1. ensure patent airway 2. adequate ventilation 3. control ext. bleed (CABC)

Trauma Flashcards by Zane Truax

Goals of prehospital

ensure patent airway
adequate ventilation
control ext. bleed (CABC)

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first step in primary survey

Rapid assessment

physical exam
monitor
ultrasound/radiography (F.A.S.T)

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FAST: primary survey

focused assessment sonography in Trauma

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FAST: primary survey

early imaging to detect bleeding
within 6 minutes of arrival

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2-4 step in primary survey

Iv access
Stat labs
ABCDEs: airway, breathing, circulation, disability, exposure.

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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

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primary goal of anesthesia team

facilitate rapid surgical management: get the patient to sleep

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meds to intubate

ketamine 1
etomidate 0.2
succinylcholine 1
rocuronium 1.2

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induction RSI

cricoid pressure 10-20 30-40 newtons
induction
OGT after ETT confirmed (not w basilar skull fracture)

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contraindications to succinylcholine

burns
spinal cord injury
renal failure
hyperkalemia

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pneumothorax s/s

hypotension
hypoxia
tachycardia
increased CVP
increased airway pressure
absence of breath sounds 1 side.

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tension pneumothorax decompression

14-gauge into the 2nd or 3rd IC space anteriorly
OR
the 4th or 5th IC space laterally.

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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.

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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.

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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

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CIRCULATORY MANAGEMENT

-6 PRBC, 6 FFP, 1 PLT
2-3 large bore IVs
Arterial line
Hemodynamic support via vasopressors

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Tranexamic Acid (TXA) dose

1 gram bolus followed by infusion (1g/8 hours)

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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.

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severity of penetrating trauma 3 determinants

velocity of missile
instrument
type of tissue passed through

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what stage in the continuum of trauma care would FAST happen?

Primary survey

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What are anesthetic implications of blunt trauma?

There may be a lot of internal bleeding.

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Lethal Triad

Hypothermia
Acidosis
Coagulopathy

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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

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s/s of hemorrhagic shock

hypotension
tachycardia and cold
clammy skin

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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 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?

Hyperventilation may be necessary prior

to opening the skull. Only hyperventilate for 15 min.limited period of time