Principles of Surgery PGY 1 and PGY 2

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Principles of Surgery - PGY 1 and PGY 2 SHOCK
EVIDENCE BASED
Sandro Rizoli, MD, FRCSC, PhD, FACS Associate
Professor Surgery and Critical Care Medicine De
Souza Trauma Research Chair CIHR New Investigator
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GOAL
1. Preparation for the exams 2. Theoretical
basis for practice
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MASTER PLAN

• Definition
• Classification
• History
• Pathophysiology
• Hypovolemic Shock
• Therapy
• Novel ideas
• Septic shock
• Definition
• Current guidelines

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QUESTION 1
With regards to the distribution and composition
of the body fluid compartments, which of the
following statements is/are correct? a) Most
intracellular water is in skeletal muscle. b) The
major intracellular cation is sodium. c) The
major intracellular anions are proteins and
phosphates. d) The major extracellular cation is
sodium.
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DEFINITION

• Inadequate tissue perfusion
• Imbalance between substrate supply (DO2)
• and demand (VO2) at a cellular level
• Dysfunction of cellular biochemistry
• cell membrane pump dysfunction
• intracellular edema
• leak intracellular contents
• inadequate regulation intracellular pH

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DEFINITION

• Initially reversible
• Cell death organ damage failure MO death
• Mortality
• septic shock 35-40 mortality
• cardiogenic shock 60-90 mortality
• hemorrhagic variable mortality

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DETERMINANTS TISSUE PERFUSION
CO HR x stroke volume (preloadcontractilityaft
erload) DO2 CaO2 x cardiac output VO2 (CaO2
- CvO2) x cardiac output O2 content (1.38 x
Hg) x O2 sat (0.03 X PaO2 ) SVR vessel
length, blood viscosity, vessel diameter
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CLASSIFICATION

• Hypovolemic decreased pre-load
• hemorrhage/fluid loss
• 2. Distributive sepsis, vasodilatory,
  pancreatitis,
• anaphylaxis, Addison, SIRS
• 3. Cardiogenic pump failure
• heart, arrhythmias, obstructive
• (PE, pneumotx, tamponade, pulm. hypert.)
• 4. Neurogenic hypotension NOT tachyc,
  vasoconstriction

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CLASSIFICATION
PCWP CO SVR SVO2 Hypovolemic
Distributive Cardiogenic
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History Shock Resuscitation
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QUESTION 2
Metabolic effects of the neuroendocrine response
to injury include which of the following
events? a) Gluconeogenesis. b) Glycogen
synthesis. c) Lipolysis. d) Proteolysis. e)
Hypoglycemia.
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PATHOPHYSIOLOGY I
Hypovolemia (decresase C.O.)
Vasoconstriction Tachycardia

• Decrease blood flow
• Splanchnic
• Loss gut barrier
• Renal redistribution
• Renin-angiotensin-aldost

Fall transmemb potential Na-K pump
Cellular dysfunction
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PATHOPHYSIOLOGY I
Intracellular water 6
Na9.9 K173 Cl3.9
Na18.4 K162 Cl11.1
Extracellular water 49
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QUESTION 3
Which of the following is/are elevated during
acute response to injury? a) Glucagon. b)
Glucocorticoids. c) Cathecolamines. d)
Insulin. e) Thyroid stimulating hormone (TSH).
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PATHOPHYSIOLOGY II
hypovolemia tissue injury pain fear
sympatho- adrenal response
hypothalamic- hypophyseal- adrenal response
catechol BP, HR contractility vasoconstriction
cortisol, glucagon
hypoxia endoth macrophages cytokines, PAF,
eicosanoid, neutrophils
ROS, coagulation reperfusion injury SIRS/MODS tra
nslocation
hypermetabolic state
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CONSEQUENCES

• Acidemia low pH, lactate, BE
• Ischemic organs
• SIRS
• MODS

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QUESTION 4

• Which of the following statements accurately
  characterizes
• fluid shifts in hemorrhagic shock?
• Loss of IV volume is fully compensated by
  interstitial fluid moving
• into the vascular space.
• b) Intracellular fluid volume decreases as fluid
  shifts from the IC
• to the EC compartment to compensate for the IV
  loss.
• c) There is movement of interstitial fluid into
  the IC space even though
• full compensation of IV losses has not yet
  occurred.
• d) Transmembrane potential falls resulting in
  increased Na permeability
• and influx of Na into the cell.

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HYPOVOLEMIC SHOCK

• Classification
• Up to 15 (compensated)
• HRlt100, RR 14-20, N urine/BP, anxious
• 30 (up to 1500ml)
• 40
• gt40

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HYPOVOLEMIC SHOCK

• Management
• ABCDE oxygen 2L NS or RL
• Identify source bleeding
• Control bleeding
• Resuscitate until perfusion corrected
• Massively transfused patients

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Control Bleeding - Surgery
Direct control of bleeding - surgery -
cauterization - topical agents -
angio-embolization
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Fluids
Restore circulating volume crystalloids vs.
colloids SAFE trial NEJM 2004 3502247 NEJM
2007 357874 - TBI severe 42 vs 22
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Blood
Replace blood losses - RBC - other blood
products TRICC trial NEJM 1999 340409 J
Trauma 2004 57563
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Crystalloid Side Effects

• Abdominal compartment syndrome
• Extremity compartment syndrome
• Pro inflammatory
• Increased organ dysfunction (ARDS)
• Increased hospital stay
• Longer ventilation days

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Diffuse Coagulopathy

• dilution
• consumption
• hypothermia
• platelet dysfunction
• excessive fibrinolysis
• DIC (????)

