This document discusses the pathology of dying in trauma patients, focusing on the triad of death - hypothermia, acidosis, and coagulopathy. It defines each component of the triad and describes how they are interrelated and can compound one another. For example, hypothermia can lead to acidosis and impair coagulation. The document reviews recent studies showing increased mortality rates associated with low body temperature, low pH, and coagulation abnormalities. It also discusses strategies for treatment and prevention of each condition to break the cycle of the triad of death in trauma patients.

1. Pathology of Dying
Dr. Isa Basuki, Dr. Meilyna Sulphiana Alam, Dr. Yufriadi Yunus
Department of Surgery, AWS General Hospital
Faculty of Medicine, Mulawarman University

2. Definition
• The active process of or associated with the process of ceasing to be or
passing from life.
• Death is the cessation of all biological functions that sustain a living
organism.
• Phenomena which commonly bring about death include biological aging
(senescence), predation, malnutrition, disease, suicide, murder and accidents
or trauma resulting in terminal injury

3. How Does the Patient Die on
Trauma?

4. Trias of Death
•Hypothermia
•Coagulopathy
•Acidosis

5. Rotondo, M,F. The damage control sequence and underlying logic. Surg
Clin North Am 1997; 77: 761-777.

6. Hypothermia
Classification Traditional Trauma
Mild 98-89.6 ⁰ F
(35-32⁰ C)
95.0-93.2⁰ F
(35-34⁰ C)
Moderate 89.6-82.4⁰ F
(32-28⁰ C)
93.2-89.6⁰ F
(34-32⁰ C)
Severe < 82.4⁰ F
< 28⁰ C
<89.6⁰ F
<32⁰ C

7. Causes of Hypothermia
• Heat loss in the field (as many as 50% of patients in one study arrived with
temps below 93.2⁰ F [34⁰ C])
• Ambient trauma room temperature  Ambient temp at which the basal rate
of thermogenesis is sufficient to offset ongoing heat losses.
• For human, the thermoneutral zone is 77-86⁰ F (25-30⁰ C)

8. Causes of Hypothermia
• Resuscitation maneuvers (infusion of fluids at room temp can lower the
temp by 0.5⁰C (0.9⁰F) for every liter of fluid infused)
• Injury severity (injuries to the pelvis, extremities, abdomen and large blood
vessels are more likely to suffer significant as opposed to moderate
hypothermia)
• Elevated blood alcohol levels (vasodilation causes increased heat loss)

9. Causes of Hypothermia
• Impaired thermogenesis
• tissue oxygen debt, hypoxic hypothalamus
• Blood transfusions (Packed red blood cells are stored at 4⁰C (39⁰F) and one
unit can lower body temp by as much as 0.25⁰C(0.45⁰F)
• Age (extremes of age unable to regulate body temp as efficiently)

10. Causes of Hypothermia
• Anesthetics and paralytics (may decrease heat production by as much as one
third)
• Exposure of body cavities during surgery (heat loss occurs with an open
peritoneum by as much as 4.6⁰C/hr (8.25⁰F)

11. How does Hypothermia affect the
body?

12. Cardiovascular System
• 95-89.6⁰ F(35-32.2⁰C)
• ↑ sympathetic activity, ↑ circulating catecholamines
• Marked vasoconstriction
• Tachycardia
• ↑ cardiac output by as much as 4-5 times
• Atrial and ventricular dysrhythmias

13. Cardiovascular System
• 89.6-82.4⁰F(32.1-28.1⁰C)
• ↓HR and cardiac output
• ↑vascular resistance
• Temps < 82.4⁰F(28⁰C) result in depression of myocardial contractility
• Temps <77⁰F(25⁰C) increase risk of VF
• Temps < 69.8⁰F(21⁰C) may result in cardiac standstill

14. Pulmonary System
• In mild hypothermia, central stimulation of the respiratory center  ↑ respiratory
rate
• As hypothermia worsens, the respiratory rate becomes increasingly depressed
• Rewarming can lead to:
• Pulmonary edema
• Depression of the cough reflex
• Excessive bronchial secretions
• Referred to as “cold bronchorrhea”

15. Central Nervous System
• Progressive depression in LOC due to linear depression of cerebral
metabolism
• Cerebral blood flow decreases by 6-7% for each 1⁰C (1.8⁰F) decrease in
body temperature

16. Renal System
• “Cold Diuresis”- 2 – 3⁰C (1.8-2.7⁰F)
• Decrease in core temperature decreases cellular enzyme activity resulting in
defects of distal tubular reabsorption of sodium and water

17. Electrolyte and Acid-Base Equilibrium
• Altered sodium- potassium pump function during hypothermia results in
hyperkalemia, with hypokalemia occurring after rewarming
• Acidosis due to ↓ tissue perfusion, shivering, and ↓hepatic clearance of lactic
acid

