Trauma physiology

Section: Trauma Curriculum: Curriculum, page 75

Overview

• Initiation
  • Direct tissue disruption → bleeding, cell death, exposure of intracellular contents (DAMPs)
• Metabolic response
  • Ebb and flow
• Immune response
  • Inflammatory cascade
• Neuro-hormonal response
  • SNS, RAAS, coritsol

Initiating Factors

• More severe the injury, greater tissue injury and greater metabolic response
• Limiting magnitude and duration of insult = Reduce extent of metabolic change
  • Usually by aggressive resus and rapid source control
  • Metabolic response
    • Larger with injury severity and tissue injury
    • Limited by good early resus
• Many factors contribute to the response to trauma
  • Non-modifiable factors - e.g. Age, gender
  • Modifiable - e.g. Timely treatment
  • Blunted in - Extremes of age, premenopausal, malnutrition, HIV
• Hypovolaemia
  • Tissue hypoperfusion
  • Multifactorial - External losses (bleeding), internal shifts, salt changes
  • Renin system activation
• Afferent Impulses
  • Hormonal and precipitated by pain
• Wound Factors
  • Endogenous factors cause tissue injury
  • SIRS via humoral and cell mediated pathways

Metabolic Response

• Trauma evokes local and systemic response
  • Local - Inflammation
  • Systemic - Protective, conserves fluid, provides energy for repair
• Ebb and Flow
  • Ebb
    • Short duration of severe shock and reduction in enzyme activity and O2 consumption
    • Hypovolaemia leads to decreased tissue perfusion causing release of catecholamines
    • Ebb is treated by good resuscitation
  • Flow (2 parts)
    • Hormonal mediators such as sympathetic system, cortisol, ADH and aldosterone leads to increased fluid conservation via sodium retention
    • Hyperdynamic state stimulated by inflammation
    • Catabolic phase - Fat/protein mobilization and weight loss
      • This is driven by the neurohormonal response and inflammatory response
        • Increase in cortisol, adrenaline, glucagon and cytokines
      • Effects
        • Increased energy expenditure
        • 3 ways it gets it
          • Protien - Increased protein breakdown and therefore urine nitrogen excretion
          • Fat - Oxidation of fat for energy
          • Carbs - Gluconeogensis and Insulin resistance
        • Fluid retention and hypoalbuminemia
      • Sequele
        • Impaired immune function
        • Delayed surgical healing
        • Impaired cardiac outout and respiratory function
        • Atrophy of smooth and skeletal muscle
        • Increase in postop morbidity and mortality
    • Anabolic phase - Fat/protein store restoration and weight gain
      • Features
      • Normal/high - BGL, glucose production, FFA, insulin, catecholamines
      • High - glucagon, O2 consumption, CO, temperature
      • Normal lactate

Immune Response

Inflammatory Pathway - many cells involved

• Cytokines - inflammatory mediators
  • Proinflammatory - TNF, IL-1, IL-8
    • Gene upregulation of mediators
    • Activate neuts, endo and epi → Tissue damage
  • Anti-inflammatory - IL-10
    • Inhibit proinflammatory cascade
• SIRS and CIRS (Compensatory Inflammatory Response Syndrome)
  • Occur simultaneously to promote homeostasis
  • If they are not balanced - Bad outcomes
  • SIRS → MODS/MOF - 50% mortality
  • More CIRS → Immune suppression, nosocomial infection in critically ill patients
  • Cytokine balance/complex interplay determines this
• Protein C activation
  • Coagulopathy causes MOF

Cellular Pathway

• Complement system - main alternative pathway in trauma
• PAMPs and DAMPS (pathogen associated molecular patterns)
  • Injury and sepsis both cause SIRS
  • Cell receptor mediated early identification of tissue damage from trauma
• Free radicals made by white cells and in response to trauma can be excessive → Organ dysfunction

Hormonal Mediators

• Increase in A/NA/cortisol and glucagon
• HPA axis
• RAA system

Effects of Various Mediators

• Hyperdynamic state with tachycardia, and increased CO
• Increased oxygen consumption
• Leading to lactic acidosis - Tissue hypoperfusion and inadequate resus
• Critically ill patients have a glucose intolerance

Clinical Relevance

• 3 factors determine survival after injury - damage extent, metabolic response and tx effectiveness
• Hypovolaemia → Tissue hypoperfusion - needs to be rectified ASAP
• Flow-on neurohormonal response can continue despite resus
• Treatment principles
  • Rapid resus | Maintenance of tissue O2 delivery | Source control

Shock

Definition

• Inadequate delivery of oxygenated blood to the tissues causing cellular hypoxia
  • Initially leading to reversible ischaemic injury then irreversible damage
• Ian Stewart Definition
  • Impaired oxygen delivery leads to hypoxia and anaerobic metabolism (pyruvate is converted to lactate and leads to decreased ATP)
  • Causes failure of cells to maintain osmotic, ionic and pH homeostasis
  • Leading to cellular oedema and death
  • Activation of inflammatory cascades, microvascular alterations, organ dysfunction.

