pathology of dying
DESCRIPTION
Presented at AW Sjahranie General Hospital, supervised by dr. Mangalindung O. SpBTRANSCRIPT
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Pathology of DyingDr. Isa Basuki, Dr. Meilyna Sulphiana Alam, Dr. Yufriadi
Yunus
Department of Surgery, AWS General Hospital
Faculty of Medicine, Mulawarman University
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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
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How Does the Patient Die on Trauma?
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Trias of Death
•Hypothermia
•Coagulopathy
•Acidosis
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Rotondo, M,F. The damage control sequence and underlying logic. Surg Clin North Am 1997; 77:
761-777.
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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
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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)
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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)
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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)
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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)
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How does Hypothermia affect the body?
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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
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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
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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”
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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
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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
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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
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GastroIntestinal and Endocrine System
• Mild ileus
• Depressed hepatic function
• Hyperglycemia- which may progress to hypoglycemia with temperatures <86⁰F (30⁰C)
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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
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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)
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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
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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%
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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
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Warming Strategies
• Passive external measures• Remove blood and saline soaked dressings and blankets
• Increase ambient room temperature
• Decrease air flow over patient
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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
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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
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Acidosis
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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
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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
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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
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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
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Treatment Strategies
• Factors which contribute to acidosis:• Hypoventilation
• Excessive saline use
• Aortic clamping
• Vasopressors
• Massive transfusions
• Impaired myocardial performance
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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
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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
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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
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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
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DIC
• Patient may demonstrate signs of tissue ischemia due to clot formation:• Metabolic acidosis
• Mottling
• Gangrene
• Organ failure
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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:
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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
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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
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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
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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
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Break the Cycle
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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.