18. GastroIntestinal and Endocrine System
• Mild ileus
• Depressed hepatic function
• Hyperglycemia- which may progress to hypoglycemia with temperatures
<86⁰F (30⁰C)

19. Metabolism
• The metabolic rate will decrease by 5% per degree of temperature drop
• Decrease in oxygen uptake and carbon dioxide production
• Increase in solubility of carbon dioxide

20. Blood and Coagulation
• Increased blood viscosity (2% increase in blood viscosity for each 1⁰C(1.8⁰F)
decrease in co temperature
• Increased hematocrit due to cold diuresis
• Inhibition of coagulation cascade
• Thrombocytopenia (reversible with rewarming)

22. Recent Studies
• Jurkovich et al.
• In a study of 71 patient stratified by injury severity, patients with a temp>34⁰C(93.2⁰F) had a mortality
of 7%, in comparison with 40% among those with a temperature <34⁰C. Temperatures below 32⁰C
(89.6⁰F) were associated with 100% mortality
• Wang et al.
• Hypothermia was independently associated with three-fold increased odds of death even when
adjusted for the confounding effects of age, injury severity and mechanism, admission SBP and
temperature measurement route
• Luna et al.
• Predicted mortalities as high as 100% are seen in patients with sever hypothermia and severe injury

23. Recent Studies
• Mortality rates in trauma patient with an ISS<25:
• Core temp <32⁰C (89.6⁰F) :100%
• Core temp 32.1-33⁰C (89.8-91.6⁰F): 69%
• Core temp 33.1-34⁰C (91.6-93.2⁰F): 40%
• Core temp >34⁰C (93.2⁰F): 7%

24. Care Implication of Hypothermia
• Nursing is integral in initiating, maintaining and monitoring a patient’s
temperature throughout the resuscitative process.
• This begins in the Emergency Department, continues in the Operating
Room and progresses on into the Critical Care Unit

25. Warming Strategies
• Passive external measures
• Remove blood and saline soaked dressings and blankets
• Increase ambient room temperature
• Decrease air flow over patient

26. Warming Strategies
• Active External Measures
• Fluid circulation, convection air and aluminum space blankets
• Placing over the patient is superior to placing under the patient
• Cover these blankets with standard cotton blankets, securing the edges
• Overhead radiant warmers
• Effectiveness unclear as they may cause inadvertent burns and when focused over blankets
may provide little direct heat exchange

27. Warming Strategies
• Active core rewarming techniques
• Airway rewarming
• Heated body cavity lavage
• Gastric lavage
• Bladder lavage
• Colonic lavage
• Pleural lavage
• Heated intravenous fluids (blood should be delivered at 42⁰C (107.6⁰F), crystalloids at 41⁰C (105.8⁰F)
• Continuous arteriovenous rewarming (CAVR)
• Use of Damage Control Surgery

30. Acidosis

31. Acidosis
• CO₂ + H₂0 ↔ H₂CO₃ ↔ H⁺ + HCO ₃⁻
• In early compensated shock, increased respiratory patterns often result in
respiratory alkalosis
• As shock progresses, tissue hypoxia ensures causing cells to shift from aerobic to
anaerobic respiration → lactic acidosis

32. Acidosis
• Acidosis results in decreasing sensitivity to catecholamine and stress hormones
resulting in:
• ↓cardiac contractility
• ↓cardiac output
• Vasodilation
• Hypotension
• ↓renal and hepatic blood flow
• Bradycardia
• ↑susceptibility to ventricular dysrhythmias

33. Recent Studies about Acidosis
• pH below 7.2 significantly enhances the deleterious effect on the
cardiovascular and the coagulation system
• Information from the Israeli army further validates that resuscitative efforts
may be futile in patients with a PH below 7.1
• Patients with an average PH of 7.29 demonstrate the highest survival
potential

35. Treatment Strategies
• Treatment is aimed at correcting hypo-
perfusion:
• Volume loading
• Transfusion
• Add inotropic support as indicated
• Continue resuscitating until indication of
cellular
• oxygenation exists through normalization of:
• Arterial PH
• Base deficits
• Lactate levels
• Gastric
‼ Because of the potential adverse effect of
sodium bicarbonate, it is typically
reserved for persistent PH of< 7.1 despite
optimal fluid loading and inotropic
support

36. Treatment Strategies
• Factors which contribute to acidosis:
• Hypoventilation
• Excessive saline use
• Aortic clamping
• Vasopressors
• Massive transfusions
• Impaired myocardial performance

37. Coagulopathies
• Hemorrhage often trauma is the result of two mechanisms:
• Mechanical bleeding (surgical bleeding)  controlled by rapid surgical control
• Coagulopathies (nonsurgical bleeding)  difficult to control and poorly understood
• Causes:
• Dilution
• Disseminated Intravascular Coagulation (DIC)
• Major Metabolic Derangements
• Hypothermia

