1. THE LETHAL TRIAD :
ACIDOSIS, COAGULOPATHY
& HYPOTHERMIA IN
TRAUMA
Trauma Intensive Care Unit
Oregon Health and Science University

2. • Outline different types of shock and specific
treatment therapies
• Identify how to initiate mass transfusion
protocol and principles of mass transfusion and
resuscitation
• Recognize risks related to coagulopathies in
diverse trauma patient populations
• Demonstrate understanding of the nursing
process and critical thinking for trauma
resuscitation
Objectives

3. P.R. is a 24 year old male arrived to the
Emergency Department following an attempted
armed robbery at a local adult superstore. When
the robber was distracted while filling his bag with
cash and other specialty adult merchandise, the
owner pulled a handgun from beneath the
counter and shot the man three times before he
collapsed.
Case Study

4. Assessment in the field
 When EMS arrived at the scene the patient was
unresponsive with agonal breathing and lying in
a large pool of blood. Initial vitals were RR 36,
BP 95/62, HR 106. P.R. was intubated at the
scene, 1 liter of LR was infused through large
bore IV
 Further assessment revealed a rapidly
hemorrhaging gunshot wound to left upper
chest. Abdomen was distended and firm,
apparently from two more gunshot wounds.

5. A path the decompensating patient follows on
the progression towards shock and death.
• Consists of coagulopathy, hypothermia, and
acidosis.
• All three factors beget each other and
contribute to a rapid and irreversible spiral to
death.
The Lethal Triad

7. Acidosis
 Poor tissue perfusion is the major contributor to acidosis in a
trauma patient
 Decreased cardiac output, anemia, and hypoxemia lead toward
cellular anaerobic metabolism, resulting in lactic acid
accumulation
 Resuscitation with unbalanced crystalloids (normal saline) can
induce a hyperchloremic acidosis
 Acidosis diminishes cardiac output and makes catecholamines
less effective, leading to worse tissue perfusion
 Acidosis is usually the initiation of coagulopathy in trauma
patients
 When the pH drops from 7.4 to 7.0, the effectiveness of the
coagulation cascade decreases by 55-70%
 Procoagulant drugs (factor VIIa) cannot work in acidic environments

8. ED Arrival
 On arrival to the ED, P.R.’s vitals are:
 BP 72/56, HR 123, RR 40, SpO2 93%, Temp 34.9c
 Physical assessment reveals:
 Pupils 3 bilateral, equal and sluggish
 7.5 ETT in place, breath sounds absent on the left, coarse on the
right
 GSW to the left chest is having a large amount of bloody drainage
 Radial pulses are weak and thready, extremities cool and clammy
 Labs:
 ABG: pH 7.21 CO2 47 HCO3 16 PaO2 88 Base Excess -4
 Chemistry: K 3.6, Na 134, Mag 1.9 BUN 14, Creatinine 0.8,

9. Hypothermia
 Maintaining normothermia requires ATP, a substance in
short supply in the hypoxic cells of a hypoperfused
patient.
 Hypothermia causes coagulapthies:
 The coagulation cascade is temperature dependent: as
temperature drops, bleeding increases dramatically
 Hypothermia can cause relative thrombocytopenia by inducing
platelet sequestration and platelet dysfunction
 All fluids infused into the sick trauma patient need to be
warmed.
 The greatest contributor to hypothermia is room temperature
crystalloids and PRBCs (kept at 4 degrees Celsius!)
 Keep patient covered and use warming blankets
 Room temp needs to be adjusted to the comfort of the patient
and not the team (80°F is ideal)

10. Coagulopathy
 Hemodilution and consumption of clotting factors can
exacerbate coagulopathy
 Crystalloid, colloid, and PRBCs, do not contain clotting factors,
leading to hemodilution
 Plasma contains clotting factors, and can improve coagulopathy
 Critically ill trauma patients consume their clotting factors in a
manner similar to disseminated intravascular coagulation
(DIC).
 Tissue trauma and the shock state can abnormally activate the
clotting cascade and cause fibrinolysis out of proportion to the
injury.
 Calcium helps activate coagulation factors in the clotting
cascades
 Hypocalcemia can be caused by dilution and by the
preservatives (citrate) contained in blood products.

