trauma adventures in night shift · etomidate some consider its use controversial as it has been...

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.