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Background:
Over many years, the terms sepsis and septicemia have referred to
several ill-defined clinical conditions present in a patient with
bacteremia. Definitions have not changed greatly since 1914, when
Schottmueller wrote, Septicemia is a state of microbial invasion from
a portal of entry into the blood stream which causes sign of illness.
In practice, these 2 terms have often been used interchangeably;
however, only about half of patients with signs and symptoms of sepsis
have positive results on blood culture. Furthermore, not all patients
with bacteremia have signs of sepsis. It follows, therefore, that sepsis
and septicemia are not in fact identical.
In the past few decades, the discovery of endogenous mediators of the
host response has led to the recognition that the clinical syndrome of
sepsis is the result of excessive activation of host defense mechanisms
rather than the direct effect of microorganisms. Sepsis and its sequelae
represent a continuum of clinical and pathophysiologic severity.
Serious bacterial infections at any site in the body (see the image
below), with or without bacteremia, are usually associated with
important changes in the function of every organ system in the body.
These changes are mediated mostly by elements of the host immune
system against infection. Shock is deemed present when volume
replacement fails to increase blood pressure to acceptable levels and
when associated clinical evidence indicates inadequate perfusion of
major organ systems, with progressive failure of organ system
functions. Although hyperlactecemia is commonly seen in severe
sepsis, its relationship to hypoperfusion is questionable and is more
often due to the acute inflammatory state, impaired lactate clearance,
and nonoxidative phosphorylation lactate production.
Multiple organ dysfunctions, the extreme end of the continuum, are
incremental degrees of physiologic derangements in individual organs
(ie, processes rather than events). Alteration in organ function can vary
widely, ranging from a mild degree of organ dysfunction to frank organ
failure. (See Multiple Organ Failure of Sepsis, Systemic Inflammatory
Response Syndrome (SIRS), Toxic Shock Syndrome, and Septic
Thrombophlebitis .)
This article does not cover sepsis of the neonate or infant. Special
consideration must be given to neonates, infants, and small children
with regard to fluid resuscitation, appropriate antibiotic coverage,
intravenous (IV) access, and vasopressor therapy. (See Neonatal
Hypovolemic shock
Obstructive shock
Distributive shock
Cardiogenic shock
Note that a patient can have a severe infection without meeting SIRS
criteria; conversely, SIRS criteria may be present in the setting of many
other illnesses not caused by an infectious pro cess.