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Introduction Introduction
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Pathophysiology of infection Pathophysiology of infection
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Inflammatory cascade Inflammatory cascade
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Early phase Early phase
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Late phase Late phase
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Anti-inflammatory cascade Anti-inflammatory cascade
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Coagulation cascade Coagulation cascade
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Anticoagulation cascade Anticoagulation cascade
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Antithrombin Antithrombin
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TFPI TFPI
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APC APC
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Fibrinolysis Fibrinolysis
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Epidemiology Epidemiology
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Clinical features and criteria for diagnosis Clinical features and criteria for diagnosis
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Differential diagnosis and clinical investigation Differential diagnosis and clinical investigation
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Treatment of sepsis Treatment of sepsis
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Antibiotics Antibiotics
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Source control Source control
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Early goal-directed resuscitation Early goal-directed resuscitation
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Treatment of hypotension Treatment of hypotension
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Corticosteroid treatment Corticosteroid treatment
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Eritoran tetrasodium, anti-Toll-like receptor (TLR)-4 Eritoran tetrasodium, anti-Toll-like receptor (TLR)-4
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Drotrecogin alfa (activated) or recombinant human activated protein C Drotrecogin alfa (activated) or recombinant human activated protein C
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Volume-limited and pressure-limited mechanical ventilation strategy Volume-limited and pressure-limited mechanical ventilation strategy
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Preventing complications and nosocomial infections Preventing complications and nosocomial infections
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Prognosis Prognosis
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Areas of uncertainty Areas of uncertainty
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Further reading Further reading
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7.1.2 Physiological changes, clinical features, and general management of infected patients
Get access-
Published:May 2010
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This version:May 2012
Updated in this version:
July 30, 2015: This chapter has been re-evaluated and remains up-to-date. No changes have been necessary.
Update:
New proinflammatory cytokines IL-17 and macrophage migration inhibitory factor.
Immunosuppression in late sepsis.
Procoagulant-anticoagulant and inflammatory interactions.
Vasopressin—role in septic shock.
Role of corticosteroid insufficiency and low-dose corticosteroid therapy.
Withdrawal of drotrecogin alfa (activated) or recombinant human activated protein C.
Failure of eritoran tetrasodium, anti-Toll-like receptor (TLR)-4.
Cite
Extract
Essentials
Introduction
The term sepsis describes the physiological consequences of the activation of the systemic inflammatory cascade that occurs in infected patients. The cascade of events in response to infectious stimuli has been well characterized using both animal and human models. This response is the main focus of this chapter. Other aspects of sepsis, including epidemiology, clinical features, treatment, prognosis, and the controversial role of corticosteroids and tight glycaemic control will also be addressed.
Pathophysiology of infection
Initial investigations suggested that inflammatory cytokines mediated the physiological responses seen in patients with sepsis. However, information from studies of the coagulation system in sepsis and the subsequent examination of autopsy specimens demonstrated microthrombi in the arterioles and venules of various organs, suggesting that the coagulation system played at least some role in the pathophysiology. It is now clear that the inflammatory and coagulation systems are intricately linked and homeostasis of both is altered in infected patients.
July 30, 2015: This chapter has been re-evaluated and remains up-to-date. No changes have been necessary.
Update:
New proinflammatory cytokines IL-17 ...More
July 30, 2015: This chapter has been re-evaluated and remains up-to-date. No changes have been necessary.
Update:
New proinflammatory cytokines IL-17 and macrophage migration inhibitory factor.
Immunosuppression in late sepsis.
Procoagulant-anticoagulant and inflammatory interactions.
Vasopressin—role in septic shock.
Role of corticosteroid insufficiency and low-dose corticosteroid therapy.
Withdrawal of drotrecogin alfa (activated) or recombinant human activated protein C.
Failure of eritoran tetrasodium, anti-Toll-like receptor (TLR)-4.
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