trauma adventures in night shift · etomidate some consider its use controversial as it has been...
TRANSCRIPT
Trauma Adventures
in
Night Shift
Dan Brady, MSN, CRNA
The Most Common
Procedures/Emergencies
Trauma (focus of this lecture)
Emergency Caesarean Sections
Orthopedic Procedures
Ectopic Pregnancies
All of the above have potential for volume
loss and therefore principles presented
apply.
Learning ObjectivesUpon completion of the lecture, the learner
will be able to:
Verbalize characteristics of trauma
induction agents.
Discuss the benefits of a high opioid
based trauma resuscitation
Verbalize manifestations of
hypothermia and acidosis on the
trauma patient.
Discuss the rationale for massive
transfusion.
The Realities of Night
Shift Anesthesia
Lack of Resources
Lack of Administration
One night may never be like the rest
Need a good working relationship with peers.
Need a good working coffee machine
TRAUMA
Trauma accounts for a significant portion
of volume at night (depending on your
hospital).
Depending on your setting likely see a
mix of blunt and penetrating trauma.
(Rural PA - 90% blunt and 10%
penetrating vs. Miami 60% blunt and 40%
penetrating)
Neither are good and will get you out of
your call room.
TRAUMA
Almost always a “suboptimal” condition.
Emergent admissions to the OR from
trauma bay often present with poorly
resuscitated patients.
Often “damage control” surgery preceded
by “damage control” resuscitation
(Sikorski, Koerner, Fouche-Weber, &
Galvagno, 2014).
TRAUMA
Tread lightly! Many injuries have yet to
“declare” themselves and past
medical/surgical history may still be
unknown.
Choose your anesthetic plan wisely!
Trauma patients often have to “earn their
anesthesia” (Sikorski, Koerner, Fouche-
Weber, & Galvagno, 2014).
BASIC PRINCIPLES OF
TRAUMAWarm fluids, warm room (80 degrees),
warm blankets, forced air warmers are a
must!
Acid-base balance is accomplished with
adequate volume resuscitation and not
pharmacology (vasopressors, bicarb).
They are “drier” than you think!
(Sikorski, Koerner, Fouche-Weber, &
Galvagno, 2014)
TRAUMA - NMB’S
Neuromuscular blockers for RSI Intubation
Succinylcholine 1-2 mg/kg
Onset 30 seconds with duration 5-10
min
ROCURONIUM 1 mg/kg
Onset approximately 60 seconds
Vecuronium usually avoided due to long
onset time.
TRAUMA - INDUCTION
AGENTS
Induction agents in trauma include:
ETOMIDATE
KETAMINE
PROPOFOL (infrequently used in my
experience)
ETOMIDATE
Etomidate
Rapid onset
Neutral hemodynamics
Dose on ideal body weight
Decreases CMRO2, CBF, ICP
May cause arterial hypotension in volume
depleted patients! (Sikorski, Koerner,
Fouche-Weber, & Galvagno, 2014).
ETOMIDATE
Some consider its use controversial as it
has been associated with mortality in
septic patients.
Single dose etomidate in the trauma
population has been associated with
increased rates of hospital-acquired
pneumonia that may be attenuated with
post-etomidate hydrocortisone therapy
(Sikorski, Koerner, Fouche-Weber, &
Galvagno, 2014).
KETAMINE
Advantageous in trauma for maintaining
adequate blood pressure in hypovolemic
patients.
Indirectly increases cardiovascular
stimulation through centrally mediated
increased sympathetic tone and
increased release of catecholamines.
(Sikorski, Koerner, Fouche-Weber, &
Galvagno, 2014)
KETAMINE
DIRECT MYOCARDIAL DEPRESSANT
Hypotension is possible in patients who
are catecholamine depleted.
Useful in asthma and reactive airway
disease for reducing bronchospasm.
May help avoid hypotension which has
been associated with poor outcomes in
TBI (controversial induction agent in TBI).
KETAMINE
Some sources have linked Ketamine to
acute stress and post-traumatic stress
disorder (PTSD).
Data is inconsistent as clinical trials
ongoing examining the use of Ketamine
as a treatment for PTSD due to its
antidepressant properties. (Sikorski,
Koerner, Fouche-Weber, & Galvagno,
2014).
PROPOFOL
Familiar, rapid onset, profound amnesia, short
duration, blunts sympathetic response to
intubation, intensifies muscle relaxation.
Decreases CMRO2, CBF, ICP. Preferred for
hemodynamically stable TBI patient.
