Bone and Joint Infections Flashcards
Osteomyelitis
types:
Etiologies (3) - common populations?
inflammation of the bone and bone marrow, typically caused by infection
Acute vs chronic
Etiologies: hematogenous, continguous spread ordirect inoculation
Hematogenous: less common, infection in the blood spreads to the bone; seein children with growing bone, vertebral osteo, usually monomicrobial
Continguous spread: most common; cellulitis infection, DM, ischemic ulcers, decubitus ulcers, trauma/ surgery —> spread to adjacent bone. polymicrobial
Direct inoculation: traumatic injuries, surgeries, open fractures
Course of Osteomyelitis
infection starts @ bone (no matter by what etiology) –> you get an immune response that blocks out the infection= inflammatory cells, try to contain the infection - killing the infected cells, sequestering the dead bone –> if left untreated, the infection will still try to spread/escape
Pathogenesis:
ACUTE: Pre-existing focus / exogenous infection –> infective embolus enters nutrient artery –> trapped in a vessel of small caliber (metaphysis) –> blocks the vessel –> active hyperemia + PMN cells exudate –> hyperemia and immbolization causes decalcificaiton –> proteolytic enzymes destroy bacteria and medullary elements –> the debris increase and intramedullary pressure increases (due to inflammatory exudates/pus stripping the periosteum)
Chronic: Inadequate treatment of acute OM/foreign implant/open fracture –> inflammatory process continues with time and persistent infection –> vascular thrombosis –> bone necrosis (sequestrum formation) –> new bone formation occur (involucrum) –> multiple openings appear in this involucrum, through which excudates and debris from teh sequestrum pass via the sinus (sinus formation – to the skin)
How can osteomyelitis differ in children?
Hematogenous form would be common in children
Bacteremia –> bacteria is deposited in metaphysis from the metaphyseal vessels (nutirent artery and vein) –> focus of infection develops in the metaphysis => cellulitis in the bone marrow –> exudate under pressure is forced laterally through the haversian systems and volkmann canals and into the cortex of the bone, wehre it can lift or rupture thorugh the periosteum
Newborns - infection spreads along the subperiosteal space and ruptures thorugh the cortex into soft tissue.
Younger – often infection spread directly to the skin vs along the bone
as children get older, infection tends to spread along the bone, instead of soft tissues. more localized.
How does OM present with contiguous etiology?
Would labs be helpful?
Contiguous:
mostly adults, especially with underlying DM, peripheral vascular disease, other skin disease
more subacute process, subtle findings
vague sx, possibly pain at site, swelling
Fevers, chills less common
Redness
Sinus tract (you can feel it down to the bone)
LABS:
Elevated WBC (not always)
Elevated sed rate (ESR), C reactive protein (CRP)
How does OM present with hematogenous etiology?
Hematogenous:
more common in pre-pubertal children, or seen with IVDU, endocarditis
typically vertebral osteo (hard to DX! often just pain)
In children, often see spread to skin, soft tissue, joints
what are the typical pathogens of OM? (5)
Gram positive more common
Staph - s. aureus, coag negative staph
Strep
Enterococcus
G. negative rods - pseudo, e coli, enterobacter…
What is the common pathogen in the following clinical scenarios?
General pop?
Open fractures/surgery related?
Sickle cell?
Neonatal period?
Vertebral?
Shoe, puncture wound?
What is the common pathogen in the following clinical scenarios?
General pop -S. Aureus MOST COMMON
Open fractures/surgery related - often poly microbial
Sickle cell - salmonella (often in children)
Neonatal period - haemophilus influenza, group B strep
Vertebral - numerous including Staph aureus, TB (potts disease of the back),
Shoe, puncture wound - pseudomonas
How is OM diagnosed?
CLINICAL PREZ - age, RF, symptoms
CULTURES- not as helpful
Blood cultures are not always positive (unless perhaps hematogenous spread!)
Cultures from sinus tract
bone biopsy with culture most useful
IMAGING
X rays - cheap, delayed by 2 weeks from time of onset
sensitivity 14%, specificity 70%
*MRI: good neg predictive value, over calls edema as osteo, limited value when hardware is present
sensitivity 98%, specificity 93%
CT: not as good as MRI
Nuclear studies
Steel probe through sinus tract to bone it is very indicative of OM
DX of OM: (4)
- Probe to bone test
- positive esp with DM foot ulcer - Culture
would swab and deep wound cultures – poor correlation with bone biopsy culture result; exception: presence of staph from deep wound culture
- Percutaneous needle biopsy - poor correlation with bone bipsy culture result
- Bone bipsy - yields positive cx 87% of the time
Tuberculosis OM
TB - mycobacteria, slow growing
endemic in many parts of the world
Typically presents a pulmonary infection – but can have bone infection
1-3% of the time complicatd pulmonary disease
usually hematogenous spread – long bones, vertebral (sometimes two in a row)
Usually solitary lesions
Histo: Granulomatous inflammation (caseous necrosis, bone destruction)
Septic Arthritis - general causes
Bacterial
- acute
- rheumatologic emergency
- rapid joint destruction, irreversible loss of funciton*
Viral
- acute
- systemic illness, often multi-joint
Fungal/Mycobacterial
- Chronic in nature
- Usually monoarticular
- More ofte in immunocompromised host but not aways
Epidemiology of Septic Arthritis
10% of pt with acute pain have septic arthritis
2-10 cases/100,000 per year of native joint arthritis (increased rates with certain risk factors)
Mortality 10-30% (30 without treatment)
Morbidity up to 50% with permanent loss of function (delayed treatment, inappropriate treatment)
Factors that INC risk for Septic Arthritis (8)
older, prosthetic joint, recent joint surgery, IVDU, endocarditis, ppl with underlying skin infection/ulcer, joint disease (RA, OA, gout), chronic dz, immunosuppressed
How can I person get Septic Arthritis?
Hematogenous
Direct Inoculation (surgery, trauma)
Spread of infection from contiguous source (bone)
Pathogenesis
Regardless of how the bacteria gets to the bone…
Bacterial and inflammatory cells enter via the leaky synovial tissue (small contained space –> INC pressure)
Acute inflammatory reponse/infiltrate occurs –> synovial membrane hyperplasia, synovial effusion, cartilage degradation
Inflammatory cells release cytokines and proteases –> cartilage damage, pressure necrosis from large synovial effusions –> cartilage / bone loss
Presentation of Septic Arthritis
[Time onset, sx, exam, lab findings]
ACUTE - hours to days
Typically mono-articular
Sx: pain, swelling, warmth, loss of fxn (both passive and active!), fevers
Exam: fevers, tenderness, limited ROM/painful, effusion, redness
Findings: elevated WBC, Sed Rate (ESR), purulent joint fluid
pathogenesis of DGI
SX :
DX:
Gonoccocal disease that is not treated –> occult bacteremia
DGI classic triad: dermatitis, tenosynovitis, migratory polyarthalgia or arthritis
see numerous painless, non-puritic macules, papules, pustular lesions; tenosynovitis more common on hands, wrists, fingers in up to 2/3s of patients; migratory polyarthalgia/arthritis could present with fever and malaises
Septic joint less common and can occur with or w/out above occuring; most often monoarticular- knees, wrist and ankles more often
DX: diagnostic tap, gram stain is only ~25% of the time [but it is a gram negative so can be r/o easier], culture only positive 50% of the time; PCR synovial fluid 80%, PCR from mucosal sites (uterine - 80-90%; urethral 50-70%)
