Etiology Bacteria are the most common pathogens in acute skeletal infections. Staphylococcus aureus is the most common infecting organism in all age groups, including newborns. Community-acquired methicillin -resistant S. aureus (CA-MRSA) isolates account for >50% of S. aureus isolates recovered from children with osteomyelitis in some reports. Group B streptococcus and gram-negative enteric bacilli ( Escherichia coli ) are also prominent pathogens in neonates
group A streptococcus constitutes <10% of all cases. After 6 yr of age, most cases of osteomyelitis are caused by S. aureus , streptococcus, or Pseudomonas aeruginosa Cases of Pseudomonas infection are related almost exclusively to puncture wounds of the foot, with direct inoculation of P. aeruginosa from the foam padding of the shoe into bone or cartilage, which develops as osteochondritis . Salmonella species and S. aureus are the two most common causes of osteomyelitis in children with sickle cell anemia. S. pneumoniae most commonly causes osteomyelitis in children <24 mo of age or children with sickle cell anemia. Bartonella henselae can cause osteomyelitis of any bone but especially in pelvic and vertebral bones. Kingella kingae may be the second most common cause of osteomyelitis in children <5 yr of age in some parts of the world
Infection with atypical mycobacteria , S. aureus , or Pseudomonas can occur after penetrating injuries. Fungal infections usually occur as part of multisystem disseminated disease; Candida osteomyelitis sometimes complicates fungemia in neonates with or without indwelling vascular catheters. A microbial etiology is confirmed in ∼60% of cases of osteomyelitis . Blood cultures are positive in ∼50% of patients.
Epidemiology The median age of children with musculoskeletal infections is ∼6 yr. The incidence of osteomyelitis in children is estimated to be 1 : 5,000. Bone infections are more common in boys than girls; the behavior of boys might predispose them to traumatic events The majority of osteomyelitis cases in previously healthy children are hematogenous . Minor closed trauma is a common preceding event in cases of osteomyelitis , occurring in ∼30% of patients. Infection of bones can follow penetrating injuries or open fractures. Bone infection following orthopedic surgery is uncommon. Impaired host defenses also increase the risk of skeletal infection.
Pathogenesis The unique anatomy and circulation of the ends of long bones result in the predilection for localization of bloodborne bacteriaIn the metaphysis , nutrient arteries branch into nonanastomosing capillaries under the physis , which make a sharp loop before entering venous sinusoids draining into the marrow. Blood flow in this area is thought to be “sluggish ,” predisposing to bacterial invasion. Once a bacterial focus is established, phagocytes migrate to the site and produce an inflammatory exudate ( metaphyseal abscess). The generation of proteolytic enzymes, toxic oxygen radicals, and cytokines results in decreased oxygen tension, decreased pH, osteolysis , and tissue destruction. As the inflammatory exudate progresses, pressure increases spread through the porous metaphyseal space via the haversian system and Volkmann canals into the subperiosteal space. Purulence beneath the periosteum may lift the periosteal membrane of the bony surface, further impairing blood supply to the cortex and metaphysis .
In newborns and young infants, transphyseal blood vessels connect the metaphysis and epiphysis, so it is common for pus from the metaphysis to enter the joint space. This extension through the physis has the potential to result in abnormal growth and bone or joint deformity. During the latter part of the 1st year of life, the physis forms, obliterating the transphyseal blood vessels. Joint involvement, once the physis forms, can occur in joints where the metaphysis is intra- articular (hip, ankle, shoulder, and elbow), and subperiosteal pus ruptures into the joint space.
Clinical Manifestations The earliest signs and symptoms of osteomyelitis , often subtle and nonspecific, are generally highly dependent on the age of the patient. Neonates might exhibit pseudoparalysis or pain with movement of the affected extremity (e.g., diaper changes). Half of neonates do not have fever and might not appear ill. Older infants and children are more likely to have fever, pain, and localizing signs such as edema, erythema , and warmth. With involvement of the lower extremities, limp or refusal to walk is seen in approximately half of patients. Focal tenderness over a long bone can be an important finding. Local swelling and redness with osteomyelitis can mean that the infection has spread out of the metaphysis into the subperiosteal space, representing a secondary soft-tissue inflammatory response.
