Trauma I Flashcards
(77 cards)
1
Q
what is the leading cause of death between 1-45 years in the US
A
trauma
2
Q
how much does care at a level 1 trauma center reduce mortality?
A
25%
3
Q
what are the three components of trauma evaluation
A
- rapid overview
- primary survery
- secondary survery
4
Q
rapid overview
A
- initial brief impression
- takes a few seconds is patient stable or unstable
5
Q
primary survey
A
- look at life-threatening injuries and how to correct them
- involves rapid evaluation for functions crucial to survival and includes ABCDE
6
Q
secondary survey
A
- detailed and systemic evaluation of each anatomic region and continued resuscitation if needed
- begins after critical life-saving actions have begin (like intubation, chest tube placement, and fluid resuscitation)
7
Q
ABCDE
A
- airway patency -is the patient talking, SOB, have an obstruction
- breathing - high flow oxygen, trachea midline, flail chest, tension pneumo, massive hemothorax (>1500 mL)
- circulation - skin temp, color, 2 large bore IVs
- disability - neuro, mentation, GCS
- exposure - take off close and examine body for injury
8
Q
three components of glasgow coma scale
A
- eye-opening response
- verbal response
- motor response
9
Q
eye-opening response
A
- 4 = spontaneous
- 3 = to speech
- 2 = to pain
- 1 = none
10
Q
verbal response
A
- 5 = oriented to name
- 4 = confused
- 3 = inappropriate speech
- 2 = incomprehensible sounds
- 1 = none
11
Q
motor response
A
- 6 = follows commands
- 5 = localizes to painful stimuli
- 4 = withdraws from painful stimuli
- 3 = abnormal flexion (decorticate posturing)
- 2 = abnormal extension (decerebrate posturing)
- 1 = none
12
Q
AVPU
A
alert
voice
pain
unresponsive
13
Q
exposure step of ABCDE
A
- final step of the primary survey that includes the complete exposure of the patient
- removal of clothing and turning to examine
- includes a brief head-to-toe search for visible injuries or deformities
14
Q
focus for the secondary survey
A
- history of injury
- allergies, medications, last oral intake
- focused medical and surgical history
15
Q
trauma airway evaluation
A
- involves diagnosis of trauma to the airway and surrounding tissue
- anticipate respiratory consequences of injury to airway
- contemplate airway management maneuvers, assume patient absolutely requires an airway and cannot be re-awakened electively
16
Q
what does airway management of trauma patients require?
A
- assisted or controlled ventilation
- self-inflating bag with a non-rebreathing valve is sufficient after intubation and for transport
- 100% oxygen is necessary until ABG is complete
17
Q
airway obstruction considerations
A
- airway edema/direct airway injury
- cervical deformity
- cervical hematoma
- foreign bodies
- dyspnea, hoarseness, stridor, dysphonia
- subQ emphysema and crepitation
- hemoptysis/active oral bleeding/copious secretions
- tracheal deviation
- JVD
- hemodynamic condition
18
Q
conisderations for airway management in trauma
A
- oxygen admin (100% oxygen)
- chin lift and jaw thrust (usually jaw thrust to minimize further injury)
- full stomach
- clearing of orophrayngeal airway
- oral and nasal airway (worry about basilar skull fracture)
- immobilization of cervical spine
- tracheal intubation if ventilation is inadequate
- consider AW adjuncts to secure AW
19
Q
nasal intubation considerations in trauma
A
- increased blood in the airway and nasal trauma
- ensure there is not a basilar skull fracture
20
Q
suspect basilar skull fractures
A
- CSF dripping out of nose
- racoon eyes
- battle sign –> bruising behind ears
21
Q
airway management techniques
A
- DL
- bougie
- video laryngoscopy
- AFOI
- RSI vs MRSI
- cricioid pressure (debated)
- manual in line cervical stabilization
