Trauma: Hemorrhagic Shock & Trauma Resuscitation

Hemorrhagic Shock

Possible Source of Occult Hemorrhage Mn

  • Street/In the Field
  • Chest
  • Retroperitoneum
  • Abdomen
  • Pelvis
  • Thighs

Hemorrhagic Shock Class Mn

Class Blood Loss HR BP Pulse Pressure RR UOP Mental Status
I < 750 cc (< 15%) Normal Normal Normal Normal Normal Slightly Anxious
II > 750 cc (15-30%) > 100 Normal Narrow > 20 < 30 Mildly Anxious
III > 1500 cc (30-40%) > 120 Low Narrow > 30 < 15 Confused, Anxious
IV > 2000 cc (> 40%) > 140 Low Narrow > 40 0 Confused, Lethargic

Pathophysiology of Hemorrhagic Shock

  • Cellular Level
    • Oxygen Delivery Unable to Meet Oxygen Demand
    • Aerobic Metabolism Converted to Anaerobic Metabolism
      • Produces: Oxygen Radicals, Lactic Acid & Inorganic Phosphates
    • Release of DAMPs Incite Systemic Inflammatory Response
    • Predictable Hemostasis Fails & Cells Die
  • Organ Level
    • Hypovolemia & Resultant Vasoconstriction Cause End-Organ Hypoperfusion & Damage
    • Hypoperfusion of the Brain & Myocardium Lead to Cerebral Anoxia & Fatal Arrhythmia within Minutes

Acute Traumatic Coagulopathy (ATC)/Trauma-Induced Coagulopathy (TIC)

  • Present in 24.4% of Trauma Patients
  • Mechanisms:
    • Activated Protein C (APC)
      • Anticoagulant – Inactivates Factors Va and VIIIa
      • Increased Activity in Trauma
        • Possibly Due to Upregulation of Thrombomodulin Activity in the Setting of Hypoperfusion
    • Endothelial Glycocalyx Layer (EGL)
      • “Shedding” of EGL After Injury Due to Yet Undetermined Mechanisms
      • Anticoagulant Components Such as Chondroitin Sulfate and Heparan Sulfate
    • Increased Fibrinolysis
      • Clotting Cascade Activated Locally
      • Distant Fibrinolytic Activity Increased
        • Believed to Prevent Microvascular Thrombosis
    • Platelet Impairment
      • Numbers are Depleted
      • Migration is Decreased
      • Function is Impaired
  • Lethal Triad Compound on Each Other and Result in Significant Morbidity and Mortality

Hemorrhagic Shock Diagnosis

  • First Step: Recognize its Presence
    • May Miss if Only Looking at Blood Pressure Due to Early Compensation
    • Earliest Signs: Tachycardia & Cutaneous Vasoconstriction
  • Second Step: Determine the Cause
    • Hemorrhagic Shock Most Common in Trauma
    • Obstructive Shock Caused by Cardiac Tamponade or Tension PTX
    • Cardiogenic, Neurogenic or Septic Shock Can Also be Present
  • Diagnosis Should Not Delay Appropriate Resuscitation

Damage Control Resuscitation

Initial Fluid Resuscitation

  • Initial Step: 1-2 L Warmed Lactated Ringer Bolus
    • *If Class III/IV Shock May Consider Immediate Transfusion to Blood/Blood Products to Limit Crystalloid Transfusions
    • Pediatrics (If < 40 kg): 20 cc/kg
  • Response:
    • Rapid Responder
      • Quick Correction that is Maintained
      • Indicates Class I Shock
    • Transient Responder
      • Initially Responds but Then Deteriorates
      • Indicates Class II-III Shock
    • Non-Responder
      • No Correction
      • Indicates Class IV Shock
  • Next Step:
    • Rapid Responder: No Further Immediate Boluses Required
    • Transient or Non-Responders: Transition to Blood or Blood Products
      • Strongly Consider Activation of Massive Transfusion Protocols (MTP) if Significant Volumes are Anticipated

Blood Transfusion

  • Initial Blood: Type O pRBC
    • Until Type & Crossmatch Available
  • Massive Transfusion Protocol (MTP)
    • Definitions:
      • ≥ 10 U pRBC in 24 Hours
      • ≥ 4 U PRBC in 1 Hour
    • Approaches:
      • Hemostatic Resuscitation (1:1:1 Ratio)
      • TEG-Guided Transfusion
      • Whole Blood

