Physiology and manifestation of Wound Infection
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 concept of a ‘magic bullet’ which could kill microbes but not their host led to early sulphonamide chemotherapy.
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 7.1) Metabolic diseases, diabetes mellitus, uraemia and jaundice may weaken defences, and disseminated cancer may also be included together with immunosuppression caused by radiotherapy, chemotherapy, steroids and acquired immunodeficiency syndrome (AIDS) (Fig 7.1 and Fig 7.2).
When enteral feeding is suspended in the perioperative period, the gut rapidly becomes colonised and bacteria, particularly Gram-negative bacilli, translocate to mesentericnodes. Release of endotoxin may follow, which further increases susceptibility to infection. In these circumstances, nonpathogens become important (opportunism).
The pathogenicity and size of bacterial inoculum also relates to the chance of developing an established wound infection after surgery. Poor surgical technique that leaves devitalised tissue, excessive dead space or haematoma may increase this risk. Foreign materials of any kind, including sutures and drains, promote infection. A logarithm reduction in the number of organisms is needed to cause a wound infection in the presence of a silk suture. These factors need consideration in prosthetic orthopaedic and vascular surgery.
In the first 4 hours after a breach in an epithelial surface and underlying connective tissues made during surgery or trauma, there is a delay before host defences can become mobilised through acute inflammatory, humoral and cellular processes. This period is called the ‘decisive period’ and it is during these first 4 hours after incision that bacterial colonisation and established infection can begin. It is logical that prophylactic antibiotics will be most effective during this time.
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.
The human body harbours approximately 1014organisms. They are released into tissues by surgery, contamination being most severe when a hollow viscus is opened (e.g. colorectal surgery). Any infection which follows may be termed primary, community acquired or endogenous. Exogenous infections are usually hospital acquired (nosocomial) and are secondary, being introduced into the tissues after surgery not during it, unless introduced via inadequately filtered air in the operating theatre.
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.
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