- surgical cricothyrotomy/trach
22
Q
indications for ETT intubation in trauma
A
- cardiac or respiratory arrest
- respiratory insufficiency/deteriorating condition
- airway protection
- need for deep sedation or analgesia (pain control)
- GCS < 8
- delivery of 100% FiO2 in presence of carbon monoxide poisoning
- facilitate work-up in uncooperative or intoxicated patient
- transient hyperventilation required
23
Q
trachetomy
A
- takes longer to perform
- requires neck extension which may cause extended neck trauma if cervical injury is present
24
Q
cricothyroidotomy
A
- surgical cricothyroidotomy
- is contraindicated in those younger than 12 years old (<12 needs needle cric)
- laryngeal damage precludes the ability to perform a circothyroidotomy
25
cricothyrotomy
- if needed greater than 72 hours then need to replace with trach
- massive facial trauma/hemorrhage
- supraglottic foreign body obstruction
- angioneurotic edema
- inhalational thermal injury
- epiglottitis/croup
26
airway management + full stomach
- full stomach is consideration for all trauma patients and impacts AW intervention
- time not available to allow pharmacologic intervention to decrease gastric contents and acidity
- emphasis placed on safe technique for securing the airway
- RSI
- cricoid pressure
- in-line stabilization
- awake intubation with topical anesthesia and sedation
- LMA use contraindicated as definitive airway
27
emergency trauma airway algorithm
- need for emergent intubation
- preoxygenate with BVM, cricoid pressure, and manual in-line cervical stabilization
- induction, muscle relaxation
- laryngoscopy 1
- laryngoscopy 2
- LMA placement
- cricothyroidotomy
- OR for definitive airway
- CONFIRM - chest rise, auscultation, EtCO2
28
induction agents for trauma
- etomidate 0.2-0.3 mg/kg IV
- ketamine 2-4 mg/kg IV OR 4-10 mg/kg IM
- propofol 2 mg/kg
- precedex
29
NMBD for trauma
- succinylcholine 1-1.5 mg/kg IV, OK in first 24 hours of burn or SCI, 30 second onset, fasciculate, 5-12 min duration
- rocuronium 1.2 mg/kg IV, 30-60 second onset, may need gentle mask ventilation (MRSI), 60-90 min duration
30
cervical spine injuries and AW management
- high suspicion for cervical injury if victim has experienced a fall, MVA, driving accidnet
- semi-rigid collar, sandbags, and backboard provide best stabilization
- manual inline stabilization (MIS) best for AW management
- stabilization is maintained until cervical injury ruled out
- orotracheal intubation is most desirable
31
when is cervical injury cleared?
- full xray of C1-C7
| - patient not obtunded or under influence of drugs and says there is no pain in neck
32
head, open eye, major vessel injury and AW management
- ensure adequate oxygenation and ventilation
- deep anesthesia and PROFOUND relaxation prior to airway manipulation and intubation (DO NOT want to increase BP/ICP/IOP)
- without sufficient depth of anesthesia these patients may have HTN, coughing, bucking, increased ICP/IOP
- must consider initial assessment of airway, if difficult you cannot use muscle relaxants or IV induction agents
33
maxillofacial injuries and AW management
- blood and debris in orophraynx may predispose patient to complete or partial airway obstruction
- aspiration of teeth or foreign bodies
- serious AW compromise may present within a few hours of penetrating facial trauma
- consider limitation of mandibular movement and trismus
- AW management technique is based on the presenting condition
34
penetrating injury
- damage depends on 3 interactive factors
- type of wounding instrument
- velocity at time of impact
- characteristics of tissue through which it passes
- clinical signs includ escape of air, hemoptysis and coughing
35
blunt injury
