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3/7/2014
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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
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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.
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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
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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
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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.
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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.
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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
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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.
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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
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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?