Robin B. Churchill and Blanca E. Gonzalez
Bone and joint infections may occur at any age but are more common in children than adults. Optimal management requires early diagnosis and aggressive initial treatment to prevent disabling sequelae. This is usually best achieved with care being provided by a multidisciplinary team of pediatricians and orthopedic surgeons experienced in the specific issues encountered in care of growing children. Soft tissue infections occur more frequently than skeletal infections but they are generally simpler to diagnose and treat with antibiotic therapy. This chapter reviews the approach to diagnosis and management of these disorders in children.
ACUTE HEMATOGENOUS OSTEOMYELITIS
Acute hematogenous osteomyelitis (AHO) is a disease of young children. The majority of cases occur before 5 years of age with up to one third occurring in children younger than 2 years of age.1,2 There is a male predilection, with males outnumbering females in most published series by approximately 2:1.1-5 However, in a more recently published series, males accounted for 52% of the patients.6 There is frequently a history of some type of minor blunt trauma2,7 or intercurrent illness, such as an upper respiratory tract infection.8 Other risk factors for AHO include immunodeficiency states, sickle cell anemia, and indwelling vascular catheters. In some areas of the United States, the incidence of osteoarticular diseases including AHO has increased with the emergence of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA).6
The majority of bone infections in children are of hematogenous origin.2 The vascular anatomy of long bones in children underlies the predilection for localization of blood-borne bacteria. In children, unlike in adults and young infants, the blood supply of the epiphysis is separate from the metaphysis.10 The nutrient artery to the metaphysis empties into a system of venous sinusoids in which sluggish flow presumably facilitates deposition of bacteria. During the cellulitic phase of acute osteomyelitis infection originates on the venous side of the system and then spreads to the nutrient artery, causing thrombosis of the nutrient artery.9 The resultant ischemia prevents host defense mechanisms from reaching the area and allows bacterial proliferation. Formation of an abscess can then occur which can rupture into the subperiosteal space with subsequent elevation of the periosteum, which is loosely adherent in children. If infection is uncontrolled, purulent material may extend up and down the diaphysis and circumferentially around the bone (see Figure 234-1). In areas in which the metaphysis is intra-articular, such as the hip and shoulder, the intraosseous abscess may rupture into the joint resulting in septic arthritis.9 In newborns and young infants, blood vessels connect the metaphysis and epiphysis, and rupture of pus into the adjacent joint space is more common.2,11
Thrombosis of blood vessels and elevation of the periosteum deprive the bone of its blood supply, resulting in necrosis, which can be extensive without early surgical drainage. Left untreated, granulation tissue forms around the dead bone, which separates from live bone and becomes a sequestrum. New bone growing around the dead bone is called an involucrum. Sinus tract formation occurs in the involucrum allowing pus to escape and eventually form sinus tracts through the skin. The involucrum is mechanically weak and may become the site of pathologic fractures.
Etiologic Agents The predominant organism in acute hematogenous osteomyelitis in all age groups is Staphylococcus aureus, accounting for 50% to 90% of cases.17,18 In recent years, CA-MRSA has emerged as a significant pathogen in AHO.6,17,19
Streptococcus pyogenes osteomyelitis accounts for approximately 10% of cases of acute hematogenous osteomyelitis (AHO) with a higher incidence in preschool and early school-aged children.21,22Streptococcus pneumoniae has been isolated as a cause of AHO in children less than 3 years of age.22-24 The use of the pneumococcal PCV-7 will likely reduce the incidence of this pathogen as overall pneumococcal invasive disease has decreased since the introduction of this vaccine.25
Kingella kingae, a gram-negative organism that may colonize the respiratory tract, is being increasingly recognized as an important pathogen in osteoarticular infections in children younger than 2 years of age. Rates ranging up to 50% in this age group have been reported in some series.26,27 Osteoarticular infections caused by this agent are, not surprisingly, often preceded by upper respiratory tract infections. The clinical course is less aggressive than that seen with other bacteria, causing fewer symptoms and minimal bone destruction.
