Trauma part 2 Flashcards
Initial response to shock is mediated by
the neuroendocrine system
- hypotension leads to vasoconstriction & catecholamine release
- heart, kidney, and brain blood flow is preserved while other regional beds are constricted
Hypotension in the state of shock leads to
vasoconstriction and catecholamine release
___________ blood flow is preserved while other regional beds are constricted.
Heart, kidney, & brain blood flow
Traumatic injuries lead to a release in
hormones that set the stage for microcirculatory response
Ischemic cells response to hemorrhage by taking up
interstitial fluid & depleting intravascular volume & producing lactate & free radicals
Inadequate organ perfusion interferes with
aerobic metabolism–> producing lactic acid & metabolic acidosis
_______ accumulate in the circulation while perfusion is diminished
lactate & free radicals
Lactate & free radicals can cause:
direct damage to cell
a toxic load that will be washed into circulation once re-established
Ischemic cells also produce inflammatory factors
(leukotrienes, interleukins, etc.)
- systemic inflammatory process
- becomes a disease process unto itself
- lays the foundation for multiple organ failure and nigh mortality rates
_______ temporarily maintain perfusion to vital organs
catecholamine release, regional vasoconstriction (adrenal/neuroendocrine)
The cellular response to shock includes:
uptake interstitial fluid–> swell
swelling may cause obstruction of capillaries–> no perfusion
this may inhibit reversal of ischemia
ischemic cells produce lactate, free radicals, and inflammatory mediators
In response to pain & hemorrhage, the following hormones are released:
renin/angiotensin vasopressin ADH growth hormone glucagon cortisol epi/norepi
Describe the CNS response to shock.
responsible for maintaining blood flow to heart, kidney, & brain at expense of other tissues
Describe the kidney/adrenal glands response to shock.
maintains GF during hypotension by selective vasoconstriction and concentration of blood flow in medulla and deep cortical areas
Describe the heart’s response to shock.
preserved via an increase in nutrient blood flow and cardiac function until later stages
Describe the lung’s response to shock
the destination of inflammatory byproducts–> accumulate in capillary beds and results in ARDS. sentinel organ for the development of MOSF
Describe the Gut/intestinal response to shock.
one of the earliest organs affected by hypo-perfusion and may be trigger for MOSF
Resuscitation includes early treatment of
acute traumatic coagulopathy
Acute traumatic coagulopathy begins in the early presence of reduced clot strength
hypotension & tissue injury–> inflammatory response—> endothelial activation of protein C
-hyperfibrinolysis due to APC formation
Base deficit reflects the
severity of shock oxygen debt changes in O2 delivery adequacy of fluid resuscitation likelihood of multi-organ failure
Admission base deficit of _____ correlates with increased mortality
5-8 mmol/L
Describe the base deficit difference in mild, moderate, and severe shock.
mild: 2-5 mmol/L
moderate: 6-14 mmol/L
severe: greater than 14 mmol/L
Blood lactate level is
less specific than base deficit but nonetheless improtant
Elevated lactate levels correlate to
hypoperfusion
Normal plasma lactate level is
0.5-1.5 mmol/L and its half life is 3 hours
Plasma lactate levels above
5 mmol/L indicate significant lactic acidosis
Failure to clear lactate within
24 hours after reversal of shock is predictor of increased mortality
Symptoms of shock include
pallor diaphoresis agitation or obtundation hypotension tachycardia prolonged capillary refill diminished urine output narrowed pulse pressure
Assessment of systemic perfusion includes
vital signs urine output systemic acid-base status lactate clearance cardiac output mixed-venous oxygenation gastric tonometry tissue specific oxygenation stroke volume variation acoustic blood flow
Urine output in assessment of systemic perfusion may be
inaccurate due to diuretic therapy, intoxication, & renal injury
Systemic acid base status is
confounded by respiratory status
Cardiac output measurement requires
PA catheter/non invasive technology
Gastric tonometry needs
time to equilibrate, subject to artifact
Stroke volume variation is
an emerging technology, uses art line
Mixed- venous oxygenation is
an accurate marker, difficult to obtain
Goals for early resuscitation include
maintain SBP at 80-100 mmHg maintain hct at 25-30% maintain PTT and PT within normal range maintain platelet count >50,000 maintain normal serum ionized calcium maintain core temp >35 degrees C maintain function of pulse ox prevent increase in serum lactate prevent worsening acidosis adequate anesthesia/analgesia
Site for emergency intravenous access in order of desirability includes:
large bore IV’s- AC vein
other large bore IV sites
subclavian vein- easiest to place and does not require neck manipulation in circumstance of cervical neck injury
femoral vein- infection risk, belly full of blood indicates possible vascular damage so could end up dumping more blood into the stomach
internal jugular vein
intraosseous
Risks of aggressive volume replacement during early resuscitation includes
increased blood pressure decreased blood viscosity decreased hematocrit decreased clotting factor concentration greater transfusion requirement disruption of electrolyte balance direct immune suppression premature reperfusion
Resuscitation goals for anesthesia include:
oxygenate & ventilate restore organ perfusion restore homeostasis/repay "oxygen debt" treat coagulopathy restore the circulating volume continuous monitoring of the response
Resuscitation goals for surgery include:
STOP the bleeding
Goals for late resuscitation include:
maintain systolic blood pressure >100 mmHg
maintain hematocrit above individual transfusion threshold
normalize coagulation status
normalize electrolyte balance
normalize body temperature
restore urine output
maximize cardiac output by invasive/noninvasive monitoring
reverse systemic acidosis
document decrease in lactate to normal range
End point for resuscitation lab levels include
serum lactate level <2 mmol/L
base deficit <3
gastric intramucosal pH >7.33
The four stops in management of shock include:
- control the source of the hemorrhage
- begin fluid resuscitation: isotonic crystalloids, hypertonic saline, colloids, PRBCs, & plasma
- Possibly use Rapid infusing system (1500 cc/min.)
