Septic shock is a very serious medical condition caused by decreased tissue perfusion and oxygen delivery as a result of infection and sepsis. It can cause multiple organ failure and death. Its most common victims are children, immunocompromised individuals, and the elderly, as their immune systems cannot deal with the infection as effectively as those of healthy adults. The mortality rate from septic shock is approximately 50%.

Definition of septic shock

To diagnose septic shock the following two criteria must be met:

1. Evidence of infection, through a positive blood culture.
2. Refractory hypotension - hypotension despite adequate fluid resuscitation and cardiac output.
• In adults it is defined as a systolic blood pressure < 90 mmHg, or a MAP < 60 mmHg, without the requirement for inotropic support, or a reduction of 40 mmHg in the systolic blood pressure from baseline.
• In children it is BP < 2 SD of the normal blood pressure.

In addition to the two criteria above, two or more of the following must be present:

• Hyperventilation (high respiratory rate) > 20 breaths per minute or, on blood gas, a P_aCO₂ less than 32 mmHg.
• White blood cell count < 4000 cells/mm³ or > 12000 cells/mm³ (< 4 x 10⁹ or > 12 x 10⁹ cells/L).

Types

A subclass of distributive shock, shock refers specifically to decreased tissue perfusion resulting in end-organ dysfunction. Cytokines TNFα, IL-1β, IL-6 released in a large scale inflammatory response results in massive vasodilation, increased capillary permeability, decreased systemic vascular resistance, and hypotension. Hypotension reduces tissue perfusion pressure and thus tissue hypoxia ensues. Finally, in an attempt to offset decreased blood pressure, ventricular dilatation and myocardial dysfunction will occur.

Causes

The process of infection by bacteria or fungi can result in systemic signs and symptoms that are variously described. In rough order of increasing severity, these are bacteremia or fungemia; septicemia; sepsis, severe sepsis or sepsis syndrome; septic shock; refractory septic shock; multiple organ dysfunction syndrome, and death.

The condition develops as a response to certain microbial molecules which trigger the production and release of cellular mediators, such as tumor necrosis factors (TNF); these act to stimulate immune response. Besides TNFα, other cytokines involved in the development of septic shock include interleukin-1β, interleukin-6 and interleukin-8.

Treatment

Treatment primarily consists of the following.

1. Volume resuscitation.
2. Early antibiotic administration.
3. Rapid source identification and control.
4. Support of major organ dysfunction.

Among the choices for pressors, a randomized controlled trial concluded that there was no difference between norepinephrine (plus dobutamine as needed for cardiac output) versus epinephrine.

However dopamine has more beta adrenergic activity and therefore is more likely to cause arrhythmia or myocardial infarction.

Antimediator agents may be of some limited use in severe clinical situations:

• Corticosteroids, especially if combined with a mineralocorticoid, can reduce mortality among patients who have relative adrenal insufficiency.
• Recombinant activated protein C (drotrecogin alpha) has been shown in large randomized clinical trials to be associated with reduced mortality (Number needed to treat (NNT) of 16) in patients with multi-organ failure. If this is given, heparin should probably be continued.

References

See also

• Anaphylactic shock
• Cardiogenic shock
• Neurogenic shock
• Sepsis
• Shock
• Systemic inflammatory response syndrome (SIRS)

Septic shock is a very serious medical condition caused by decreased tissue perfusion and oxygen delivery as a result of infection and sepsis. It can cause multiple organ failure and death. Its most common victims are children, immunocompromised individuals, and the elderly, as their immune systems cannot deal with the infection as effectively as those of healthy adults. The mortality rate from septic shock is approximately 50%.

Definition of septic shock

To diagnose septic shock the following two criteria must be met:

1. Evidence of infection, through a positive blood culture.
2. Refractory hypotension - hypotension despite adequate fluid resuscitation and cardiac output.
• In adults it is defined as a systolic blood pressure < 90 mmHg, or a MAP < 60 mmHg, without the requirement for inotropic support, or a reduction of 40 mmHg in the systolic blood pressure from baseline.
• In children it is BP < 2 SD of the normal blood pressure.

In addition to the two criteria above, two or more of the following must be present:

• Hyperventilation (high respiratory rate) > 20 breaths per minute or, on blood gas, a P_aCO₂ less than 32 mmHg.
• White blood cell count < 4000 cells/mm³ or > 12000 cells/mm³ (< 4 x 10⁹ or > 12 x 10⁹ cells/L).

Types

A subclass of distributive shock, shock refers specifically to decreased tissue perfusion resulting in end-organ dysfunction. Cytokines TNFα, IL-1β, IL-6 released in a large scale inflammatory response results in massive vasodilation, increased capillary permeability, decreased systemic vascular resistance, and hypotension. Hypotension reduces tissue perfusion pressure and thus tissue hypoxia ensues. Finally, in an attempt to offset decreased blood pressure, ventricular dilatation and myocardial dysfunction will occur.

Causes

The process of infection by bacteria or fungi can result in systemic signs and symptoms that are variously described. In rough order of increasing severity, these are bacteremia or fungemia; septicemia; sepsis, severe sepsis or sepsis syndrome; septic shock; refractory septic shock; multiple organ dysfunction syndrome, and death.

The condition develops as a response to certain microbial molecules which trigger the production and release of cellular mediators, such as tumor necrosis factors (TNF); these act to stimulate immune response. Besides TNFα, other cytokines involved in the development of septic shock include interleukin-1β, interleukin-6 and interleukin-8.

Treatment

Treatment primarily consists of the following.

1. Volume resuscitation.
2. Early antibiotic administration.
3. Rapid source identification and control.
4. Support of major organ dysfunction.

Among the choices for pressors, a randomized controlled trial concluded that there was no difference between norepinephrine (plus dobutamine as needed for cardiac output) versus epinephrine.

However dopamine has more beta adrenergic activity and therefore is more likely to cause arrhythmia or myocardial infarction.

Antimediator agents may be of some limited use in severe clinical situations:

• Corticosteroids, especially if combined with a mineralocorticoid, can reduce mortality among patients who have relative adrenal insufficiency.
• Recombinant activated protein C (drotrecogin alpha) has been shown in large randomized clinical trials to be associated with reduced mortality (Number needed to treat (NNT) of 16) in patients with multi-organ failure. If this is given, heparin should probably be continued.

References

See also

• Anaphylactic shock
• Cardiogenic shock
• Neurogenic shock
• Sepsis
• Shock
• Systemic inflammatory response syndrome (SIRS)