Surgical infections are those best treated by operative intervention or those that follow surgical procedures and occur in the operative wound or at a distant site. Surgical infections may be classified as primary infections occurring spontaneously, those following tissue injuries, or those following planned surgical trauma such as an operation.

The unique feature of all surgical infections is tissue necrosis. In post-traumatic surgical infection tissue necrosis is induced by mechanical or other physical trauma, while in primary or spontaneous surgical infection tissue necrosis is induced by the pathophysiological process. Inflammation is the response to tissue necrosis, leading to the events visible at the surface which were well described by Celsus and refined by Galen as rubor (redness), tumor (swelling), calor (heat), dolor (pain), and functio laesa (loss of function). These symptoms describe the effects of the host responses which, when controlled and properly regulated, result in elimination of necrotic material and prepare the way for tissue repair. The same mechanisms of inflammation are employed to eliminate invading micro-organisms.

Inflammation is characterized by increased blood flow, increased vascular permeability, recruitment of cells that phagocytose microbes and damaged tissue, secretion of preformed mediators, generation of additional mediator compounds, and the local or regional accumulation of these biochemically active compounds and inflammatory cells. The magnitude of the inflammatory response and of its symptoms is dependent on the burden of tissue injury and on the number and pathogenicity of the invading micro-organisms. If toxins or other bacterial products continuously destroy tissue, or exceed the capability of the host to confine the challenge to body integrity, the inflammatory process will continue and may then result in multisystem malfunction.

The sequence of events occurring early in the inflammation process is the result of activation of inter-relating systems that provide considerable duplication of biological effects. For example, the peptides of the clotting, kinin, and complement systems may each produce vasodilation. Duplication maintains the integrity of the response even in the face of dysfunction of one component part; it also provides the basis for additive and even deleterious effects recognized clinically as autoaggressive multisystem organ failure.

Surgical infections take a relatively uniform course once initiated. First, there is local inflammation following the initial tissue injury. Macrophages may not be capable, however, of phagocytosing all the dead cells and detritus, and remaining necrotic tissue is an excellent nutrient medium for bacterial growth. Bacteria, in turn, release toxins that destroy additional tissue and thus fuel the infectious challenge. Bacteria may invade surrounding tissue slowly or rapidly, depending on their production of specific toxins (spreading factors). The host, in turn, answers with further inflammation in an attempt to confine the infection. If successful, dead tissue, foreign bodies, and micro-organisms are destroyed and removed, and a scar is formed.

If the extent of tissue injury and number of bacteria exceed the capability of the host to terminate an infection locally, an abscess may form (Fig. 1) 18. During the early phases of inflammation there is exudation of plasma, and thus fibrin, through widened spaces between endothelial cells and through open injured vessels. As the infection progresses, this inflammatory process spreads centrifugally from the initial focus of infection, with macrophages and fibrin deposition attempting to confine the infection faster than bacterial toxins can destroy the tissue. The progress of the infection is eventually stopped through the formation of a pyogenic membrane, inside which dying phagocytes and bacteria release toxins that liquefy the abscess contents. The resulting high osmolarity attracts water, increasing the pressure inside the abscess capsule, while oxygen and nutrients diffuse poorly through the abscess capsule, promoting anaerobic glycolysis. An abscess is therefore characterized by high pressure, low pH, and low oxygen tension, and represents an ideal environment for the multiplication of anaerobic bacteria. It is poorly permeated by antibiotics. This is particularly true of aminoglycosides, which are inactive at the pH commonly found in an abscess. The best treatment of an abscess is drainage: local host defences are so intensely concentrated around the abscess capsule that additional antibiotic therapy, except for the period immediately before and during drainage, is rarely indicated.

If local circumscription of infection is not possible, either by removing the bacteria or by abscess formation, micro-organisms eventually invade the bloodstream and may reach distant organs. The presence of bacteria in the bloodstream (bacteraemia) transiently occurs in healthy individuals. In patients, bacteria often will be found on the intravascular portion of catheters. Non-toxin producing, mostly non-multiplying bacteria can sometimes be isolated by blood culture, but these cause no or only mild systemic symptoms: bacteraemia may, however, progress to systemic disease, especially in immunocompromised and postoperative patients. If the condition is persistent and associated with multiplication of bacteria in the bloodstream, and with the death of large numbers of bacteria as a consequence of host defence mechanisms, then a serious state of infection termed sepsis or septicaemia ensues. Septicaemia is characterized not only by invasion and multiplication in the bloodstream of large numbers of bacteria but also by the potential for subsequent sudden overload of the host with endotoxin and cytokines, leading to septic shock. Sepsis is the clinical symptomatic state resulting from the host response to septicaemia. Liberated bacterial exo- and endotoxins are deleterious to many organ functions; equally, cytokine mediators of host defences are potentially damaging if there is failure of their down-regulation. It not treated successfully, the patient may die immediately of septic shock, or later following multisystem organ failure: 1 ng endotoxin/kg body weight results in irreversible shock and death within 2 h.

Clinically, symptoms of sepsis resemble those of endotoxaemia. Fever usually is high, spiking, and accompanied by chills. Tachycardia accompanies or precedes fever and is proportional to it. The total leucocyte count may not be particularly abnormal in sepsis and may even be low due to consumption of polymorphonuclear white cells. The differential count is more reliable: there is always a shift to the left. Petechial lesions may be seen in the skin or conjunctivae of patients suffering from septicaemia caused by streptococci, meningococci, or pseudomonads. Anaemia secondary to haemolysis may appear rapidly when septicaemia is due to staphylococci, pseudomonads, coliforms, or clostridia. During the initial hyperdynamic phase of septic shock, the peripheral vasodilation is explained by a circulatory response which aims to compensate for the inability of cells to use oxygen. The last stage of septic shock is hypodynamic due to exhaustion. Shock is common in septicaemia caused by Gram-negative organisms, but occurs relatively less often with Gram-positive infection. Metastatic abscesses, especially of the bone, brain, or spleen, are not unusual after an episode of septicaemia: any injured tissue is easily infected during septicaemia. Diagnosis is aided by a high index of suspicion.

Thermolabile exotoxins are released by living bacteria, particularly Gram-positive organisms, while thermostabile endotoxins are released by all bacteria after death. Endotoxins are complex moieties of high molecular weight consisting of phospholipids, polysaccharides, and proteins derived from the outer cell wall, particularly of Gram-negative rods such as Escherichia coli. Clinically measurable effects of endotoxin include fever, consumptive coagulopathy, increased vagotonus, hyperglycaemia followed by hypoglycaemia, leucopenia or leucocytosis, increased levels of plasma lipids, release of hepatic enzymes, thrombocytopenia, and reduced serum iron concentration.

Low doses of endotoxin primarily affect the reticuloendothelial system. Animal studies have shown a marked reduction of clearance of particulates such as colloidal carbon during endotoxaemia. Mediators such as collagenases, pyrogenic prostaglandins, and coagulation factors are released from macrophages, and after 7 days antibodies against endotoxin are produced. Endotoxins act directly on the hypothalamic temperature regulation centre to cause fever, reinforcing the activity of pyrogenic substances released from dying neutrophilic granulocytes. Erythropoiesis is shifted from the bone marrow to the spleen, resulting in leucopenia followed by leucocytosis after 2 to 6 h. In small doses, endotoxins increase phagocytic activity and bacterial killing. Thrombocytopenia, accompanied by thrombocyte aggregation and lysis, results in the release of ADP, vasoactive amines, histamine, serotonin, and platelet factor III, which in turn may lead to consumptive coagulopathy. In the extrinsic coagulation system, endotoxins cause release of a tissue factor derived from macrophages, as well as platelet factors and thromboplastins. In the intrinsic system, factor XII (Hageman factor) is activated, leading to disseminated intravascular coagulation.

