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Advanced Principles- Fall 2018 > Trauma > Flashcards

Flashcards in Trauma Deck (62)
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What are the trauma statistics?

  • 9% of total annual mortality
  • 1.24 million traffic accident fatalities
    • usually pedestriants, cyclists, and motorcyclists
  • 1.5 million deaths d/t violence
  • Most deaths d/t high energy mechanixm of injury
    • 1.3 die within first 4 hours
    • deaths d/t low energy impact higher after 7 days
  • Leading cause of mortality is head trauma, 2nd is hemorrhagic shock


What is the pathophysiology of hemorrhagic shock?

  • Problem of supply vs demand: imbalance occurs between systemic O2 delivery and O2 consumption
  • hemodynamic instability, coagulopathy, decreased O2 delivery, decreased tissue perfusion, and cellular hypoxia
  • Initial response: macrocirculatory and mediated by neuroendocrine system
    • release of: renin, antiotensin, vasopressin, ADH, GH, glucagon, cortisol, epinephrine, norepi
      • renal and adrenal systems play major role in this
    • this sets stage for the microcirculatory response


What is the " shock cascade?"

(flow chart)

  • Ischemia in any part of body will trigger an inflammatory response that will affect the non-ischemic organs even after perfusion has been restored.
    • individual ischemic cells respond to hemorrhage by taking up interstitial fluid, further depleting intravascular fluid
    • cellular edema can block adjacent capillaries which prevents reversal of ischemia even with good macroperfusion
  • Ischemic cells produce lactate--this washes back into central circulation and sets up for SIRS and Multi organ failure


How does CNS system respond to Hemorrhagic shock?

  • CNS is the prime trigger of the neuroendocrine response
    • controls selective perfusion to heart, kidney, and brain
    • reflexes and cortical electrical activity are both depressed (this is reversible in mild hypoperfusion)


How does the cardiac system respond to hemorrhagic shock?

  • Cardiac system is preserved from ischemia
    • lactate, free radicals, and other humoral factors released by ischemic cells all act as negative inotropes
  • Somebody with cardiac disease (esp fixed stroke volume) is at greater risk for decompensation d/t hypovolemia and anemia
  • cardiac dysfunction is a LATE SIGN and often a terminal event


How does the pulmonary system respond to hemorrhagic shock?

  • The lungs are the filter for the inflammatory by-products of the ischemic cells in body.  
    • immunE complex and cellular factors accumulate in pulmonary capillaries and lead to neutrophil and platelet aggregation, increased capillary permeability, destruction of lung, and ARDS


How does the renal system respond to hemorrhagic shock?

  • Neuroendocrine response
  • GFR maintained with selective vasoconstriction
  • Prolonged hypotension affects the ability to concentrate urine
    • also tubular epithelial necrosis and renal failure


How does hemorrhagic shock affect the gut/intestines?

  • One of first organs affected by hypoperfusion
  • Intestinal cell death causes a breakdown in the barrier function of the gut that allows bacteria into the liver and lungs
    • this potentiates ARDS


How does the liver respond to hemorrhagic shock?


Skeletal muscles?

  • Failure of synthetic function of the liver--cannot make things like coagulation factors
    • this can be lethal
  • Skeletal muscles
    • tolerate ischemia better than other organs
    • release lactic acid and free radicals that can potentiate the ARDS


What are the steps for a Trauma assessment?

  1.  Initial rapid assessment- is pt stable, unstable, or dead
  2. Primary survey: ABCDE
    1. ABC- airway patency, breathing, circulation
    2. D- disability: brief neurological examination 
    3. E- expose:  Undress and inspect for external injuries
    4. Must decide to proceed immediately to surery or continue on to secondary survey
  3. Secondary survey: detailed multi-system exam and history
    1. further diagnostic evaluation


What are the details of ABCDE?

(flow chart)


How is the airway managed for a trauma patient?

  • Stabilize C-spine
  • provide 100% FiO2 (until you have ABG)
  • For obstruction if spontaneously breathing:
    • Initial- chin lift, jaw thrust, suction, OPA (nasal ok, but avoid if any possibility pt has basilar skull fx or maxillofacial injury)
    • Still inadequate- consider BMV or SGA
  • Proceed to intubation
    • awake vs RSI vs cricothyroidotomy


How does the airway algorithm change when dealing with a trauma?

What is best choice?

  • You do not have the option to awaken the patient if you cannot get the airway
  • If something does not work, you MUST change something 
  • Best choice: RSI or awake intubation with topical anesthesia
  • Steps:
    • Locate cricothyroid membrane
    • pre-oxygenate
    • perform RSI
    • look with video laryngoscopy and attempt intubation
    • consider SGA but do not delay
    • proceed to cricothyrotomy if no view


What are the indications for intubation in trauma patients?


Strong indication

discretionary indication


How are cervical spine injuries diagnosed or ruled out?

Gold standard?


