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Trauma Flashcards

1
Q

Primary trauma survey

A
  1. Stable, unstable,
    moribund?
    o Airway
    o Breathing
    o Circulation

• Neurologic function
• Physical examination

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2
Q

Trauma secondary survey

A

Detailed full body exam

Systematic evaluation of injury
-by anatomic region, includes imaging

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3
Q

Causes of airway obstruction

A

Object
Soft tissue trauma
Edema
Bleeding/secretions
Altered LOC

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4
Q

Airway obstruction management trauma

A

Jaw thrust
Clear oropharynx
Oral airway

-verify existing airways

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5
Q

Tips for RSI in trauma patient

A

Trauma ALWAYS assumed full stomach

Propofol/ketamine/etomidate-based on hemodynamics

Succinylcholine DRUG OF CHOICE

Cricoid with caution, may cause further injury

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6
Q

LMAs in trauma

A

Bridge to ETT

Only if unable to intubate/ventilate

May protect lungs from upper airway hemorrhage

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7
Q

Airway trauma considerations

A

Type of injury

Nature of airway compromise

Hemodynamics and oxygenation

Urgent vs emergent

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8
Q

C-spine injury causes

A

High-speed MVAs
Falls
Diving accidents
Gunshots
Head injury with low GCS

7-15% are unstable

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9
Q

C-spine injury airway management

A

CT chest and neck first if possible

MRI gold standard

Rigid c-collar

Manual inline stabilization

Recommended fiberoptic**

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10
Q

MILS

A

Manual inline stabilization

C-collar in place

3 people technique- shoulders/head/airway

Makes DL more difficult

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11
Q

Blind nasal intubation in trauma- 3 risks

A

Epitaxis

Coughing

DO NOT attempt in basilar skull fracture

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12
Q

GCS

A

Motor response 1-6

Verbal response 1-5

Eye opening 1-4

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13
Q

Mandibular fx or Lefort airway management

A

Tracheostomy

Retrograde

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14
Q

Retrograde intubation

A

Topicalize airway-patient awake or in K hole?

Wire through cricothyroid

Thread up into oropharyx

Use as a guidewire to enter trachea with ETT

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15
Q

TBI

A

Cause of 40% of trauma related deaths

Exacerbated by hypotension and hypoxia

Therapeutic:
-normalize ICP-mannitol.hypertonic
-maintain CPP
-Adequate O2

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16
Q

Cushing REFLEX

A

Response to cerebral ischemia from high ICP

ICP increased
MAP increased to maintain CPP
Baroreceptor

Needs decompression!

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17
Q

Cushing triad

A

HTN
Bradycardia
Respiratory irregularity

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18
Q

Is succinylcholine acceptable in open globe injury?

A

YES

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19
Q

GCS score requiring ETT

A

<8

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20
Q

2 most important things in ICP management according to andrea (in red)

A

Euglycemia < 200

Maintain O2 >95%

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21
Q

ICP management

A

Hyperventilation (6 hrs)
Positioning
CSF drainage
Decompression Sx
Mannitol/hypertonic
Euthermia
Euvolemia

