10
3/7/2014 1 The Triangle of Death: Hypothermia, Acidosis and Coagulopathy Allen C. Wolfe Jr., MSN, RN, CCRN, CFRN, CMTE Clinical Education Director/Critical Care Clinical Air Methods Corporation Denver, Colorado Objectives 1. Discuss the significance of hypothermia, acidosis and coagulopathy in the survival of the critical care patient. 2. Discuss the importance of recognizing the components of the triangle of death. 3. Analyze important lab values in recognition of the triangle of death. 4. Integrate treatment options for patients in the triangle of death. At the end of the session the participant will be able to: Trauma Statistics Ages 1-44 1/10 of all deaths are due to trauma Worldwide Uncontrollable Hemorrhage is the 2nd leading cause of traumatic death And, the leading cause of preventable traumatic death World Journal of Surgery, 2007 Death Hypothermia Coagulopathy Acidosis Mikhail, Judy (1999). The trauma triad of Death: Hypothermia, Acidosis, and Coagulopathy. AACN Clinical Issues. 10 (1), 85-89 The Triangle of Death Facts In Trauma Patients: Hypothermia accompanied with acidosis and coagulopathy increase your mortality by 90% Spahn, R and Rossaint, R.(2005) Coagulopathy and blood components Transfusion in trauma. British Journal of Anesthesia (95) 130-139. How does Hypothermia in trauma patients differ from patients undergoing Cardiac surgery? Trauma Patients start with oxygen deficits, shock and hemorrhage

PowerPoint Presentationnursingnetwork-groupdata.s3.amazonaws.com/AACN/Heart_of_Illinois... · Malone DL, Hess JR, Fingerhut A. Comparison of practices around the globe and suggestion

  • Upload
    hahanh

  • View
    221

  • Download
    4

Embed Size (px)

Citation preview

Page 1: PowerPoint Presentationnursingnetwork-groupdata.s3.amazonaws.com/AACN/Heart_of_Illinois... · Malone DL, Hess JR, Fingerhut A. Comparison of practices around the globe and suggestion

3/7/2014

1

The Triangle of Death: Hypothermia, Acidosis and Coagulopathy

Allen C. Wolfe Jr., MSN, RN, CCRN, CFRN, CMTE

Clinical Education Director/Critical Care Clinical

Air Methods Corporation

Denver, Colorado

Objectives

1. Discuss the significance of hypothermia, acidosis and coagulopathy in the survival of the critical care patient.

2. Discuss the importance of recognizing the components of the triangle of death.

3. Analyze important lab values in recognition of the triangle of death.

4. Integrate treatment options for patients in the triangle of death.

At the end of the session

the participant will be able to:

Trauma Statistics

• Ages 1-44

• 1/10 of all deaths are due to trauma Worldwide

• Uncontrollable Hemorrhage is the 2nd leading cause of traumatic death

• And, the leading cause of preventable traumatic death

World Journal of Surgery, 2007

Death

Hypothermia Coagulopathy

Acidosis

Mikhail, Judy (1999). The trauma triad of Death: Hypothermia,

Acidosis, and Coagulopathy. AACN Clinical Issues. 10 (1), 85-89

The Triangle of Death Facts

In Trauma Patients:

Hypothermia accompanied with acidosis and coagulopathy increase your mortality by 90%

Spahn, R and Rossaint, R.(2005) Coagulopathy and blood components

Transfusion in trauma. British Journal of Anesthesia (95) 130-139.

How does Hypothermia in trauma patients differ from patients undergoing Cardiac surgery?

Trauma Patients start with oxygen deficits, shock and hemorrhage

Page 2: PowerPoint Presentationnursingnetwork-groupdata.s3.amazonaws.com/AACN/Heart_of_Illinois... · Malone DL, Hess JR, Fingerhut A. Comparison of practices around the globe and suggestion

3/7/2014

2

Triangle of Death

• Hypothermia induced by heat loss on scene

• Cold IV fluids in ED

• Temperature decrease have a greater impact on platelets reducing activation

• Thrombin generation is < 50% at 7.20

• < ph increases fibrinolysis

Theusinger, O., Madjdpour, C and Spahn, D. Resuscitatiion and transfusion management in trauma patients: emerging concepts. Current Opinion in Critical Care 2012, 18:661-670

Wolber, A, etc. A systematic evaluation of the effect of temperature on coagulation enzyme activity and platelet function. J Trauma 2004: 56:1221-1128.

