surgical
Recent developments
in surgical sepsis
Every surgical operation is an experiment in bacteriology – Moynihan
Ramya Kalaiselvan
MBBS MPhil FRCS
Gordon Carlson
BSc(Hons) MB ChB
(Hons) MD FRCS
FRCSGen FRCSEd
(Ad Hom)
Department of General
and Colorectal Surgery,
Salford Royal NHS
Foundation Trust,
Manchester, UK
It is almost a century since Moynihan famously
noted that, “every surgical operation is an
experiment in bacteriology.” 1 While the basic
components of that experiment (the host, the
bacterial flora and the factors which alter the
balance between bacterial capacity for invasion
and host resistance) have not changed, the
outcome of surgical procedure, even when
complicated by infection, has improved markedly.
The last century has seen overwhelming advances
in reducing the incidence of surgical (and other)
infections, as well as an ability to treat them more
effectively. These have resulted from (inter alia),
better nutrition and overall public health, a better
understanding of factors which contribute to
infection such as temperature maintenance,
oxygenation, blood glucose control, and aseptic
technique, and of course the development of
powerful antibiotics for both prophylaxis and
treatment of infection complicating surgical care.
However, despite these measures, infection
remains a common and life-threatening problem
and the sepsis, which results from this infection,
continues to be a significant cause of avoidable
mortality, morbidity and health expenditure.
Some of the most devastating adverse
consequences of infection result not from the
direct pathogenic effects of the invading bacteria
but from the immunological consequences of the
host response. While a coordinated pro- and
anti-inflammatory response is essential for
localisation, bacterial killing, and resolution,
infection can trigger an overwhelming host
inflammatory response, resulting in shock,
multi-organ dysfunction, and death.
The definitions of sepsis, septic shock, and
organ dysfunction were based on an international
consensus conference, 2 which focused on the
then-prevalent view that sepsis developed as part
of a host systemic inflammatory response
syndrome (SIRS), triggered by an infectious insult,
noting that sepsis could arise in response to
multiple infectious causes and that ‘septicaemia’
was neither a necessary condition nor a helpful
term. It was proposed that sepsis complicated by
organ dysfunction was termed severe sepsis,
which could progress to septic shock, defined as
“sepsis-induced hypotension”, persisting despite
adequate fluid resuscitation or by
hyperlactataemia. In 2001, a second consensus
panel endorsed most of these concepts, with the
caveat that signs of a systemic inflammatory
response, notably tachycardia or an elevated
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white-cell count, also occur in many non-
infectious conditions and therefore are not
helpful in distinguishing sepsis from other
conditions. 3 In addition, severe sepsis and sepsis
were sometimes used interchangeably to describe
the syndrome of infection complicated by acute
organ dysfunction. Attempts to take account of
the fact that critical illness might arise as
a consequence of infection, without the
requirement for the patient necessarily to
exhibit the fever, tachypnoea, tachycardia and
leukocytosis required of SIRS led to a third
International consensus for sepsis and septic
shock, at which sepsis was defined as life-
threatening organ dysfunction caused by
a dysregulated host response to infection. 4
This new definition also recommended using