Sepsis is a clinical syndrome characterized by fever, leukocytosis or
leukopenia, tachycardia, increased cardiac index, reduced systemic vas
cular resistance, and hypercatabolism. It is generally believed to be
a response to invasive infections, although an infectious source canno
t always be identified in patients with sepsis. Over an 18-month perio
d 287 patients were admitted for more than 48 hours to a noncardiac ad
ult surgical intensive care unit. Data were collected concurrently and
recorded in a computer database. Seventy-three patients (25%) develop
ed sepsis, and 50 (68% of those with sepsis) had bacteremia, with a me
an of 1.5 organisms and 3.5 positive blood cultures per patient. Only
22 of 50 patients with bacteremia had a potential infectious source, a
nd there was a concordance of cultures from the putative source and th
e blood stream in only 10 patients. Forty-one patients with sepsis (56
%) had no apparent infectious source, but 28 of these (68%) had bacter
emia, often with multiple organisms. Forty of the 73 patients with sep
sis died in the hospital. Mortality in sepsis could not be predicted b
y the presence of an infectious source (P > 0.35) and was not related
to bacteremia (P > 0.75). Mortality was strongly associated with the d
evelopment of multiple organ failure (P < 0.0001). Sepsis is a generic
response to a number of physiologic insults and does not require infe
ction for expression. This inflammatory response may have survival val
ue by increasing oxygen delivery to sites of injury, but uncontrolled
inflammation may cause dysfunction in several vital organ systems. The
associated immunosuppression results in bacterial colonization of sit
es from which bacteria ordinarily are excluded. These colonizations ar
e not invasive infections, they are not necessarily the cause of sepsi
s, and they do not affect the outcome of patients with sepsis.