FIGURE 234-1. Magnetic resonance imaging scan axial stir sequence at the level of the distal tibia and fibula demonstrating an extensive subperiosteal abscess surrounding the cortex of the fibula (arrow) secondary to methicillin-resistant Staphylococcus aureus (MRSA).
Streptococcus agalactie and gram-negative organisms occur almost exclusively in neonates. Salmonella is the most common organism isolated in patients with sickle cell anemia with osteomyelitis.29Pseudomonas infections are usually a result of puncture wounds to the feet. Anaerobic, gram-negative, and polymicrobial infections can result after puncture wounds or open fractures. Haemophilus influenzae type B, an important pathogen in older series, is now rarely seen in countries that routinely use the H influenzae conjugate vaccine. Less common organisms causing osteomyelitis include Bartonella henselae (the organism of Cat Scratch Disease), Brucella, and Mycobacterium tuberculosis.
CLINICAL MANIFESTATIONS AND DIFFERENTIAL DIAGNOSIS
Early signs of skeletal infection may be subtle, especially in the neonate who typically does not appear ill.9,12,13 One of the earliest signs of osteomyelitis in infants is failure to move the affected extremity (pseudoparalysis), pain on passive movement, or both.1 Older children frequently present with fever, pain at the site of infection, and refusal to use the affected extremity.3,4 Nonspecific constitutional symptoms can occur but are not prominent. There is intense tenderness over the metaphysis of the bone on palpation, and muscles of the adjacent joint are frequently in spasm. The joint is held in a position of comfort, usually mild flexion, but to a lesser degree than with septic arthritis.9 Soft tissue changes of swelling, erythema, and heat are generally late findings in osteomyelitis. After several days, a sympathetic sterile effusion may occasionally form in a nearby joint, presenting a problem in differentiation from septic arthritis.9 It is imperative for the evaluating physician to remember that any infant or child with fever and failure to bear weight or use an extremity needs to be evaluated for potential musculoskeletal infection.
Long bones are most often involved in acute hematogenous osteomyelitis in children.1,3,4,14,15 The most common sites of involvement are the lower femoral and upper tibial metaphyses. Next in frequency are the proximal femoral metaphysis and distal metaphyses of the radius and humerus.9 Infection in flat bones occurs most often in the pelvis and calcaneus in children.1,3,4,14,15
The differential diagnosis of osteomyelitis includes cellulitis, septic arthritis, pyomyositis, malignancy, collagen vascular disease, and trauma. In differentiating cellulitis from bone infection, tenderness disproportionate to physical findings suggests osteomyelitis. Septic arthritis may be differentiated from osteomyelitis by its more discrete joint findings and its greater degree of joint immobility, in addition to a lack of metaphyseal tenderness.16 History, clinical scenario, and radiologic studies are helpful in differentiating skeletal infection from other diagnoses. Recovery of the causative organism is best obtained by biopsy or aspiration, which not only establishes the diagnosis, but also facilitates susceptibility testing and rules out other pathologic processes.
Special Clinical Situations
Neonatal Osteomyelitis Diagnosis of osteomyelitis in an infant who is less than 1 month of age requires a high index of suspicion. Young infants with bone infections often lack fever and other systemic signs of illness.1,30Symptoms may be confined to failure to move an extremity and fussiness.2 Predisposing factors include prematurity, preceding infection, bacteremia, exchange transfusions, and the presence of intravascular catheters.30-32S aureus, group B streptococcus, and enteric gram-negative bacteria are the most common etiologic agents.31,33 Candida must also be considered, especially in the premature infant who has had previous antibiotic therapy and placement of intravascular catheters.34,35 Neonates are more likely to have multifocal disease and decompression of pus into the adjacent joint resulting in an associated septic arthritis.30
Pelvic osteomyelitis often presents a diagnostic dilemma. Most patients present with fever, limp or refusal to bear weight, and pain that seems to be localized to the hip, groin, or buttocks.36-38 Initial diagnostic impressions often include intraabdominal pathology, other intrapelvic problems, and septic arthritis of the hip joint. In these cases, imaging studies such as bone scans, MRI, or computerized tomography (CT), may be particularly helpful in establishing the diagnosis.
