Physiology
and manifestation
Background. It is clear that the Egyptians knew about infection. They
certainly were able to prevent putrefaction which is testified in their skills
of mummification. Their medical papyruses also describe the use of salves and
antiseptics to prevent wound infections. This had also been known, although less
well documented, by the Assyrians and the Greeks, particularly in Hippocratic
teachings, which had refined the use of antimicrobial practice. The use of wine
and vinegar to irrigate open infected wounds before successful secondary closure
was practised widely. Common to all these cultures, and the later Roman
practitioners, was a dictum that whenever pus developed in an infected wound it
needed to be drained.
Galen
recognised that localisation of infection (suppuration) in wounds inflicted in
the gladiatorial arena often heralded recovery, particularly after drainage of
the pus (pus bonum et Iaudabile). Sadly, this dictum was misinterpreted
by many until well into the Renaissance; many practitioners actually promoted
suppuration in wounds by application of many noxious substances, including
faeces, in the misbelief that healing could not occur without pus formation.
There was occasional light in this long, dark tunnel: Theodoric of Cervia,
Ambroise Pare and Guy de Chauliac all realised that clean wounds, closed
primarily, could heal without infection or suppuration.
The
understanding of the causes of infection came in the nineteenth century~
Microbes had been seen under the microscope, but Koch laid down the first
definition of infective disease (Koch’s postulates). These were basically
that a particular microbe could be considered responsible for an infection when
it was found in adequate numbers in a septic focus, could be cultured in pure
form from specimens taken from the focus and could cause similar lesions when
injected into another host.
The
Austrian obstetrician, Ignac Semmelwe is, showed that maternal mortality caused
by puerperal sepsis could be reduced from over 10 per cent to under 2 per cent
by the simple act of hand washing between postmortem examinations and the
delivery suite.
Louis
Pasteur recognised that microorganisms spoilt wine and Joseph Lister applied
this knowledge to the reduction of organisms in compound fractures allowing
surgery without infection. However, his toxic phenol spray and principles of
antiseptic surgery soon gave way to aseptic surgery at the turn of the century
— a technique still employed in modern operating theatres.
The antibiotic penicillin, the discovery of which is ascribed to
Alexander Fleming, was isolated by Florey and Chain. The first patient to
receive penicillin was Police Constable Alexander, who had a severe
staphylococcal illness. He made a partial recovery before the penicillin ran out
but later relapsed and died. Since then there has been a huge increase in
antibiotic groups with improved antibacterial spectra. Few staphylococci are now
sensitive to penicillin but streptococcal illnesses respond, although they are
seen increasingly rarely in surgical practice. Many bacteria develop resistance
through the acquisition of beta-lactamases which can break up the 3-lactam ring,
common in the formula of many antibiotics. In general surgery, the synergy of
aerobic Gram-negative bacilli with anaerobic Bacteroides spp. presents
the most challenging infection. Wide-spectrum antibiotics can be given
empirically to treat such infections, or more specific, narrow-range antibiotics
given based on culture and sensitivity. The range of surgery now practised owes
much to rational antibiotic use —faecal peritonitis may not be considered to
be lethal, and wounds made in the presence of such contamination can heal
primarily without infection in 80—90 per cent of patients. Patients undergoing
prosthetic surgery or who are immunosuppressed can be spared infection in
their wounds by the appropriate use of prophylactic antibiotics.
Bacteria are normally prevented from causing infection in tissues by
intact epithelial surfaces, but these are broken down by surgery. In addition to
this mechanical barrier, there are other protective mechanisms, i.e. chemical
(such as the low gastric pH), humoral (antibodies, complement and opsonins) and
cellular (phagocytic cells, macrophages, polymorphonuclear cells and killer
lymphocytes).
Host
response is weakened by malnutrition which may present as obesity as well as
recent rapid weight loss (Table
When
enteral feeding is suspended in the perioperative period, the gut rapidly
becomes colonised and bacteria, particularly Gram-negative bacilli, translocate
to mesenteric
Local and systemic
manifestation
Infection of a wound can be defined as the invasion of organisms
through tissues following a breakdown of local and systemic host defences.
Sepsis is the systemic manifestation of a documented infection, the signs and
symptoms of which may also be caused by multiple trauma, burns or pancreatitis.
Bacteraemia should not be confused with this systemic inflammatory response
syndrome (SIRS) although the two may coexist (see Table
7.2). Septic
manifestations are mediated by release of cytokines [such as interleukins (IL)
and tumour necrosis factor (TNF)] and other modules from polymorphonuclear and
phagocytic cells and, in its most severe form, presents as multiple system organ
failure (MSOF). Infection may cause SIRS through the release of
lipopolysaccharide endotoxin from the walls of dying Gram-negative bacilli
(mainly Escherichia coli) and other toxins, which in turn causes release
of cytokines (Fig. 7.3). A reduced defence to wound infection follows.
Pathogens resist host defences by release of toxins, particularly in
unfavourable anaerobic conditions, which favours their spread in wound
infections. Clostridium perfringens, which is responsible for gas
gangrene, releases many spreading proteases such as hyaluronidase, lecithinase
and haemolysin. Many resistant pathogens can produce beta-lactamases which destroy
the beta lactam ring of antibiotics. This resistance can be acquired and passed on
through plasmids.
A
major wound infection is defined as a wound which discharges pus and may need a
secondary procedure to be sure of adequate drainage (Fig.
7.4). There may be
systemic signs of tachycardia pyrexia and a raised white count (SIRS). The
patient may be delayed in returning home beyond the planned day. Minor wound
infections may discharge pus or infected serous fluid but should not be
associated with excessive discomfort, systemic signs or delay in return home (Fig. 7.5).
The differentiation of major and minor wound infection is
important in audit trials of antibiotic prophylaxis and is of relevance to
‘league tables’ of hospital infection as major wound infections must be
accounted for.