The Triangle of Death

• Ph 7.10

• Temp. 34

• SBP 70 for > 70 mins.

Schreiber, M.(2005) Coagulopathy in the Trauma Patient.

Current Opinion in Critical Care. 11:590-597.

98%

Chance of coagulopathy

High Cl¯(154meq/l) solutions like NS that have a Ph of 5

may attribute to acidosis. Some attendings use LR (buffer)

with a PH 6.5 for this reason.

NS can exacerbates lactic acidosis

What Fluids do we use for resuscitation?

Hypothermia

Hypothermia in Trauma Statistics

• 66% of Trauma Patient arrive to the ER Hypothermic

• Greatest loss of temperature (57%) occurred in the ED rather than in the field

• Hypothermia has protective effects but can be harmful clinically

Classic: Gregory, J., Flancbaum, L., Townsend, M., Cloutier, C., Jonasson, O.

(1991) Incidence and timing of hypothermia in seriously injured patients.

Journal of Trauma. 31.795-800.

Physiological Effects of Hypothermia with Multiple Trauma Injured Patients

• In response to hypothermia, the

normal sympathetic nervous

system releases catecholamines

and causes alterations in the

coagulation cascade.

• This is enhanced by the Systemic

Inflammatory Response (SIRS),

making the effects faster and more

complicated.

Page 3: PowerPoint Presentationnursingnetwork-groupdata.s3.amazonaws.com/AACN/Heart_of_Illinois... · Malone DL, Hess JR, Fingerhut A. Comparison of practices around the globe and suggestion

3/7/2014

3

Physiology of Temperature Control

Conduction Transfer of heat by direct contact down

the temperature gradient.

Convection Transfer of heat by movement of

heated material. (i.e. wind)

Radiation

- Loss of heat from non-insulated areas

H2O Evaporation Loss of heat through exhalation

Hypothermia Classification

• MILD 32 – 35 degrees C (90 to 95F)

- thermogenesis still possible

• MODERATE 28 – 32 degrees C (82-90F)

- progressive failure of thermogenesis

• SEVERE less than 28 degrees C

- spontaneous cardiac arrest poikilothermic (cold blooded)

Thermogenesis is the process by which the body generates heat, or energy,

by increasing the metabolic rate above normal

Naked in

A cold room Cold

Fluids

Intoxication

And

Paralysis

Decreased

02

consumption

Effects of Hypothermia

General

Mild

(32.2 C – 35.0 C) Moderate

(28.0 C– 32.2 C)

Severe

(<28.0 C)

Shivering

↑ 02 consumption

Confusion

Acidosis

Neuro

Cardiovascular

Renal

Coagulation

↑ CO, ↑HR,↑MAP

Peripheral Vasoconstriction

but is delayed in injured

vessels

Osborne (J Waves)

Bradycardia

Atrial fib.

V Fib.

Asystole

Cold diuresis

Thrombocytopenia Impaired clotting activity

Coma Lethargy

OLIGURIA

Evidence Base Medicine Hypothermia: Factors effected by Temperature

• Demonstrated on animals • In induced hypothermia:

– Impaired hemostasis occurs at ph 7.20 – Impaired Platelet function

Classic: Dunn, E., Moore, E., Breslich. D., et. Al.(1979)

Acidosis induced Coagulopathy. Surgical Forum. 30, 471-478.

Evidence Base Medicine Hypothermia: Factors effected by Temperature

(cont.)

In 112 Trauma Patients analyzed the effects of hypothermia on trauma patients

Hypothermia accounts for 6 times variation in acidosis than injury severity.

Acidosis therefore appears to be a sequela of hypothermia rather than injury severity.

This study supports acidosis contributes to Coagulopathy as a result of hypothermia and not independent of it.