Endotoxin has a profound effect on metabolism. Initially, it induces hyperglycaemia, which is followed after several hours by hypoglycaemia. Hyperlipidaemia results from altered metabolism of free fatty aids, cholesterol, phospholipids, and triglycerides. Protein synthesis by the liver is stimulated; lactate dehydrogenase transaminases and phosphokinases are released, increasing the serum concentration of these enzymes. Release of adrenocorticotrophic hormone, cortisone, and growth hormone is increased; thyrotropin and luteinizing hormone are not affected. Plasma iron and total iron binding capacity are reduced. A vagotonic effect results in loss of thirst and appetite, stomach emptying is delayed, and diarrhoea may occur.

The early accurate diagnosis of surgical infections is essential: delayed treatment can result in overwhelming sepsis and multisystem organ failure. The history and physical examination are the surgeon's most important diagnostic tools. The classical signs of tumor, rubor, calor, dolor and functio laesa are indicative of localized surgical infections. Clinical symptoms of systemic sepsis include disturbed sensorium, tachypnoea, tachycardia, hypotension, fever, oliguria, and high output heart failure. In postoperative patients, the sudden appearance of tachypnoea and hypotension suggests Gram-negative septicaemia. The condition has a potential mortality rate of 30 to 50 per cent, but early diagnosis and treatment markedly improves the chance of survival.

The entire body must be examined; all dressings should be removed. Inspection and palpation of an area of suspicion might reveal the first three of the classical signs of infection. Removal of an intravenous cannula dressing may reveal purulent drainage or thrombophlebitis. Rectal examination may show tenderness and induration as signs of a developing pelvic abscess. Auscultation of the chest may reveal the presence of pneumonia before it is evident on a chest radiograph.

The patient should be examined for clues to the source of infection such as pain or redness in the surgical wound or at an intravenous infusion site, or purulent sputum, cough, pleuritic pain, rales, or dullness in the chest, diarrhoea, dysuria, or flank pain. Pain in the shoulder and an immobile diaphragm suggest a subphrenic abscess. A pelvic or prostatic mass on rectal examination may indicate an abscess, and headache or nuchal rigidity may indicate a central nervous system infection.

Most bacterial infections produce an increase in the leucocyte count and a shift to the left in the differential count, or a relative lymphopenia. This increase in the proportion of the more immature forms of polymorphonuclear leucocytes may signal infection before a rise in the total leucocyte count is evident. The differential count may also reveal lymphocytosis in viral infections, monocytosis in tuberculosis, eosinophilia in parasitic infections or hypersensitivity reactions (drug allergy), and toxic granulation of leucocytes in acute bacterial infection. A leukaemoid response (a total white count over 25 000 cells/mm³), may be seen in septicaemia, pneumococcal pneumonia, liver abscess or cholangitis, suppurative pancreatitis, necrotic bowel, or retroperitoneal phlegmon. Leucopenia is a sign of overwhelming bacterial infection and carries a bad prognosis. Viral infection, typhoid perforation of the bowel, or tuberculosis may also present with leucopenia. Anaemia may be associated with infection caused by bacteria, such as Clostridium perfringens, group A streptococci, or coagulase-positive staphylococci, which produce haemolytic enzymes.

Routine chest films may reveal generalized or focal atelectasis, or may indicate intra-abdominal infection through signs of gastrointestinal leakage or free air identified under one of the diaphragms. In the investigation of patients with suspected intra-abdominal infection, flat, upright, and decubitus films may reveal a localized air–fluid level, suggesting an intra-abdominal abscess, or a spreading air bubble pattern suggestive of infection with a gas-producing organism. Specialized radiological procedures are often helpful in confirming the diagnosis of intra-abdominal abscess. These studies include ultrasonography and computerized tomography (CT); the choice of technique depends primarily on the expertise of the local radiologist. Although a gallium scan may be helpful in special circumstances, this examination is subject to appreciable error and is difficult to interpret in a patient who has had a recent operation.

Observation of exudates and secretions such as wound drainage, urine, and sputum for odour, colour, and consistency may be useful in diagnosing. Grape-like odours occur with pseudomonal infections, urea-like odours with Proteus infections, and faeculent odours with anaerobic organisms such as Bacteroides, fusobacteria, clostridia, and peptostreptococci. A Gram stain offers the earliest clue to the cause of an infection, particularly when a specific monobacterial infection is suspected. If multiple infecting organisms are present the Gram stain usually shows a variety of pathogenic bacteria. Notes should be taken of the numbers of polymorphonuclear leucocytes on the slide (few, many, loaded) and whether organisms can be seen inside them. Acid-fast and fungus stains can be used if such infections are likely. Pathogens recovered most frequently from the exogenous and endogenous flora are shown in Fig. 2 19. Bacteria often responsible for intra-abdominal infections are listed in Table 1 5.

Purulent material from the deepest aspect of the wound should be aspirated into a syringe and any air evacuated. Pus is the best medium in which to preserve bacteria for transport to the laboratory. The capped syringe is sent for aerobic and anaerobic culture and for determinations of antibiotic sensitivity. Alternatively, a moist swab can be used to obtain bacteria from a site of suspected infection. Ideally, anaerobic specimens should be transported immediately in a CO&sub2;-filled tube and plated within 1h of sampling; fastidious organisms may otherwise die, resulting in a false-negative culture result. If the specimen is held overnight, it should be placed in an anaerobic sterile vial or tube; under no circumstances should an anaerobic specimen be refrigerated. Generally speaking, Escherichia coli (aerobe) and Bacteroides fragilis (anaerobe) are the usual causes of wound infection following gastrointestinal or gynaecological operations, while staphylococci are the usual causative organisms when intra-abdominal viscera have not been resected or opened.

Blood cultures are indicated in the investigation of all serious infections. Following careful disinfection of the venipuncture site with an iodophor preparation, blood samples should be obtained for aerobic and anaerobic culture. Blood should not ordinarily be drawn for culture through an existing intravenous needle or catheter. It is important to obtain a number of blood cultures from different sites and at different times; if possible, they should be obtained at the start of a chill or the beginning of a fever spike to increase the likelihood of culturing from a specimen drawn during the septicaemic peak. If the patient is receiving treatment with antimicrobial drugs a drug removing device is helpful in obviating antimicrobial action during culture.

Biopsy of skin lesions and lymph nodes may be helpful, although lymph node biopsies in the inguinal region should be avoided. If no nodes are palpable and the diagnosis is obscure, a blind scalene node biopsy may sometimes be productive. Specimens should be sent for routine bacteriological, acid-fast bacillus, and fungal cultures, as well as for histological examination. Skin tests, except for tuberculosis, have limited use: serological tests are more reliable then skin tests for the diagnosis of fungal disease.

While culture and sensitivity tests are essential, the latter results need to be interpreted appropriately since the tests are not always reproducible and must be viewed with caution. Sensitivity reports are an oversimplification of the complex foundations on which antimicrobial chemotherapy is based and are usually based on disc diffusion tests, which are highly sensitive to small technical and environmental changes. They may not correlate with the actual minimal inhibitory or bactericidal concentration of an antibiotic or with the concentration of antibiotic achieved at the site of infection. Routine disc sensitivity tests are generally of little value to the clinician. The minimal inhibitory concentration or the minimal bactericidal or fungicidal concentration is more useful clinically.

