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2015 ; 28
(2
): 227-36
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The coagulopathy of acute sepsis
#MMPMID25590467
Simmons J
; Pittet JF
Curr Opin Anaesthesiol
2015[Apr]; 28
(2
): 227-36
PMID25590467
show ga
PURPOSE OF REVIEW: Sepsis, defined by the presence of infection and host
inflammation, is a lethal clinical syndrome with an increasing mortality rate
worldwide. In severe disease, the coagulation system becomes diffusely activated,
with consumption of multiple clotting factors resulting in disseminated
intravascular coagulation (DIC). When present, DIC portends a higher mortality
rate. Understanding the mechanisms that tie inflammation and diffuse thrombosis
will allow therapeutic interventions to be developed. The coagulopathy of acute
sepsis is a dynamic process that is time and disease burden specific. Whole-blood
testing of coagulation may provide more clinically useful information than the
classical tests. Natural anticoagulants that regulate thrombosis are
downregulated in sepsis. Patients may benefit from the modulation of the
coagulation system when systemic inflammation and hypercoagulopathy exist. Proper
timing of anticoagulant therapy may ultimately lead to decreased incidence of
multisystem organ dysfunction. RECENT FINDINGS: The pathogenesis of coagulopathy
in sepsis is driven by an upregulation of procoagulant mechanisms and
simultaneous downregulation of natural anticoagulants. Inflammation caused by the
invading organism is a natural host defense that cannot be eliminated during
treatment. Successful strategies to prevent multisystem organ dysfunction center
on stratifying patients at high risk for DIC and restoring the balance of
inflammation and coagulation. SUMMARY: The prevention of DIC in septic patients
is a key therapeutic target in preventing death from multisystem organ failure.
Stratifying patients for therapy using thromboelastometry, specific markers for
DIC, and composite scoring systems is an area of growing research.
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