Prevention of infection is key to successful orthopaedic surgery. Meticulous attention to aseptic technique in the operating room, proper skin preparation and surgical scrub, the use of modern gown and mask techniques, planning the operation to shorten the time the tissues are exposed to air, laminar flow air, and prophylactic antibiotics1–4 are all important in the prevention of infection. However, none is as critical as meticulous debridement of wounds and careful handling of tissues to prevent cell death.4 When infection does occur following an operation or from hematogenous origin, early diagnosis and prompt effective treatment can prevent disastrous complications.
I. PREVENTION
A. Elective surgery. Refer to Chapters 2, III, and 11, I, for techniques described for the prevention of operative and posttraumatic infections.
B. Early diagnosis
- Whenever a patient’s postoperative or postinjury status does not follow the normal or expected course, the surgeon should be alert to the possibility of infection. A respiratory problem such as mild atelectasis may be a cause of persistent postoperative temperature elevation (this is especially common in patients who smoke), but such a potential diagnosis should not lull the surgeon into complacency. Wound infection may be the cause, or the two could be concurrent. Large hematomas can themselves be the cause of fever, but hematomas also represent the best culture media for bacteria and hence should be avoided or evacuated if present. Always obtain a culture of any evacuated hematoma.
- When there is concern regarding a wound infection, inspect the wound and document the findings at least daily, using sterile technique. Inspect the wound for swelling, erythema, and serous or bloody drainage. Culture any drainage. Tense skin, erythema, and abnormal tenderness or swelling are frequently signs of low-grade inflammation and infection.
- If the patient does not respond promptly to treatment or if the wound remains indurated, aspiration should be carried out using aseptic technique with a large needle inserted into the wound area but away from the suture line.
- A low-grade fever in patients who have had antibiotics is not uncommon. In such instances, the temperature rarely exceeds 37.8°C (100°F) and may show a mild afternoon elevation. The patient frequently feels lethargic and has mild anorexia.
- Be alert to the possibility of infection. Establish the diagnosis through cultures whenever possible, and treat the infection aggressively. If in doubt, the best course is generally to return the patient to the operating room and open the wound, irrigate and debride it to remove hematoma and necrotic wound tissue, and reclose the wound using the most “tissue friendly” suture technique (see Chapter 11). If a low-grade inflammatory process involves a joint, the patient complains of pain from passive motion of the joint, which should alert the surgeon to the possibility of a septic joint.
Consultation with another experienced surgeon can be helpful.
C. Treatment. Once the diagnosis of a musculoskeletal infection has been established, treatment proceeds as for acute osteomyelitis or septic arthritis. The principles of treatment include removal of all dead tissue and any hematoma along with appropriate antibiotic therapy. The wound is nearly always left open for secondary closure except when the infection involves a joint. If the wound is closed, a suction drain is mandatory.
II. BONE AND JOINT INFECTIONS
A. Bones and joints represent special problems for the host defense mechanisms. Normal bone has an excellent blood supply, although there is slowing of the circulation in the metaphyseal region in children. Once pus forms under pressure, the vascular supply to bone is lost because of its rigid structure, resulting in areas of infected, devitalized bone. Septic emboli in bone or vascular thrombosis can cause additional devascularization. Ligaments and tendons are relatively avascular structures and do not handle infection well. Joints, with their avascular cartilage and menisci, pose a particular problem. Local phagocytic function can be deficient, and it is often difficult to ensure adequate delivery of humoral factors (antibodies, opsonins, complement). In addition to the direct destructive effect of cell breakdown on cartilage, the pus under pressure interferes with cartilage nutrition and blood supply to the periarticular structures. At particular risk is the epiphyseal blood supply, and avascular necrosis may be the result. Antibiotics can inhibit or cure an infection only when they can reach the infecting organism in bacteriostatic or bactericidal concentrations. Infections producing pressure in a bone or joint as well as in relatively avascular tissues can impede or prevent antibiotics from reaching the primary site of infection.