Classification

• Hypovolaemic
• Cardiogenic
• Obstructive
• Distributive
• Neurogenic

CO = SV x HR

• Tachy in trauma to increase to improve CO
• SV
  • Preload reduced - Hypovolaemia
  • Contractility initial increase with stress hormones but reduces with contusion and acidosis
  • Afterload affected by trauma due to vasoconstriction response
• Compensatory methods
  • Cutaneous and visceral vasoconstriction (preserve kidney/heart/brain)
  • Hormones - Histamine, bradykinin, stress hormones
  • Wound factors - systemic inflammatory response

Hypovolemic Shock

• Definition
  • Global hypoperfusion leading to cellular hypoxia cause by reduced intravascular volume
• Pathophysiology
  • Reduced intravascular volume → Reduced SV and tachycardia maintain CO initially

Classification

Class	Blood Loss (%)	Volume (mL)	HR	BP	PP	RR
I	< 15	< 750	< 100	N	Normal	14-20
II	15-30	750-1500	> 100	N	Narrow	20-30
III	30-40	1500-2000	> 120	Decreased	Narrow	30-40
IV	> 40	> 2000	> 140	Decreased	Narrow	> 35

Hemorrhagic shock

• Haemorrhagic shock is classified into 4 classed with increasing severity based on haemodynamic and end organ parameters
  • Key feature: May be no significant signs until 1-1.5L of blood loss
• Class 1
• < 750mL blood loss
  • < 15% loss of blood volume
  • HR <100
  • BP normal
  • Pulse P normal or elevated
  • RR 14-20
  • UO > 30ml/hr
  • Slightly anxious
• Class 2
  • 750mL-1500mL blood loss
  • 15-30% loss of blood volume
  • HR >100
  • BP normal
  • PP reduced
  • RR 20-30
  • UO 15-30ml/hr
  • Mildly anxious
• Class 3
  • 1500mL - 2000mL blood loss
  • 30-40% loss of blood volume
  • HR >120
  • BP reduced
  • PP reduced
  • UO 5-15ml/hr
  • Anxious and confused
• Class 4

  • 2000mL blood loss

  • 40% loss of blood volume

  • HR >140
  • BP and PP reduced
  • UO negligible
  • Confused and lethargic

Measurement of Shock

• CO is determined by preload, myocardial contractility and afterload (wall tension during LV ejection)
• Indirect flow measures (useful measures as they are quick and easy)
  • Cool peripheries and reduced CRT form cutaneous vasoconstriction
  • Pallor from cutaneous vasoconstriction
  • UO - Renal blood flow preservation
  • Confusion/mentation - Rerebral blood flow preservation
• Direct flow measures
  • CVL
    • Routes
      • Subclavian
        • Good for when C-spine status unclear
        • Least line sepsis
        • Risks - PTX/Arterial puncture
      • Jugular
        • C-spine not clear and has a neckline, discomfort
      • Femoral
        • Thrombosis, infection and intra-abdominal cannulation risk
  • Systemic arterial BP - BP cuff or arterial line
  • Pulmonary Artery Wedge Pressure - uncommon
  • CO - Thermodilution technique

End-Points in Shock Resuscitation

• Needs to closely monitor acid base status → Blood gas
• Metabolic acidosis and lactic acidosis!

Management of the Shocked Patient

• Primary goal - early establishment of adequate oxygen delivery
• Within 3 - 5mins of trauma shock, respiration switches to anaerobic
  • Requires restoration of adequate oxygenated blood flow
  • By controlling AW and ventilation
• Restoration of optimal circulating BV and enhancing CO with pressors, acid base correction and treating sepsis
• Trauma shocked pts goal of treatment is to restore cellular aerobic metabolism
  • Rapid balance resuscitation
  • Monitoring progression/improvement of metabolic/lactic acidosis
  • I.e. ICU style monitoring with regular VBG for acid base status and lactate