Therapeutic Discussions – Bone and Joint Infections
Pathophysiology
Hematogenous osteomyelitis (bone infection)
- most cases occur in patients < 16 y/o
- vascular structure within long bones predisposes bone for hematogenous infections to begin
within the metaphyses
o infection initiated in bend of arterioles
 blood flow slows through hairpin turns within arterioles and then into wider
venous structures  slowing allows bacteria present within bloodstream to
settle and initate an inflammatory response
 less phagocytosis within metaphysis
o infection settles  avascular necrosis occurs from occlusion of nutrient vessels and
release of bacterial enzymes
- exudate forms within bone = increased pressure
o 12-18 mo olds – infection in metaphysis of long bone prevented from spreading into
joint due to growth plate; exudate expands laterally through thin outer cortex & raises
loose periosteum (thick and not easily broken) with pus remaining subperiosteal 
soft-tissue abscess if significant periosteal damage
o adults – periosteum tightly bound and cortex is thick  infection will remain
intramedullary and can spread to adjacent bones
o neonates – blood vessels through cortex of metaphyses and into epiphyses  infection
to spread easily to involve the joint as well as the periosteum
Contiguous-Spread Osteomyelitis
- direct entrance of organisms from penetrating wounds, open fractures, various invasive
orthopedic procedures
- secondary to pressure ulcers
- 80% occur after internal fixation of hip fracture/femoral or tibial shaft fracture
Infectious/Septic Arthritis (Joint infection)
- synovial tissue highly vascular and no basement membrane  organisms can easily reach fluid
- gain access to joint from deep-penetrating wound, intra-articular steroid injection, arthroscopy,
prosthetic joint surgery, continuous OM
o after access in joint, bacteria begin to multiply and produce a persistent purulent
effusion
 > 7 days present = irreversible damage via cartilage destruction by increasing
leukocyte enzyme acitivty
Etiology
Osteomyelitis
 Hematogenous – spread through bloodstream
Contiguous – spread from adjoining soft tissue infection or direct inoculation
 Acute – onset usually several days to 1 week
Chronic – symptoms > 1 month or relapses of initial infection
Hematogenous osteomyelitis (bone infection)
- Single organism isolate – S. aureus most frequent in children
- Neonatal – S. aureus, group B streptococcus, E. coli
- Vertebral – S. aureus (60%), GNB (E. coli), mycobacterium tuberculosis
- IVDU – vertebral most common; GNB (88%) – P. aeruginosa (78%), Klebsiella, Enterobacter,
Serratia; Stapylococcal, Streptococcal
- Sickle cell anemia – Salmonella
Contiguous-Spread Osteomyelitis
- S. aureus = most common
- CoNS second common
- GN bacilli = frequently; P. aeruginosa, streptococcus, E. coli, Staphylococcus epidermidis and
anaerobes
- Puncture wound to feet = P. aeruginosa
- Vascular insufficiency = multiple organisms – staph, strep, enterobacteriaceae, enterococci,
anaerobes (B. fragilis, B. melaninogenicus)
- Rare – candidia  requires treatment of 6-12 months
Infectious Arthritis
 Mostly infect a single joint – monarticlar infections
 Hematogenous dissemination – comprises majority of infections
Contiguous – spread of infection from adjacent bone infection
Direct contamination of joint space
 Risk factors
o Systemic CCS use, pre-existing arthritis, athrocentesis, distant infection, DM, trauma,
immunosuppressive states (cancer, liver dz)
 Chronic inflammation makes joint more susceptible to infection
o IVDU
Pathogens
- S. aureus = most common (48%)
- Streptococcal (18%)
- GNB – E. coli most common; P. aeruginosa most frequent in IVDU
- Neonates = GNB most common
- 18-30 y/o or women = N. gonorrhoeae
- Prosthetics have more weird and wonderfuls (anaerobes, enterococcus) < 10%
