Trauma Part 1 Flashcards
trauma is the leading cause of death between ____ years of age
1-45
WHO estimates trauma is leading cause of death world wide between _____ years of age
15-44
3 sequential components of evaluation
- rapid overview (stable v unstable)
- primary survey (5-10 minutes max), ABCDE
- secondary survey
Primary Survey ABCDE stands for
airway, breathing, circulation, disability, exposure
Primary Survey: airway
potency. obstruction? agitated (hypoxia), gurgling, stridor, tracheobronchial obstruction, paradoxical chest movement, pneumothorax, or talking and fine
Primary survey: breathing
how to maintain: high flow oxygen, trachea midline, flail chest (3 or more fractured segments of ribs), tension pneumothorax, massive hemothorax (>1500cc of blood)
primary survey: circulation
pale, tachycardic, bleed that needs tamponade. large bore IV’s (two 16gauges would be lit)
Primary Survey: Disability
mentation (neuro, GCS)
Primary Survey: exposure
strip them to examine for contusions, deformities, foreign objects. See if they need emergent OR, log roll patient when turning.
GCS: eye opening response
4: spontaneous
3: to speech
2: to pain
1: none
GCS: verbal response
5: oriented to name
4: confused
3: inappropriate speech
2: incomprehensible sounds
1: none
GCS: motor response
6: follows commands
5: localizes to painful stimuli
4: withdraws to painful stimuli
3: abnormal flexion (decorticate)
2: abnormal extension (decerebrate)
1: none
percent mortality of GCS <8
35%
Secondary Survey
begins after critical life saving actions including intubation, chest tube placement, fluid resuscitation. focus is history of injury, allergies, medications, last oral intake. focused medical and surgical history
ex) also think: obese, older, those kinds of assessments and implications of.
airway: most trauma patients require
assisted or controlled ventilation, self inflating bag with non rebreathing valve is sufficient after intubation and for transport. 100% oxygen is necessary until ABG is complete.
airway obstruction considerations
airway edema/direct aw injury (jaw injury, trismus?)
cervical deformity (think cervical injury, sandbags or c collar.)
cervical hematoma
foreign bodies (gsw. internal and external ex) knocked tooth and aspirated, bite tongue off)
dyspnea, hoarseness, stridor, dysphonia
SQ emphysema and crepitation (palpate neck. laceration or tracheal tear with hoarseness or stridor are signs)
hemoptysis/active oral bleeding/copious secretions (fiberoptic not best, you’ll just see red!)
tracheal deviation
JVD (chest wound, stab wound, narrowed PP, muffled heart, hypo perfusion)
hemodynamic condition
airway management considerations
100% oxygen administration ma'am chin lift and jaw thrust (CAN DO if neck is injured) full stomach (SNS response) clearing of oropharyngeal aw oral and nasal aw immobilization of cervical spine tracheal intubation if ventilation is inadequate consider aw adjuncts to secure aw
tracheal intubation considerations
if NT tube, smaller hole so switch to ett as soon as you can. sinusitis is SE.
naso tracheal intubation: when you can and cant!
basilar skull fx (battle signs behind ear, raccoon eyes, CSF leak are sx) NO
lefort 1 and 2 if you have to~~
lefort 3, nah fam
if you go to ED/ICU and patient is intubated, check tube placement via
breath sounds and capnometry at the least.
what happens to your CO2 if your pt is hypotensive
low CO2 ma’am.
difference between RSI and MRSI
modified is trying to ventilate. like if theyre hypoxic af or obese. but really dont want to put more air in the stomach so like, proceed with caution.
cricoid pressure?
dont “have to” anymore, not in algorithm.
indications for ETT
cardiac or respiratory arrest
respiratory insufficiency/deteriorating condition
aw protection
need for deep sedation or analgesia (pain control)
GCS <8
delivery of 100% FiO2 in the presence of carbon monoxide poisoning
facilitate w/u in uncooperative or intoxicated patient
transient hyperventilation require
facial burns, consider protecting that airway
flail chest, need ETT?
