Types of Infection
A wound abscess presents all the Celsian clinical features of acute inflammation: calor(heat), rubor (redness), dolor (pain)and tumour(swelling),to which can be added functio leasa (loss of function ) .it hurts the infected part is not used). Pyogenic organisms, predominantly Staphylococcus aureus, cause tissue necrosis and suppuration. Pus is also composed of dead and dying white blood cells which release damaging cytokines, oxygen-free radicals and other molecules. An abscess is surrounded by an acute inflammatory response, and a pyogenic membrane composed of fibrinous exudate and oedema, and the cells of acute inflammation. Granulation tissue (macrophages, angiogenesis and fibrobbasts) forms later around the suppuration and beads to collagen deposition. If excessive or partly sterilised by antibiotics (antibioma), a chronic abscess may result. Abscesses usually track along planes of least resistance and point towards the skin. Wound abscesses may spontaneously discharge through a surgical incision but most take 7—9 days to form after surgery. Many infections may present after the patient has left hospital.
Abscesses may need débridement and curettage with an exploration to break down all loculi before resolution can occur. Persistent chronic abscesses may lead to sinus or fistula formation. In a chronic abscess, lymphocytes and plasma cells are seen with sequestration and later calcification. Certain organisms are related to chronicity, sinus and fistuba formation, e.g. mycobacteria and actinomyces, and should not be forgotten.
Perianastomotic abscesses may be the cause or result of anastomotic leakage. Deep cavity abscess (pleura or peritoneum) may be difficult to diagnose or locate even when there is strong clinical suspicion (Fig. 7.6). Plain or contrast radiographs may not be helpful, whereas ubtrasonography,computerised tomography, magnetic resonance imaging and isotope scans are usually accurate and may allow guided aspiration without the need for surgical intervention.
The role of antibiotics in the treatment of wound abscesses is controversial unless there are signs of spreading infection (ceblulitis or lymphangitis). Surgical decompression and curettage must be adequate and may allow resuture without antibiotics but this is also controversial. Delayed primary or secondary suture is safer.
Cellulitis and lymphangitis
This is the nonsuppurative invasive infection of tissues. In addition to the cardinal signs of inflammation, there is poor bocabisation. Spreading infection is typical of organisms such as f3-haemolytic streptococci (Fig. 7.7), staphylococci (Fig. 7.8) and C. perfringens. Tissue destruction and ulceration may follow, caused by release of streptokinase, hyaburonidase and other proteases.
Systemic signs (toxaemia) are common: SIRS, chills, fever and rigors. These follow release of exotoxins and cytokines but blood cultures are often negative.
Lymphangitis is caused by similar processes but presents as painful red streaks in affected lymphatics. Cellulitis is usually located at the point of injury and subsequent tissue infection. Lymphangitis is often accompanied by painful lymph node groups in the rebated drainage area.
Bacteraemia and septicaemia
These are unusual in superficial wound infections but common after anastomotic breakdown. They are usually transient and follow procedures undertaken through infected tissues (particularly instrumentation in infected bile or urine).Bacteraemia is important when prosthetics have been implanted, particularly cardiac valves. Septicaemia commonly relates to colonisation and translocation in the gastrointestinal tract and may follow anastomotic breakdown accompanied by MSOF (Fig. 7.3). Aerobic Gram-negative bacilli are mainly responsible but S. aureus and fungi may be involved, particularly after the use of broad-spectrum antibiotics.
Specific wound infections
Gas gangrene is caused by C. perfringens. The Gram-positive, spore-bearing bacilli are widely found in nature, particularly soil and faeces, which is relevant to military and traumatic surgery, and colorectab operations. Patients who are immunocompromised, diabetic or have malignant disease are at risk, particularly when anaerobic wound conditions are present with necrotic or foreign material. Wound infections are associated with severe local wound pain and crepitus (gas in the tissues which may also be noted on plain radiographs). The wound presents a thin, brown, sweet-smelling exudate, from which bacteria can be recognised on Gram staining. Oedema and spreading gangrene follow the release of collagenase, hyaburonidase, other proteases and a-toxin. Systemic complications with circulatory collapse and MSOF supersede without appropriate intervention.
Prophylaxis in patients at risk should always be considered, particularly amputation for peripheral vascular disease. Once established, barge doses of intravenous penicillin and aggressive débridement of affected tissues are required. The use of hyperbaric oxygen is controversial.
Synergistic spreading gangrene (necrotising fasciitis) is not caused by cbostridia. A mixed pattern of organisms is responsible — cobiforms, staphylococci, Bacteroidesspp., anaerobic streptococci and pepto-streptococci have been implicated. Synonyms have been associated with abdominal wall infections (Meleney’s synergistic hospital gangrene) and scrotal infection (Fournier’s gangrene, Fig. 7.9). Patients are almost always immunocompromised (such as diabetes mebbitus). The initial wound may have been minor, but severely contaminated wounds are more likely to be the cause. Severe wound pain, signs of spreading inflammation with crepitus and smell lead on to widespread gangrene. The extent of subdermal spread of gangrene is always much more extensive than at first is apparent. Wide-spectrum antibiotic therapy must be combined with aggressive circulatory support and wide excision and laying open of affected tissue. Débridement may need to be extensive. Patients who survive need barge areas of skin grafting.
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