P&P : Sepsis and Shock

Part 1: Sepsis Overview

Learning Outcomes

  • Identify principal causes and risk factors of septicaemia and sepsis.

  • Understand pathophysiological changes and clinical manifestations related to shock.

  • Apply knowledge of shock progression in clinical observations and interventions.

  • Describe treatments and management principles specific to sepsis.

Complete Lecture Plan

  • Review the circulatory system and its "protected status".

  • Pathway entry into circulation leading to sepsis.

  • Exploration of shock and its various types.

  • Management strategies for dealing with shock.

  • Additional considerations concerning sepsis, including Systemic Inflammatory Response Syndrome (SIRS) and Multiple Organ Dysfunction Syndrome (MODS).

Circulatory System Details

  • Systemic Circulation: Transports oxygenated blood to upper and lower body via aorta, veins, and renal/liver arteries.

  • Pulmonary Circulation: Involves the entry and exit of blood through lungs via pulmonary arteries and veins for gas exchange.

Breaching the Barrier

  • Mechanical forces contribute to infections:

    • Unintentional: Perforating wounds, burns.

    • Intentional: Intravenous sites, surgical procedures.

  • Risk of infections increases when the protective barrier (skin) is compromised.

  • Alcohol Prep Pads can mitigate risks during invasive procedures.

Defences Against Parenteral Infections

  • Parenteral infections involve pathogens entering through blood, e.g., Total Parenteral Nutrition (TPN).

  • Key Defenses:

    • Blood flow and circulation of inflammatory and immune cells.

    • Role of the liver and spleen in systemic immunity.

Conditions Promoting Parenteral Infections

  • Large or continuous organism delivery into the bloodstream.

  • Impaired blood flow due to conditions such as infective endocarditis.

  • Pathogens capable of evading immune responses.

  • Presence of immunocompromised hosts (weak immune systems).

Definition of Sepsis

  • Sepsis is a condition marked by the presence of bacteria in the bloodstream, leading to systemic inflammation and response.

Pathophysiology of Sepsis

  • Sepsis is triggered by organisms infusing inflammatory response chemicals into the blood.

  • Vascular damage results from severe inflammation and leads to impaired organ perfusion.

  • Increased presence of cytokines and activation of leukocytes contribute to systemic inflammation.

Inflammatory Response Reminder

  • Injury to tissues leads to immune responses:

    1. Phagocyte activation to consume pathogens.

    2. Chemical signals release (e.g., histamine).

    3. Dilation of capillaries, leading to fluid leakage.

    4. Migration of more immune cells to the infected area.

Systemic Inflammation Mechanisms in Sepsis

  • Leads to intravascular clotting from hyperactive coagulation responses.

  • Drop in mean arterial pressure (MAP) due to systemic vasodilation.

  • Increased vascular permeability and tissue edema.

Part 2: Shock Overview

  • Shock results from blood circulation failure to deliver adequate oxygen.

  • Insufficient tissue perfusion triggers cellular waste accumulation and metabolic distress.

Types and Causes of Shock

  • Loss of blood volume leads to:

    • Hypovolaemic shock (e.g., dehydration, hemorrhage).

    • Cardiogenic shock (e.g., heart failure).

    • Obstructive shock (e.g., blockage in vessels).

  • Loss of vasomotor tone leading to

    • Neurogenic shock.

    • Septic shock.

    • Anaphylactic shock.

Mechanism Leading to Hypovolaemic Shock

  1. Blood volume decreases.

  2. Drop in venous return to the heart.

  3. Reduced stroke volume and cardiac output.

  4. Resulting lower MAP.

Mechanism of Cardiogenic Shock

  • Failure of the heart's pumping ability reduces blood output and MAP.

Obstructive Shock Mechanism

  • Blockage reduces circulation return, decreasing stroke volume and cardiac output leading to lower MAP.

Neurogenic Shock Mechanism

  • Central nervous system damage leads to vasodilation, loss of peripheral resistance, and reduced venous return.

Septic and Anaphylactic Shock Comparison

  • Both involve systemic vasodilation and increased capillary permeability.

  • Can occur in response to pathogens or allergens, leading to low MAP and decreased perfusion.

Manifestations of Shock

  • Signs include marked hypotension, oliguria, poor tissue perfusion, nausea, and fainting.

  • Adaptive responses activate sympathetic nervous system:

    • Increased heart rate, pallor, clamminess, emotional responses.

Manifestations of Septic Shock

  • Symptoms include fever, edema, and elevated laboratory markers:

    • White blood cell count (WBC).

    • Lactate levels.

    • C-reactive protein.

    • Blood culture results.

Treatment of Shock

  • Address underlying causes of shock, particularly for sepsis:

    • Broad-spectrum antibiotics, reassessing after blood cultures.

    • Fluid resuscitation for hypotension.

    • Vasopressors if necessary for blood pressure management.

    • Oxygen delivery for hypoxia.

    • Fibrinolytic drugs for coagulation issues.

    • Bicarbonate infusion for addressing acidosis; monitor blood sugar levels.

Types of Shock Summary

  1. Hypovolaemic Shock: Caused by a sudden reduction in blood volume.

  2. Cardiogenic Shock: Heart failure.

  3. Obstructive Shock: Blockage to circulation.

  4. Neurogenic Shock: Loss of vasomotor tone.

  5. Septic Shock: Pathogen-induced systemic inflammation.

  6. Anaphylactic Shock: Allergic response leading to systemic effects.

Part 3: Progressive (Septic) Shock Overview

  • The cascade of dysfunction leading from sepsis to septic shock includes severe inflammatory responses, organ dysfunctions, and potential multi-organ failure.