Mikhail, Judy (1999). The trauma triad of Death: Hypothermia,

Acidosis, and Coagulopathy. AACN Clinical Issues. 10 (1), 85-89

Page 4: PowerPoint Presentationnursingnetwork-groupdata.s3.amazonaws.com/AACN/Heart_of_Illinois... · Malone DL, Hess JR, Fingerhut A. Comparison of practices around the globe and suggestion

3/7/2014

4

Hypothermia Osborn Wave

Pelter, M., Kozik, T., and Carey, M. (2006) American Journal of Critical Care. Nov. Vol. 15,6.

J-wave (Osborn wave) camel-hump sign Highly suggestive of hypothermia May appear at any temp < 32 C Commonly seen in lead 2 or V6 V3 and V4 in severe

Measurement Instruments

• Tympanic

• Skin

• Oro-Nasopharynx

• Esophagus

• Bladder

• Rectal

• PA Catheter

• ▲in ambient temp.

• ▲in ambient temp.

• Varies based on location • Varies based on where probe is

position because of gas movement in trachea

• Closest to PA

• Presence of gas and feces

Drawbacks Routes

Eddy, V., Morris, J., and Cullinane, D. (1999) Hypothermia, Coagulopathy and Acidosis

Surgical Clinics of North America (80) , 3, 845-854.

Schreiber, M.(2005) Coagulopathy in the Trauma Patient.

Current Opinion in Critical Care. 11:590-597.

Hypothermia Management

Passive

• Remove wet clotting

• Insulating blanket

• Raise ambient Temp.

• Keep patient dry

• Humidified Air

• Warm IV fluids and blood

Active

• Body Cavity Lavage

• Heated Inspired Air

• Bair Hugger

• CPB

• CAVR- MAP dependent

Hypothermia Rewarming Rates

• Warmed fluids/Heated O2/Warm Blankets – 1.2 ° C/hr

• Bair Huggers 2.4° C/hr.

• Pleural and Peritoneal Lavage 6°C/hr.

• CAVR - 3 ° C/hr

• CPB 0.5°C – 3.5°C/20minutes

Acidosis

Acidosis Pathophysiology

Ph < 7.20 =decrease in cellular function causing failure to produce ATP (energy stores) to transport proteins across cells and slows or stops transmission of messages

Page 5: PowerPoint Presentationnursingnetwork-groupdata.s3.amazonaws.com/AACN/Heart_of_Illinois... · Malone DL, Hess JR, Fingerhut A. Comparison of practices around the globe and suggestion

3/7/2014

5

Definition in Multiple Trauma Patient Acidosis

• Shock induced Metabolic Acidosis -Results from inadequate tissue perfusion

• Tissue hypoxia alters cellular function shifts from aerobic to anaerobic metabolism resulting in lactic acidosis.

Arrhythmias

Poor Cardiac performance

Vasodilatation, lost of responsiveness

Catecholamines Hypotension which

further perpetuates shock and acidosis Mikhail, Judy (1999). The trauma triad of Death: Hypothermia,

Acidosis, and Coagulopathy. AACN Clinical Issues. 10 (1), 85-89

Schreiber, M.(2005) Coagulopathy in the Trauma Patient.

Current Opinion in Critical Care. 11:590-597.

Base Deficit

Base Deficit is the amount of alkali buffer required to titrate 1 L of blood to a Ph

7.40 at normal body temperature

Farah, A. et. Al. (2003)Serum Lactate and base deficit as predictors

of mortality and morbidity. The American Journal of Surgery. 185, 485-491.

Base Deficit

• Sensitive to overall metabolic acidosis

– renal failure

– respiratory alkalosis

– DKA

– toxicants

• “Washout phenomenon “

• Reperfusion of previously hypoperfused tissue will cause increases BE.

Martin, M., et.al.(2006) Discordance between lactate and base deficit in the surgical intensive Care Unit: which one do you trust? The American Journal of Surgery. 191, 625-630.

