Paper I
Question
Define shock. Classify shock. Discuss the etiopathogenesis of septic shock. Discuss the different stages of shock. (1+4+5+5)
Answer
Definition of shock
- Shock is a state of systemic hypoperfusion of tissues, resulting from either reduced cardiac output or reduced effective circulating blood volume, leading to cellular hypoxia and, if uncorrected, irreversible cell injury and multi-organ failure
Classification of shock
- Hypovolaemic shock — inadequate circulating volume from loss of red cell mass and plasma (haemorrhage) or plasma alone (burns, dehydration from vomiting/diarrhoea, excessive diuretic use, acute pancreatitis)
- Cardiogenic shock — acute circulatory failure from a sudden fall in cardiac output despite normal blood volume, from deficient emptying (myocardial infarction, cardiomyopathy, cardiac rupture, arrhythmia), deficient filling (cardiac tamponade), or outflow obstruction (pulmonary embolism, tension pneumothorax, dissecting aortic aneurysm)
- Septic (toxaemic) shock — from severe bacterial infection, most often Gram-negative septicaemia (endotoxic shock — E. coli, Klebsiella, Pseudomonas), less often Gram-positive (exotoxic shock — streptococci, pneumococci)
- Other types: traumatic shock (initially hypovolaemic, with ongoing plasma loss into injured tissue even after haemorrhage is controlled); neurogenic shock (interrupted sympathetic vasomotor supply — high cervical cord injury, high spinal anaesthesia, severe head injury); hypoadrenal shock (failure of the normal stress response from adrenal insufficiency)
(Note: anaphylactic shock, a Type I IgE-mediated hypersensitivity phenomenon, is conventionally classified separately from “true”/secondary circulatory shock, since its underlying mechanism is immunological rather than a primary derangement of blood volume, cardiac output, or septic mediator release — though it produces a similar end-state of hypotension and hypoperfusion.)
Etiopathogenesis of septic shock
- Most commonly triggered by Gram-negative bacterial infection (endotoxin/LPS) or Gram-positive bacterial exotoxins/superantigens
- Pathogen-associated molecular patterns (e.g., LPS) bind pattern recognition receptors (e.g., TLR4) on innate immune cells, triggering a massive systemic release of pro-inflammatory cytokines (TNF-α, IL-1, IL-6) — the “cytokine storm”
- This produces:
- Widespread vasodilatation and hypotension
- Increased vascular permeability, causing fluid loss into the interstitium
- Activation of the coagulation cascade, potentially leading to disseminated intravascular coagulation
- Myocardial depression
- Endothelial injury and metabolic derangements (hypoglycaemia in later stages)
- Progressive hypoperfusion leads to multi-organ dysfunction and, if uncorrected, death
Stages of shock
- Non-progressive (compensated) stage: Compensatory neurohumoral mechanisms (baroreceptor reflexes, catecholamine release, renin-angiotensin activation) maintain perfusion to vital organs (heart, brain); tachycardia, peripheral vasoconstriction
- Progressive stage: Compensatory mechanisms begin to fail; tissue hypoperfusion causes widespread tissue hypoxia and metabolic (lactic) acidosis, which further impairs vascular tone; vasodilatation and worsening hypotension ensue
- Irreversible stage: Cellular injury becomes so severe that even correction of the haemodynamic abnormality cannot prevent death; widespread cell death, lysosomal enzyme leakage, and multi-organ failure occur