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| Septic shock Classification and external resources |
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| ICD-10 | A41.9 |
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| ICD-9 | 785.52 |
Septic shock is a very serious medical condition caused by decreased tissue perfusion and oxygen delivery as a result of infection and sepsis, though the microbe may be systemic or localized to a particular site[1]. It can cause multiple organ failure and death[1]. 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% [1].
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Definition of septic shock
To diagnose septic shock[2] the following two criteria must be met:
- Evidence of infection, through a positive blood culture.
- 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:
- Tachypnea (high respiratory rate) > 20 breaths per minute or, on blood gas, a PaCO2 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[1]. Finally, in an attempt to offset decreased blood pressure, ventricular dilatation and myocardial dysfunction will occur[1].
Causes
The process of infection by bacteria or fungi can result in systemic signs and symptoms that are variously described. Approximately 70% of septic shock cases are due to gram-negative bacilli that produce endotoxins[1]. 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.
- Volume resuscitation.
- Early antibiotic administration.
- Rapid source identification and control.
- 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.[3]
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.[4]
- 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.[5] If this is given, heparin should probably be continued.[6]
See also
- Anaphylactic shock
- Cardiogenic shock
- Neurogenic shock
- Sepsis
- Shock
- Systemic inflammatory response syndrome (SIRS)
References
- ^ a b c d e f Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; & Mitchell, Richard N. (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 102-103 ISBN 978-1-4160-2973-1
- ^ Tslotou AG, Sakorafas GH, Anagnostopoulos G, Bramis J. Septic shock; current pathogenetic concepts from a clinical perspective. Med Sci Monit. 2005 Mar;11(3):RA76-85. PMID 15735579 Full Text.
- ^ Annane D, Vignon P, Renault A, et al (2007). "Norepinephrine plus dobutamine versus epinephrine alone for management of septic shock: a randomised trial". Lancet 370 (9588): 676–84. doi:. PMID 17720019.
- ^ Annane D, Sebille V, Charpentier C, Bollaert PE, Francois B, Korach JM, Capellier G, Cohen Y, Azoulay E, Troche G, Chaumet-Riffaut P, Bellissant E. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA. 2002 Aug 21;288(7):862-71. PMID 12186604
- ^ Bernard GR, Vincent JL, Laterre PF, LaRosa SP, Dhainaut JF, Lopez-Rodriguez A, Steingrub JS, Garber GE, Helterbrand JD, Ely EW, Fisher CJ Jr; Recombinant human protein C Worldwide Evaluation in Severe Sepsis (PROWESS) study group. Efficacy and safety of recombinant human activated protein C for severe sepsis. N Engl J Med. 2001 Mar 8;344(10):699-709. PMID 11236773
- ^ Levi M, Levy M, Williams MD, et al (2007). "Prophylactic heparin in patients with severe sepsis treated with drotrecogin alfa (activated)". Am. J. Respir. Crit. Care Med. 176 (5): 483–90. doi:. PMID 17556722.
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- This page was last modified on 9 September 2008, at 08:19.
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