Decreases SVR, has myocardial depressant
effects must be used with EXTREME
CAUTION in trauma.
(Sikorski, Koerner, Fouche-Weber, & Galvagno,
2014)
PROPOFOL
Simply reducing the dose may not be
sufficient to maintain MAP and CPP.
Doses of 0.5 mg/kg or lower WITH
BOLUSES of Phenylephrine 100 mcg to
maintain MAP in hypovolemic patients.
(Sikorski, Koerner, Fouche-Weber, &
Galvagno, 2014)
LIDOCAINE &
ATROPINEData on Lidocaine and it’s effects on ICP
are inconclusive. Has been associated
with decreased blood pressure during
RSI. Dose of 1 - 1.5 mg/kg is usually
used.
Atropine - consider its use in peds, those
with increased vagal tone and those at
risk of bradycardia (patients on digoxin,
beta and calcium channel blockers,
amiodarone). Dose of 0.01 mg/kg.
EARNING THE
ANESTHETIC
RESUSCITATION NECESSITATES THAT
THE TRAUMA PATIENT “EARN THEIR
ANESTHESIA” BASED ON HEMODYNAMIC
STABILITY
Be aware of injuries and titrate accordingly.
Retroperitoneal bleeding/pelvic
fractures/bleeding into “occult” compartments
due to fractures may require unanticipated
amounts of volume resuscitation.
EARNING THE
ANESTHETIC
Avoid high-dose opioid loading until
surgical hemostasis achieved.
High blood product ratio-driven manner
(1:1 blood loss/replacement ratio) to
maintain SPB greater than 90 mmHg or
MAP greater than 50 in patient without
TBI.
EARNING THE
ANESTHETIC
Anesthetizing the patient may be challenging.
Awareness occurs in 0.1 to 0.2% of elective
surgery, but prevalence is higher in trauma.
Awareness may be a trigger for PTSD.
(Sikorski, Koerner, Fouche-Weber, & Galvagno, 2014)
EARNING THE
ANESTHETIC - BENZOS
Benzodiazepines are advantageous in
trauma.
Amnesia
No vasodilation
Midazolam or Diazepam are good
choices.
(Sikorski, Koerner, Fouche-Weber, &
Galvagno, 2014)
SCOPOLAMINE
Scopolamine (anticholinergic amnestic)
has been used in doses of 0.2mg x 1.
HAS A LONG HALF LIFE (4.5 HOURS)
May confound neurological examination
due to pupillary dilatation.
(Sikorski, Koerner, Fouche-Weber, &
Galvagno, 2014)
VOLATILE
ANESTHETICSHave been identified as effective modulators
of the inflammatory response.
Their effect on the inflammatory response,
coagulation system and outcomes of trauma is
unknown.
ONCE HEMODYNAMICALLY STABLE (SBP
90 mmHg) titrate to 1/2 MAC. In TBI keep less
than 1 MAC to avoid decreases in CBF.
(Sikorski, Koerner, Fouche-Weber, & Galvagno,
2014)
VOLATILE
ANESTHETICS
SOME PATIENTS ARE JUST TOO SICK
TO HANDLE VOLATILE AGENTS.
Slow titration, vigilance are essential.
(Sikorski, Koerner, Fouche-Weber, &
Galvagno, 2014)
NITROUS OXIDE
Generally avoided in trauma.
Expands all gas spaces:
Worsens PTX, pneumocephaly, small bowel
obstructions, expands ET tube cuffs.
Decreases hypoxic drive, increases pulmonary
vascular resistance and can cause diffuse
hypoxia.
(Sikorski, Koerner, Fouche-Weber, & Galvagno,
2014)
NITROUS OXIDE
In those with TBI, nitrous oxide increases
CMRO2 and ICP.
May disturb CBF-CMRO2 coupling.
Evidence exists that nitrous may alter
immunological responses to infection,
cause apoptosis, increase homocysteine
levels, and mask myocardial depression.
(Sikorski, Koerner, Fouche-Weber, &
Galvagno, 2014)
BASIC PRINCIPLES OF
TRAUMA RESUCITATION
The ultimate goal of trauma resuscitation
is the return of adequate micro-circulatory
flow.
Increases in SBP with resuscitation
indicates increased MACRO-
CIRCULATORY pressure, NOT
NECESSARILY MACRO or MICRO
circulatory flow.
(Sikorski, Koerner, Fouche-Weber, &
Galvagno, 2014)
HIGH DOSE OPIOID
TECHNIQUE
Once adequate SBP rises, Fentanyl in doses
of 50 to 100 mcg is carefully titrated.