  • C-spine injuries can be missed on initial trauma assessment
  • CT (with < 3mm cuts) is typical diagnostic tool
    • soft tissue and ligament injuries can only be detected on MRI
    • MRI is gold standard
  • *It is very rare to cause cervical cord injury with airway management but we still take precautions
  • If pt is wake and sober, check for posterior midline neck tenderness
    • if this test is negative with no other distracting injuries, there is low likelihood if c-spine injury


How are c-spine precautions maintained during airway management?

  • All airway maneuvers cause some s-spine movement
  • Rigid collar is NOT enough
  • Manual inline stabilization is preferred
  • Pt may have unopposed vagal tone during airway manipulation causing severe brady
    • may want to premedicate


How is manual inline stabilization done?

  • Ideally anesthesia provider + two people
  • One perso stabilizes and aligns the head in neutral position without applying cephalad traction
  • other person stabilizes both shoulders by holding them agains bed
  • anterior portion of collar may be removed to improve mouth opening
  • MILS can obstruct glottic view


Blunt airway injuries:


preferred airway management

  • Symptoms:  
    • hoarseness/muffled voice
    • dyspnea/stridor
    • dysphagia
    • odynophagia (painful swallowing)
    • cervical pain and tenderness
    • ecchymosis
    • subQ emphysema
    • flattening of adams apple
  • preferred airway management:
    •  Fiberoptic bronch or surgical airway
    • CT before intervention if stable
  • 70% of blunt airway injuries also have C-spine injuries
  • blunt airway injuries can be missed


Penetrating airway injury:



  • Symptoms:
    • air bubbling through wound
    • hemoptysis
    • coughing
  • managment:
    • ETT inserted in wound
    • tracheostomy distal to wound
    • oral intubation


What are pulmonary complications seen in trauma?

  • Tension pneumothorax
    • no time to confirm with CT or Xray
    • must do needle decompression or chest xray
  • Flail chest- two or more sites of at least three adjacent ribs (costocondal separation or sternal fx)
    • will decompensate over 3-6 hours
    • ARDS likely if lung contusion >20%
  • Open pneumothorax
    • risk for vascular air entrainment


What are symptoms of tension pneumothoras?

Where do you do needle decompression of pneumothorax?

Where does chest tube go?

  • Symptoms:
    • cyanosis
    • tachypnea
    • hypotension
    • neck vein tistension (unless hemorrhaging)
    • tracheal deviation
    • diminished breath sounds on affected side
  • Needle decompression:
    • midclavicular line of 2nd intercostal space
    • remember nerves/veins, arteries are high in intercostal space
      • walk off top of third rip
  • Chest tube mid-axillary 5th intercostal space


How do you treat flail chest?

  • Automatic intubation is NOT recommended
  • focus on analgesia to maintain adequate excursion and ventilation/oxygenation
    • epidural or thoracic paravertebral blocks preferred with O2 and non-invasive PPV


What are the different classes of shock?

blood loss (ml)

blood loss (%)

pulse rate

systolic BP

pulse pressure



CNS/mental state


Information about shock:

difinitive treatment?

When should you expect major bleeding?

Ideal SBP?

goal Hgb?

  • Difinitive tx- operative control of bleeding at the source
  • expect major bleeding with falls >6 ft, high energy deceleration, or high velosity like GSW
    • free fluid on Xray or CT warrants immediate intervention
  • Ideal SBP = 100-110,
    • especially in elderly (90's ok in young/healthy)
    • Goal Hgb = 7-9


What does the base deficit tell us?

  • Base deficit is more reliable than pH in:
    • reflecting the severity of shock
    • oxygen debt
    • changes in O2 delivery
    • adequacy of fluid resuscitation
    •  likelihood of multi-organ failure


What are the principles of damage control?

  • 1st phase (arrival)- recognize the severity of injury; control bleeding, rapid transport to OR
    • limit crystalloids
    • permissive hypotensive
    • active rewarming
    • early FFP and platelets at high ratios with PRBCs
  • 2nd phase (in OR)
    • surgeons rapidly control bleeding; leave abdomen open
    • goals:
      • maintain intravascular volume
      • temp
      • acid/base status
      • coagulation
  • 3rd phase: ICU management with same goals
  • 4th phase: multiple returns to OR at 24 and 48 hour intervals for organ repair, washout, and debridement



  • Permissive hypotension (except TBI, spinal cord injury, or elderly)
  • rapid control of bleeding
  • Avoid large volume of crystalloid- can cause ARDS and abdominal compartment syndrome by worsening endothelial dysfunction
  • Early administration of plasma and other product in balanced racio with PRBCs (1:1:1)
  • tranexamic acid
  • New PRBCs preferred (<14 days old)- lower incidence of reaction


What kind of blood do you use for uncrossmatched patient?





What is the lethal triad of hemorrhage?

  • Hemorrhage causes acidosis, hypothermia, and coagulopathy
    • acidosis and hypothermia cause factor and platelet dysfunction, enhancing coagulopathy
      • this causes MORE bleeding


What are the two components of coagulopathy in trauma?

  • Acute traumatic coagulopathy-occurs shortly after trauma
    • hyperfibrinolysis and severe tissue injury releases tissue factor--this activates coagulation pathways
  • Resuscitation-associated coagulopathy
    • Caused by hypothermia, dilution with crystalloids