Osteomyelitis in the Child with Sickle Cell Anemia
Aseptic bone infarcts are common in children with sickle cell disease. The signs, symptoms, and radiographic changes mimic those of acute osteomyelitis, making differentiation between the diagnoses difficult. Neither bone scan nor MRI reliably discriminates between the two conditions.39-41 Ultrasonography has been reported as a method assisting in differentiation between infarction and infection.42,43Diagnostic aspiration of the site should be done in an attempt to recover the organism and confirm the diagnosis. Salmonella species, followed by S aureus, are the most frequent causes of bone infection in the sickle cell patient.29,44 Aggressive surgery and prolonged parenteral therapy may be necessary for treatment of osteomyelitis in the child with sickle cell disease.
Vertebral osteomyelitis and discitis are two entities that may present similarly with patients complaining of back pain, limp, or refusal to bear weight. Vertebral osteomyelitis accounts for 1% to 2% of osteomyelitis in children. It is seen in older children and adolescents who are usually febrile on presentation and may have had symptoms for several weeks or months. The lumbosacral area is most commonly involved.45Staphylococcus aureus is the predominant organism isolated. Discitis is seen more frequently in children less than 5 years of age where blood supply to intervertebral discs is rich. These patients are seldom ill appearing, and fever is uncommon.45
Plain radiographs may show narrowing of the intervertebral space with destruction of vertebral endplates in discitis. Destruction of the vertebrae is seen in vertebral osteomyelitis, but findings may not appear until later in the disease course. MRI has become the modality of choice to differentiate one entity from the other.
Figure 234-2 outlines an approach to the diagnosis and management of a patient with suspected acute hematogenous osteomyelitis. No specific laboratory test for the diagnosis of osteomyelitis exists, with the exception of isolation of a pathogen from bone.
Bone Needle Aspiration and Biopsy
These procedures are usually performed by an experienced orthopedic surgeon, or interventional radiologist. Bone cultures are positive in 38% to 91% of cases and confirm the diagnosis.1,7,14,15 Blood cultures are very useful, demonstrating the organism in 30% to 76% of cases.3,47 The highest diagnostic yield occurs when both blood and bone specimens are submitted for culture. Recovery of organisms is enhanced by inoculating the bone aspirates into blood culture bottles. This is particularly important when fastidious organisms such as Kingella are suspected which may require up to a week of incubation before being evident.48 Alternatively, bone or joint aspirates can be submitted for amplification of 16SrRNA and specific real-time PCR (for Kingella) when trying to establish a diagnosis in culture-negative osteomyelitis.26,28,49
FIGURE 234-2. An algorithmic approach to the management of a patient with suspected acute hematogenous osteomyelitis. (©1995 American Academy of Orthopaedic Surgeons. Volume 3(4), pp. 183-193, with permission.)
The ability to recover an organism from blood or bone cultures decreases with prior antimicrobial therapy. Therefore, if the patient is stable, and blood and bone cultures are done in a timely fashion, it is preferable to delay the initiation of antibiotics until cultures are obtained.
Other Laboratory Studies
Peripheral white blood count (WBC) and differential may or may not be abnormal. The erythrocyte sedimentation rate (ESR) rises slowly and initially may be normal or minimally elevated. ESR usually peaks 3 to 5 days after the initiation of therapy and returns to normal in 3 to 6 weeks.50 Many experts find C-reactive protein (CRP) to be a more responsive measure of the efficacy of therapy, because it rises earlier, peaks within 48 hours of onset of symptoms, and returns to normal after approximately 1 week of efficacious therapy.50 Surgical intervention itself increases inflammatory markers so baseline ESR and CRP values used for monitoring disease progression should be repeated after surgical intervention when drainage procedures are necessary.
Plain films begin to show destructive changes approximately 7 to 14 days after the onset of bone infection. Subtle osteopenic changes may sometimes be discerned after 5 days. Plain films may be helpful acutely in demonstrating changes in the deep soft tissue adjacent to the affected bone or joint effusion. To detect alterations of the soft tissue, identical views of the contralateral limb are recommended.