Reduction in SBP following titration of
narcotics/volatiles may indicate reduce
vascular tone and indicates the need for
continued resuscitation for target SBP >/= 90
mmHg.
(Sikorski, Koerner, Fouche-Weber, & Galvagno, 2014)
HIGH DOSE OPIOID
TECHNIQUESikorski et al advocate a step-wise
increase in opioids as the dose-response
becomes minimal with subsequent doses
of fentanyl.
They continue this dose-response
regimen until the patient tolerates a single
bolus of approximately 250 mcg of
Fentanyl.
(Sikorski, Koerner, Fouche-Weber, &
Galvagno, 2014)
RESUSCITATION
CONTINUES......When there is no longer a response to
Fentanyl while goal directed resuscitation
continues AND there is evidence of tissue
hypoperfusion as noted by increased
lactated and a base deficit, they add an
additional OPIOID such as Methadone in
10 mg increments to a maximum of 20-30
mg if the QTc is WNL.
(Sikorski, Koerner, Fouche-Weber, &
Galvagno, 2014)
METHADONE/OPIOIDS
Additional Methadone may cause vasodilation
and additional resuscitation.
This technique can only by carried out if the
patient’s perfusion pressure is adequate and
hemorrhage controlled.
If Methadone contraindicated, Dilaudid titrated
in 0.2 to 0.4 mg increments to a max dose of 2
mg .
(Sikorski, Koerner, Fouche-Weber, & Galvagno,
2014)
OPIOIDS
Morphine is generally avoided due to
concerns about histamine, which may
exacerbate hypotension.
Theorized that high dose opioids may
improve tissue perfusion.
(Sikorski, Koerner, Fouche-Weber, &
Galvagno, 2014)
OPIOIDS - BENEFICIAL
IN TRAUMABlunting of the deleterious activation of the
sympathetic nervous system and altering
microcirculation in a way that may prevent
further tissue damage in hemorrhagic shock.
High levels of catecholamines are associated
with an increase in biomarkers that indicate
endothelial damage, glycocalyx breakdown
and perpetuation of hyper fibrinolysis.
(Sikorski, Koerner, Fouche-Weber, & Galvagno,
2014)
OPIOIDS - BENEFICIAL
IN TRAUMA
Biomarkers related to ongoing catecholamine
release are also related to coagulopathy,
which increases mortality.
Restoration of adequate micro-circulatory
blood flow is crucial in shock reversal, as well
as protection of the endothelial glycocalyx.
(Sikorski, Koerner, Fouche-Weber, & Galvagno,
2014)
OPIOIDS - BENEFICIAL
IN TRAUMAEssential in order to minimize leukocyte-
endothelial interaction, as well as
maintaining he integrity of the vascular
basement membrane.
As the lactate and base deficit normalize
and the vasodilatory response to an
opioid becomes minimal, two central, but
unequivocal goals are achieved.
(Sikorski, Koerner, Fouche-Weber, &
Galvagno, 2014)
OPIOIDS - BENEFICIAL
IN TRAUMAResuscitation goals achieved when there is
return of micro-circulatory flow and the
correction of the acute coagulopathy of
trauma, and blunting of the catecholamine
response.
Opioids have been shown to precondition
skeletal and myocardial tissue, promote
hemodynamic recovery and provide protection
against acute ischemia.
(Sikorski, Koerner, Fouche-Weber, & Galvagno,
2014)
OPIOIDS - BENEFICIAL
IN TRAUMAMorphine has been shown to attenuate
microvascular hyperpermiability after
hemorrhagic shock, possibly due to
dependence on protein kinase.
Studies are ongoing to elucidate the
impact of opioids on coagulation and
inflammatory responses.
(Sikorski, Koerner, Fouche-Weber, &
Galvagno, 2014)
COAGULOPATHY AND
MASSIVE TRANSFUSION
Historically defined as the replacement by
transfusion of 10 units of red cells in 24
hours.
In response to massive and uncontrolled
hemorrhage.
Associated with a number of hemostatic
and metabolic complications.
MASSIVE
TRANSFUSION
Requires careful selection of products
and consideration of:
Volume Status
Tissue Oxygenation
Management of bleeding and
coagulation abnormalities
Changes in ionized calcium, potassium
and acid-base balance.
MASSIVE TRANSFUSION -
RED CELL AND VOLUME
REPLACEMENTCrystalloids play a role in maintaining
hemodynamic stability, but red cells
improve and maintain tissue oxygenation.
