Classification
of wounds
Potential
for infection
The best measure of wound contamination at the end of an operation, and
the risk of developing infection, is to sample tissue in the wound edge.
Bacteria will already be affected if antibiotic prophylaxis has been given, but
the theoretical degree of contamination relates well to infection rates (Table
7.6). When wounds are heavily contaminated or an incision is made into an
abscess, continuing prophylaxis as therapy is justified. Infection rates after
nonprosthetic clean surgery may be higher if looked for. Antibiotic prophylaxis
is controversial.
Bacteria
involved in wound infection
Streptococci form chains and are Gram positive on staining (Fig.
7.16).
The most important is the 13-haemobytic streptococcus which resides in the
pharynx of 5—10 per cent of the population. It is in group A of the Lancefiebd
A—G carbohydrate antigens. The alternative name of Streptococcus pyogenes is
deserved because of its tendency to spread (cellubitis) and to cause tissue
destruction through release of
Staphylococci
form clumps and are Gram positive (Fig. 7.17). Staphylococcus aureus is
the most important pathogen in this group and resides in the nasopharynx of up
to 15 per cent of the population. It can cause exogenous suppuration in wounds
(and implanted prosthetics), and MRSA can be involved in epidemics. Doctors and
nurses may need to be swabbed and carriers identified and treated in an
epidemic. Infections are usually localised (see Wound abscess above). Most
hospital S. aureus strains are now f3-lactamase producers and are
resistant to penicillin. Sensitivity to flucloxacillin, vancomycin,
aminoglycosides, some cephabosporins and fusidic acid (used in osteomyelitis) is
still high.
Staphylococcus
epidermidis (syn. albus and
most conventionally coagulase-negative Staphylococcus) was regarded
Clostridial
organisms are Gram-positive, obligate anaerobes which produce resistant spores (Fig.
7.18). Clostridium perfringens is the cause of gas gangrene
(Specific wound infections above). Clostridium tetani causes tetanus
following implantation in the tissues or a wound by release of the exotoxin
tetanospasmin. A short prodromal period is related to development of severe
spasms including opsithotonus, respiratory arrest and death. A longer prodromal
period of 4—5 weeks is associated with a much milder form of the
disease. Prophybaxis with toxoid is the best preventative treatment but, once
established, minor débridement with benzyl penicillin and rebaxants (even with
ventilation) may be required. The use of antitoxin is controversial.
Clostridium
difficile is the cause of
pseudomembranous colitis but is not involved in wound infection.
Aerobic
Gram-negative bacilli (AGNB) are normal inhabitants of large bowel. Escherichia
coli and Klebsiella spp. are lactose fermenting; Proteus is
nonlactose fermenting. Most organisms in this group act in synergy with Bacteroides
to cause wound infections after bowel operations (in particular
appendicitis, diverticubitis and peritonitis). The pseudomonads tend to cobonise
burns and tracheostomy wounds, as well as the urinary tract (all members of this
group are a cause of urinary tract infection). Pseudomonads may be regarded as
markers and cobonise wards and intensive care units from which they may be
difficult to eradicate. Surveillance of cross-infection is important in
outbreaks. Hospital strains become resistant to 3-lactamase which can be
transferred by pbasmids and individual sensitivity testing may be needed. Wound
infections only need antibiotic therapy when there is progressive or spreading