All wounds whether made at the operating table or resulting from trauma, provide an environment for bacterial growth. Infections can be minimized if wound management follows the principles below.

1.Tissue should be handled gently, and operative trauma kept at a minimum.

2.Further contamination should be minimized by use of aseptic techniques.

3.Devitalized tissue, debris, and traumatic foreign bodies should be removed.

4.Complete haemostasis should be achieved.

5.Blood supply is essential for healing and should not be impaired.

6.Formation of dead space should be avoided during closure.

7.The wound should be closed with layer-to-layer approximation without tension.

8.Operative time should be kept to a minimum to reduce the numbers of bacteria entering the wound.

9.The wound may be irrigated with liberal amounts of sterile saline Ringer's lactate solution prior to closure.

Resistance of the host to infection is intimately involved with the magnitude of trauma and the early inflammatory response. Three primary factors interact in infection: the extent of tissue injury, the inoculum (quantity) and toxic products (quality) of infecting micro-organisms, and the host defence capacity. Meticulous, atraumatic technique is important: the extent of tissue injury is crucial in the development of subsequent bacterial infection. Debridement is important to reduce the amount of necrotic material, allowing phagocytes to concentrate on invading micro-organisms. If the initial wound is contused and fringed with loose tissue, scalpel excision of the wound edges often leaves less traumatized issue. Any fresh wound almost invariably becomes contaminated as long as it is exposed to the environment. In this index, the operating room is not sterile, and bacteria can be isolated from the wound exudate of even primarily healing wounds. Bacteria require 6 to 8 h to multiply to a concentration which is virulent and which is accompanied by invasion of adjacent tissues. During this time debridement of necrotic tissue and primary wound closure carries little risk of infection. However, infections frequently complicate healing of wounds if primary closure is completed later than 6 to 8 h after injury.

Non-localized infections (cellulitis, lymphangitis) should be treated with antibiotics, preferably penicillin G in high doses, as well as local heat, rest, immobilization, and elevation. Local moist heat relieves pain and increases blood and lymph flow: it is best applied by intermittent moist compresses, which hastens localization. Prolonged application of heat encourages oedema and satellite infection. Surgical incision and drainage are not usually indicated.

In a localized infection (abscess, infection of a closed space), the most important therapeutic modality is the operative reduction or elimination of invading and multiplying bacteria and the removal by drainage of factors promoting bacterial growth. Antimicrobial therapy is effective only in conjunction with operative reduction of the bacterial inoculum. Incision and drainage is thus indicated whenever infection is localized or occurs in a closed space. Fluctuance of most superficial abscesses signals the appropriate time for drainage. When in doubt, needle aspiration may be diagnostic, especially in deeper infections. The incision must be large, placed in the most dependent area of the abscess, and kept open to prevent skin closure before the deepest site of infection is controlled. Superficial wound abscesses should be packed lightly with gauze after drainage, while deeper abscesses are kept open by sump drains or tubes.

The goal of antibiotic therapy is to achieve a concentration of antibiotic in the infected tissue that exceeds the minimum inhibitory concentration for at least three-quarters of the time between successive doses. Drug pharmacokinetics vary considerably with patient age and disease. Antibiotics are usually given in insufficient doses, particularly at the onset of treatment, if only manufacturers' recommendations and disc sensitivity data are used to determine the dose and dosing interval. Clinically appropriate doses are recorded in a review by the authors (Condon and Wittmann 1992) which should be consulted for further information. Suggestions about initial empiric therapy for surgical infections originating from various sources are recorded in Table 2 6.

Systemic antibiotics are not usually indicated for the treatment of uncomplicated wound abscess which can be drained through an incision which does not open new tissue planes or expose new tissue to contamination by the contents of the abscess. Since overlying tissues must be opened to drain deep abscesses, antibiotics should be administered during the period immediately before and during incision and drainage. A longer period of therapy with parenteral antibiotics is indicated in immunocompromised patients, or when there is evidence of septicaemia (systemic toxicity, high fever), or progression of infection despite adequate drainage. If infection persists the first question to be asked, before systemic antibiotics are given, is whether incision and drainage has been adequate, and whether there may be another unrecognized and undrained surgical infection.

Antimicrobial treatment should be specific: that is, directed against the causative pathogens based on either the clinical diagnosis or a specific bacteriological diagnosis. When the bacteriological diagnosis is uncertain, empirical or calculated antibiotic therapy should be targeted at the most likely pathogens and the following points should be considered.

1.The spectrum of pathogens known to be typical.

2.The pathogenicity, synergism, and antagonism exhibited by bacteria in various mixed infections.

3.The concentration of antibiotic which can be achieved at the site of infection.

4.The side-effects of antimicrobials.

5.The negative interaction of antibiotics with host defence mechanisms.

6.The results of well controlled clinical studies of unselected patients.

Antibiotics that reliably kill bacteria should be given preference, such as penicillin for infections by group A streptococci or clostridia and cefotaxime against E. coli and Klebsiella.

Several factors increase the risk of a patient acquiring infection (Table 3) 7. These risk factors may be related to the patient's capability to defend against an infectious threat, the infectious challenge itself, as represented by the number and pathogenicity of bacteria, the extent of associated injury, and environmental factors such as the hospital bacterial flora. The surgeon should be alert to these factors and tailor therapeutic or preventive strategies to the specific circumstances. For example, antibiotic prophylaxis is usually not indicated before a clean or aseptic operative procedure, but may very well be useful in an insulin-dependent diabetic. The dilemma for the surgeon is to decide when bacteriological contamination of an open ulcer, for example, becomes a clinically significant risk or is associated with tissue-penetrating disease.

Improper preoperative management is an organizational problem and can increase the postoperative infection rate. Common errors include failure to give a preoperative bath with antiseptic soaps or solutions, and shaving of the operative site the night before operation. Shaving is probably not indicated in most patients; when practised, it should be limited to the immediate preoperative period.

Changes in the microbial flora of the skin, respiratory tract, and gastrointestinal tract are seen in the most seriously ill patients, regardless of the underlying disease. Resistant Gram-negative organisms, staphylococci, and fungi usually colonize such patients shortly after admission to the hospital. Factors increasing the incidence of colonization are antibiotic administration, use of inhalation therapy equipment, immunosuppressive or irradiation therapy, and depressed neurological status. Administration of multiple potent antimicrobials disturbs the patient's microbial ecological system since not only pathogenic but also symbiotic bacteria are eliminated. For example, therapy with imipenem often leads to elimination of too many bacteria, and, in the susceptible patient, allows superinfection with fungi or other resistant bacteria which are normally of low pathogenicity. These situations should be avoided by discontinuing antimicrobials at the earliest possibility or changing early to a narrow spectrum regimen directed only at pathogenically important micro-organisms.

Many scoring systems have been developed to assess the severity of disease. The Surgical Infection Society currently proposes the use of the APACHE-II system to compare treatment regimens. The APACHE score consists of an Acute Physiology Score and a Chronic Health Evaluation (Fig. 3) 20,21. There are disease-specific weighting factors to calculate mortality. For patients with intra-abdominal infection, a score of 21 correlates with a mortality risk of 50 per cent (Fig. 4) 22.