11. Resuscitation goals
 Blood pressure can be deceiving. The goal of resuscitation is
tissue perfusion
 Pulse Pressure = SBP – DBP : (ie 120/80  PP of 40
 Narrow pulse pressure indicates low stroke volume and is
the first change seen in blood pressure in hypovolemic shock
 PP less than 25% of SBP suggests significant blood loss
 BP of 88/68 : 88 - 68 = Pulse pressure of 20 (25% of 88 is 22)
 MAP best represents actual organ perfusion and is less
subject to artifact
 The literature suggests no advantage to tissue perfusion with
MAP > 65
 MAPs above this level may increase the pressure to bleeding
vessels and dislodge clot without any perfusion benefit

12. Stop the Bleeding
 Use diagnostic exams to identify the cause of bleeding
 The patient may need emergent interventions in the
Operating Room or Interventional Radiology to stop internal
bleeding
 Stopping the bleeding is the most important resuscitative step
we can take, as it prevents further blood loss
 Bleeding extremity- apply a blood pressure cuff and inflate it to
twice the systolic blood pressure and continue resuscitation
efforts. As soon as the patient begins to stabilize, take down the
cuff and re-assess the extremity.
 Scalp wound- These cannot be allowed to continue bleeding
during the initial resuscitation. Be aware that when the patient is
hypotensive, the wound may appear dry, only to start pumping
out blood when the BP rises. Remember after the patient
stabilizes proper cleansing and suturing needs to occur.

13. Admission to 7A
P.R is transported to 7a by the CRN and trauma team to the TICU for
stabilization:
 Vitals: BP 75/48, HR 122, RR 20, SpO2 94%, Temp 35.1
 P.R. remains hypotensive despite 2 liters of crystalloid and 2 units of
blood given in the ED. A liter of LR is hanging to gravity and blood
tubing is dry with the 2nd unit of blood just finished.
 The CRN tells you the chest X-ray reveals a hemothorax on the left
 Abdomen is distended and firm. No urine output with foley catheter
placement
 Pt arrived with a box of blood, 4 units left of PRBC

14. Administration of Fluids and
Product
 Important to administer bolus as rapidly as possible into large bore
IV
 Introducer, Rapid Infusion Catheter 7-8.5g (RIC) or 14-18g PIV in AC
 Quicker the infusion, the less volume needs to infuse.
 A positive response to 250 ml infused in 30 sec should show:
 Increase in radial pulse strength
 Increase in MAP
 Improvement in pulse oximetry waveform
 When the same 250 takes 10 minutes
 Response to the therapy is impossible to see.
 Fluid is just left wide open and the rest of the liter is given
 The team is distracted with other aspects of the resuscitation
and forgets to evaluate immediate response
 It is difficult to observe the response to components when infused
by gravity through relatively small catheters

15. PRBCs
 If no response to 2 liters of crystalloid, move on to
product
 Red cells should be utilized early in critical hemorrhagic shock
 Prioritize cross matching the patient, since the blood
bank only has a limited supply of uncrossmatched O
negative blood, therefore it is imperative that a type and
screen is completed ASAP
 250 cc of warmed normal saline to run into the blood bag
before infusing will decrease the viscosity and increase
the flow rate (unnecessary step if you are using a Level I)

16. Fresh Frozen Plasma and
Platelets
 Coagulation factors need to be added early to trauma
resuscitation
 Ideal ratio of 1unit PRBC: 1 unit FFP: 1pack platelets
 Because of the PROPPR study, the OHSU blood bank
now keeps 12 units of plasma thawed at one time.
 If you anticipate the patient needs FFP give the blood
bank notice so they have time to thaw additional units
 Platelets live for about 5 days
 Consider adding platelets if no response in stability after
the first 6-8 units of PRBCs.

