severity of penetrating trauma 3 determinants
velocity of missile
instrument
type of tissue passed through
what stage in the continuum of trauma care would FAST happen?
Primary survey
What are anesthetic implications of blunt trauma?
There may be a lot of internal bleeding.
Lethal Triad
Hypothermia
Acidosis
Coagulopathy
Defined as a pathologic event that is triggered by the loss of circulating blood volume and results in a reduction in oxygen delivery to the tissue.
hemorrhagic stock
s/s of hemorrhagic shock
hypotension
tachycardia and cold
clammy skin
why are hemorrhagic shock patients cold and clammy?
shunting the blood away from periphery and into vital organs
hemorrhagic shock resuscitation
Two whole blood right away with positive fast
OR –> MTP
1:1:1
RBC and clotting
40% of patients with blunt trauma present with a
tension pneumo
blunt abdominal trauma needs
fluid
40% of deaths in the first 24 hours of trauma
hemorrhage
acidosis causes
coagulopathy –> acidosis
cell ischemic leads to
anaerobic metabolism –> lactate –> acidosis
1:1:1
mimics whole blood
6 PRBC, 6u FFP, 6pk platelets
A negative feedback control mechanism of the circulation tries to return the cardiac output and arterial pressure to normal levels.
compensated shock
don’t correct HR
Associated with cardiac depression caused by ischemia, vasomotor failure, thrombosis of small vessels, increased capillary permeability, release of endotoxins by ischemic tissues, and generalized cellular degeneration.
progressive shock
HR:100
BP:70/30
SaO2: 98%
tachy, but not enough to maintain BP
less responsivle to catecholamines
This stage occurs when adenosine triphosphate reserves are depleted and toxic substances are released from apoptotic cells.
irreversible shock
death
cellular ischemia cannot be overcome even though resuscitated
where to keep BP prior to surgical control of bleeding?
lower than normal
systolic >85-90
MAP >60
what stage of shock is tachycardia and hypotensive?
stage 2
coagulopathy is caused by 3 things
hypothermia (30-40%)
acidosis / endothelial dysfunction (7.4-7)
hemodilution
independent predictor of mortality
PT on coagulopathy on admission
coagulopathy develops in what % of trauma patients?
25-35%
ph 7.4–> 7.0
lose 50% of clotting cascade
acute traumatic coagulopathy is associated with shock and hypoperfusion
endogenous: initial injury
coagulopathy arises from effects of dilution resulting from fluid resuscitation and consumption through bleeding and loss of clotting factors
exogenous
sodium bicarb does not help with _____.
acidosis.
it increased CO2 and hypocalcemia, which are direct myocardial depressants.
Each unit of packed red blood cells (PRBCs) will increase hemoglobin (HGB) by
1 g/dL, and hematocrit (HCT) by 3%
factors in FFP
5
8
Consider that factor after the second round of MTP, used for cessation of coagulopathic bleeding
Recombinant Factor 7
50-100 mcg/kg
(pH dependent)
Before giving factor 7 you need to
correct acidosis >7.2
surgical control of bleeding
must be within 3 hours
given to correct citrate toxicity
calcium
for those on antiplatelet therapy
DDAVP
Coumadin w/ TBI
Factor 7
guide the hemostatic resuscitation of bleeding injured patients, promote targeted transfusion therapy with specific coagulation factor(s)
TEG
What 3 things does TEG measure
speed
strength
duration of clot formation
time to start forming clot
R time
Trearment for long R time
FFP
Time until clot reaches a fixed strength
K time
Treatment for K time
Cryro
speed of fibrin accumulation
alpha angle
treatment for the alpha angle
cryoprecipitate
highest verticle amplitude of the TEG
MA
MA treatment
Platelets or DDAVP
% of amplitude reduction 30 m after MA
LY30
Treatment for LY30
TXA
Aminocaproic Acid
When a TEG is being processed, the speed at which the sample coagulates in depends on…?
R time –> depends on coagulation factors. Give FFP
Injury that happens in the field. bones, spinal column, ligaments, cord through hemorrhage, compression, vasospasm
Primary SCI
what is secondary SCI?
Hypoxia and hypotension –> cord ischemia –> inflammatory response
complete transection of T6 or below we lose ______ __________.
sympathetic innervation –> no tachycardia or HTN. Warm, pink.
inducing SCI
manual inline stabilization
c spine collar
lose chest wall innervation, paradoxical respiratory motion and an inability to clear secretions
C6-C7 injury
is not recommended in acute SCI
succinylcholine –> Roc 1.2mg/kg
spinal shock (T6 or higher)
Test question
Hypotension
Bradycardia
Hypothermia
No sympathetic innervation
parasympathetically functioning
T6 and above injuries
Very HIGH vagal tone
How is secondary SCI different than primary SCI?
We can mitigate secondary
Which anesthetic interventions can be used to prevent secondary SCI?
Perfusion, warm, correct acidosis
Primary goal of TBI
prevent secondary brain damage
prioritize oxygenation
maintain BP for CPP
normal adult ICP
is defined as 5 to 15 mm Hg
ICP values of 20 to 30 mm Hg
= intracranial hypertension
The Monro-Kellie doctrine states that the skull is a rigid compartment and contains three components:
V brain
V blood
V cerebrospinal fluid (csf)
=herniation
If an increase occurs in the volume of one component, the volume of one or more other components must decrease, or ICP will be elevated
Monro-Kellie Doctrine
can you use nitrous in trauma?
No
can aggravate pneumocephalus and/or pneumothorax
NGT with basililar skull fracture?
No
Hyperventilation may be necessary prior
to opening the skull. Only hyperventilate for 15 min.limited period of time
have steroid been shown to improve outcome or reduce ICP?
no