Lactic Acidosis vs. Base Deficits

Mikhail, Judy (1999). The trauma triad of Death: Hypothermia,

Acidosis, and Coagulopathy. AACN Clinical Issues. 10 (1), 85-89

Lactate is a direct correlation with byproduct of anaerobic metabolism

elevated in hypoperfused states and prevents pyruvate from entering the kreb cycle

total oxygen debt (imbalance between needs and consumption)

Magnitude of hypoperfusion

Severity of Shock

< 4 goal for lactate

Base Deficit

good prognostic guide to resuscitation efforts after the acute phase.

< 6 goal for resuscitation

Lactic Acidosis vs. Base Deficit (cont.)

• If lactic acid or base deficit is worsening ----the type of resuscitation should be re-evaluated.

• The lactic acid remains sensitive to lactate and anaerobic metabolism

• If normal lactate clearance occurs within 24 hours. Survival rates increase 90%

• Bicarbonate will alter relationship

Farah, A. et. Al. (2003)Serum Lactate and base deficit as predictors of mortality and morbidity. The American Journal of Surgery. 185, 485-491.

Page 6: PowerPoint Presentationnursingnetwork-groupdata.s3.amazonaws.com/AACN/Heart_of_Illinois... · Malone DL, Hess JR, Fingerhut A. Comparison of practices around the globe and suggestion

3/7/2014

6

Acidosis Intervention

• Improve tissue oxygenation and perfusion

– treat hypothermia

– maintain hemodynamic stability

– ensure patient is well oxygenated

– Try to avoid IV bicarbonate…may cause alkalosis

– Ph 7.20

Mikhail, Judy (1999). The trauma triad of Death: Hypothermia,

Acidosis, and Coagulopathy. AACN Clinical Issues. 10 (1), 85-89

Schreiber, M.(2005) Coagulopathy in the Trauma Patient.

Current Opinion in Critical Care. 11:590-597.

Oxygen Dissociation Curve

• In the hypothermic trauma patient: 02 cannot be released from the hemoglobin to the tissue

Shivering

Mottling

Acidosis Intervention The Oxygen Consumption and Oxygen Demand

(1.39 x Hb) x art. saturation + (PaO2 x 0.003) = ml O2 / 100 ml blood = CaO2

CaO2 x CO x 10 = DO2

Cardiac Output Hemoglobin

Oxygen

Saturation

Coagulopathy

Coagulopathy

• Hemorrhage is the leading cause of death • Bleeding from wounds

• DIC

• Hypothermia slows clotting, production of factors and platelet aggregation

• Acidosis affects platelets and fibrinolysis

Coagulopathy Pathophysiology

• In temperatures ~33C, pt.s clotting factor act similarly to conditions where clotting factors are 50% concentration.

• Remember Lab values are done at 37C

• Lab values may disguise coagulopathy

• In studies involving pigs decreased clotting time was

observed when lactic acid was added.

Schreiber, M.(2005) Coagulopathy in the Trauma Patient.

Current Opinion in Critical Care. 11:590-597.

Page 7: PowerPoint Presentationnursingnetwork-groupdata.s3.amazonaws.com/AACN/Heart_of_Illinois... · Malone DL, Hess JR, Fingerhut A. Comparison of practices around the globe and suggestion

3/7/2014

7

Coagulopathy Pathophysiology

• Hemodilution is a cause of coagulopathy.

• Amount of volume is directly proportional to coagulopathy regardless of fluid type.

• Colloids – fibrinogen dysfunction produces poor clot stability

• Coagulopathy occurs the first half hour

• Hypoperfusion increases this process.

Theusinger, O., Madjdpour, C and Spahn, D. Resuscitatiion and transfusion management in trauma patients: emerging concepts. Current Opinion in Critical Care 2012, 18:661-670

Coagulopathy Definition

• PT > 14 seconds (1.5 x norm) • PTT > 34 seconds (1.5 x norm) • Platelets < 100,000 in severely injured patients • Raised hematocrit (@2% per degree temp drop)

Clinical Assessment of Coagulopathy • Ongoing blood loss • Oozing wounds • Oozing vascular sites • Oozing oral mucosa

There is no single reliable laboratory test to confirm Coagulopathy

Consumption Coagulopathy Resuscitation Treatment

• Increase INR > 2.0 plus ↑ PTT – FFP • Increase PT and PTT – Vitamin K • Fibrinogen Levels – Cryoprecipitate, Platelets • D Dimer – use of fibrin products for clotting • 1unit of plts/kg. • 1 unit cryo./kg. • 1 unit pRBC’s = 3 % points

Eddy, V., Morris, J., and Cullinane, D. (2000) Hypothermia, Coagulopathy and Acidosis

Surgical Clinics of North America (80) , 3, 845-854.