Radiophosphate bone scintigraphy using technetium (99Tc) is the most commonly used procedure. Although bone scans have a high degree of sensitivity, they do not make the diagnosis of skeletal infection. Bone scans indicate abnormal areas of bone without revealing whether the abnormality is due to infection, tumor, or injury. Bone scans are not required in the diagnostic workup of every child with presumed bone infection. If the site of infection is able to be localized by physical examination, a bone scan is not necessary prior to aspiration. It has been shown experimentally that aspiration of bone or joint does not compromise results of subsequent bone scans.51 Bone scans are particularly helpful in cases where the site of infection is not readily apparent by physical examination or when multiple sites of involvement are suspected.
Gallium scans or indium-labeled leukocyte scans are less commonly used techniques in the diagnosis of skeletal infection. Indium-labeled leukocyte scans, which reflect migration of white blood cells into areas of inflammation, are useful in diagnosis of osteomyelitis associated with trauma, recent surgery, or prosthetic devices.52
Magnetic Resonance Imaging
MRI is an effective modality for imaging bone and is quite sensitive and specific in diagnosis of musculoskeletal infections.53-56 It is not recommended as a screening study but is very useful when there is an indication where the pathology is localized either from physical examination or radionuclide scanning. It can be especially helpful in cases in which the spine or the pelvis is the site of infection, conflicting clinical data exist, or in planning surgical intervention.56 Many orthopedic surgeons request a preoperative MRI because the spatial resolution of MRI is far superior to bone scan. Additionally, conditions requiring surgical intervention such as bone abscesses, subperiosteal abscesses, joint effusions, and pyomyositis are readily determined by MRI.41
The need for surgery in osteomyelitis depends on the extent of the pathologic process in individual patients and probably somewhat on the aggressiveness of specific pathogens. In children who present early in the “cellulitic phase,” antibiotic therapy alone is usually sufficient for treatment. If pus is encountered during diagnostic aspiration, if a subperiosteal or intramedullary abscess is detected by ultrasound or MRI, or if a bone lesion is evident on plain films, surgical intervention is warranted. Patients initiated on medical therapy who do not promptly improve should also be evaluated for the need for surgery. Surgical drainage and debridement remove inflammatory products more rapidly than do host defense mechanisms, providing a more effective environment for antibiotic penetration and preventing further bone necrosis. Drainage of an abscess reduces the inoculum of bacteria present, and debridement of necrotic and avascular bone eliminates areas prone to poor penetration where bacteria can persist.8 Any patient with a lytic lesion on plain films should have, in addition to cultures sent, a bone biopsy sent to pathology for histology and special stains to rule out other pathologic processes such as malignancy and to evaluate for unusual organisms such as fungi.57
Initial antibiotic therapy for osteomyelitis should be based on Gram-stained specimens obtained from bone aspiration, when possible. The importance of obtaining the exact bacteriologic diagnosis by blood or bone culture cannot be overemphasized. In the absence of such data, initial therapy is empiric and must be directed at likely pathogens based on age of child and considering underlying medical conditions.
Because S aureus is the major pathogen of acute hematogenous osteomyelitis (AHO), empiric therapy for all age groups should include an appropriate antistaphylococcal agent. Before the emergence of CA-MRSA, nafcillin, oxacillin or a first-generation cephalosporin were the antibiotics of choice for coverage of S aureus. Currently, it is important to know the rates of infection caused by CA-MRSA locally, prior to choosing empiric treatment regimens. Some authors have suggested that when methicillin resistance among S aureus exceeds 10%, clindamycin or vancomycin should be used initially rather than a β-lactam agent.22 Several studies have proven the effectiveness of clindamycin in the treatment of osteomyelitis.58-60 However, certain strains of S aureus may develop resistance to this drug. The presence of inducible resistance may be detected in vitro with a D-test. When the inducible resistance rates in the community are greater than 10% to 15%, clindamycin alone should not be used for initial treatment.22
Vancomycin and clindamycin are also effective for the treatment of most AHO caused by Group A Streptococci and S pneumoniae. Kingella kingae is susceptible to most beta-lactam agents as well as second- and third-generation cephalosporins that are also effective against Haemophilus influenzae type B.