Each unit of PRBC contains
approximately 200 ml of red cells and in
the adult will raise Hct roughly 3
percentage points unless bleeding
continues.
RED CELL
REPLACEMENTAmerican Society of Anesthesiologists
recommend that hemoglobin below 6
g/dl be avoided in healthy individuals,
with higher values necessary in those
with active cardiovascular disease.
COAGULOPATHY
May be caused by activation and
consumption of coagulation factors
secondary to tissue trauma, head injury,
muscle damage, prolonged shock,
hypoxia, hypothermia.
Acute DIC - microvascular oozing,
prolongation of PT/PTT, decreased
fibrinogen and increased levels of D-
dimer.
ACIDOSIS
Interferes with assembly of coagulation
factor complexes involving calcium and
negatively-charged phospholipids.
As a result the activity of factor Xa/Va
prothombinase complex is reduced by:
50% at a pH of 7.2
70 % at a pH of 7.0
80% at a pH of 6.8
ACIDOSIS
The resulting delayed production and
reduced concentration of generated
thrombin lead to delayed fibrin production,
altered fibrin structure and increased
susceptibility to fibrinolysis.
Acidosis with coagulopathy in trauma
patients leads to mortality.
HYPOTHERMIA
Reduces the enzymatic activity of plasma
coagulation proteins.
Prevents the activation of platelets via
traction on the glycoprotein 1b/IX/V
complex by Von Willebrand factor.
Pathway stops functioning in 50% of
individuals at 30 degrees and markedly
diminished in the rest.
HYPOTHERMIA
This effect on platelet-mediated primary
hemostasis means that massive bleeding
in conjunction with a core temperature of
less than 30 degrees is rarely survived.
Onset of this effect is seen at core
temperatures of 34 degrees and below.
COAGULATION
PROTEINS
Replacing blood loss with RBCs and
crystalloids ONLY will result in a gradual
dilution of plasma clotting proteins, leading to
prolongation of the PT and PTT.
10% decrease in concentration of clotting
proteins for each 500 ml of blood loss
replaced.
MASSIVE TRANSFUSION
IN TRAUMA
Results from a number of studies on
massive transfusion in trauma advocate a
1:1:1 (FFP:platelets:RBCs) ratio (i.e., the
“damage control approach”).
Pathophysiology supporting this approach
derives from the acute coagulopathy of
trauma and the dilute nature of
conventional blood products.
MASSIVE TRANSFUSION
IN TRAUMA
Patients with uncontrolled hemorrhage
and shock have typically lost between 30
to 40% of their blood volume.
Conventional resuscitation with crystalloid
will rapidly lead to greater than 50%
dilution of coagulation factors and a
diminution of thrombin generation.
1:1:1 Ratio in Massive
Transfusion
Resuscitation with this method means
that the actual blood being given has a
coagulation factor concentration of 65%
of normal, a platelet count of 88x10g/L
and a hematocrit of 29%.
COMPLICATIONS OF
MASSIVE TRANSFUSIONMETABOLIC ALKALOSIS - each mmol of
citrate generates 3 mEq of bicarbonate
Free hypocalcemia - due to citrate binding
10% Calcium Chloride - 2 to 5 ml for
every 500 ml of blood
Hypothermia
Hyperkalemia - due to large volume
infusion of stored PRBC
MASSIVE TRANSFUSION
SUMMARYPrimary reason for transfusion is
prevention of ischemia which can be
accomplished by aggressive volume
expansion/blood transfusion.
As volume replaced, pay attention to
coagulation parameters, platelet count
and metabolic status.
Frequent monitoring of PT, PTT,
fibrinogen, platelets or TEG preferably
after each 5 units of PRBC.
MASSIVE TRANSFUSION
SUMMARY
If PT/PTT exceed 1.5 times normal, give at
least 2 units FFP. If platelet count below
50,00, six units of platelets.
Best approach to transfusion in trauma (1:1:1
vs 1:2:1) is unknown.
In military, plasma as the primary choice of
resuscitation fluid has been advocated.
Use a blood warmer.
Monitor pH, potassium and calcium levels.
References
Hess, J., R. (2016, July 15). Massive blood
transfusion. Retrieved from:
https://www.uptodate.com/contents/massive-blood-
transfusion?source=search_result&search=massiv
e%20transfusion%20protocol&selectedTitle=1~15
0
Sikorski, R. A., Koerner, A. K., Fouche-Weber, L.
Y., & Galvagno, S. M. (2014). Choice of general
anesthetics for trauma patients. Current
Anesthesiology Report, 4: 225-232.