not always. may need pain management so they take deep breaths and ventilate
tracheostomy versus cricothyroidotomy
tracheostomy takes longer to perform, requires neck extension which may cause extended neck trauma if cervical injury is present
cricothyroidotomy is contraindicated in those younger than 12. do a needle cric if <12y. laryngeal damage precludes the ability to perform a cricothyroidotomy.
consider cricothyroidotomy when
massive facial trauma/hemorrhage supreglottic foreign body obstruction angioneurotic edema inhalation thermal injury epiglottis/croup tracheal/laryngeal damage
complications of cricothyroidotomy
esophageal perforation
SQ emphysema
bleeding/hemorrhage
gold standard airway technique for spinal injury and cervical spinal injurries
fiberoptic
aw management and full stomach
full stomach is consideration for every trauma patient. no time for pharmacological intervention to decrease gastric contents and acidity. so, RSI (cricoid pressure?) and manual inline stabilization or awake intubation with topical anesthesia and sedation if pt cooperative.
LMA use is contraindicated as a definitive aw (yah)
suggested emergency aw algorithm for trauma
- need for emergent intubation
- preoxygenate with bag valve mask, cricoid pressure and manual in line stabilization
- induction, muscle relaxation
- laryngoscopy #1
- if unsuccessful, laryngoscopy #2 with bougie
- if unsuccessful, LMA placement
- if unsuccessful, cricothyroidotomy
- if unsuccessful (or even successful), OR for definitive aw
succinylcholine for burns and SCI
ok in first 24 hours, contraindicated after
induction drug suggestions for trauma (and doses)
etomidate .2-.3mg/kg IV (.2-.4)
ketamine 2-4mg/kg IV (except for head injuries)
ketamine 4-10mg/kg IM
propofol 2mg/kg IV (vasodilation tapered if given slowly)
NMB drug suggestions for trauma
succinylcholine 1-1.5mg/kg IV (head/globe injury, no succ)
rocuronium 1.2mg/kg IV (30-60 second onset, may need gentle mask vent or MRSI, 60-90m DOA)
succinylcholine defasciculating dose
for head/globe injury, can admin defasciculating dose of 3-5mg roc
anesthetic drugs in trauma, other drugs to consider
scopolamine .4mg IV (amnesia, Ach inhibition)
precedex
benzodiazepines
cervical spine injuries and aw management: high suspicion in these situations
fall, MVA, diving accident
cervical spine injuries management includes
semi rigid collar, sandbags, backboard. always log roll, manual in line stabilization (MIS) best for aw management. stabilization maintained until cervical injury ruled out. orotracheal intubation most desirable
how to rule out cervical spine injury
XR C1-7 and patient is not obtunded/high/drunk so they are awake and can communicate pain
how to do manual in line stabilization (MILS)
hold near mastoid process and can take front part of collar off if needed
head, open eye, major vessels injuries and aw management
ensure adequate oxygenation and ventilation
deep anesthesia and profound relaxation prior to aw manipulation and intubation
head, open eye, major vessels injuries and aw management: without sufficient depth of anesthesia, patients may present with
HTN, coughing/bucking, increased ICP, IOP, and intravascular pressure
head, open eye, major vessels injuries and aw management: initial assessment considerations
if its a difficult aw, cannot use muscle relaxants or IV induction agents. 4% lido to inhale or to help with cough/bucking.
maxillofacial injuries and aw management
blood and debris in oropharyngeal cavity may predispose to partial or complete aw obstruction
aspiration of teeth or foreign bodies
serious aw compromise may present within few hours of penetrating facial trauma
consider limitation of mandibular movement and truisms
aw mangement technique is based on presenting condition
leave them in whatever position they are with ventilation until they are ready to ventilate
cervical injuries and aw management: penetrating injury. damage depends on 3 interactive factors
type of wounding instrument
velocity at time of impact
characteristic of tissue through which is passes.
clinical signs include escape of air, hemoptysis, and coughing
cervical injuries and aw management: blind injury
includes direct impact, deceleration, shearing, and rotary forces. laryngotracheal damage
clinical signs include hoarseness, muffled voice, dyspnea, stridor, dysphagia, cervical pain and tenderness, flattening of thyroid cartilage
cervical injuries and aw management: ways to establish secure aw
intubation of trachea should be with fiberoptic scope or aw should be established surgically
C4-5 injury and aw
intubate!