Pelvic osteomyelitis can manifest with subtle findings such as hip, thigh, or abdominal pain. Back pain with or without tenderness to palpation overlying the vertebral processes is noted in vertebral osteomyelitis . Long bones are principally involved in osteomyelitis the femur and tibia are equally affected and together constitute almost half of all cases. The bones of the upper extremities account for one fourth of all cases. Flat bones are less commonly affected.
There is usually only a single site of bone or joint involvement. Several bones are infected in <10% of cases; the exception is osteomyelitis in neonates, in whom two or more bones are involved in almost half of the cases. Children with subacute symptoms and focal finding in the metaphyseal area (usually of tibia) might have a Brodie abscess, with radiographic lucency and surrounding reactive bone.
Diagnosis The diagnosis of osteomyelitis is clinical; blood cultures aspiration or biopsy of bone or subperiosteal abscess for Gram stain, culture, and possibly bone histology The white blood cell count and differential, erythrocyte sedimentation rate (ESR), or C-reactive protein (CRP) The leukocyte count and ESR may be normal during the first few days of infection, and normal test results do not preclude the diagnosis of skeletal infection. Monitoring elevated ESR and CRP may be of value in assessing response to therapy or identifying complications.
Plain Radiographs -Within 72 hr of onset of symptoms of osteomyelitis , plain radiographs of the involved site using soft-tissue technique and compared to the opposite extremity, if necessary, can show displacement of the deep muscle planes from the adjacent metaphysis caused by deep-tissue edema. Lytic bone changes are not visible on radiographs until 30-50% of the bony matrix is destroyed. Tubular long bones do not show lytic changes for 7-14 days after onset of infection. Infection in flat and irregular bones can take longer to appear.
CT can demonstrate osseous and soft-tissue abnormalities and is ideal for detecting gas in soft tissues MRI is more sensitive than CT or radionuclide imaging in acute osteomyelitis and is the best radiographic imaging technique for identifying abscesses and for differentiating between bone and soft-tissue infection. MRI can also demonstrate a contiguous septic arthritis, pyomyositis , or venous thrombosis. Radionuclide imaging can be valuable in suspected bone infections, especially early in the course of infection and/or if multiple foci are suspected or an unusual site is suspected, as in the pelvis
Differential Diagnosis Cellulitis Pyomyositis & Myositis Appendicitis, urinary tract infection, and gynecologic disease are among the conditions in the differential diagnosis of pelvic osteomyelitis leukemia Neuroblastoma with bone invoivement Primary bone. In patients with sickle cell disease, distinguishing bone infection from infarction may be challenging.