Infections with a single organism usually follow minor trauma, and are limited to the skin and subcutaneous tissues. However, even minuscule lesions may become life threatening; examples are streptococcal erysipelas, cellulitis, phlegmon or lymphangitis, clostridial infections including gas gangrene, tetanus, and some staphylococcal infections.

Group A streptococci may cause cellulitis and erysipelas: once inoculated beneath the skin, the defensive barriers are easily breached by the toxins released by streptococci; in addition the lymphatic system is frequently involved. Clinically, there is oedema with reddening of the skin (Fig. 5) 23. Penicillin G is the treatment of choice since it kills all group A streptococci, a remarkable property that has not changed since the introduction of this drug more than 45 years ago. Before the discovery of penicillin, invasive group A streptococcal infection had a mortality rate of 90 per cent. Anaerobic streptococci (peptostreptococci) are part of the normal flora of the mouth and gastrointestinal tract. In contrast to other streptococcal wound infections, these organisms produce a thin, brown discharge, often with crepitation in the infected tissue (anaerobic cellulitis). Treatment consists of wide incision and drainage, and administration of 10 million units (6 g) of penicillin G 6-hourly. Cephalosporins, clindamycin, chloramphenicol, and metronidazole are second choice agents against anaerobic cocci.

These infections are usually due to Staphylococcus aureus, although in patients receiving antibiotics, Gram-negative bacteria and Candida may be the cause. Folliculitis originates within one hair follicle; furunculosis represents infection of several hair follicles in a circumscribed area; a carbuncle (boil) is a confluent infection involving multiple contiguous follicles in which the infection is limited to the subcutaneous tissue by thick overlying skin and dense subcutaneous fascia. Carbuncles usually are found on the back of the neck and torso. Warm skin compresses and good local hygiene are usually sufficient therapy for folliculitis and most cases of furunculosis. Carbuncles require incisions for drainage and treatment with antistaphylococcal penicillins, erythromycin or clindamycin.

This infection of apocrine sweat glands is usually seen in young adults and is due to staphylococci or anaerobes (especially peptostreptococci). Often, only complete excision of the infected tissue down to deep fascia, with subsequent grafting or delayed closure, is curative.

Human bite wounds are contaminated with a combination of aerobic non-haemolytic streptococci, anaerobic streptococci, B. melaninogenicus, spirochaetes, and staphylococci. The original wound must be treated by debridement, thorough irrigation, and immobilization. Systemic antibiotics, usually penicillin, must be administered. If the infection becomes established, radical debridement of the infected area is imperative and must be accompanied by antibiotic therapy.

Infections of dog and cat bite wounds are caused by Pasteurella multocida in 25 to 50 per cent of cases; otherwise, the spectrum of bacteria is the same as that seen in human bite wounds. The antibiotics of choice are high dose penicillin G, amoxicillin/clavulanic acid or oral cefuroxime.

Chronic progressive bacterial gangrene is caused by the synergistic action of microaerophilic non-haemolytic streptococci, and aerobic haemolytic staphylococci (Fig. 6) 24. The incubation period is 7 to 14 days. Cellulitis is followed by gangrenous ulceration that is progressive unless treated. Radical excision of the ulcerated lesion and its gangrenous borders is imperative, along with administration of large system doses of penicillin. Burrowing ulcers are caused by a combination of microaerophilic streptococci and staphylococci (Meleney's ulcer). Such lesions have a characteristic metallic sheen, cause necrosis of large areas of skin, and may produce sinus tracts in the underlying tissue. These should be incised, drained, and treated with high doses of penicillin (10 million units every 6 h).

Non-clostridial gangrenous cellulitis caused by B. melaninogenicus and anaerobic streptococci is typified by a progressive gangrenous infection of the skin and adjacent areolar and fascial tissues. Prompt incision and drainage, and administration of large doses of penicillin are necessary. Supportive treatment is imperative, since toxaemia with dehydration, fever, and prostration rapidly develops.

Clostridial cellulitis is a serosanguineous, crepitant, septic process of subcutaneous, retroperitoneal, or other areolar tissue, caused principally by C. perfringens (also known as C. welchii). It differs from gas gangrene in that the infection does not involve muscle (Fig. 7) 25, but spreads rapidly via fascial planes. Extensive gangrene results from vascular thrombosis. Systemic effects are moderate if the infection is treated promptly with early surgical debridement and penicillin therapy.

Clostridial myonecrosis (gas gangrene) is an anaerobic infection of muscle characterized by profound toxaemia, extensive local oedema, massive necrosis of tissue, and a variable degree of gas production (Fig. 8) 26. The causative organisms are the clostridia which abound in soil, dust, and the alimentary tract of most animals and which are usually saprophytic. C. perfringens, which is the most common cause, produces a variety of potent toxins, including hyaluronidase, collagenase, four different haemolysins, five necrotizing lecithinases, and six other necrotizing lethal toxins. All clostridia owe their pathogenicity to elaboration of such soluble exotoxins that destroy tissue and blood cells. Clostridia enter a wound, multiply in the presence of devitalized muscle, and use iron from myoglobin to produce necrotizing exotoxins. Disruption and fragmentation of normal muscle cells and capillaries result in further necrosis, haemorrhage, and oedema. There is no fibrin formation or polymorphonuclear leucocytic reaction. The affected muscles are at first red and friable, but progress to a purplish black, stringy, pulpy mass. The presence of gas is variable. The affected area swells and discharges a brownish, malodorous fluid. The overlying skin initially shows blotchy ecchymoses (marbling), then blackens, and finally sloughs.

The diagnosis of gas gangrene is based on typical clinical findings, as well as on the presence of large Gram-positive rods in the wound fluid. Delay in diagnosis, even for just a few hours, greatly increases the mortality. Immediate removal of involved muscle groups is necessary: amputation is indicated if the remaining viable muscles are insufficient for useful function. High intravenous doses of penicillin and whole blood are given preoperatively and postoperatively. Multiple treatments with hyperbaric oxygen (oxygen at 3.03 kPa) may reduce the amount of debridement necessary and lower the mortality, but muscle resection should not be delayed in anticipation of hyperbaric therapy. Untreated gas gangrene is always fatal; the fatality rate in treated patients ranges from 25 to 40 per cent.

This is caused by a spore-forming obligate anaerobe, Clostridium tetani, found in the faeces of humans and animals and capable of prolonged survival in soil. Two exotoxins are produced: tetanospasmin, a neurotoxin, and tetanolysin, a haemolysin. Dead muscle and clotted blood provides an ideal culture medium for germination of tetanus spores, and compound fractures with devitalization of muscle are very susceptible to such infection, as are small puncture wounds harbouring a clot deep in the tissues. Locally produced tetanolysin contributes to optimal growth conditions through its lecithinase, gelatinase, esterase, and lipase activities. Tetanospasmin, the neurotoxin responsible for the clinical features of the disease, does not act peripherally or locally but is carried to and acts on the central nervous system. In order to neutralize blood-borne toxin, antitoxin must be present before tetanospasmin becomes fixed by nerve cells. Antitoxin given when symptoms are apparent only limits further intoxication of nerve cells and cannot reverse developing symptoms.

There is considerable variability in progression of the disease from onset. There may be a prodromal period of headache, stiff jaw muscles, restlessness, yawning, risus sardonicus, and wound pain, typically beginning 1 to 2 weeks after trauma but occasionally as early as 1 day or as late as 2 months after injury. The active stage follows in 12 to 24 h, with trismus, facial distortion, opisthotonos, pain, clonic spasms, and seizures. Acute asphyxia is a major hazard and may result from either spasm of the respiratory muscles or aspiration. The shorter the incubation period, the poorer the prognosis.