Permissive Hypotension (Hypotensive Resuscitation/Controlled Resuscitation)

  • Initial Goal SBP: ≥ 70 mmHg Until Definitive Hemostasis Achieved
  • Rapid Resuscitation Exacerbates Bleeding By:
    • Dislodging Fragile Clots
    • Decreasing Blood Viscosity
    • Exacerbating Lethal Triad
  • Contraindicated in TBI – Maintenance of Cerebral Perfusion Pressure Essential to Prevent Secondary Brain Injury
    • Age 15-49: ≥ 110 mmHg
    • Age 50-69: ≥ 100 mmHg
    • Age ≥ 70: ≥ 110 mmHg

Damage Control Resuscitation – Approach to Blood Transfusion

Hemostatic/Balanced Resuscitation

  • pRBC:FFP:Plt at Ratio 1:1:1
  • Closest Approximation to Whole Blood Available
  • Concentration After Dilution & Storage:
    • Hematocrit: 29% (5-10% Are Lost After Transfusion)
    • Platelet Count: 88,000 (Only 2/3 Are Viable After Transfusion)
    • Coagulation Factors: 65% of Normal
  • Effective Concentration (After Dilution, Storage & Immediate Losses):
    • Hematocrit: 26%
    • Platelet Count: 59,000
    • Coagulation Factors: 65% of Normal
    • *Adding More of One Component Dilutes the Other Two & Adding Fluids Dilutes All Three
    • Barely Keeps Levels Above Traditional Transfusion Indications

Thrombelastography (TEG)

Whole Blood

  • Better Access in Military with “Fresh Blood” from a “Walking Blood Bank” of Prescreened Soldiers
    • Less Available in Civilian Populations
  • Concentration After Dilution & Storage:
    • Hematocrit: 35-38%
    • Platelet Count: 150,000-200,000
    • Coagulation Factors: 85% of Normal
  • May Decrease Transfusion Requirements & Mortality Although Evidence Insufficient

Damage Control Resuscitation – Adjuncts

Tranexamic Acid (TXA)

  • Inhibits Plasminogen Conversion to Plasmin, Inhibiting Fibrinolysis & Clot Breakdown
  • Off-Label Use in the US
  • Dosing: 1 g Bolus & Second 1 g Infusion Over 8 Hours
    • If Given Within 3 Hours: Reduces Mortality and Blood Transfusions
      • Debated
    • If Given After 3 Hours: Increased Mortality
  • Recommended for Significant Hemorrhage if Given Within 3 Hours

Recombinant Activated Factor VIIa (rVIIa)

  • Activates Factor X & Thrombin Formation
  • Off-Label Use in the US
  • Insufficient Evidence to Guide Use

Cryoprecipitate

  • Replaces Fibrinogen – The First Factor to Reach Critically Low Concentrations in Major Blood Loss
  • Insufficient Evidence to Guide Use

Vasopressors

  • Increased Mortality for Most Vasopressors in Hemorrhagic Shock
    • *Evidence is However Poor with High-Risk of Bias Through Observational Studies
  • Arginine Vasopressin (AVP)
    • Dosing: 4-U Bolus and 0.04-U/min Infusion
    • Decreased Transfusion Requirements but No Change in Mortality
    • No Increased Risk of Complications but May Decrease Risk of DVT

Pneumatic Antishock Garment (PASG)/Military Antishock Trousers (MAST)

  • Historical Tool, No Longer Used Today
  • Inflatable Garment Promotes Hemostasis and Manually Increases PVR
    • 3 Inflatable Compartments: Abdomen/Pelvis and 2 Legs
    • Each Inflated/Deflated Separately
  • Was Previously Used in Pre-Hospital Setting
  • Compartments Released One-At-A-Time Once in ED
  • Contraindicated by Thoracic Trauma
  • No Improvement in Mortality
  • Can Cause Lower Extremity Ischemia/Compartment Syndrome

PASG/MAST

Mnemonics

Possible Source of Occult Hemorrhage

  • “SCRAPT”
    • Street/In the Field
    • Chest
    • Retroperitoneum
    • Abdomen
    • Pelvis
    • Thighs

Hemorrhagic Shock Class (Percent Blood Loss)

  • Tennis Scoring System – Similar to How Tennis is Scored
  • 0-15-30-40

References

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