Treatment Antibiotic Therapy In neonates-an antistaphylococcal penicillin, such as nafcillin or oxacillin (150-200 mg/kg/24 hr divided q6h IV), and a broad-spectrum cephalosporin, such as cefotaxime (150-225 mg/kg/24 hr divided q8h IV), provide coverage for the S. aureus , group B streptococcus, and gram-negative bacilliIf methicillin -resistant Staphylococcus is suspected, vancomycin is substituted for nafcillin
In patients with sickle cell disease with osteomyelitis , gram-negative enteric bacteria (Salmonella) are common pathogens as well as S. aureus , so a broad-spectrum cephalosporin such as cefotaxime (150-225 mg/kg/24 hr divided q8h) is used in addition to vancomycin or clindamycin . Clindamycin (40 mg/kg/24 hr divided q6h IV) is a useful alternative drug for patients allergic to β- lactam drugs
For most infections including those caused by S. aureus , the minimal duration of antibiotics is 21-28 days, provided that the patient shows prompt resolution of signs and symptoms (within 5-7 days) and the CRP and ESR have normalized; a total of 4-6 wk of therapy may be required. For group A streptococcus, S. pneumoniae , or H. influenzae type b, treatment duration maybe shorter. A total of 7-10 postoperative days of treatment is adequate for Pseudomonas osteochondritis when thorough curettage of infected tissue has been performed. Immunocompromised patients generally require prolonged courses of therapy, as do patients with mycobacterial or fungal infection
Changing antibiotics from the intravenous route to oral administration when a patient's condition clearly has improved and the child is a febrile for ≥48-72 hr, may be considered. For the oral antibiotic regimen with β- lactam drugs for susceptible staphylococcal or streptococcal infection, cephalexin (80-100 mg/kg/24 hr q8h) or oral clindamycin (30-40 mg/kg/24 hr q8h) can be used to complete therapy for children with clindamycin -susceptible CA-MRSA or for patients who are seriously allergic or cannot tolerate β- lactam antibiotics
Surgical Therapy Physical Therapy
Prognosis When pus is drained and appropriate antibiotic therapy is given, the improvement in signs and symptoms is rapid. Failure to improve or worsening by 72 hr requires review of the appropriateness of the antibiotic therapy, the need for surgical intervention, or the correctness of the diagnosis. Acute-phase reactants may be useful as monitors. The serum CRP typically normalizes within 7 days after start of treatment, whereas the ESR typically rises for 5-7 days, and then falls slowly, dropping sharply after 10-14 days. Recurrence of disease and development of chronic infection after treatment occur in <10% of patients. Because children are in a dynamic state of growth, sequelae of skeletal infections might not become apparent for months or years; therefore, long-term follow-up is necessary with close attention to range of motion of joints and bone length.
Septic arthititis
Inflammation of a joint Infection may follow –penetrating injuries(direct inoculation) -Hematogenous -contagious
Etiology Haemophilus influenzae type b- accounted for more than half of all cases of bacterial arthritis in infants and young children Staphylococcus aureus - the most common infection in all age groups Group A streptococcus Streptococcus pneumoniae ( pneumococcus ) is most likely in the first 2 years of life Kingella kingae is recognized as a relatively common etiology with improved culture and polymerase chain reaction (PCR) methods in children <5 yr old In sexually active adolescents, gonococcus Group B streptococcus is an important cause of septic arthritis in neonates Chronic arthritis- Fungal infections ,tuberculosis
Pathogenesis Septic arthritis primarily occurs as a result of hematogenous seeding of the synovial space Less often, organisms enter the joint space by direct inoculation or extension from a contiguous focus. The synovial membrane has a rich vascular supply and lacks a basement membrane, providing an ideal environment for hematogenous seeding The presence of bacterial products ( endotoxin or other toxins) within the joint space stimulates cytokine production (tumor necrosis factor-α, interleukin-1) within the joint, triggering an inflammatory cascade
Phatogenesis … The cytokines stimulate chemotaxis of neutrophils into the joint space, where proteolytic enzymes and elastases are released by neutrophils , damaging the cartilage. Proteolytic enzymes released from the synovial cells and chondrocytes also contribute to destruction of cartilage and synovium . Bacterial hyaluronidase breaks down the hyaluronic acid in the synovial fluid, making the fluid less viscous and diminishing its ability to lubricate and protect the joint cartilage. Damage to the cartilage can occur through increased friction, especially for weight-bearing joints.
Phatogenesis The increased pressure within the joint space from accumulation of purulent material can compromise the vascular supply and induce pressure necrosis of the cartilage. Synovial and cartilage destruction results from a combination of proteolytic enzymes and mechanical factors Synovial inflammation - increased vascular permeability - increased fluid production-fluid collected under pressure -compression/thrombosis of intra articular joint vesseles - avascular necrosis Extension of infection to bone may occur.