Human immune globulin, 3000 units intramuscularly, should be given immediately to neutralize circulating toxins. An additional 1000 units are injected into and immediately proximal to the wound, followed by wide debridement. Five hundred units of intramuscular immune globulin may be given daily subsequently. If symptoms persist for longer than 2 weeks, the large initial doses of immune globulin may be repeated. An airway must be established; tracheostomy will be needed in every patient with more than prodromal symptoms and should be performed before the situation becomes urgent. Respirator support and oxygenation may be needed. Muscle spasms may be controlled with intravenous midazolam or diazepam, or with intramuscular meprobamate or chlorpromazine. If spasms persist, curare or another muscle blocker should be given. Additional sedation is usually not needed if muscle relaxant therapy has been adequate, but is best achieved with intramuscular barbiturates if required. The patient should be placed in a quiet room, with environmental stimulation kept at a minimum to avoid triggering seizures. Intravenous thiopental (Pentothal) may be needed to control seizures. High doses of penicillin G (5–10 million units) will establish a sufficient antibacterial tissue concentration. With appropriate early care, 75 per cent of patients survive with no neurological impairment.

Tetanus is absolutely preventable by prior active immunization. Effective active immunization (not associated with a fresh wound) is accomplished by injection of 0.5 ml fluid or adsorbed toxoid, repeated after 2 and 20 months.

Immediate meticulous surgical care of the fresh wound is of prime importance. Removal of devitalized tissue, blood clots, and foreign bodies, obliteration of dead space, and prevention of tissue ischaemia in the wound are the objectives of initial treatment. If the wound is grossly contaminated, penicillin should be administered. Wounds which are seen late or are grossly contaminated should be left unsutured after debridement, protected by a sterile dressing for 3 to 5 days, and closed by delayed primary suture if the tissues appear clean and healthy. Active and passive immunization should be accomplished with 0.5 ml tetanus toxoid and tetanus immune globulin, 250 to 1000 units, as outlined in Table 4 8. Patients not previously immunized should receive injections of 0.5 ml fluid or adsorbed toxoid, repeated after 2, 6, and 20 months.

The most common hand infections are paronychia, pulp infection, and subcutaneous abscesses, including felon and bacterial tenosynovitis. The therapeutic goal is to restore full hand function. Elevation, immobilization in the position of function, and heat in the form of hot wet packs changed every 2 to 4 h are helpful. Hot soaks may be used for 20 min every 4 h. Ten million units of penicillin 6-hourly are effective in severe infections. Abscesses and other local collections of pus should be drained promptly; generally the volar aspect is incised. Important principles of managing hand infections are summarized in Table 5 9.

Anaerobic and staphylococcal infections of the breast occur in two forms: puerperal (postpartum) and spontaneous (non-puerperal). A puerperal breast abscess is usually caused by staphylococci; non-puerperal breast abscesses (Fig. 9) 27 may also be due to anaerobes, usually Peptostreptococcus magnus (Table 6) 10. Excision of the involved duct through a periareolar incision is indicated for persisting or recurring non-puerperal breast abscess.

A subcutaneous area located in the intergluteal cleft over the sacrum becomes infected when ingrown hair leads to formation of a foreign body sinus and triggers growth of mixed bacterial species, often with a predominance of anaerobes. Initial lesions are treated by unroofing, leaving the deep epithelialized wall of the sinus track intact, accompanied by epilation of surrounding skin and allowing secondary healing. No additional antibiotic therapy is required, although wide excision and healing by secondary intention may be required if infection is recurrent or persistent.

Anaerobic infections of the perianal soft tissue originate from anal ducts and glands and present as localized subcuticular or subcutaneous foci immediately adjacent to the pigmented epithelium of the anal verge and canal. They do not burrow into deeper tissues, but must be clearly differentiated from perirectal and deeper abscesses by digital rectal examination. If tenderness precludes adequate investigation a thorough examination can be completed under anaesthesia. Before fluctuance occurs, antibiotic therapy for 2 to 3 days together with twice-daily sitz baths will often resolve the infection. If a fluctuant collection is present, perianal incision allows drainage; antibiotics are discontinued but sitz baths should continue until all inflammation has resolved.

Burrowing, intersphincteric, ischiorectal, and supralevator abscesses originate in the rectal crypts and glands at the upper end of the anal canal. Goodsall's rule is incorrect; burrowing abscesses may originate at any point of the anorectal circumference. Typically, the abscess burrows directly radially from the infected gland or crypt of origin to present on the perianal skin at a slight distance from the anal verge. Burrowing may also occur in the subcutaneous tissues around the anus to form a more or less complete ‘horseshoe abscess’. Alternatively, the infection may burrow between the anal sphincters or through the sphincters into the ischiorectal space, from which it may extend superiorly into the supralevator space, before dissecting subcutaneously to perianal skin. All forms of perirectal abscess are potentially more dangerous than a simple perianal abscess, and the two infections should not be confused. Examination under anaesthesia (regional block or general) is essential to make an accurate diagnosis. Drainage through a wide perianal incision is the treatment of choice. Bacteroides species, clostridia, and peptostreptococci predominate as causative organisms; the most common causative aerobe is Proteus mirabilis. The drainage wound should be packed open, packs changed frequently, and sitz baths taken twice daily. Additional antibiotic therapy after completion of drainage is not necessary in patients with normal immunological function.

Lung infection may follow chest trauma which includes pulmonary contusion or rib fractures. Pulmonary infections may be caused by a variety of micro-organisms: aspiration following major trauma is a common cause of bronchopneumonia, usually caused by oral anaerobes. Treatment consists of a broad spectrum cephalosporin, such as cefotaxime, in combination with clindamycin.

Pleural empyema may follow haemothorax as well as pneumonia or other pulmonary infection, and is usually due to the same organisms as those which caused the lung infection. It may also follow elective thoracotomy. Empyema always requires closed tube drainage. If the lung does not completely expand, open pleural debridement (decortication is a misnomer) is essential. Antimicrobial therapy is directed against causative bacteria which may include anaerobes. Pulmonary infections, particularly those which follow aspiration of oral or gastric fluids, may progress to intrapulmonary abscess. Obligate oral anaerobes are often involved, but these may be difficult to isolate in routine culture. Percutaneous needle aspiration is often helpful for diagnosis. Antibiotic therapy should include anaerobic coverage with metronidazole, and open drainage may be required.

Surgical infections of the heart include endocarditis and pericarditis. Tuberculous pericarditis may require pericardiectomy, and endocarditis due to enterococci, Streptococcus viridans, pneumococci, and other bacteria also may require operative treatment. Subacute bacterial endocarditis is usually caused by streptococci of the viridans group (70 per cent of cases), Enterococcus faecalis, or group D streptococci. All streptococci are sensitive to parenteral penicillin at a dose of 6 million units (3.6 g) every 24 h for 4 weeks. The penicillin sensitivity of Enterococcus faecalis is variable; ampicillin is the best treatment for infections with this organism. Enterococci are generally resistant to cephalosporins and aminoglycosides.