Schreiber, M.(2005) Coagulopathy in the Trauma Patient.

Current Opinion in Critical Care. 11:590-597.

PATIENT RESUSCITATION

Massive Blood Transfusions

Sensitive to Lungs

and other cells

Capillary leaks

T.R.A.L.I

Hess, J. R., and Zimirin, A.B. (2005) Massive Transfusion for

Trauma. Current Opinion Hematology. 12, 488-492.

Neutrophil Activation

Sensitive to Endothelial

cells

MSOF

Biologically active

cell membrane

breakdown products

platelet activating

factors

and dialkylglycerol

Malone DL, Hess JR, Fingerhut A. Comparison of practices around the globe

and suggestion for a massive transfusion protocol.

J Trauma, 2006

• Reviewed massive transfusion protocols from well-developed trauma systems in Denver, Houston, Helsinki, Sydney, and Baltimore.

• This group then presented a massive

transfusion protocol based on the best data from their review.

–1:1:1

Page 8: PowerPoint Presentationnursingnetwork-groupdata.s3.amazonaws.com/AACN/Heart_of_Illinois... · Malone DL, Hess JR, Fingerhut A. Comparison of practices around the globe and suggestion

3/7/2014

8

INDICATIONS FOR EARLY FFP, CRYOPRECIPITATE, AND PLATELET TRANSFUSION IN TRAUMA

Lloyd Ketchum, John R. Hess and Seppo Hiippala J Trauma, 2006

• If clinically evident coagulopathy is prevented by the early use of FFP, subsequent blood product consumption is likely to be less.

• In massive transfusion, 1:1:1

PRBC: Plasma:platelets are indicated

Massive Transfusion Tidbits

• Monitor H/H

• Monitor Coags. – Give factors

– Give all coags at the same time

• Warm all blood

• Autotransfusion – CPD - Phosphorous

• Monitor Calcium – Give Calcium

Coagulopathy Treatment

• Stop the Hemorrhage – Apply pressure

• Ligation of Bleeders

• Early Operative Management

• Damage Control Surgery

• Fluid Resuscitation

- Permissive Hypotension in Penetrating Trauma

• Decreases mortality, Coagulopathy and survival

Schreiber, M.(2005) Coagulopathy in the Trauma Patient.

Current Opinion in Critical Care. 11:590-597.

Resuscitation Concepts

• High volume pre-hospital worsens ED coagulation

• > 2000ml – worse coagulation , required more blood, higher organ failure and overall mortality.

• < 1500ml – less effects on system

Wafaisade, A. et al. Drivers of acute coagulopathy afer severe trauma: a multivariate analysis of 1987 pateints. Emerg Med J 2010; 27:934-939.

Colloid vs Crystalloid

• Perel Systematic reviews 2011

• 65/90 Randomized controlled trials of crystalloid and colloids respectively.

– Resuscitation with colloids reduces the risk of death compared to resuscitation with crystalloids.

– Recommendation

• use of crystalloids if they are effective rather than liberal use of colloid

Theusinger, O., Madjdpour, C and Spahn, D. Resuscitatiion and transfusion management in trauma patients: emerging concepts. Current Opinion in Critical Care 2012, 18:661-670

Perel, R and Roberts, I. Colloids vs crystalloids for fluid resuscitation in critically ill patients. Cochrande Database Systematic Review 2011. CD00567

Hypertonic Saline

Reduction in ICP by improving CO, oxygenation and decreasing edema administration of small volumes of hypertonic saline in TBI

• 2011 Burger – no significance difference in mortality at 28 days

• Study stopped due to mortality increases in subgroup receiving hypertonic saline but no blood transfusions within first day.

