+++
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.
++
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 The
majority of strains circulating in the community harbor the genes
encoding for the exotoxin Panton Valentin leukocidin (PVL). This
important virulence factor has been associated with severe musculoskeletal
infections in children.18,20 Studies have shown
that osteomyelitis caused by PVL-positive S aureus strains
(methicillin-resistant or -sensitive Staphylococcus aureus)
are of greater severity and are characterized by the more frequent presence
of subperiosteal and intraosseous abscesses as well as complications
such as multifocal disease and deep venous thrombosis.17,20
++
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. Child-to-child transmission may occur as seen
in several reports of outbreaks in daycare centers.27,28
++
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.29 Pseudomonas 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.1,30 Symptoms
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 intra-abdominal 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.42,43 Diagnostic 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/Discitis
++
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
++
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.
++
In a recently published study, the combination of amplification
of 16SrRNA, specific real-time PCR for Kingella and culture yielded
an etiologic diagnosis in 66% of cases compared to 45% of
cases when cultures alone were submitted.26
+++
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.
+++
Radionuclide
Scanning
++
Radiophosphate bone scintigraphy using technetium (99Tc)
is the most commonly used procedure. Isotope accumulates to a greater
degree in areas of increased vascularity and rapid bone turnover,
resulting in a hot spot reflected on the scan.
Conversely, infected areas may have associated compromise of the
vascular supply, causing the area to appear cold or
normal, resulting in a false-negative interpretation. 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
++
It is well accepted that Pseudomonas osteochondritis is
mainly a surgical disease. When thorough curettage and debridement
is achieved, 10 days of antipseudomonal therapy is usually sufficient.
++
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 pyogenes, 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. It
has been shown to be effective in step-down therapy of AHO by gram-positive
organisms.66 Long-term therapy (greater than 2
weeks) has been associated with anemia and thrombocytopenia, and
thus, weekly blood counts are required when using this drug.67 Other
adverse effects described include optic neuritis, peripheral neuropathy,
and serotonin syndrome when used in combination with serotonin reuptake
inhibitors (SSRIs) and sympathomimetic drugs.22,68
++
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.
++
If sequential parenteral/oral therapy is implemented,
the oral drug chosen should be active against the identified pathogen,
or if the pathogen has not been isolated, it should be identical
in spectrum of activity to the parenteral drug to which the patient
has shown clinical response. Contraindications to oral therapy include
the inability to swallow or retain medication, lack of an effective
oral agent, and failure to demonstrate adequate clinical response
to parenteral antibiotics. Some experts also feel that failure to
demonstrate the etiologic agent and an inability to monitor the
degree of drug absorption also constitute contraindications to oral
therapy. Especially in young children, palatability of oral suspensions
is an important feature. In general, cephalosporins are more palatable than
penicillins. Clindamycin is an excellent drug for staphylococcal
osteomyelitis in older children, but many young children will not
tolerate the taste of the oral solution.
++
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
+++
Chronic Osteomyelitis
++
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
++
With the increase of PVL-positive S aureus strains,
especially CA-MRSA, there has been an increase in cases of severe
sepsis in adolescents with the involvement of multiple sites of osteomyelitis
and septic arthritis.70 Deep venous thromboses
have also been encountered more frequently in patients with CA-MRSA
osteomyelitis.71-73 The thromboses are usually
in a vein adjacent to the infected bone site. Septic embolisms have
been seen in such patients leading to severe respiratory compromise.
In patients who have evidence of septic emboli or persistent bacteremia,
evaluation for deep venous thrombosis by Doppler ultrasonography
should be considered.
+++
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 consider75and 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.
+++
Clinical Manifestations
++
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. Ultrasonography 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