Contamination of the abdominal cavity may follow penetrating abdominal trauma or blunt trauma associated with intestinal rupture. Such patients usually undergo early operation, and intra-abdominal infection does not occur; unless operated on within 24 h of traumatic perforation, an intra-abdominal infection is likely. Secondary peritonitis may follow a variety of pathological conditions, including peptic ulcer perforation, pancreatitis, gallbladder perforation, bowel ischaemia due to strangulation or vascular compromise, small or large bowel perforation, genitourinary infection, and perforation of an intra-abdominal abscess. The source of infection must be controlled by closure or exteriorization, and the abdominal cavity must be cleansed of bacteria, toxins, and adjuvants such as bile, mucus, barium, blood, and necrotic tissue. Additional further influx of bacteria or adjuvants must be prevented. Multiple planned relaparotomies (staged abdominal repair) may be required for advanced cases with an APACHE-II score of 14 or greater.

These are almost always associated with calculous disease. The infection progresses from acute cholecystitis to cholangitis or empyema of the gallbladder and, occasionally, to internal fistula formation; alternatively, the acute infection may settle into repetitive episodes of chronic cholecystitis. Uncomplicated gallstones are associated with bacteribilia (culture-positive bile) in 30 to 50 per cent of cases. The most important and frequently recovered pathogenic bacteria are E. coli, klebsiellae, and clostridia. Treatment consists of cholecystectomy and drainage of the bile duct system, following which infection usually resolves with antibiotic therapy. In immunocompromised patients broad-spectrum penicillins and third-generation cephalosporins are indicated.

This may be due to amoebae, salmonellae, or to a mixed bacterial population, and usually follows appendicitis, bacterial or other forms of colitis, or biliary tract infection. Echinococcal cysts occasionally become secondarily infected. Obligate anaerobes are found in over 50 per cent of liver abscesses. Percutaneous drainage is needed if the abscess has developed a rind or wall within the liver. Specific antibiotic treatment will cure the infection, provided that the underlying condition is eliminated.

Pancreatitis begins as a chemical inflammation, but more than half of the fatalities are due to infection. Pancreatic abscesses develop within the necrotic pancreatic tissue and require drainage; planned multiple laparotomies have been advocated for severe cases. Antibiotic therapy includes a third-generation cephalosporin combined with metronidazole; imipenem or sulbactam/ampicillin are good alternatives.

Appendectomy (Fig. 10) 28,29 is required. Antibiotics given prior to surgery are effective mainly for prophylaxis of infection in the incisional wound, and in uncomplicated appendicitis need not be continued following completion of the operation. Continued administration of antibiotics is indicated when the disease has progressed to gangrene, perforation, abscess, or diffuse peritonitis. Abscesses may be drained percutaneously with the help of ultrasound or CT, or open drainage by laparotomy may be established. Obligate anaerobes are always present. E. coli may cause lethal sepsis. In severe cases of diffuse peritonitis, a third-generation cephalosporin must be combined with metronidazole for therapy; ampicillin/sulbactam also has been successful.

More than half of patients over 50 years of age in the Western world have colonic diverticula, but only a minority develop symptoms. Diverticulitis may occur at any time and is usually treated with bowel rest and antibiotics. The disease is due to anaerobic organisms; 500 mg metronidazole every 12 h is the treatment of choice. If septicaemia develops, a third-generation cephalosporin may be included. Other drug combinations active against B. fragilis and E. coli may be used. Perforation of a diverticulum results in either diffuse peritonitis or a peridiverticular abscess (Fig. 11) 30. The abscess itself may secondarily perforate and cause diffuse peritonitis; laparotomy and resection of the diseased colon segment is the treatment of choice. Primary anastomosis has been successful in selected cases; if this is not appropriate or possible, an end-colostomy and mucus fistula may be performed, but Hartmann's procedure should be avoided if possible. Later restoration of bowel continuity entails some further risks of mortality and morbidity, but the magnitude of such risks is generally exaggerated in reports in the literature.

Infections of this region are mostly non-surgical (in the sense that operative drainage or debridement of tissue is not usually necessary to control the infection), and the mainstay of therapy is the administration of appropriate antibiotics. Sexually transmitted infections are diagnosed by the presence of specific microorganisms in cultures of cervical exudate. Pelvic inflammatory disease is usually due to gonococci, while endometritis, adnexitis, and myometritis are caused by mixed infection with aerobic and anaerobic intestinal bacteria. These infections are treated with antibiotics; transvaginal drainage is needed in some cases. Occasionally, a persisting tubal abscess may need resection.

The most common form of urinary tract infection involves only the urinary bladder, occurs primarily in women due to the relatively short length of the urethra, and is caused by coliform organisms. Such infections usually respond readily to increased fluid intake and administration of an oral penicillin or cephalosporin, although recurrence is common. Urinary bladder infection is also common following the placement of a Foley catheter. Although closed urinary drainage systems delay the onset of bladder infection, infection always occurs eventually if the catheter remains in place, the route of infection being through the urethra external to the catheter. Such infections are usually caused by coliform bacteria. Antibiotics should not ordinarily be used to treat this form of urinary bladder infection unless the catheter can be removed; the continued presence of the catheter assures continuing infection and administration of antibiotics only results in emergence of resistant organisms. Acidifying bladder washes are partially effective in controlling bladder infection in this situation.

If the ureteropelvic junction is incompetent, backwash of infected bladder urine into the ureter and renal pelvis may result in acute pyelitis, accompanied by septicaemia and even septic shock. Chronic pyelonephritis is usually haematogenous in origin and may result in a nephric or perinephric abscess which may rupture and cause peritonitis. Drainage is required and antibiotic treatment should be specific and should include a drug active against anaerobes such as metronidazole.

This is seen primarily in unstable fractures in which moving fragments continuously produce friction and necrotic tissue; unless the fracture is stabilized, the infection cannot be controlled. Staphylococci are the predominant causative micro-organisms but P. aeruginosa is isolated in 10 per cent of cases. Obligate anaerobes are present in more than 10 per cent of the cases, but are usually missed by routine culture techniques, and Gram-negative facultative anaerobes may become a problem. Following operative stabilization of the fracture, specific intravenous antimicrobial therapy should be continued for 4 weeks. The bone concentration of the chosen antibiotic should be greater than its minimum inhibitory concentration for the infecting bacteria.

In adults, antimicrobial therapy should be specific for the infecting organism and should achieve a bone concentration above its minimum inhibitory concentration. A swab is insufficient as a bacteriological specimen; open biopsy to obtain a piece of infected tissue for culture and determination of antibiotic sensitivity is preferred. Haematogenous osteomyelitis in adults (usually immunocompromised individuals) may require operative drainage and sequestrectomy. Haematogenous osteomyelitis in children can be treated successfully if parenteral antibiotics are administered early in the disease, but if a large subperiostal abscess or a sequestra forms, operative management is required. Osteomyelitis of the spine may present as a groin abscess and is usually seen in immunocompromised patients: staphylococci, mycobacteria, and salmonellae are the most common causative micro-organisms. Specific antimicrobial therapy is mandatory and bone biopsy may be required to provide adequate samples for culture and sensitivity studies. The chosen antibiotic needs to reach bone concentrations above their minimum inhibitory concentration for the pathogen involved.

Subdural empyema accounts for 10 to 32 per cent of intracranial suppurations. Acute frontal sinusitis and mastoid infections are the most common antecedent cause, but infected subdural collections occur in 2 per cent of patients following meningitis and are most commonly caused by Gram-positive cocci. Early drainage is essential to prevent a further increase of intracranial pressure (neurosurgical emergency).

Metastatic and primary brain abscess may follow meningitis, or may be due to haematogenous or direct spread from mastoiditis or nasal sinus infection. Anaerobic bacteria and Staphylococcus aureus are most commonly found in these conditions. Prompt incision and drainage is required.