17. Lab Trap
 Type and Cross is most important lab during
an unstable trauma admission
 Coagulation panels and CBC will lag far
behind the induced coagulopathy of bleeding
and resuscitation
 The thromboelastogram (TEG) is a far superior
test, but unfortunately we are unable to use
results to help direct resuscitation

18. Disseminated Intravascular
Coagulation (DIC)
 DIC leads to the formation of small blood clots
inside the blood vessels throughout the body.
 As the small clots consume coagulation proteins and
platelets, normal coagulation is disrupted and
abnormal bleeding occurs from the skin wounds, GI
tract, respiratory tract and surgical wounds.
 The small clots also disrupt normal blood flow to
organs which can lead to MODS (multi organ
dysfunction syndrome).
 Trauma patients are at increased risk for DIC d/t
widespread areas of tissue injury

19. Factor VII
 Endogenous Factor VII is produced in
the liver
 It is key in the extrinsic pathway of the
coagulation cascade
 The ultimate result is improved thrombin
production
 Factor VII is vitamin K dependent
 Consider replacing Vitamin K during
resuscitation
 Use of warfarin or similar anticoagulants
decreases hepatic synthesis of Factor VII.
 Recombinant Factor VII is safe and
easy to give
 Expensive: $7,000 per dose

20. Tranexamic Acid
 A fibrinolysis inhibitor/anti-fibrinolytic that competitively
inhibits the conversion of plasminogen to plasmin
 Prevents clot breakdown
 Dose 1gram/10 minutes, followed by 1gm/8 hours
 At OHSU this dose is indicated if a massive transfusion is
activated and the patient has received more than 4 units of
PRBC in 2 hrs
 Works best within the first 3 hours of injury
 Administration after 3 hours; research showed an increase
in mortality
 Not expensive, costing less than $100 USD per dose
 Research showed a decrease in mortality and risk of
death due to bleeding

21. Prothrombin Complex Concentrate
(PCC)
 Combination of blood clotting factors II, VII, IX and X, as well
as protein C and S.
 Reverses the effect of warfarin/coumadin
 Contains factor II, IX, X and very little VII
 Useful in cases of significant bleeding with a coagulopathy
 Expensive $4,000 USD per dose
 Advantages over FFP
 Rapidly available
 No large volume transfusion
 Decreased infectious risk- Multiple viral inactivation steps
 Decreased TRALI risk lack of anti-HLA/anti – granulocyte
antibodies
 3000 IUs increases factors 40 – 80%

22. Patients at increased risk for
* The Lethal Triad *
1) All trauma patients are at risk for hypotension, and therefore
acidosis
 Trauma related injuries can be diffuse, and widespread tissue
damage can predispose patient to coagulopathies such as DIC
 Patients can become hypothermic d/t severe weather,
hypoperfusion, or length of time before treatment initiated
 Motor vehicle accident in the winter during severe conditions
 Patient being pulled from the river after suicide attempt/near drowning
 Ground level fall of an elderly patient who lives alone
2) Previous anticoagulation
 What is their past medical history?
 What meds are they currently taking?
3) Liver injury
 The liver is where the clotting factors are made and where the
clotting cascades are initiated. Liver injury could lead to clotting
dysfunction

23. Previous Anticoagulation and
Reversal
 History of Atrial Fibrillation
 Patient is most likely on Coumadin
 If INR > 1. 5 should consider reversal with
 Vitamin K – monitor for hypotension
 Prothrombin Complex Concentrate (PCC)
 FFP - Repeat INR 10 minutes after completion of
infusion
 History of a Stent
 Patient is most likely on antiplatelet therapy
 Aspirin or Plavix (clopidogrel)
 Antiplatelet effects last the lifespan of the platelets
(about 10 days)
 Consider giving 1 pack platelets (6 units)

24. P.R. goes to the O.R
 P.R. was transfused 4 more units of PRBC,
two units FFP, and a left chest tube was
inserted. His pressure stabilized at 95/58, at
which point the trauma surgeons decided to
take him to the OR. He was found to have a
ruptured diaphragm and a grade 4 liver
laceration, along with a severely punctured
lung. In the OR he was transfused 16 more
units of PRBC, 4 more of FFP, 2 units of
platelets, and a second chest tube on the left
was inserted.