In the neonate, staphylococci and group B streptococci are the major pathogens, but coverage for enteric gram-negatives must be included. An appropriate initial therapeutic regimen includes an antistaphylococcal agent plus a third-generation cephalosporin, such as cefotaxime or an aminoglycoside.
In children less than 5 years of age, a regimen providing coverage for S aureus, S pyo-genes, Kingella, and S pneumoniae should be used. Clindamycin or vancomycin plus a third-generation cephalosporin provides appropriate coverage.
In immunocompromised children or those with underlying medical conditions, broader-spectrum coverage may be appropriate. If Pseudomonas is a consideration, an antipseudomonal penicillin plus an aminoglycoside or cefepime can be used.
Once an organism is identified, therapy should be guided by susceptibilities. If an methicillin-sensitive Staphylococcus aureus (MSSA) is identified, nafcillin, oxacillin, or a first-generation cephalosporin are the agents of choice. Cefazolin and other cephalosporins have been shown to reach adequate concentrations in bone tissue, provide more convenient dosing schedules,63,64 and are generally better tolerated.
In addition to vancomycin and clindamycin, newer antimicrobials have shown to be acceptable alternatives for the treatment of methicillin-resistant Staphylococcus aureus (MRSA) osteomyelitis. Linezolid is a promising agent for the treatment of MRSA osteomyelitis.65 It achieves excellent levels in bone and has equivalent intravenous and oral bioavailability.
When cultures remain sterile, treatment should be continued based on the most common organism for the age group, usually S aureus. If possible, initiating treatment with a single agent is preferred. If there is no response, less common organisms may be suspected. In children under 3 with negative cultures, Kingella kingae should strongly be considered.
There are several options for delivery of antibiotic therapy in the treatment of osteomyelitis. The entire course of therapy may be delivered parenterally through a central venous catheter or a peripherally inserted central catheter (PICC). Another common option is to initiate therapy parenterally, followed by orally administered drugs after the clinical condition has stabilized and any necessary surgical procedures have been performed. Oral therapy usually is initiated after 5 to 14 days of parenteral therapy and is equally efficacious when the responsible organism and its susceptibilities are defined. The selected option depends on a patient’s particular situation considering factors such as location, extent, and severity of disease, as well as the patient’s ability to tolerate oral therapy and the likelihood of compliance. It is important to recognize that exact length of parenteral or parenteral-oral therapy is dependent on a patient’s response and may need to be extended in severe disease or in the immunocompromised patient.
Dosages of oral antibiotics required in sequential intravenous-oral regimens are 2 to 3 times those used for minor infections. It is desirable to monitor absorption of oral antibiotics and compliance by measurement of serum bactericidal levels against the isolated organism or measurement of antibiotic serum levels; however, in practice, these are frequently not done.
The minimum or optimum duration of antimicrobial therapy for acute osteomyelitis is unknown. The usual recommended duration is 4 to 6 weeks but depends on the cause and extent of infection as well as clinical and laboratory response. Older literature suggests that courses of 3 weeks or less are associated with a greater likelihood of relapse or recurrence.7 Each patient must be evaluated individually, taking into account the speed of clinical response, whether surgical debridement was done, normalization of C-reactive protein or erythrocyte sedimentation rate, and radiologic findings.
COMPLICATIONS AND OUTCOME
The most common complication in acute hematogenous osteomyelitis is chronic or recurrent osteomyelitis, which occurs in fewer than 5% of cases. Development of chronic osteomyelitis is more common following nonhematogenous osteomyelitis. The hallmark of chronic osteomyelitis is bone necrosis. Therapy is primarily surgical with adjunctive long-term antibiotics. A bone biopsy should be obtained in chronic osteomyelitis for histopathology and culture and to exclude chronic recurrent osteomyelitis, Langerhans cell histiocytosis, primary bone tumors, and other malignancies.69
Other Complications and Outcome
Pathologic fractures can occur but are rare. If the bone growth plate is involved, there is a risk of abnormal length of affected bone. In general, the outcome of well-managed cases of acute osteomyelitis in pediatric patients is favorable.