Any purulent discharge from a closed surgical incision (not just from around a suture) with inflammation of the surrounding tissue, with or without a positive culture, should be considered as a wound infection. A rare case of sterile fat necrosis will be included, but this is better than overlooking a true infection. Superficial (suprafascial) wound infection in the early postoperative period is diagnosed on clinical findings, as well as on the results of a Gram stain of needle-aspirated material. The earliest sign of such infections is induration, accompanied by erythema and increasing pain: excessive wound pain is a commonly overlooked sign, particularly in patients with wound infections caused by Gram-negative organisms. Immediate therapy consists of reopening the wound and evacuating the pus; antibiotics are not usually required.

Deep wound infections involving fascia and muscle are more serious, and are usually accompanied by infection in one of the main body cavities or in bone or a joint. They usually occur as the result of a technical error. Drainage, control of any source of continuing infection, and antibiotic therapy are indicated.

This is a serious mixed infection due to a haemolytic streptococci or staphylococci and peptostreptococci, and associated with excessive collagenase production, leading to dissolution of connective tissue. The infection involves the epifascial tissues of an operative wound, laceration, abrasion, or puncture. It may be immediately fulminant or may remain dormant for 6 or more days before beginning to spread rapidly. Subcutaneous and fascial necrosis accompanies extensive undermining of the skin, resulting in gangrene. Treatment is excision of the entire area of fascia affected, administration of large doses of penicillin (12–30 million units/day), and appropriate systemic support.

Fifteen to 30 per cent of all intra-abdominal infections occur following an operation. The diagnosis is usually delayed. The most common cause is a technical error compromising the vascular supply to an anastomosis, resulting in necrosis and leakage of intestinal contents into the peritoneal cavity. Iatrogenic perforation of a hollow viscus is another cause. An intra-abdominal haematoma may become secondarily infected, resulting in an abscess. Treatment is operative, as in other forms of secondary peritonitis, although non-operative drainage with ultrasound or CT guidance is a valid option for an abscess not associated with an anastomosis (Fig. 12) 31. Antimicrobial therapy is more difficult due to the possible selection of resistant bacteria by preoperative antibiotic therapy. Antibiotics administered should not only cover the specific bacteria isolated, but should also be effective against possible pathogens from the facultative and obligate anaerobic bowel flora; usually a third-generation cephalosporin plus metronidazole is sufficient. Other options are imipenem or ampicillin-sulbactam. If a resistant Pseudomonas, Enterobacter, or Serratia presents problems for treatment, the synergism seen between aminoglycosides and &bgr;-lactam antibiotics should be exploited. Enterococci rarely cause a problem and need not be treated specifically when otherwise adequate aerobic and anaerobic antibiotic coverage is provided.

These are common following thoracic and upper abdominal operations. Pain and the supine posture interfere with adequate diaphragmatic and chest wall respiration resulting in atelectasis, and subsequent bronchopneumonia or lobar pneumonia. Treatment of mild cases involves physical therapy and adequate analgesia to allow for full expansion of the lungs. If antimicrobial therapy is likely to be required for suspected pneumonia, transtracheal aspiration should be used to obtain a specimen for culture before therapy is started. If indicated, infected secretions can be removed by bronchoscopy, and a reliable specimen can be obtained for Gram stain, culture, and determination of antibiotic sensitivity. A variety of micro-organisms, such as streptococci, pneumococci, staphylococci, meningococci, gram-negative anaerobes, and fungi may be isolated. The result of the Gram stain will help in choosing the initial antibiotic for calculated therapy. Aspiration pneumonia is usually due to anaerobic oral bacteria. If gastric juice is also aspirated, a severe infection may result (Mendelson syndrome) which has a high mortality risk. Pleural empyema may develop following thoracic or abdominothoracic operations, or following postoperative pneumonia. The contribution of anaerobic organisms is usually underestimated. Tube thoracostomy drainage and rethoracotomy are treatment options. Initial antimicrobial therapy should be based on the result of a Gram stain and should also include a drug such as metronidazole or clindamycin, active against anaerobes.

This carries a high mortality and is most commonly seen following oesophageal resection. Treatment consists of adequate operative drainage and administration of antimicrobials fully active against endotoxin-producing Gram-negative bacteria and obligate anaerobes; a third-generation cephalosporin, combined with metronidazole will cover most pathogenic bacteria. Imipenem may be required. Interpretation of bacteriological results is difficult since antibiotics will usually have been given before a proper specimen can be obtained during the operative drainage procedure. The gaps in bacterial coverage of antibiotics previously given should influence the current choice of antibiotic. Sternum infection is seen following median sternotomy and most commonly is due to staphylococci. If antibiotic treatment is not initially successful, the sternum must be reopened to allow for drainage.

A Foley catheter, if required, should be connected to a closed drainage system and should be removed as soon as possible. Specimens of urine should be sent for culture and sensitivity testing every 5 days, and at the time of catheter removal. Suprapubic urinary bladder catheterization is preferable for long-term bladder drainage since the risk of infection is considerably reduced. A colony count of 10&sup6;/ml bacteria in fresh urine is highly suggestive of active infection. Dysuria is not always present. Hemorrhagic cystitis is usually caused by E. coli. If the infecting organism is unknown, a Gram stain will help in selecting an appropriate antibiotic.

One-third of intravenous catheters become colonized with bacteria within 2 days of placement. Bacteraemia will occur in 1 per cent of patients with an intravenous catheter in place for longer than 48 h, and the risk of septicaemia increases to 5 per cent with increasing duration of catheterization. An intravenous catheter should always be removed and cultured whenever bacteraemia is suspected. Intra-arterial catheters may also be the site of sepsis and should be similarly handled.

Infections of vascular prostheses are most commonly due to staphylococci. Treatment may require removal of the artificial vascular graft. Antimicrobial wound treatment without graft removal succeeds in selected situations.

The scientific basis for the use of prophylactic antibiotics in surgery was laid by Miles and Burke in the late 1950s when they were able to show that infections could be prevented only when antimicrobials were given prior to or at the time of the infectious challenge. Antibiotics given 3 h following a challenge with infectious bacteria were ineffective in preventing infection. A surgical incision exposes normally sterile tissues to a non-sterile environment; some contamination occurs with any operation. Bacteria may start multiplying before effective host defences are established, and if initially present in a concentration exceeding 100000 organisms/g tissue, may exceed the host defence capacity. Host defences also recognize damaged and dead tissue, which are eliminated by the same humoral and cellular mechanisms as those used to defeat invading bacteria. Thus, there is a need for gentle operative technique to minimize the volume of damaged tissue and for adherence to principles of aseptic surgery to reduce the level of bacterial contamination.

Following closure of the wound, its environment is sealed by local intravascular coagulation and the events of early inflammation which initiate wound healing: this may explain why postoperative administration of antibiotics is ineffective in preventing wound infection. Antibiotics administered preoperatively diffuse into the peripheral compartment, in this case the wound fluid; since the wound is saturated with antimicrobials at the time it becomes contaminated, potentially invading bacteria are inhibited from multiplying and many are killed.