• No trials providing compelling evidence to support use of hypertonic saline

Bulger, EM et al. Out of Hospital hypertonic resuscitation after traumatic hpovolemic shock: a randomized, placebo controlled trial. Ann Surg 2011; 253;431-441.

Hashiguchi, N. et.al. Hypertonic saline resuscitation efficacy may require early treatment in severely injured patients. J Trauma 2007; 62:299-306.

Page 9: PowerPoint Presentationnursingnetwork-groupdata.s3.amazonaws.com/AACN/Heart_of_Illinois... · Malone DL, Hess JR, Fingerhut A. Comparison of practices around the globe and suggestion

3/7/2014

9

Concepts of Damage Control

• Goals – Stop the bleeding – surgical intervention

• avoid prolong operative procedures – temporary

• Paired with massive fluid resuscitation reduces mortality

– Stop hypoperfusion

– Correcting acidosis

– Reversing hypothermia

– Coagulation under control

– Definitive corrective surgery later

Theusinger, O., Madjdpour, C and Spahn, D. Resuscitatiion and transfusion management in trauma patients: emerging concepts. Current Opinion in Critical Care

2012, 18:661-670

Case Study

Case Study

GSW to Hand

• 50 year old

• GSW to hand 9 months ago

• The patient used an ice pick to remove the bullet with Heroin as anesthesia

• No Medical Attention

• Continued to use an ice pick to debrided the wound when he felt “it looked bad”

• Came to the Hospital because of bleeding!

Clinical Assessment Case Study

• Airway - Patent

• Breathing – 24/min.

• Circulation – Pulse…Bleeding

• Disability (Neuro) – GCS 15

• Pain – 0/10!

• Temperature 35.0

• History – Heroin Addiction, Asthma

• Treated with Keflex po by relative with access to medications

Case Study Initial Treatment

• Supplemental 02

• IV Access (#16 Left Hand)

• All other systems Ok

• Labs sent

• Basic warming methods started

– Blankets and Bear Hugger

– Warm IV fluids - NS

Time Ph BE Temp Lactate coags VS Fluids

1230 7.32 -6.6 35.0 2.9 PT 16.7

PTT 43

Plt. 140

BP 80,

HR 110,

RR 26

2L in

field

1330 7.22 -10.1 34.5 3.9 PT 21,

PTT 48

Plt. 51

BP 78,

HR

124,

RR - V

1LNS

2

pRBC’s

1430 7.16 -10.0 33.8 10.5 PT 18.3

PTT 37.8

Plt. 49

D Dimer 950

Fibrinogen

186

BP 60,

HR 108,

RR -V

1L NS

2

pRBCs

OR

1545 7.29 -13 35.5 5.9 PT 25

PTT 45

D Dimer

1600

Plt 33

BP 101,

HR 118,

RR - V

OR

10 plts

6 FFP

1

pRBC’s

Sequence of Events

Page 10: PowerPoint Presentationnursingnetwork-groupdata.s3.amazonaws.com/AACN/Heart_of_Illinois... · Malone DL, Hess JR, Fingerhut A. Comparison of practices around the globe and suggestion

3/7/2014

10

Sequence of Events (cont.)

Time Ph BE Temp Lactate Coag

s

VS Fluids

1615 7.35 8.5 35.6 4.5 PT 18.3

PTT 37.8 BP

108

HR

108

6 FFP

250 LR

1645 7.39 6.5 36.0 2.4 PT 15.4

PTT 43

Plt. 64 Fibrinogen

186

D Dimer

350

BP

110

HR

102

LR 500

ml

Case Study Clinical Findings

- Brachial Artery Bleeding

- To OR for repair, amputation and debridement

Case Study

• Post Op bleeding occurred

• Oozing from Incision site

• Decreased BP high 70’s for approx. 2 hours

• Re-intubated

• Temperature decrease to 340C

• 2 #16 Peripheral IV,RSC Central line

• Patient Live after significant extremity lost.

Triangle of Death Summary Trauma

Bleeding Resuscitation Hemodilution

Hypothermia Acidosis

Coagulopathy

More Bleeding MSOD

mortality by 90%

QUESTIONS?

[email protected]