Clinical Manifestations fever and pain, with localizing signs such as swelling, erythema , and warmth of the affected joint. Decreased the range of motion With involvement of joints of the pelvis and lower extremities, limp or refusal to walk is often seen Septic arthritis in neonates and young infants is often associated with adjacent osteomyelitis caused by transphyseal spread of infection, although osteomyelitis contiguous with an infected joint can be seen at any age In neonates irritability, poor feeding , pseudoparalysis Multiple joint involvement and contigous osteomyelitis common in infants
Diagnosis Blood cultures Aspiration of the joint fluid for Gram stain and culture- the definitive diagnostic. A microbial etiology is confirmed in about 65% of cases of septic arthritis Synovial fluid analysis for cell count, differential, protein, and glucose has limited usefulness because noninfectious inflammatory diseases, such as rheumatic fever and rheumatoid arthritis, can also cause exuberant reaction with increased cells and protein and decreased glucose. Nevertheless, cell counts >50,000-100,000 cells/mm 3 generally indicate an infectious process.
Diagnosis .. The white blood cell count and differential, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) are generally elevated in children with joint infections but are nonspecific and might not be helpful in distinguishing between infection and other inflammatory processes. The leukocyte count and ESR may be normal during the first few days of infection, and normal test results do not preclude the diagnosis of septic arthritis. Monitoring elevated ESR and CRP may be of value in assessing response to therapy or identifying complications.
Plain Radiographs shows widening of the joint capsule, soft-tissue edema, and obliteration of normal fat lines Ultrasonography Ultrasonography is particularly helpful in detecting joint effusion and fluid collection in the soft tissue and subperiosteal regions. Ultrasonography is highly sensitive in detecting joint effusion, particularly for the hip joint, where plain radiographs are normal in >50% of cases of septic arthritis of the hip.
Computed Tomography and Magnetic Resonance Imaging Radionuclide Imaging Radionuclide imaging compared to radiographs is more sensitive in providing supportive evidence of the diagnosis of septic arthritis; a scan may be positive within 2 days of the onset of symptoms.
Differential Diagnosis For the hip, toxic synovitis , Legg-Calve- Perthes disease, slipped capital femoral epiphysis, psoas abscess, and proximal femoral, pelvic, or vertebral osteomyelitis as well as diskitis should be considered. For the knee, distal femoral or proximal tibial osteomyelitis , pauciarticular rheumatoid arthritis, and referred pain from the hip should be considered. Other conditions such as trauma, cellulitis , pyomyositis , sickle cell disease, hemophilia, and Henoch-Schonlein purpura can mimic purulent arthritis. When several joints are involved, serum sickness, collagen vascular disease, rheumatic fever, and Henoch-Schonlein purpura should be considered. Arthritis is one of the extraintestinal manifestations of inflammatory bowel disease. Reactive arthritis following a variety of bacterial (gastrointestinal or genital) and parasitic infections, streptococcal pharyngitis , or viral hepatitis can resemble acute septic arthritis (Chapter 151).
Treatment Antibiotic Therapy- In neonates, an antistaphylococcal penicillin, such as nafcillin or oxacillin (150-200 mg/kg/24 hr divided q6h IV), and a broad-spectrum cephalosporin, such as cefotaxime (150-225 mg/kg/24 hr divided q8h IV), provide coverage for the S. aureus , group B streptococcus, and gram-negative bacilli. If MRSA is a concern, vancomycin is selected in favor of nafcillin or oxacillin . If the neonate is a small premature infant or has a central vascular catheter, the possibility of nosocomial bacteria ( Pseudomonas aeruginosa or coagulase -negative staphylococci) or fungi (Candida) should be considered. In older infants and children with septic arthritis, empirical therapy to cover for S. aureus , streptococci, and K. kingae includes cefazolin (100-150 mg/kg/24 hr divided q8h) or nafcillin (150-200 mg/kg/24 hr divided q6h).
Surgical Therapy Infection of the hip is generally considered a surgical emergency because of the vulnerability of the blood supply to the head of the femur. For joints other than the hip, daily aspirations of synovial fluid may be required. Generally, one or two subsequent aspirations suffice. If fluid continues to accumulate after 4-5 days, arthrotomy or video assisted arthroscopy is needed .