Sepsis and septic shock

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

Sepsis, Pediatric Sepsis, Treatment of Sepsis and Septic Shock in

Children, Shock in Pediatrics, and Shock and Hypotension in the
Newborn.)

Shock Classification, Terminology, and Staging

Shock is identified in most patients by hypotension and inadequate
organ perfusion, which may be caused by either low cardiac output or
low systemic vascular resistance. Circulatory shock can be subdivided
into 4 distinct classes on the basis of underlying mechanism and
characteristic hemodynamics, as follows:

Hypovolemic shock

Obstructive shock

Distributive shock

Cardiogenic shock

These classes of shock should be considered and systematically

differentiated before a definitive diagnosis of septic shock is
established.
Hypovolemic shock results from the loss of blood volume caused by
such conditions as gastrointestinal (GI) bleeding, extravasation of
plasma, major surgery, trauma, and severe burns. Patients suffering
from hypovolemic shock demonstrate tachycardia, cool clammy
extremities, hypotension, dry skin and mucous membranes, and poor
turgor.
Obstructive shock results from an intrinsic or extrinsic obstruction of
circulation. Pulmonary embolism and pericardial tamponade both result
in obstructive shock.
Distributive shock is caused by excessive vasodilation and impaired
distribution of blood flow (eg, direct arteriovenous shunting), and it is
characterized by decreased resistance or increased venous capacity
from the vasomotor dysfunction. Patients with this type of shock have
high cardiac output, hypotension, a large pulse pressure, a low
diastolic pressure, and warm extremities with good capillary refill.
These findings on physical examination strongly suggest a working
diagnosis of septic shock.
Cardiogenic shock is characterized by primary myocardial dysfunction,
which renders the heart unable to maintain adequate cardiac output.
Affected patients demonstrate clinical signs of low cardiac output while
showing evidence of adequate intravascular volume. The patients have

cool clammy extremities, poor capillary refill, tachycardia, a narrow

pulse pressure, and low urine output.

Definitions of key terms

The basis of sepsis is the presence of infection associated with a
systemic inflammatory response that results in physiologic alterations
at the capillary endothelial level. The difficulty in diagnosis comes in
knowing when a localized infection has become systemic and requires
more aggressive hemodynamic support. No criterion standard exists
for the diagnosis of endothelial dysfunction, and patients with sepsis
may not initially present with frank hypotension and overt shock.
Clinicians often use the terms sepsis, severe sepsis, and septic shock
without following commonly understood definitions. In 1991, the
American College of Chest Physicians (ACCP) and the Society of Critical
Care Medicine (SCCM) convened a consensus conference to establish
definitions of these and related terms.
Systemic inflammatory response syndrome
The term systemic inflammatory response syndrome (SIRS) was
developed in an attempt to describe the clinical manifestations that
result from the systemic response to infection (fever or hypothermia,
tachycardia, tachypnea, and hyperleukocytosis or leukopenia). Criteria
for SIRS are considered to be met if at least 2 of the following 4 clinical
findings are present:

Temperature higher than 38C (100.4F) or lower than 36C

(96.8F)

Heart rate (HR) higher than 90 beats/min

Respiratory rate (RR) higher than 20 breaths/min or arterial

carbon dioxide tension (PaCO 2) lower than 32 mm Hg

White blood cell (WBC) count higher than 12,000/L or lower

than 4000/L or with 10% immature (band) forms

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.