- includes direct impact, deceleration, shearing, and rotary forces (laryngotracheal damage)
- clinical signs = hoarseness, muffled voice, dyspnea, stridor, dysphagia, cervical pain, and tenderness, flattening of thyroid cartilage
36
factors that alter respiration and interefrere with breathing
- tension pneumo
- flail chest
- open pneumo
- hemothorax
- pulmonary contusion
- diaphragmatic rupture
- chest wall splinting
37
hemothorax
- presence of blood in the pleural cavity
- hallmark symptoms = hypotension, hypoxemia, tachycardia, increased CVP
- treatment = aim to eliminate and correct
- anesthetic considerations = include placing a chest tube and one lung ventilation
38
pneumothorax
- disruption of the parietal or visceral pleura presence of gas within the pleural space
- 3 categories = simple, communicating, tension
- treatment = chest tub if PTX > 20% of lung collapsed
39
tension pneumo
- occurs with rib fractures and barotrauma due to mechanical ventilation
- hallmark symptoms - hypotension, hypoxemia, tachycardia, increased CVP, diminished BS on the affected side
- treatment is needle decompression
40
flail chest
- results from - communicated fractures of at least 3 ribs, rib fractures associated with costrochondral separation, sternal fracture
- respiratory insufficiency and hypoxemia over several hours with deterioration of CXR and ABG
- consider pain management (blocks, opioids, multimodal, incentive spirometry, CPAP, BiPAP) over mechanical ventilation
41
circulation/shock
- hemorrhage is the most common cause of traumatic hypotension and shock in trauma patients
- circulatory failure leading to inadequate vital organ perfusion and oxygen delivery
- resuscitation refers to the restoration of normal circulating blood volume, normal vascular tone, and normal tissue perfusion
42
physiologic response to shock
- initial response = mediated by neuroendocrine system
- hypotension leads to vasoconstriction and catecholamine release
- heart, kidney, brain, blood flow is preserved while other regional beds constricted
- traumatic injuries --> release in hormones that set the stage for mircocirculatory response
- ischemic cells respond to hemorrhage by taking up interstitial fluid and depleting intravascular volume and producing lactate and free radicals
- inadequate organ perfusion interferes with aerobic metabolism --> producing lactic acid and metabolic acidosis
- lactate and free radicals accumulate in the circulation while perfusion is diminished
- lactate and free radicals can cause damage to cell and a toxic load that will be washed into circulation once it is re-established
- ischemic cells also produce inflammatory factors (leukotrienes, interleukins) --> systemic inflammatory process, becomes disease process unto itself, lays foundation for MODS
43
CNS response to shock
-responsible for maintaining blood flow to heart kidney and brain at expense of other tissue
44
kidney/adrenal response to shock
-maintains GF during hypotension by selective vasoconstriction and concentration of blood flow in medulla and deep cortical areas
45
heart response to shock
-preserved via increase in nutrient blood flow and cardiac function until later stages
46
lung response to shock
- destination of inflammatory byproducts --> accumulate in capillary beds and results in ARDS
- sentinel organ for the development of MOSF
47
gut/intestinal response to shock
-one of the earliest organs affected by hypo-perfusion and may be trigger for MOSF
48
acute traumatic coagulopathy
- begins in early presence of reduced clot strength
- hypotension and tissue injury --> inflammatory response --> endothelial activation of protein C (APC)
- hyperfibrinolysis due to APC formation
- resuscitation includes early treatment of ATC
49
what does base deficit reflect?