B. An acute infection of bone (hematogenous osteomyelitis), in its earliest phase, is a medical disease and can often be cured by prompt, appropriate antibiotic therapy. However, the time between initial infection and bone infarct is often short. If effective treatment is delayed and devascularization of the involved tissues results, surgical treatment is a necessary adjunct to the antibiotic therapy. Even under the best of circumstances, late treatment (perhaps as early as 48 hours after the infection starts) may result in the loss of or abnormal function of the joint. Thus, appropriate antibiotic therapy must be initiated as early as possible. Appropriate therapy requires knowledge of the etiologic agent and its sensitivities. Every effort should be made to obtain a bacterial culture and determine sensitivity. Once the culture specimen is obtained, it is important to institute antibiotic therapy based on a probable diagnosis using the most effective broad-spectrum antibiotics.
C. Diagnosis
- The earliest symptom or sign that may help differentiate a bone or joint infection is usually pain or localized tenderness in the periarticular region. In the infant, refusal to move or use an extremity may be noted first. The cardinal signs of infection—redness, heat, and swelling—may appear later than the pain and tenderness, or not at all. When examining a child with a fever of unknown origin, note any pain or alteration of the normal range of motions of a joint and carefully palpate all metaphyseal areas to determine local tenderness. Roentgenograms are of little value in making the early diagnosis, although careful comparison with the opposite side may show abnormal soft-tissue shadows. Roentgenographic evidence of bone or joint destruction is seen during the chronic phase of the disease. Osteomyelitis should always be included in the differential diagnosis for a patient with the radiographic appearance of a bone tumor.5 Radioisotopic bone scanning, especially indium imaging, is helpful in early localization of bone infection.6 Many authorities have advocated the use of magnetic resonance imaging in the diagnosis of osteomyelitis,7–10 but clinical context is of paramount importance in the evaluation of any abnormal findings. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) serum levels are useful in laboratory evaluations.11–14
- Identification of the infecting organism is essential. In the early stages of the disease, particularly if there is a spiking temperature, blood cultures can often identify the organism. If acute metaphyseal tenderness is present, the organism can frequently be obtained by inserting a needle into the site of maximum tenderness. A serrated biopsy needle is useful if subperiosteal pus is not encountered. If a joint is involved, the effusion should be aspirated before joint lavage. Processing the aspirates should include the following:
a. Immediate Gram stain.
b. Culture for aerobic and anaerobic bacteria.
c. White blood cell count and differential.
d. Determination of the character of the hyaluronic precipitate, the presence of fibrin clots, and any disparity between the glucose in the aspirate and blood glucose may prove helpful, but the Gram stain, culture, and cell count are most valuable.
D. Differential diagnosis. Care must be taken to differentiate soft-tissue infection, or cellulitis, from an infection involving a bone or joint. This is a particularly important precaution when the infection overlies a joint because any aspiration of a reactive sterile effusion by passing a needle through the soft-tissue infection may create a pyarthrosis. Tenderness and swelling from unrecognized trauma over a bone, particularly with some periosteal reaction, can present a confusing picture, but the absence of fever and systemic signs is helpful. Nonbacterial inflammatory arthritis, including viral and toxic synovitis and rheumatoid arthritis, must be included in a differential diagnosis, but until proved otherwise, think first of septic arthritis. Spontaneous hemorrhages in patients with hemophilia and fractures in paraplegic patients, particularly patients with meningomyelocele, are special situations that can confuse the picture.
E. Bacterial considerations1,4,12
- In acute hematogenous osteomyelitis, Staphylococcus aureus is the most common etiologic agent in all age groups. In recent years, an increasing number of isolated strains have been found to be methicillin resistant. In infants younger than 1 month, a diversity of other bacteria must also be considered. Group B streptococci and gram-negative organisms such as Escherichia coli, Proteus species, Pseudomonas aeruginosa, Klebsiella pneumoniae, and Salmonella species are all possible pathogens. In infants with a complicated medical history, particularly those who have had prolonged indwelling venous catheters, extensive surgery, or intensive prior antibiotic therapy, coagulase-negative staphylococci, and rarely anaerobic organisms such as Bacteroides fragilis and fungal agents such as Candida albicans (hard to diagnose) must also be considered.
- In septic arthritis and osteomyelitis among infants younger than 1 month, S. aureus is the predominant etiologic agent. After the neonatal period and up to 4 years of age, Haemophilus influenzae is also a major cause of septic arthritis in those who have not had the Hib vaccine. In later childhood, the etiologic agents are the same as for adults, with S. aureus predominating. Neisseria gonorrhoeae
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