Trauma Flashcards

1
Q

Goals of prehospital

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

first step in primary survey

A

Rapid assessment

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

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3
Q

FAST: primary survey

A

focused assessment sonography in Trauma

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4
Q

FAST: primary survey

A

early imaging to detect bleeding
within 6 minutes of arrival

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5
Q

2-4 step in primary survey

A
  1. Iv access
  2. Stat labs
  3. ABCDEs: airway, breathing, circulation, disability, exposure.
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6
Q

what is secondary survery goal?

A

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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7
Q

primary goal of anesthesia team

A

facilitate rapid surgical management: get the patient to sleep

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8
Q

meds to intubate

A

ketamine 1
etomidate 0.2
succinylcholine 1
rocuronium 1.2

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9
Q

induction RSI

A

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

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10
Q

contraindications to succinylcholine

A

burns
spinal cord injury
renal failure
hyperkalemia

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11
Q

pneumothorax s/s

A

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

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12
Q

tension pneumothorax decompression

A

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

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13
Q

etiology of ARDS in trauma

A

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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14
Q

Pathology of ARDS

A

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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15
Q

ARDS VENTILATION

A

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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16
Q

CIRCULATORY MANAGEMENT

A

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

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17
Q

Tranexamic Acid (TXA) dose

A

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

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18
Q

Newtons first law

A

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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19
Q

severity of penetrating trauma 3 determinants

A

velocity of missile
instrument
type of tissue passed through

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20
Q

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

A

Primary survey

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21
Q

What are anesthetic implications of blunt trauma?

A

There may be a lot of internal bleeding.

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22
Q

Lethal Triad

A

Hypothermia
Acidosis
Coagulopathy

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23
Q

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.

A

hemorrhagic stock

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24
Q

s/s of hemorrhagic shock

A

hypotension
tachycardia and cold
clammy skin

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25
Q

why are hemorrhagic shock patients cold and clammy?

A

shunting the blood away from periphery and into vital organs

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26
Q

hemorrhagic shock resuscitation

A

Two whole blood right away with positive fast
OR –> MTP
1:1:1
RBC and clotting

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27
Q

40% of patients with blunt trauma present with a

A

tension pneumo

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28
Q

blunt abdominal trauma needs

A

fluid

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29
Q

40% of deaths in the first 24 hours of trauma

A

hemorrhage

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30
Q

acidosis causes

A

coagulopathy –> acidosis

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31
Q

cell ischemic leads to

A

anaerobic metabolism –> lactate –> acidosis

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32
Q

1:1:1

A

mimics whole blood

6 PRBC, 6u FFP, 6pk platelets

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33
Q

A negative feedback control mechanism of the circulation tries to return the cardiac output and arterial pressure to normal levels.

A

compensated shock

don’t correct HR

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34
Q

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.

A

progressive shock

HR:100
BP:70/30
SaO2: 98%

tachy, but not enough to maintain BP

less responsivle to catecholamines

35
Q

This stage occurs when adenosine triphosphate reserves are depleted and toxic substances are released from apoptotic cells.

A

irreversible shock

death

cellular ischemia cannot be overcome even though resuscitated

36
Q

where to keep BP prior to surgical control of bleeding?

A

lower than normal
systolic >85-90
MAP >60

37
Q

what stage of shock is tachycardia and hypotensive?

A

stage 2

38
Q

coagulopathy is caused by 3 things

A

hypothermia (30-40%)
acidosis / endothelial dysfunction (7.4-7)
hemodilution

39
Q

independent predictor of mortality

A

PT on coagulopathy on admission

40
Q

coagulopathy develops in what % of trauma patients?

A

25-35%

41
Q

ph 7.4–> 7.0

A

lose 50% of clotting cascade

42
Q

acute traumatic coagulopathy is associated with shock and hypoperfusion

A

endogenous: initial injury

43
Q

coagulopathy arises from effects of dilution resulting from fluid resuscitation and consumption through bleeding and loss of clotting factors

A

exogenous

44
Q

sodium bicarb does not help with _____.