Clinical Presentation (think head to toe)
Hematogenous OM
Vitals: fever; tachycardia
CNS: night sweats; malaise; neurological symptoms if spinal cord compression
GI: weight loss
DERM/MSK: decreased limb motion; edema over affected area; pain that worsens with movement;
localized tenderness, warmth, and erythema
HEME: increased WBC, neuts, ESR, CRP; positive blood cultures
Chronic OM – don’t feel well; non-specific symptoms
Acute Infectious Arthritis
Vitals: fever
DERM/MSK: painful swollen joint in absence of trauma; effusion of joint; restriction of joint motion;
tenderness; wound drainage if prosthetic joint; purulent fluid with low synovial glucose level
HEME: increased ESR, WBC, neuts, positive blood cultures
FLUID: synovial WBC count elevated (non-gonococcal)
Diagnostic Tests
OM
Radiographs of involved area – bone changes not seen for at least 10-14 days after onset of infection;
soft tissue swelling; bone lesions seen 10 days after infection
Bone scan – Gallium or WBC scan – can see within 1 day of symptoms
CT/MRI – if spine affected
CRP/ESR
S. aureus and bacteremic – will do ECHO to rule out IE
Infectious arthritis
Radiographs – distention of joint capsule with soft tissue swelling in adjacent space; loosening of
prosthesis
CT/MRI for infected hip
CRP/ESR
S. aureus and bacteremic – will do ECHO to rule out IE
Goals of Therapy
Prevent mortality
Cure the infection
Maintain limb function
Prevent long-term sequelae  sepsis, septic shock, bacteremia, amputation, abscesses, diskitus
Normalize surrogates (imaging, blood cultures, WBC, neut, ESR/CRP, temp)
Prevent adverse events
Modifiable risk factors – DM, vascular insufficiency
Therapeutic Alternatives
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Non-Pharmacologic
o OM
 Surgical debridement to remove all dead bone and necrotic material
o Infectious Arthritis
 Surgical debridement and retention of prosthetic
 Joint drainage can be repeated daily for 5-7 days
 Joint rest – no weight bearing
 Removal of prosthetic (1 stage or 2 stage)
o Abscess
 Drain abscess
Pharmacologic – wait for at least blood cultures to be drawn
o OM  IV preferred
 Cloxacillin 2 g IV q4h
 Cefazolin 2 g IV q8h  will also help with easy GNB
 FQ – GNB
 Cipro – reserve for pseudomonas; poor GPB coverage and no anaerobic
 Levo – good GPB coverage and a bit of anaerobic
 Moxi – best anaerobic coverage of FQs
 Septic  vancomycin
o Infectious Arthritis
 < 1 mo old – cloxacillin + AMG
 < 5 y/o and immunized against H. flu – cloxacilin, cefazolin
 > 5 y/o – cloxacillin; MRSA – clindamycin, vanco, linezolid
 IVDU – combination therapy with AMG
 Gonococcal – ceftriaxone then switch to amoxicillin, doxy if sensitive
o Bone penetration difficult to correlate to clinical practice; most studies completed in
rabbits
Duration
o OM – 4-6 weeks
 Failure rates ~20% in children who receive < 3 weeks
o Infectious Arthritis – 4 weeks in nongonococcal infections in native joint; 6 weeks for
prosthetic joint
 Disseminated gonocococcal infections – 7-10 days
PO meds for OM if:
 Confirmed OM
 Initial clinical response to IV abx
 Suitable oral agent available
 Compliance ensured
 Adults w/o DM or PVD
o Populations that have benefited = children responding to initial IV; adults with organism
that is sensitive to FQ
PO meds for infectious arthritis
o Children can be converted after initial IV therapy
Therapeutic recommendations
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Evidence
o Ceftriaxone 2 g IV daily x 6 weeks for S. aureus OM = cure rate of 77%
o SR: acute hematogenous OM; compared < 7 days IV + PO abx vs. > 7 days IV + PO abx 
NSS between groups; cure rates of ~95%
Therapeutic controversies
o Empiric coverage of MRSA when staphylococcal infection suspected?
o FQ use in OM