C6-7 injury and aw
intubate because they lose respiratory muscle function and lung compliance (diaphragm, airway reflexes)
breathing abnormalities that require intubation
tension pneumothorax flail chest (probably, not always) open pneumothorax hemothorax pulmonary contusion diaphragmatic rupture chest wall splinting
hemothorax symptoms, tx, anesthetic considerations
sx: HoTN, hypoxemia, tachycardia, increased CVP
tx: eliminate/correct
anesthetic considerations: 1 lung ventilation. first put in regular ett to establish aw asap then in a controlled environment switch for a double lumen tube. will likely need CT, assess how much blood and if transfusion is warranted.
pneumothorax categories (3) and tx
simple (not open to the world), communicating (open to the world), tension
tx: chest tube if pneumothorax is creating >20% lung collapse
tension pneumothorax hallmark symptoms and tx
sx: HoTN, hypoxemia, tachycardia, increased CVP, diminished BS on affected side
tx: decompression. most common between 2nd and 3rd ICS MCL anteriorly
flail chest results from
comminuted fractures of at least 3 ribs, rib fractures associated with costochondral separation, sternal fracture (possible pulmonary contusions)
flail chest sx, considerations, tx
sx: respiratory insufficiency and hypoxemia over several hours with deterioration of cxr and abg
consider: pain management over mechanical ventilation
tx: pain relief and oxygen. ex) epidural anesthesia, intercostal blocks. if patient decompensates, then intubate if necessary. CPAP/BiPAP ok as well
most common cause of traumatic HoTN and shock in trauma patients
hemorrhage
resuscitation refers to:
restoration of normal circulating blood volume, normal vascular tone, normal tissue perfusion
physiologic response to shock
- initial response mediated by neuroendocrine system (HoTN leads to vasoconstriction and catechol release. blood flow to heart, kidney, brain preserved while others restricted.)
- ischemic cells respond to hemorrhage by taking up interstitial fluid and depleting intravascular volume and producing lactate and free radicals. “trapped in cell=cell swelling”.
- inadequate organ perfusion interferes with aerobic metabolism producing lactic acid and metabolic acidosis. lactate and free radicals accumulate in circulation while perfusion is diminished
- ischemic cells also produce inflammatory factors, lays foundation for multiple organ failure and high mortality rates
lactate and free radicals can cause
direct damage to the cell, toxic load that will be washed into circulation once it is re established. this is self perpetuating.
blunt trauma can be responsible for what type of shock
cardiogenic
neurogenic trauma can be responsible for what type of shock
distributive
hormones released during shock include
renin, angiotensin, vasopressin, ADH, growth hormone, glucagon, cortisol, epi/norepi
organ responses to shock: CNS
responsible for maintaining blood flow to heart kidney and brain at expense of other tissue
organ responses to shock: kidney/adrenal
glands maintains BF during HoTN by selective vasoconstriction and concentration of BG in medulla and deep cortical areas
organ responses to shock: heart
preserved via increase in nutrient blood flow and cardiac function until later stages
organ responses to shock: lung
is the destination of inflammatory byproducts, accumulate in capillary beds and results in ARDS. sentinel organ for development of MSOF
organ responses to shock: gut/intestinal
one of earliest organs affected by hypo perfusion and may be trigger for MSOF
acute traumatic coagulopathy pathophys cascade
begging in early presence of reduced clot strength. HoTN and tissue injury->inflammatory response->endothelial activation of APC. hyperfibrinolysis d/t APC formation
resuscitation includes early tx of ATC
base deficit reflects
the severity of shock, oxygen debt, changes in O2 delivery, adequacy of fluid resuscitation, likelihood of multiple organ failure
base deficit: mild shock
2-5mmol/L
base deficit: moderate shock
6-14mmol/L
base deficit: severe shock
> 14mmol/L
admission base deficit of ____correlates with increased mortality
5-8mmol/L
is blood lactate or base deficit more specific?
