Pathology of dying


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Presented at AW Sjahranie General Hospital, supervised by dr. Mangalindung O. SpB

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Pathology of dying

  1. 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. 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. 3. How Does the Patient Die on Trauma?
  4. 4. Trias of Death •Hypothermia •Coagulopathy •Acidosis
  5. 5. Rotondo, M,F. The damage control sequence and underlying logic. Surg Clin North Am 1997; 77: 761-777.
  6. 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. 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. 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. 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. 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. 11. How does Hypothermia affect the body?
  12. 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. 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. 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. 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. 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. 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. 18. GastroIntestinal and Endocrine System • Mild ileus • Depressed hepatic function • Hyperglycemia- which may progress to hypoglycemia with temperatures <86⁰F (30⁰C)
  19. 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. 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)
  21. 21. 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
  22. 22. 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%
  23. 23. 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
  24. 24. Warming Strategies • Passive external measures • Remove blood and saline soaked dressings and blankets • Increase ambient room temperature • Decrease air flow over patient
  25. 25. 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
  26. 26. 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
  27. 27. Acidosis
  28. 28. 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
  29. 29. 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
  30. 30. 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
  31. 31. 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
  32. 32. Treatment Strategies • Factors which contribute to acidosis: • Hypoventilation • Excessive saline use • Aortic clamping • Vasopressors • Massive transfusions • Impaired myocardial performance
  33. 33. 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
  34. 34. 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
  35. 35. 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
  36. 36. 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
  37. 37. DIC • Patient may demonstrate signs of tissue ischemia due to clot formation: • Metabolic acidosis • Mottling • Gangrene • Organ failure
  38. 38. 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:
  39. 39. 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
  40. 40. 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
  41. 41. 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
  42. 42. 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
  43. 43. Break the Cycle
  44. 44. 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.