A

acidosis.

it increased CO2 and hypocalcemia, which are direct myocardial depressants.

45
Q

Each unit of packed red blood cells (PRBCs) will increase hemoglobin (HGB) by

A

1 g/dL, and hematocrit (HCT) by 3%

46
Q

factors in FFP

A

5
8

47
Q

Consider that factor after the second round of MTP, used for cessation of coagulopathic bleeding

A

Recombinant Factor 7
50-100 mcg/kg

(pH dependent)

48
Q

Before giving factor 7 you need to

A

correct acidosis >7.2
surgical control of bleeding
must be within 3 hours

49
Q

given to correct citrate toxicity

A

calcium

50
Q

for those on antiplatelet therapy

A

DDAVP

51
Q

Coumadin w/ TBI

A

Factor 7

52
Q

guide the hemostatic resuscitation of bleeding injured patients, promote targeted transfusion therapy with specific coagulation factor(s)

A

TEG

53
Q

What 3 things does TEG measure

A

speed
strength
duration of clot formation

54
Q

time to start forming clot

A

R time

55
Q

Trearment for long R time

A

FFP

56
Q

Time until clot reaches a fixed strength

A

K time

57
Q

Treatment for K time

A

Cryro

58
Q

speed of fibrin accumulation

A

alpha angle

59
Q

treatment for the alpha angle

A

cryoprecipitate

60
Q

highest verticle amplitude of the TEG

A

MA

61
Q

MA treatment

A

Platelets or DDAVP

62
Q

% of amplitude reduction 30 m after MA

A

LY30

63
Q

Treatment for LY30

A

TXA
Aminocaproic Acid

64
Q

When a TEG is being processed, the speed at which the sample coagulates in depends on…?

A

R time –> depends on coagulation factors. Give FFP

65
Q

Injury that happens in the field. bones, spinal column, ligaments, cord through hemorrhage, compression, vasospasm

A

Primary SCI

66
Q

what is secondary SCI?

A

Hypoxia and hypotension –> cord ischemia –> inflammatory response

67
Q

complete transection of T6 or below we lose ______ __________.

A

sympathetic innervation –> no tachycardia or HTN. Warm, pink.

68
Q

inducing SCI

A

manual inline stabilization
c spine collar

69
Q

lose chest wall innervation, paradoxical respiratory motion and an inability to clear secretions

A

C6-C7 injury

70
Q

is not recommended in acute SCI

A

succinylcholine –> Roc 1.2mg/kg

71
Q

spinal shock (T6 or higher)

Test question

A

Hypotension
Bradycardia
Hypothermia

No sympathetic innervation

72
Q

parasympathetically functioning

A

T6 and above injuries

Very HIGH vagal tone

73
Q

How is secondary SCI different than primary SCI?

A

We can mitigate secondary

74
Q

Which anesthetic interventions can be used to prevent secondary SCI?

A

Perfusion, warm, correct acidosis

75
Q

Primary goal of TBI

A

prevent secondary brain damage

prioritize oxygenation
maintain BP for CPP

76
Q

normal adult ICP

A

is defined as 5 to 15 mm Hg

77
Q

ICP values of 20 to 30 mm Hg

A

= intracranial hypertension

78
Q

The Monro-Kellie doctrine states that the skull is a rigid compartment and contains three components:

A

V brain
V blood
V cerebrospinal fluid (csf)

=herniation

79
Q

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

A

Monro-Kellie Doctrine

80
Q

can you use nitrous in trauma?

A

No

can aggravate pneumocephalus and/or pneumothorax

81
Q

NGT with basililar skull fracture?

A

No

82
Q

Hyperventilation may be necessary prior

A

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

83
Q

have steroid been shown to improve outcome or reduce ICP?

A

no

84
Q
A