For years the basic principles concerning appropriate timing in administering antibiotics for prophylaxis were not accepted. Although a controlled trial demonstrating the efficacy of antibiotic prophylaxis in potentially contaminated operations was reported by Bernard and Cole, other reports produced conflicting conclusions. Nearly 10 years after the description of the decisive or vulnerable period by Burke, the data from a controlled clinical trial proving that antibiotics were effective only when given in the immediate preoperative period were reported and widely accepted by surgeons. Doubts about the efficacy of antibiotic prophylaxis persisted well into the 1970s, but during the last two decades many excellent studies have been published, so that today antibiotic prophylaxis is an established practice and the principles for optimal preventive antibiotic administration are widely accepted.

1.Use an antibiotic with efficacy against the bacteria likely to contaminate the wound as demonstrated in a controlled clinical trial.

2.Use full doses of the chosen antibiotic.

3.Administer the antibiotics preoperatively at a time such that effective tissue concentrations will have been achieved when intraoperative contamination occurs.

4.If the operation is prolonged beyond 3 or 4 h, give another dose. Otherwise, single dose prophylaxis is effective in most clinical situations.

5.Employ antibiotic prophylaxis whenever the risk of wound infection is increased.

The first prospective controlled trial which investigated the proper postoperative duration of antibiotic prophylaxis was performed by Strachan and colleagues in 1977. A single preoperative dose of cefazolin was compared with a regimen of cefazolin given for a period of 5 days after operation. The infection rate following a single dose of antibiotic was 3 per cent; that following multiple postoperative dosing was 5 per cent. Although there was no statistically significant difference between these figures, the slight numerical difference in favour of the single dose seen in this study was also found in many subsequent studies which tested the same hypothesis for various indications. The most prudent and conservative interpretation of the results of all of these studies is that, at the very least, single dose prophylaxis is as effective as multiple dosing, and is preferable because it is less likely to alter antibiotic resistance patterns of bacteria in a hospital. It is astonishing in the presence of this evidence (Table 7) 11 that multiple dose prophylaxis still is used today in many institutions.

The risk of developing a wound infection has traditionally been determined by stratifying operations into classes: clean, clean-contaminated, contaminated, and dirty, based on the relative degree of intraoperative bacterial contamination. This scheme ignores other important factors, such as the functional state of host defences and the amount of tissue trauma engendered by the operation, which also help to determine the risk of developing a wound infection. Regression analysis of outcome in a very large number of surgical patients has indicated that the factors controlling the risk of developing a wound infection are: heavy bacterial contamination as reflected in an operation classed as contaminated or dirty; impaired host defences as reflected in an ASA score of 3 or higher; and long duration of operation. The critical time is procedure-specific (Table 8) 13.

Any patient exhibiting one or more of these risk factors should be given antibiotic prophylaxis. In addition, prophylaxis should be administered whenever a prosthesis is to be inserted during the operation.

In the discussion of selected specific clinical circumstances, we have used the results of published controlled studies which fulfil most of these following criteria: prospective conduct of the study, definition of entrance criteria and drop-out conditions, consideration of risk factors, unbiased randomization, double-blind assessment of clinical and bacteriological outcome, and appropriate statistical analysis.

The risk of wound infection following colorectal operations without prophylaxis is of the order of 40 per cent. A single dose of parenteral antibiotics or effective oral antibiotic bowel preparation can reduce the incidence of postoperative infection to less than 10 per cent. The two essential steps in effective prophylaxis for an elective colon operation are thorough mechanical cleansing of the bowel, preferably by polyethylene glycol purgation, and oral administration of antibiotics: neomycin and erythromycin base are effective. Parenteral antibiotics alone are less reliable in this situation. Since the risk associated with administering a single parenteral dose of a &bgr;-lactam antibiotic is minimal, we now employ combined oral and systemic prophylaxis (Table 9) 12. The use of parenteral antibiotics alone is not recommended in an elective surgery situation, but is the only regimen available for emergency operations.

Antibiotic prophylaxis for patients undergoing surgery for acute appendicitis includes a treatment aspect for the intra-abdominal infection, as well as a prophylaxis aspect as regards infection of the abdominal wound. Antibiotics are of questionable therapeutic value in simple acute appendicitis, but are certainly therapeutic when perforated appendicitis and peritonitis are present. For all other circumstances, single dose prophylaxis is justified. The high risk of wound infection following perforation justifies leaving the subcutaneous wound open.

The best results are obtained with antibiotics active against aerobic as well as anaerobic bacteria. In studies in which an aminoglycoside or a cephalosporin was used in combination with either clindamycin or metronidazole, only seven of 261 patients (2.7 per cent) developed a wound infection. The best current regimen seems to be metronidazole combined with cefazolin.

The incidence of postoperative wound infections following stomach operations correlates directly with the number of bacteria within the stomach which, in turn, correlates with the acidity of the stomach and the underlying pathology. The ‘acid barrier’ which effectively kills swallowed bacteria in normal individuals may be altered by H&sub2;-receptor antagonists given during the 12 h before operation. All groups of antibiotics have been studied as prophylaxis for gastroduodenal operations. First-generation cephalosporins are as effective as any other group of &bgr;-lactam drugs and are as effective as aminoglycosides.

Recommended prophylaxis for gastroduodenal operations involves interdicting use of acid secretion blocking or neutralizing agents for 1 or 2 days preoperatively, including when ordered as part of the anaesthetic premedication, and administration of 2 g of cefazolin on induction of anaesthesia.

Although the normal biliary tree rarely harbours any bacteria, in the presence of disease the biliary tract should be viewed as bacterially contaminated. The number of bacteria is influenced by a variety of factors, primarily the presence of biliary stones or a stricture (Table 10) 15. The risk of infection following an operation for biliary disease without antibiotic cover is about 16 per cent. Numerous clinical trials have employed a variety of antibiotic regimens in biliary operations (Table 11) 14.

Single dose antibiotic prophylaxis is appropriate in bile tract surgery. Although enterococci are frequently recovered from bile, their presence can be ignored in choosing an antibiotic for prophylaxis when cholecystectomy is being performed for calculous disease. The agent of choice remains 2 g of cefazolin given about 30 to 45 min prior to the operation. Second choice agents may be cefuroxime, cefamandole, sulphamethoxazole-trimethoprim, or cefotaxime. The use of ceftriaxone is not recommended because of its long half-life. Cholangitis (fever, chills, jaundice) involves a more faeculent spectrum of bacteria, including the regular presence of anaerobes. In this circumstance, ampicillin-sulbactam, 2 g, is preferred.

The risk of infection is increased by the clinical setting in which most vascular reconstructions are performed: electively for arterial insufficiency, implying some degree of tissue ischaemia, or as an emergency for trauma. The frequent need for insertion of a prosthesis for bypass or repair further disables host defence mechanisms and increases the risk of infection. Overall, the risk of infection following vascular surgery is of the order of 4 per cent. The bacteria of concern are S. aureus, E. coli and other enteric Gram-negative rods, which are the cause of early postoperative infections, and the S. epidermidis group of organisms which cause indolent late graft infections. A few controlled clinical trials have been reported (Table 12) 16, but recent increases in resistance among staphylococci, especially S. epidermidis, mandate care in the choice of antibiotic for prophylaxis.

Recommended prophylaxis is cefazolin administered at induction of anaesthesia, as long as two-thirds or more of S. epidermidis group isolates in the hospital are sensitive to this antibiotic. If S. epidermidis resistance is a problem, ampicillin-sulbactam or sulphamethoxazole-trimethoprim are currently effective alternatives. If methicillin-resistant staphylococci are a problem, vancomycin (for the staphylococci) plus cefotaxime or aztreonam (for the coliforms) should be effective.

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