38. Dilutional Coagulopathy
• Crystalloid Resuscitation prior to arrival → 20 minutes
• Clotting studies drawn after patient arrival → 15 minutes
• Lab must run clotting studies → 45 minutes
• ED continues to resuscitate with crystalloid or PRBC → 10 minutes
• Physician receives lab results and decides to transfuse FFP→ 30 minutes
• FFP must be prepared and thawed

39. Coagulopathies and Trauma
• Kearney et al.
• 41% of trauma patients with head injury developed DIC, 25% of trauma patients without head injury
developed DIC
• Keller et al.
• All patients with a GCS < 5 were coagulopathic
• ISS and Coagulopathy:
• ISS 30-44 = coagulopathy 41% of the time
• ISS 45-59= coagulopathy 59% of the time
• ISS 60-57= coagulopathy 79% of the time

40. DIC
• Stage 1 ↑clotting:
• ↑capillary permeability →thick sludgy blood
• Mediator and free oxygen radicals injure inside of blood vessels
• Increased coagulation:
• Mediators
• Acidosis
• Vasoconstriction increases contact of clotting factors with blood vessel walls

41. DIC
• Patient may demonstrate signs of tissue ischemia due to clot formation:
• Metabolic acidosis
• Mottling
• Gangrene
• Organ failure

42. DIC
• Stage 2 Anticoagulation:
• Clotting factors are consumed
• Existing clots release fibrin degradation products → anticoagulation of the systemic
system
• Patients will demonstrate increased signs of bleeding:

43. Coagulopathies and Acidosis
• It has been demonstrated that acidosis contributes to coagulation disorders:
• Ment et al. found that activated Factor X and the activity of activated Factor VII is
substantially reduced in PH below 7.4 (and is actually increased in alkaline
environments)
• Dunn et al. found impaired hemostasis at a pH below 7.2

44. Coagulopathies and Hypothermia
• Hypothermia impairs platelet aggregation and potentiates coagulopathy in factor
deficient plasma
• Johnson et al. found that at 95⁰F(35⁰C) without dilution there were decreases of
function in all factors
• Clotting factors XI and XII only functioned at 65% of normal (at 91⁰F, 33⁰C), their
activities fell to 17% and 32% respectively
• Patients with a high trauma score (15 or 16) had significantly less blood loss when
body temperature was maintained above 35⁰C when compared to patients whose
temperature was 33⁰C

45. Recognition of Coagulopathies
• Basic tests of coagulopathies:
• Platelets- maintenance of platelets at 50,000 or higher results in less microvascular
bleeding
• PT, INR is sensitive to low levels of Factor VII and is not indicative of severe
coagulation defects, although it may be mildly elevated in trauma
• PTT reflects multiple steps in the coagulation cascade and elevations with trauma
indicate multiple and severe defects
• Fibrinogen – excessive bleeding has been reported with fibrinogen levels under
50mg/dL

46. Treatment Strategies
Abnormal Lab Result Treatment Consideration
Platelet Count < 50-75,000 6-8 pack of single donor platelet concentration
Fibrinogen level <100 mg/dL 10 units of cryoprecipitate
INR over 2.0 with an abnormal PTT 2-4 unit of fresh frozen plasma
PTT > 1.5 times normal 2-4 units of plasma

47. Break the Cycle

48. References
• Deloughery, T.G. (2004). Coagulation defects in trauma patients: etiology and recognition and therapy. Critical Care Clinics, 20 13-24.
• Dutton, R.P., McCunn, M. & Hyder, M. (October, 2004). Factor V11a for correction of traumatic coagulopathy. The Journal of Trauma,
57(4), 709-719.
• Hilderbrand, F., Ginnaudis P.V. & Van Griensven, M. (2004). Pathophysiologic changes and effect of hypothermia on outcome in elective
surgery and trauma patients. The American Journal of Surgery, 187 363-371
• Ho, A. M., Karmakar, M.K.& Dion, P.W. (2005). Are we giving enough coagulation factors during major trauma resuscitation? The American
Journal of Surgery, 190 479-484.
• Kelley, D.M. (March 2005). Hypovolemic Shock: an overview. Critical Care Nursing Quarterly, 28(1), 2-19.
• Mikhail, J.(1999). The trauma trial of death: Hypothermia, Acidosis, and Coagulopathy. AACN Clinical Issue Advanced Practice in Acute
Critical Care, 10 (1), 85-94.
• Moore, F.A., McKinley, B.A. & Moore, E.E. (2004). The next generation of shock resuscitation. The Lancet, 363 1988-1996.
• Wang, H.E., Calloway, C.W.& Peitzman, A.B. (2005). Admission hypothermia and outcome after major trauma. Critical Care Medicine, 33(6),
1296-1300.