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22
Q

CPP in TBI

A

Maintain CPP>50-70

=MAP>80-90mmhg

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23
Q

2 categories of spinal injury

A

Complete- sensory perception absent

Incomplete- intact sensory perception over sacral distribution

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24
Q

Spinal shock

A

Flaccidity and loss of reflexes below injury

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25
Injuries above this level require mechanical ventilation
C4
26
ASCI anesthetic management
Airway -C-collar, thoughtful approach Euvolemia MAP> 85mmhg -for spinal perfusion -steroids
27
Anterior spinal artery syndrome
hypoperfusion to anterior spinal artery = post-operative motor weakness. Prevent by monitoring MEPs during the case.
28
Autonomic dysreflexia
Weeks to months after injury in 60-80% of patients HTN response to stimuli below injury Symptoms -HTN -HA -diaphoretic -flushing Prevent with dense spinal block and general anesthesia
29
Treating autonomic dysreflexia
Calcium channel blockers, nitrates, hydralazine
30
Pneumothorax
-subcutaneous emphysema -respiratory distress -hyperresonance -diminished breath sounds
31
Tension pneumothorax symptoms
• Cyanosis, tachypnea, hypotension, & neck vein distention • Shift of mediastinal structures toward contralateral lung • Hemodynamic instability and potential for cardiovascular collapse if not treated promptly
32
Treating tension pneumothorax
Needle decompression 14g Angiocath 2nd intercostal Midclavicular
33
34
Flail chest
Fx to at least 2 or more sites on 3 adjacent ribs -flail section moves independently and opposite of the rest of the chest • Pulmonary contusion with increased elastic recoil & increased work of breathing = hypoxemia and/or concomitant respiratory failure -POSITIVE PRESSURE WITH PEEP
35
Becks triad
JVD Hypotension Muffled heart sounds =pericardial tamonade -Pulsus paradoxus….
36
Signs and symptoms of pericardial tamonade
Tachycardia Hypotension Becks triad
37
Anesthetic implications of pericardial tamponade
Avoid myocardial depression Maintain spontaneous ventilation until fluid drained Artline!!! Pericardiocentesis as soon as fucking possible-ASAFP
38
Anesthetic implications of abdominal trauma
Ex lap usually Prepare for bleeding Abdominal compartment syndrome- bowel ischemia/edema with respiratory insufficiency
39
Abdominal compartment syndrome
Elevated diaphragm Decreased CO and UOP Increased CVP/PAP/SVR Intrabdominal pressure>25mmg
40
Definition of hemorrhagic shock
Insufficient oxygen deliver to sustain aerobic metabolism of vital cells in essential organs
41
Final common denominator in all forms of shock
Low blood flow state to vital organs
42
Hemorrhagic shock classification based on HR and blood loss
Class one <750ml HR<100 Class two 750-1500cc HR >100 Class three 1.5-2L. HR>120 Class four >2L HR >140
43
Compensated shock- 3 mechanisms
Neural Hormonal Biochemical -SNS activation/hyperventilation/RAAS
44
Progressive shock
Occurs when first two stages do not compensate for volume loss • Na-K pump: failure • Metabolic Acidosis = worsens • Capillary permeability = increases • Micro-embolic phenomena occurs • Inflammatory cytokines → released • Cell death occurs → compromises vital organ function
45
Initial state of shock
Tissue hypoxia due to hypoperfusion…
46
Refractory shock
IRREVERSIBLE Complete depletion of ATP -vital organ failure and brain damage
47
Why might tachycardia be absent in 30% of shock patients?
Bezold-Jarisch reflex- increase in vagal tone
48
Anesthetic resuscitation needs in shock
IVs Fluids Blood Lab support Extra set of hands on induction
49
Tissue factor (thromboplastin)
Cofactors of extrinsic clotting pathway -recruits platelets and activates factor VII
50
Von willebrand factor
Acts as bridge between collagen and glycoprotein Ib platelet receptor
51
Gp1b receptor
platelet membrane glycoprotein → receptor for von Willebrand factor (VWF)
52
Gp11b/111a receptor
helps regulate platelet “stickiness” by signaling the process for them to stick together
53
Adrenaline in clot formation
Helps with platelet aggregation
54
Thromboxane
Hormone released from platelets -promotes aggregation
55
Factor IIa (thrombin)
Enzyme that converts fibrinogen to fibrin
56
Ionized calcium in clotting
Helps activate prothrombin
57
3 steps in fibrinlysis
Plasminogen is activated-plasmin Plasminogen acts-fibrin Fibrin degrades-fibrin degradation products are washed away
58
DIC labs
PT/INR aPTT Platelet Fibrin and fibrin byproducts
59
Cascade of DIC