- reasonable blood pressure (early resusc. 80-100 vs. late >100)
Describe the use of isotonic crystalloids:
monitor electrolytes & lactate will direct fluid therapy plasmalyte is a good option
Describe the use of hypertonic saline:
traumatic brain injury HS is used as an osmotic agent in the management of increased ICP
Describe the use of colloids:
rapid plasma volume expansion
Describe the use of FFP:
2 units of FFP with every 4 units of PRBC when massive transfusion is anticipated or ongoing
Describe the use of PRBCs:
provided to adequate oxygen carrying capacity- mainstay of hemorrhagic shock
blood loss replacement:
-1:1 with RBC
3:1 with crystalloid
Rh negative blood is preferable if crossmatch is not complete (ABO & Rh)
especially if woman of childbearing age
Damage control with hemostatic resuscitation includes
administration of set protocol of blood & hemostatic products to mimic whole blood
massive transfusion protocol
limited crystalloid
Goal directed therapy with hemostatic resuscitation includes:
utilizes “point of care” visoelastic (TEG) monitoring to direct therapy
Tranexamic acid is a
antifibrinolytic
-benefit when instituted within 1 hour of admission
Additional hemostatic agents include
recombinant activated human coagulation factor VII
it’s expensive so not commonly kept on hand
Describe the lethal triad***
acidosis
hypothermia
coagulopathy
Principle goal of early management of the hemorrhaging trauma patient is
to avoid the development of the lethal triad
________ are major factors in the induction of coaguloapthy
acidosis & hypothermia
Resuscitation with fluids & PRBC without hemostasis properties can
dilute already dysfunctional platelets
Fluid inflation system is an
active mechanical pump that enables fluid administration rates up to 1500 mL/min.
The fluid inflation system is compatible with
crystalloid, colloid, PRBCs, washed salvaged blood & plasma
Additional facts regarding the fluid inflation system include:
reservoir allows for mixing of products in preparation for rapid blood loss
fluids infused at a controlled temperature (38-40 C)
able to pump simultaneously through multiple intravenous lines
accurate recording of fluid volume administration
portable enough to travel with patient between units
Hypothermia causes worsening of
acid base disorders coagulopathy myocardial function shifts oxygen-hgb curve to left decreases the metabolism of lactate, citrate, and some anesthetic drugs
Hypothermia results in
vasoconstriction***; can ultimately make BP appear higher than volume status really is… BP may drop as patient warms
Hypothermia leads to
abnormal potassium and calcium homeostasis
impairs platelet and clotting function
left shift of oxygen dissociation curve- decreased tissue oxygenation
Combined disorders of platelet & clotting factors
massive transfusion causes dilution of factors and platelets
hypothermia slows coagulation and causes sequestering of platelets
At 29 degrees C _____ increase 50%
PT & PTT
At 29 degrees C _____ decrease 40%
platelets
Activation of the clotting cascade causes
consumption of clotting factors
Blood loss causes a loss of
clotting factors
_______ further dilutes clotting factors
Hemodilution
Severely injured trauma patients become
hypercoagulable
Treatment of coagulopathy includes
avoidance or reversal of the lethal triad
judicious resuscitation… avoid hemodilution
treat coagulopathies
Trauma disrupts the equilibrium between
hemostatic and fibrinolytic processes
Changes are complex and can either result in
hypercoagulable or hypocoagulable states
Avoidance or reversal of the lethal triad includes
control hemorrhage
avoid/correct hypothermia
actively re-warm
