Septic 🦠⚡️Shock


Septic shock is a severe and potentially fatal condition resulting from sepsis, which occurs when the body’s response to an infection causes widespread inflammation and vasodilation. This inflammation and vasodilation lead to dangerous drops in blood pressure and organ dysfunction, even when fluids are administered. It is a subset of sepsis characterised by profound circulatory, cellular, and metabolic abnormalities that significantly increase mortality.

Definition: Septic shock is defined as sepsis with persisting hypotension requiring vasopressors to maintain MAP ≥ 65 mmHg and having a serum lactate level > 2 mmol/L despite adequate volume resuscitation.

Pathophysiology:
The pathophysiology of septic shock involves a complex interplay of infection, immune response, inflammation, and coagulation abnormalities:

  1. Infection and Immune Response:
  • Pathogen Entry: The process begins with the entry of pathogens (bacteria, viruses, fungi, or parasites) into the body.
  • Recognition: Immune cells recognise these pathogens through pattern recognition receptors (PRRs) on their surface, leading to activation of the immune response.

2. Systemic Inflammation:

  • Cytokine Release: Recognition of pathogens triggers the release of pro-inflammatory cytokines (e.g., TNF-α, IL-1, IL-6) that recruit more immune cells to the site of infection.
  • Endothelial Dysfunction/Damage: Inflammatory cytokines cause endothelial cells lining blood vessels to become activated, leading to increased vascular permeability and leakage of fluid into tissues.

3. Vasodilation and Hypotension:

  • Widespread Vasodilation: Inflammatory mediators cause widespread vasodilation, reducing systemic vascular resistance.
  • Hypotension: The combination of fluid leakage and vasodilation leads to a significant drop in blood pressure, which persists even after adequate fluid resuscitation.

4. Coagulation Abnormalities:

  • Coagulation Cascade Activation: Inflammatory mediators activate the coagulation cascade, resulting in microvascular thrombosis.
  • Disseminated Intravascular Coagulation (DIC): Widespread clotting can lead to the consumption of clotting factors and subsequent bleeding.

5. Organ Dysfunction: (Organ Failure)

  • Hypoperfusion: Reduced blood pressure and fluid leakage impair tissue perfusion, leading to hypoxia and metabolic acidosis.
  • Multi-organ Failure: Prolonged hypoperfusion and hypoxia result in cellular injury and death, causing dysfunction in multiple organs, including the kidneys, liver, lungs, and heart.

Identification:
Early recognition of septic shock is critical for effective treatment. Identification involves clinical assessment and diagnostic testing:

  1. Clinical Symptoms:
  • Persistent hypotension despite fluid resuscitation
  • Signs of poor perfusion (e.g., mottled skin, delayed capillary refill)
  • Altered mental status (confusion, disorientation)
  • Rapid heart rate (weak pulse -tachycardia)
  • Rapid breathing (tachypnea)
  • Low urine output (oliguria)
  • Cold, clammy skin (in later stages)

2. Diagnostic Criteria:

  • Blood Cultures: To identify the causative pathogen.
  • Lactate Levels: Elevated lactate indicates tissue hypoperfusion.
  • Arterial Blood Gases (ABGs): To assess oxygenation, acid-base balance, and metabolic status.

Management:
Management of septic shock focuses on early recognition, rapid administration of antibiotics, fluid resuscitation, and supportive care to stabilise organ function:

  1. Initial Resuscitation:
  • Fluid Resuscitation: Administer 30 mL/kg of IV crystalloid fluids within the first three hours.
  • Vasopressors: Use norepinephrine to maintain MAP ≥ 65 mmHg if hypotension persists after fluid resuscitation.
  • Antibiotics: Administer broad-spectrum antibiotics within one hour of recognising septic shock, then tailor based on culture results.

2. Source Control:

  • Identify and Eliminate Source of Infection: Drain abscesses, remove infected devices, and perform surgery if necessary.

3. Supportive Care:

  • Oxygen Therapy and Mechanical Ventilation: Provide supplemental oxygen or mechanical ventilation for respiratory failure.
  • Renal Replacement Therapy: Dialysis may be necessary for patients with acute kidney injury.
  • Nutritional Support: Ensure adequate nutritional intake through enteral or parenteral feeding.

4. Adjunctive Therapies:

  • Corticosteroids: Consider IV hydrocortisone (200 mg/day) for patients with refractory septic shock.
  • Glucose Control: Maintain blood glucose levels ≤ 10 mmol/L.

5. Monitoring and Follow-up:

  • Frequent Monitoring: Monitor vital signs, urine output, and laboratory parameters regularly to assess response to treatment.
  • Adjust Treatment: Continuously reassess and adjust treatment strategies based on the patient’s clinical status and response to therapy.

Conclusion:
Early identification and prompt, aggressive treatment are crucial to improving outcomes in patients with septic shock. Comprehensive management involves addressing the underlying infection, restoring haemodynamic stability, and providing ongoing support to maintain organ function.

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