base deficit
elevated lactate levels correlate with
hypoperfusion
normal plasma lactate level and half life is
.5-1.5mmol/L and half life is 3h
plasma level above ____ is significant lactic acidosis
> 5mmol/L
failure to clear lactate within ____ hours after reversal of shock is predictor of increased mortality
24 hours
assessment of systemic perfusion includes
VSS (will not indicate occult hypo perfusion)
UOP (may be inaccurate r/t diuretics, intoxication, renal injury)
systemic acid base status (confounded by resp status)
lactate clearance (time to obtain lab result)
CO (requires PA cath/non invasive technology)
mixed venous O2 (accurate, difficult to obtain)
gastric tonometry (needs time to equilibrate, subject to artifact)
tissue specific oxygenation (emerging technology)
SVV (emerging technology, arterial line)
acoustic BF (investigational technology)
symptoms of shock
pallor diaphoresis agitation or obtundation HoTN tachycardia prolonged capillary refill diminished UOP narrowed PP
sites for emergency IV access in order of desirability
- large bore IV’s in AC
- other large bore IV site
- subclavian vein (easiest to place and does not require neck manipulation in circumstance of cervical neck injury)
- femoral vein (infx risk, access above diaphragm best r/t injuries)
- IJ
- IO (tibia)
goals for early resuscitation
maintain SBP 80-100mmHg maintain Hct 25-30% maintain PTT and PT WNL maintain platelets >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
risks of aggressive volume replacement during early resuscitation
increased BP decreased blood viscosity decreased HCT decreased clotting factor concentration greater transfusion requirement disruption of electrolyte balance direct immune suppression premature reperfusion
resuscitation goals: anesthesia considerations
oxygenation and ventilation restore organ perfusion restore homeostasis, repay oxygen debt tx coagulopathy restore circulating bolume continuous monitoring of response SURGERY STOPS BLEEDING NOT U OKAI
goals for late resuscitation (late not as in near death, late as in you were successful with early resuscitation)
“normalize” is buzz word
maintain SBP >100
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
end point for resuscitation
lactate <2mmol/L
base deficit <3mmol/L
gastric intramucosal pH >7.33
blood loss replacement
1:1 with PRBC for trauma (1:2 normally)
3:1 with crystalloid
Rh negative blood is preferable if crosmatch is not complete (ABORh). esp if woman is child bearing age.
blood loss replacement and FFP
2U FFP with every 4U PRBC when massive transfusion is anticipated or ongoing
hemostatic agents to consider during trauma
TXA (antifibrinolytic). benefits when instituted within 1 hour of admission
recombinant activated human coagulation factor VII (rFVIIa)
fluid inflation system (rapid transfuser?) pearls
1500ml/min transfusion infused at controlled temp allows for mixing of products compatible with crystalloid, colloid, PRBC, washed salvaged blood, plasma accurate recording of fluid volume admin portable
lethal triad
acidosis
hypothermia
coagulopathy
hypothermia worsens
acid base DO's coagulopathy myocardial fx shifts oxygen hgb curve to left decreases metabolism of lactate, citrate, and some anesthetic drugs causes vasoconstriction (BP looks higher than it is) abnormal K and Ca hemostasis causes sequestering of platelets!
coagulopathy in the trauma patient pearls
activation of clotting cascade causes consumption of clotting factors
blood loss causes loss of clotting factors
hemodilution further dilutes clotting factors
severely injured trauma patients because hypocoagulable
massive transfusion causes dilution of
factors and platelets
at 29c, PT and PTT ______ and platelets ______
PT and PTT increase 50% and platelets decrease 40%
tx of coagulopathy
avoidance or reversal of lethal triad
avoid hemodilution during resuscitation
treat coagulopathies
can be hypo coagulable or hyper coagulable state r/t trauma. treat accordingly.