Delayed or inadequate treatment of the septic joint can result in permanent joint damage with subsequent disability. Septic arthritis is most common in children less than 3 years of age.2,74,75 In most cases, a single, large joint is involved, usually in the lower extremity.75-77 As with osteomyelitis, males are affected more frequently.2,77 There may be a history of trauma or recent infection of the skin or upper respiratory tract. Underlying medical conditions such as immunodeficiencies and hemoglobinopathies are predisposing factors.
The anatomy of the synovial joint provides an environment conducive to bacterial infection.8 The synovial tissue lining the joint lacks a basement membrane and therefore secretes a transudate of serum. The rest of the joint surface is composed of avascular cartilage. Bacteria enter the joint by hematogenous seeding, direct extension from an adjacent focus, or direct inoculation during a joint aspiration, arthrotomy, or trauma. Initially, after bacterial invasion occurs, the synovial membrane swells and produces increased amounts of fluid, distending the joint. If infection persists without treatment, pus accumulates in the area and destruction of cartilage follows. Subluxation or dislocation of the joint with increased intra-articular pressure occurs when the joint capsule is distended by purulent fluid. This increased pressure may compromise blood supply in certain areas. In the hip, this may lead to avascular necrosis of the femoral head.74
As in osteomyelitis, etiologic agents of septic arthritis vary by age. S aureus (MSSA and MRSA) is the leading organism in all age groups.77,79,80 In neonates, group B streptococcus and enteric gram-negative organisms are also important to consider75 and may be isolated from an affected joint as a consequence of an adjacent osteomyelitis. Staphylococcus aureus, S pyogenes, Kingella kingae, and S pneumoniae are the most prominent causative pathogens in children less than 3 years of age.26Haemophilus influenzae type b, the most common organism in this age group in the past, is no longer a prominent agent in septic arthritis. In children older than 5 years, S aureus including MRSA and S pyogenes are the chief pathogens.81
Other organisms reported to cause septic arthritis in children include Neisseria meningitidis, P aeruginosa, and enteric gram-negative organisms including Salmonella.75,77Neisseria gonorrhoeae is a consideration in neonates and sexually active adolescents.2 Salmonella species are isolated more frequently in patients with sickle cell disease.
Children generally present acutely with a painful, erythematous, warm joint, and refusal to move or bear weight on the affected extremity. Fever, toxicity, and irritability are often accompanying features. The joint is held in the position of most comfort, usually mild flexion. When the hip is involved, joint swelling is generally not obvious, but the affected hip is held in a position of flexion, abduction, and external rotation.74,78 Young children may exhibit the phenomenon of “referred pain,” in which symptoms from an infected hip joint are referred to the ipsilateral knee. The differential diagnosis of septic arthritis includes reactive arthritis, juvenile rheumatoid arthritis, cellulitis, transient synovitis, and arthritis associated with systemic disease or malignancy.
Because of the risk of long-term orthopedic complications, septic arthritis is an orthopedic emergency. Joint aspiration is the most important component of the diagnostic evaluation. Other laboratory tests and radiologic studies are generally non-specific but findings may be useful to direct the evaluation.
Patients in whom the diagnosis is suspected should undergo immediate joint aspiration to rapidly confirm the diagnosis. Synovial fluid should be sent for Gram stain, aerobic and anaerobic cultures, and cell count with a leukocyte differential. Fungal cultures may be considered in some instances. Joint fluid cultures are positive in 30% to 60% of cases.2,77,79,82 Inoculation of joint fluid into blood culture bottles increases the yield of cultures, particularly when the etiologic agent is fastidious such as in the case of Kingella kingae.83,84 Leukocyte counts in the range of 50,000 cells/mm3, with a predominance of segmented neutrophils, are suggestive of bacterial arthritis, even in the absence of a positive culture. However, it should be recognized that white blood cell counts in infected joint fluid can vary widely, ranging from 2000 to 300,000 per mm3.74,85,86 Synovial fluid glucose and protein may be measured but are nonspecific.