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Triangle of Death
massive transfused (10-20U RBC)
hypothermia
death
acidosis
coagulopathy
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• Damage control resuscitation
• 5 massively bleeding
• Restrict crystalloids
• Reconstituted whole blood
• RBC 11 FFP (1 platelet)

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Evidence 1FFP1RBC

• Borgman (J.Trauma 200763805)
• Retrospective chart review
• 246 at US Combat Army Hospital
• 10U RBC/24h (including whole blood)
• mortality death by exsanguination
• 18 65 92
• 12 34 78
• 11 19 37

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Evidence 1FFP1RBC

• Borgman (J.Trauma 200763805)
• Survivorship bias
• Crystalloids
• mortality crystalloids
• 18 65 1.8L/h
• 11 19 0.5L/h

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Evidence 1FFP1RBC

• Kashuk (J. Trauma 2008, 65261)
• Retrospective (Civilian - Denver)
• 133 patients gt10 RBC in 6h
• 11 NO survival benefit
• Crystalloids NOT risk factor coagulopathy
• Temperature risk factor (ISS ??)

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Guidelines ATLS (95 patients) Endpoints Trauma
Room
85 inadequate tissue O2
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Current Resuscitation
Endpoints ICU Global Regional supranormal
DO2 gastric tonometry mixed venous O2
sat skin/brain blood flow RVEDV - LVP base
deficit lactate
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THERAPY
GOAL-DIRECTED SUPRANORMAL VALUES Shoemaker (late
80s) post op, trauma pre-op patients Boyd
Hayes (1999) no improvement overall reduced
mortality if 8-12h (8RCT) 92 survival if
achieved 24h 93 mortality if not and lactate
high gt24h
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• 598 patients
• penetrating
• BP ? 90 mmHg

• NO FLUID
• n 289
• 90 cc p.h.
• 280 cc ER

• STANDARD
• n 309
• 870 cc p.h.
• 1608 cc ER

62 survived
70 survived
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• TIMING for fluids
• Bleeding surgical hemostasis
• NO TBI allow hypotension

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HYPOVOLEMIC SHOCK

• Management
• ABCDE oxygen 2L NS
• Identify control bleeding
• Resuscitate until perfusion corrected
• Massively transfused patients
• Blood-based resuscitation
• Reconstituted whole blood (11 RBCFFP)
• Restrict crystalloid

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QUESTION 5
Which one or more of factors determines cardiac
output? a) End-diastolic volume. b)
Afterload. c) Contractility. d) Heart rate. e)
Ventricular interaction.
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QUESTION 6
Which factors directly affect oxygen
delivery? a) Blood transfusions. b) Oxygen
consumption (VO2). c) Cardiac output (CO). d)
Fraction of inspired oxygen (FiO2). e)
Metabolic alkalosis.
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SEPTIC SHOCK
SIRS Sepsis documented infection Severe
sepsis lactic acidosis, oliguria (lt0.5ml/h),
mental, platelet lt100,000, cap refill 3sec,
mottled Septic shock hypotension despite
fluids (40-60 ml/Kg)
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DEFINITION SIRS

• At least two of
• RRgt20 or PaCO2lt32mmHg
• HRgt90
• Temperature gt380C or lt350C
• WBCgt12,000 or lt4,000

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THERAPY

• FLUIDS
• DIAGNOSIS
• SOURCE CONTROL
• ANTIBIOTICS

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THERAPY

• FLUIDS
• CVP 8-12
• MAP ? 65
• U.O. ? 0.5cc/h
• SvO2 ? 70 (or SVCO2)

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Rivers NEJM 2001
control CVP, MAP, U.O.
intervention CVP, MAP, U.O., SvO2
more fluid more blood more inotropes
0 to 6h
more fluid more blood more inotropes MORE DEATHS
7 to 72h
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THERAPY
5. PRESSOR (2nd line, nor, epi or dopamine) 6.
INOTROPES (dobutamine)
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THERAPY

• 7. STEROIDS (ACTH, low raise lt9mcg/dl hemod
  effect)
• rhAPC (PROWESS APACHEgt25, MOD x2
• ADDRESS not for low risk death)

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THERAPY

• 9. TRANSFUSION TRIGGER
• PROTECTIVE VENTILATION
• TV 6ml/k PPlt30, PEEP
• 11. SEDATION, PARALYSIS
• 12. NUTRITION, GLUCOSE CONTROL

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CONCLUSIONS

• Shock
• Definition, classification
• Overview physiopathology
• Hypovolemic shock
• Stop bleeding then volume
• Damage control resuscitation
• Septic shock
• Definition
• Current guidelines

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