Looking at SIRS more
specifically, there are four key response mediators at work - neutrophils,
macrophages, platelets, and endothelial cells. Some are working directly on
platelet aggregation; others are stimulated to produce the chemical mediators. There are five sub-groups of these chemical
mediators, cytokines, plasma enzyme cascades, lipid mediators; toxic oxygen
related mediators, and two unclassified mediators, nitric oxide and proteases.
In a synergistic effort to fight the triggering mechanism, our body mounts a
hormonal response as well. The stress hormones catecholamines, glucagon,
cortisol and growth hormone are released along with suppression of the thyroid
gland and a hormonal suppression of the fluid electrolyte and balances
(Kleinpell and Burns 2007).
Sepsis is a manifestation of SIRS
in the presence of a known infection, usually bacterial in nature (Pugin 2008).
Each year approximately 215,000 deaths are reported due to severe sepsis. It is also associated with a mortality rate
of 28%-50%. Annually, it is estimated that cost of treating patients with
sepsis is about 16 billion dollars yearly just in the US. Risk factors for sepsis include extremes of
age, surgical or invasive procedures, malnutrition, and use of broad-spectrum
antibiotics, chronic illness, immune deficiency disorders and increasing
numbers of drug resistant microorganisms (Kleinpell 2003).
As a manifestation of SIRS,
sepsis has a continuation of the systemic exposure of the pro-inflammatory
cytokines. This can overwhelm the actions of the anti-inflammatory cytokines.
Excessive systemic inflammation occurs, leading to impaired tissue function and
organ damage. The pro-inflammatory cytokines (interleukin and tumor necrosis
factor-?) that are now being produced without regulation by the
anti-inflammatory cytokines stimulate the release of tissue factor, a cell
surface glycoprotein produced by the monocytes and endothelial cells. This
action triggers the coagulation pathway (Kleinpell 2003), which can lead to
DIC.
Comments (0):