Other Laboratory Tests
In addition to cultures of joint fluid, it is important to obtain blood cultures, which are positive 30% to 40% of the time.2,77 The combination of blood and joint fluid cultures reveals an etiologic agent in approximately 70% of cases.77,80 As in osteomyelitis, peripheral white blood count, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) may be useful in the workup of the patient with suspected joint infection but are nonspecific. Although frequently abnormal, they do not confirm or exclude the diagnosis. CRP and ESR are valuable adjuncts in gauging response to therapy.
Plain films may demonstrate evidence of soft tissue swelling or widening of the joint space. In the hip, lateral displacement or subluxation of the femoral head may be evident. Normal plain films do not eliminate the possibility of pyogenic arthritis of a joint. Ultra-sonography is a reliable method of detecting joint fluid, especially in the hip.74,87 It has the advantage of being noninvasive, usually does not require sedation, and generally is more readily available than MRI. MRI is also a sensitive method for detecting joint fluid and may demonstrate abnormalities in adjacent bone or soft tissue if present. The decision on the need for MRI should be made in conjunction with the consulting orthopedic surgeon.
Figure 234-3 illustrates an approach to the diagnosis and management of septic arthritis. An orthopedic surgeon experienced in the treatment of children should be involved in the management of the child with septic arthritis. The goals of therapy are decompression of the joint space and removal of inflammatory debris by adequate drainage; sterilization of the joint through the use of appropriate antimicrobial agents; relief of pain; and prevention of joint deformity.74,81
Drainage of the infected joint may be achieved through repeated aspiration, arthroscopic lavage, or open drainage with lavage. Repeated aspiration may be appropriate in a setting where no surgeon is readily available to perform arthroscopic or open drainage, but drainage with lavage, either arthroscopic or open, is superior because it allows thorough cleansing and removal of inflammatory debris that cannot be evacuated by aspiration. Arthrotomy has been considered the standard treatment for septic arthritis of the hip but an alternative management approach using arthroscopic techniques has less morbidity and similar efficacy.88-90
Antimicrobial therapy should be instituted immediately after blood cultures and joint fluid samples are obtained. Empiric, initial antibiotic choice is based on the likely pathogens at various ages, the results of Gram stain of the joint aspirate, and any special considerations dictated by the patient’s underlying medical problems or clinical situation.
Regimens for all age groups should include an antistaphylococcal agent with coverage for MRSA as dictated by local prevalence. Otherwise, empiric choice of agents is similar to that recommended for osteomyelitis. If N gonorrhoeae is a consideration, ceftriaxone or cefotaxime should be used. Parenteral antibiotics are used initially and continued until there is no further need for surgical intervention and the child is afebrile with clinical improvement and normalization of laboratory parameters. Exact length of therapy is dependent on the clinical situation, the patient’s response, and the particular organism. Therapy is usually continued for at least 2 weeks after the patient is afebrile, joint fluid accumulation has resolved, and laboratory parameters have normalized. Therefore, the usual duration of therapy in septic arthritis is 3 to 6 weeks.
PROGNOSIS AND OUTCOMES
Sequelae of septic arthritis include joint deformity and residual dysfunction, abnormal bone growth, and in the hip, avascular necrosis of the femoral head. Risk factors for subsequent complications include delay in drainage, age < 1 year, involvement of the hip or shoulder, adjacent osteomyelitis, and infection with S aureus.75-77
FIGURE 234-3. An algorithmic approach to the management of a patient with suspected septic arthritis. (©1995 American Academy of Orthopaedic Surgeons. Volume 3(4), pp. 183-193, with permission.)
