THE LETHAL TRIAD : ACIDOSIS,

COAGULOPATHY & HYPOTHERMIA IN

TRAUMA

Trauma Intensive Care Unit

Oregon Health and Science University

• 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

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

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.

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

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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

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,

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)

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.

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

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.

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

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

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)

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.

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

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

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

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

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%

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

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)

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.