- severity of shock
- oxygen debt
- changes in O2 delivery
- adequacy of fluid resuscitation
- likelihood of multi-organ failure
50
mild shock
base deficit between 2-5 mmol/L
51
moderate shock
base deficit between 6-14 mmol/L
52
severe shock
base deficit between 14 mmol/L
53
base deficit of 5-8 mmol/L
correlates with increased mortality
54
blood lactate level
- blood lactate level is less specific than base deficit but nonetheless important
- elevated lactate levels correlate to hypoperfusion
- normal plasma lactate level is 0.5-1.5 mmol/L and half life is 3 hours
- plasma lactate level above 5 mmol/L indicate significant lactic acidosis
- failure to clear lactate within 24 hours after reversal of shock is predictor of increased mortality
55
assessment of systemic perfusion
- VS
- UOP
- systemic acid-base status
- lactate clearance
- cardiac output
- mixed venous oxygenation
- gastric tonometry
- tissue specific oxygenation
- SVV
- acoustic blood flow
56
symptoms of shock
- pallor
- diaphoresis
- agitation or obtundation
- hypotension
- tachycardia
- prolonged capillary refill
- diminished UOP
- narrowed pulse pressure
57
sites for emergency IV access
- large bore IVs antecubital vein
- other large bore IV sites
- subclavian vein (easiest place and does not require neck manipulation in circumstance of cervical neck injury)
- femoral vein (but infection risk, and if bleeding into abdomen could pour stuff in)
- IJ
- IO
58
goals for early resuscitation
- maintain SBP at 80-100 mmHg
- maintain Hct at 25-30%
- maintain PTT and PT within normal range
- maintain plt count >50,000
- maintain normal serum iCal
- maintain core temp > 35 celsius
- maintain function of pulse ox
- prevent increase in serum lactate
- prevent worsening acidosis
- adequate anesthesia/analgesia
59
risks of aggressive volume replacement during early resuscitation
- increased blood pressure
- decreased blood viscosity
- decreased Hct
- decreased clotting factor concentration
- greater transfusion requirement
- disruption of electrolyte balance
- direct immune suppression
- premature reperfusion
60
anesthesia resuscitation goals
- oxygenate and ventilate
- restore organ perfusion
- restore hemostasis/repay oxygen debt
- treat coagulopathy
- restore circulating volume
- continuous monitoring of the response
61
surgery resuscitation goals
-stop the bleeding
62
goals for LATE resuscitation
- maintain SBP > 100 mmHg
- maintain Hct above individual transfusion threshold
- normalize coagulation status
- normalize electrolyte balance
- normalize body temperature
- restore UOP
- maximize CO by invasive/noninvasive monitoring
- reverse systemic acidosis
- document decrease in lactate to normal range
63
end point for resuscitation
- serum lactate level < 2 mmol
| - base deficit < 3
64
management of shock
- control the source of hemorrhage
- begin fluid resuscitation - isotonic crystalloid, hyperteonic saline, colloids, PRBCs, plasma)
- possible use rapid infusing system (RIS) (1500 cc/min)
- early resuscitation 80-100 mmHg and late >100 mmHg
65
hypertonic saline
-traumatic brain injury HS is used as an osmotic agent in the management of increased ICP
66
colloids
rapid plasma volume expansion
67
PRBCs
- provided to adequate oxygen carrying capacity - mainstay of hemorrhagic shock
- blood loss replacement (1:1 with RBC, 3:1 with crystallloid, Rh negative blood preferable esp for women of childbearing age)
68
FFP
2 units of FFB with every 4 units PRBC when MTP is anticipated or ongoing
69
hemostatic resuscitation damage control
- administration of set protocol of blood and hemostatic products to mimic whole blood
- MTP
- limited crystalloid
70
hemostatic resuscitation goal directed
-utilizes point of care viscoelastic (TEG) monitoring to direct therapy
71
hemostatic agents
- TXA - antifibrinolytic; benefit when instituted within 1 hour of admission
- recombinant activated human coagulation factor VII
72
lethal triad
- acidosis
- hypothermia
- coagulopathy
* acidosis and hypothermia are major factors in the induction of coagulopathy*
73
shock and hypothermia
- acid base disorders
- coagulopathy
- myocardial function
- shifts oxygen-Hgb curve to the left
- decreases the metabolism of lactate, citrate and some anesthetic drugs
74
hypothermia
- left shift of oxygen hgb dissociation curve - decreased tissue oxygenation (bc left loves)
- impairs plt and clotting enzyme function
- abnormal potassium and calcium homeostasis
- causes vasoconstriction, can ultimately make BP appear higher than volume status actually is so BP may DROP as patient warms
75
coagulopathy in trauma patient
- activation of clotting cascade causes consumption of clotting factors
- blood loss causes a loss of clotting factors
- hemodilution further dilutes clotting factors
- severely injured trauma patients become hypercoagulable
76
29 degrees celcius
PT and PTT increase by 50%
| plts decrease by 40%
77
treatment of coagulopathy
- avoidance or refersal of lethal triad
- judicious resuscitation avoid hemodilution
- trauma disrupts equilibrium between hemostatic and fibrinolytic processes
- changes are complex and can either result in hypocoagulable or hypercoagulable states