SKIN AND SOFT TISSUE INFECTIONS
In many areas of the United States, the emergence of CA-MRSA has been accompanied by a marked increase in the incidence of skin and soft tissue infections that are one of the most common manifestations of this pathogen.91
It is important to differentiate uncomplicated cellulitis from other more serious disorders that require more aggressive therapy. For example, it is often difficult to determine if there may be an underlying osteomyelitis or septic arthritis present. Tenderness disproportionate to the soft tissue findings suggests involvement of deeper structures. It is also very important to differentiated uncomplicated cellulitis from the more serious condition of group A streptococcal necrotizing fasciitis, discussed in more detail in Chapter 285. Single or multiple skin abscesses often develop in conjunction with cellulitis caused by S aureus. Periorbital cellulitis is discussed separately due to important differences in management.
Cellulitis is an acute localized infection of the skin involving the subcutaneous tissues. Infection usually develops as a result of a breach in skin integrity or an associated skin lesion. Gram-positive organisms, primarily S aureus(including methicillin-resistant Staphylococcus aureus) and S pyogenes, account for the majority of infections involving the skin. Other organisms may occasionally be involved, particularly in neonates, in the immunocompromised host, or after trauma. Extremities are frequent sites of infection because they are more subject to minor trauma that may go unnoticed.
The presence of cellulitis is usually easily recognized clinically by findings of erythema, warmth, and edema of an area. Pinpointing the exact etiologic agent in the absence of an associated abscess or skin lesion is frequently difficult. Blood cultures may be obtained but are positive in a minority of cases. If there is an abscess or purulent skin lesion present, material for Gram stain and culture should be obtained during incision and drainage, which should be performed.91 Some literature discusses skin aspiration from the point of maximal inflammation92; however, in practice, this is seldom performed.
Therapy in the immunocompetent child should be aimed at S aureus and S pyogenes and based on local susceptibility patterns for MRSA and S pyogenes. Incision and drainage constitute the primary therapy for purulent skin and soft tissue infections.91 Failure to perform incision and drainage has been associated with a lack of clinical response in patients with S aureus skin and soft tissue infections in a recent series.93 In the afebrile, nontoxic child, drainage alone is sometimes sufficient treatment. Oral therapy for cellulitis alone or as an adjunct to the treatment of abscesses should include agents with coverage for MSSA, MRSA, and S pyogenes. Clindamycin is a reasonable choice in areas where most MRSA and S pyogenes are susceptible. Doxycycline is an alternative for older children but may not provide adequate coverage for all S pyogenes strains. Bactrim is also an option if S pyogenes is unlikely based on Gram stain results. Parenteral therapy should be used in the febrile patient if progression is rapid or if associated lymphangitis or lymphadenitis is present. Again, initial Gram stain results, if available, can be used to guide selection of therapy. Seven to 10 days of therapy is usually sufficient duration and can be achieved by sequential parenteral-oral therapy when the patient’s condition warrants.
Infection of the tissue and skin that surround the eye deserves separate consideration due to its potential for severe morbidity with vision loss. Infection can result from local trauma including insect bites, or can spread from contiguous structures. Hematogenous spread can occur or infection can result secondary to sinusitis. Typically, children present with sudden fever and rapid swelling of the tissues around the eye. If the infection affects orbital structures there may be proptosis and decreased extraocular movement.
The most common organism causing these types of cellulitis are Staphylococcus aureus, Streptococcus pyogenes, and Haemophilus influenza type B (HIB). The incidence of HIB as the cause of periorbital cellulites has declined dramatically in developed countries since the introduction of the HIB vaccination. Prompt antibiotic treatment directed at the likely causative organisms and diagnostic imaging are important to prevent morbidity. If systemic involvement is suspected, a full evaluation including lumbar puncture may be indicated. Most pediatric patients require admission for intravenous antibiotics. These may be changed to oral antibiotics following clinical improvement.
CT scanning to rule out orbital and subperiosteal involvement, or a cavernous sinus thrombosis, is indicated if one cannot perform a full evaluation of the eye due to edema. It should also be performed in any patients with proptosis, ophthalmoplegia or decreased visual acuity, bilateral periorbital edema or in those not improving with antibiotic therapy within 24–36 hours. If orbital involvement is demonstrated, emergent ophthalmologic consultation is necessary to consider drainage procedures.