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Monday, March 4, 2013

Shock - Definition, Types, Morphology, Stages and Clinical Course

Find out everything you need to know about shock: definition, types, pathogenesis, morphological changes in the body, clinical features, stages and treatment of cardiogenic, hypovolaemic and septic shock...


What is SHOCK?

Shock is a disorder that result from systemic hypo-perfusion due to reduction either in cardiac output or in the effective circulating blood volume.
Common Causes of shock are profuse haemorrhage, large myocardial infarction, severe diarrhoea, severe vomiting, extensive burn, trauma, bacterial sepsis, and pulmonary embolism.

Effects of Hypo-perfusion:

Due to hypo-perfusion there is less supply (hypoxia) of oxygen and nutrients to the cells and tissues and inadequate removal of metabolites. 
Hypoxia leads to less aerobic and more anaerobic metabolism with increased production of lactic acid. At first there is reversible injury to cells which passes on to irreversible injury with persistence or severe shock (see stages of shock below). Finally there may be necrosis of cells or even death of the patient.



Types of shock:

  • Cardiogenic shock
  • Hypovolaemic shock
  • Septic Shock




Cardiogenic shock:

Cardiogenic shock is caused by any form of severe heart failure:
Cardiogenic shock
  1. Myocardial infarction
  2. Arrhythmias
  3. Sudden Mitral regurgitation
  4. Sudden aortic regurgitation
  5. Prosthetic valve dysfunction
  6. Rupture of the heart
  7. Acute massive pulmonary embolism
  8. Cardiac tamponade

How does Cardiac Shock develop?

Cardiac shock develops as a result of myocardial pump failure due to intrinsic myocardial damage, or extrinsic obstruction of blood flow.


Development of Cardiac Shock
Development of Cardiac Shock



Hypovolaemic Shock:

Hypovolaemic shock
Hypovolaemic shock occurs due to any condition that leads to a major reduction in blood volume: loss of blood, plasma, or fluid.

Causes of hypovaemic shock:

  1. Haemorrhagic Shock - occurs with acute loss of blood of aboput 1250 ml (about 25% of total blood)
  2. Traumatic Shock - Primarily due to blood loss
  3. Severe burn - due to loss of plasma
  4. Sever diarrhoea - loss of fluid
  5. Sever vomiting - loss of fluid
  6. Others - Diabetic coma, Acute pancreatitis, Peritonitis, acute poisoning

How does Hypolaemic shock develop?


Development of Hypovolaemic Shock

Septic Shock:

Septic shock is caused by systemic microbial infection which causes peripheral vasodilation and pooling of blood- leading to stasis of blood > hypoperfusion > shock.

Causes of septic shock: 

Septic shock results mostly in overwhelming microbial infection from a initially localized infection (eg abscess, pneumonia).


The organisms that usually cause septic shock are:
  1. Endotoxin producing Gram negative bacilli(most common). They produce endotoxin  and so it is also called endotoxic shock. Endotoxins are bacterial cell wall lipopolysaccharides (LPS) having a toxic lipid core and a polysaccharide coat (including O antigens). LPS are released when the cell walls of bacteria are degraded.
  2. Common Gram negative bacilli are Escherichia coli, Lebsiella pneumoniae, Proteus, Pseudomonus aeruginosa. 
  3. Gram positive septicaemia.
  4. Meningococcal septicaemia.
  5. Super-antigens: Super-antigens are substance (as an enterotoxin) that acts as an antigen capable of stimulating much larger numbers of T cells than an ordinary antigen. These cause syndromes similar to septic shock, eg toxic shock syndrome toxin-1 of Staphyloccus aureus.
  6. Fungal sepsis.
Septic shock

Pathogenesis of Septic Shock:

Septic shock occurs with moderate to severe infections. Endotoxic shock develops with high quantities of LPS. LPS binds to blood LPS-binding protein forming LPS-protein complex. LPS-protein complex binds to CD14 molecules followed by binding of LPS to TLR-4(Toll-like receptor 4) on monocytes, macrophages, and endothelial cells. These cells are activated and a large number of cytokine mediators are released by them. LPS induces production of TNF by mononuclear phagocytes. TNF induces production of IL-1 by mononuclear phagocytes. TNF and IL-1 activate endothelial cells to produce IL-6 and IL-8 . Cytokine induced secondary mediators particularly NO and PAF are produced. LPS and thus cytokines, chemokines, and other mediators in low quantities produce local inflammatory effects. With moderate quantities systemic effects occur. At high quantities syndrome of septic shock occur, which are:
  1. Hypo-tension
  2. Acute respiratory distress syndrome (ARDS)
  3. Disseminated intravascular coagulation (DIC)
  4. Multi-organ system failure, such as failure of kidneys, central nervous system, liver and other organs.

Clinical features of Shock:

Shock is a progressive disorder. If not managed properly it leads to death. Threat to life depends on the cause of shock(eg myocardial infarction, severe haemorrhage, uncontrolled bacterial infection).
The clinical manifestations depend on the cause. Skin is cool, clammy and cyanotic in hypovolemic and cardiogenic shock. Skin may be initially warm and flushed due to peripheral vasodilatation in septic shock. The pulse is weak and more than 100/min. Tachypnoea, hypotension (systolic BP <100 mm Hg), and oliguria (urine output <30ml/hr).
Death may occur rapidly in cases like a large infarct of left ventricle.


Stages of Shock:

Shock is divided into three stages:

1. Non-progressive phase or compensated phase:

During this phase of shock, neurohumoral mechanisms help to maintain cardiac output and blood pressure. These include baroreceptor reflexes, release of catecholamines, activation of renin-angiotensinsystem, and antidiuretic hormone secretion. If recovery occurs then it is labelled "reversible shock".

2. Progressive or de-compensated phase:

If compensatory mechanisms fail to prevent circulatory insufficiency then there is a rapid pulse, further lowering of blood pressure, respiratory difficulties, low urine output (oliguric phase) and metabolic acidosis. Hypoperfusion starts to develop leading to circulatory and metabolic imbalances.

3. Irreversible stage:

The patient deteriorates due to failure of the compensatory mechanisms. There is so severe cellular and tissue injury that death occur even if the haemodynamic defects are corrected.

Morphology changes of the body in Shock:

Kidneys: shows "acute tubular necrosis" due to ischaemic injury. Oliguria, anuria and electrolyte imbalance occur.
Heart: shows sub-endocardial haemorrhages and necrosis of individual myofibres or zonal lesions and scattered contraction bands within myocytes.
Brain: may develop hypoxic (ischaemic) encephalopathy
Lungs: in hypovolaemic shock lungs are usually not affected. In cardiogenic and septic shock there may be severe pulmonary oedema and shock lung (Acute Respiratory Distress Syndrome ARDS)
Liver: may show fatty changes and central necrosis.
Other organs: like gastrointestinal tract, adrenal and pituitary glands may be affected

Treatment of a case of Shock:


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