Endothelial damage Clotting factors and platelets are consumed=bleeding worsens Thrombocytopenia Systemic microemboli form
60
Treatment of DIC
Cryoprecipitate Treat causative factors FFP and platelets may help
61
What is in cryoprecipitate?
Factor VIII and fibrinogen
62
Acute traumatic coagulopathy
Occurs in 25% of trauma patients Prolonged PT and aPTT Increased mortality and complications Multi factorial consumptive coagulopathy -tissue damage and hyperfibrinolysis
63
Treating hemorrhagic shock
Control bleeding?! Normothermia Limit crystalloid Blood 1:1:1 RBC FFP platelets- crit of 29% 1g TXA early
64
Labs and BP in hemorrhagic shock resuscitation
BE> -2 Lactate 0.5-1.5 Maintain systolic at 90mmhg under 65 years old At 110mmhg over 65
65
TXA
Synthetic derivative of. Lysine Inhibits activation of plasminogen via tissue plasminogen activator competition -impairing fibrinolysis 10x more potent than amicar Half-life of 2 hours 1gm- outcomes not improved with higher doses
66
Stats on PRBCs
Hematocrit of 70% 1 unit increases crit by 3% and hemoglobin by 1gm/dl
67
Increase when given 1 platelet concentrate
7k-10,000
68
FFP stats
Fresh frozen plasma 1 unit increases clotting factors by 2-3% Coagulation is normal if levels are >30% of normal
69
What’s in whole blood?
Volume 500ml Hct- 38-44% Platelet 150,000-400,000 100% activity of coagulation factors with 600mg of fibrinogen
70
What would cause increased Pt/INR with normal aPTT
Factor VII deficiency • Vitamin K deficiency • Coumadin • Sepsis
71
What would cause normal PT/INR with increased aPTT
Heparin contamination • Isolated factor deficiency ➢VIII, IX, XI, XII
72
Causes of elevated PT/INR and aPTT
Multiple coagulation factor deficiencies • DIC • Liver disease • Low fibrinogen (<50mg/dL) • High heparin levels
73
What does TEG evaluate?
Platelet reactions Coagulation Fibrinolysis
74
Interpreting TEG pic Think Normal, anticoagulants, fibrinolysis, Hypercoagulability, DIC
75
Definition of massive transfusion
Replacement of 1-1.5 of patients blood volume in 24hrs 8-10 units prbcs Citrate toxicity! Give calcium
76
Blood product complications
Dilutional coagulopathy DIC Citrate toxicity Hypo/hyperkalemia Acidbase imbalance Hypothermia Immunomodulation-delayed wound healing TRALI
77
Mechanism of impaired hemoglobin function in setting of MTP
2,3 DPG levels are potentially decreased, shifting oxyhemoglobin curve to the left
78
Factor VII
Increasing off label use Currently only approved in hemophilia -2 doses given after large volume resuscitation found to stop persistent bleeding
79
Choosing blood products based on lab results with active bleeding*
• Platelets <50-75k: Give 6-8 pack (1 unit) of Platelet concentrate • HCT < 21-28%: Give PRBCs • INR >2.0 (and aPTT >1.3x control): Give 2-4 units FFP • Fibrinogen <125mg/dl: Give 10 units cryoprecipitate
80
3 components of a lethal burn
Inhalational >40% TBSA Age > 60years old =90% mortality
81
How do severe burns cause systemic disease?
Inflammatory mediators——interleukins and TNF (leading to wound edema)
82
1st degree burn
Sunburn
83
2nd degree burn
Deep partial thickness -deep dermis, require excision and grafting
84
3rd degree burn
Full thickness No blanching, insensate May cause sepsis
85
4th degree burn
Down to the bone Patient will have limited function
86
Rule of nines
Head = 9 % Upper extremities = 18% (4.5 each side) Whole trunk = 36% Lower extremities = 36%
87
1st phase (Burn shock)
First 1-2 days PVR/SVR increase Hematocrit increase Oliguria/ myoglobinuria
88
2 phase of a burn injury
Hyper metabolic/dynamic Decreased SVR/increased CO Decreased hematocrit Increased GFR but decreased tubular function
89
Signs of thermal airway burn
Singed facial hair Facial burns Cough Swallowing difficulties
90
Lower airway burn injury
Increased surfactant/mucocilliary function Mucosal necrosis and ulceration,edema and tissue sloughing/secretions=bronchial obstruction leading to air trapping and bronchopneumonia
91
Treating airway burns
High O2 Fiberoptic is a handy way to look at lower airways
92
Parkland formula
4ml crystalloid/kg/%burn in first 24 hours 20-60% of calculated plasma volume as colloid replacement in second 24 hrs
93
Stop burn resuscitation if
• Urine output = 0.5-1ml • Pulse = 80-140 bpm • MAP = adults > 60mmHg • Base deficit < 2
94
Anesthetic considerations in burns
Artline TEE for volume UOP Temp control Pain is high, decrease induction doses
95
Meds that may be less effective in burns
Opioids/ketamine/benzos -downregulation of Mu and upregulation of protein kinase and NMDA receptors
96
After the first 2 hours what are we avoiding in burn patients?
Sux
97

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