Download Bone infection lecture oct 2013

Bone infection
Dr. Sami Abdalla
Definition
• An inflammation of the bone caused by an infective
organism, leading to inflammatory destruction of
bone, necrosis and new bone formation.
Classification
• Based on :
 Duration and type of symptoms.
 According to the mechanism.
 Host response.
Risk factors
• Systemic:
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Malnutrition.
Sickle cell anaemia.
Diabetes.
Immuno-suppressive conditions.
• Local:
– Trauma.
– Foreign body.
– contiguous infection.
Acute haematogenous
osteomyelitis.
• Causal organism:
– Staph. aureus 80%
– Strept., Pneumococcus, H. infleunzae (<2yrs),
– Pseudomonas  heroin addicts.
– Salmonella  sickle cell anaemia.
Sources fo infection
• Minor skin abrasion, boil, septic tooth.
• Infected umbilical cord.
• Urethral catheterization.
Pathogenesis
• The organism usually settle in the metaphysis
of :
– Proximal tibia.
– Proximal and distal femur.
– Proximal end of the humerus.
• Acute inflammatory reaction:
– Increase intra-osseous pressure.
– Obstruction to the blood flow.
– Intravascular thrombosis.
• Suppuration:
– Pus forms within the bone in the 2nd and 3rd day.
– Through volkman’s canal  subperiosteal abscess
forms.
• Bone necrosis:
– By the end of the first week.
– Due to
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infective thrombosis
Periosteal stripping.
Bacterial toxin.
Leucocyte enzymes.
• New bone formation;
– By the end of the 2nd week.
• Resolution:
Clinical features
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Constitutional symptoms.
Severe pain.
Tenderness,
Lymphadenopathy.
In adult  backache and mild fever.
Investigation
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Blood culture  +ive in 50% .
Blood test.
Culure aspirate.
Ulrasoud.
M.R.I.
Radiography.
Bone scan.
Differential diagnosis
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Cellulitis.
Strep. Necrotizing myositis.
Acute suppurative arthritis ,
Acute rheumatism.
Sickle cell crisisl
Gaucher’s disease.
Treatment
• Supportive treatment.
• Splintage
• Antibiotic therapy
– Best guess.
– Gm stain.
– Culture and sensitivity.
• Surgical treatment;
– Unresponsiveness within 36 hrs of starting
treatment.
– Signs of deep pus.
Complication
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Septicaemia.( rare).
Metastatic infection ( infants)
Suppurative arthrits.
Altered bone growth.
Chronic osteomyelitis.
Subacute haematogenous
osteomyelitis.
• Differ from AHO in severity of symptoms and
signs.
• Common in distal femur, proximal and distal
tibia.
• Staph. Aureus and epidermis are the
predomint organisms.
Clinical picture
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The patient is usually a child or adolescent.
Pain for severa weeks or even months.
Mild constitutional symptoms.
Limping and slight swelling.
Muscle wasting and local tenderness.
• This indolent course is due to
– increase host resistance.
– Lower bacterial virulence.
– Antibiotic administration.
Investigation
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TWB normal.
ESR 50%
Blood culture  usually are not +ive.
Culture of bone aspirate or biopsy 60%.
X-ray.
Treatment
• Conservative :
– For typical lesions.
– Antibiotics for 6/52.
• Biopsy and curretage;
– For aggressive lesion.
– If the diagnosis is in doubt.
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Post-traumatic osteomyelitis
• Most common cause in adults.
• Common organisms
– Staph.aureus.
– Gm –ive coliform.
– An aerobic organisms,
Clinical picture
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Constitutional symptoms.
Sero-purulent discharge.
Delayed union.
Leucocytosis and increase in ESR
Treatment
• Prophylaxis.
– Cleaning and debridement of open #
– Provision of drainage by leaving the wound open.
– Immobilization of the #
– Antibiotics.
• Pyogenic wound infection;
– Regular wound dressing.
– Debridement.
– External fixation for unstable fracture.
– If these failed:
• The management is essentially that of chronic
osteomyelitis.
Chronic osteomyelitis
• Used to be due to acute haematogenous osteomyelitis, but
nowadays it more frequently follows an open fracture or
operation.
• The usual organisms (mixed infection) are staph.aureus, E.coli,
strept.pyogenes, proteus and pseudomonos.
Chronic osteomyelitis
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Pathology:
– The disease may take one 2 forms:
1. Pus + sequestrum surrounded by vascular tissue
beyond which is an area of sclerosis.
Sequestra act as substrates for bacterial adhesions,
ensuring persistence till they are removed or
discharged through a draining sinus
Chronic osteomyelitis
– Two factors are responsible for the chronicity of
the disease :
1.presence of dead infected bone
2.the intra-osseous cavity can’t be obliterated because of
the rigid walls and as a result, the body’s normal
defense mechanisms and antibiotics are unable to
reach all the bacteria in the bone
Chronic osteomyelitis
2. Brodie’s abscess:
– This form is closely contained creating chronic abscess
within the bone (pus or jelly-like granulation tissue)
surrounded by sclerotic bone. This may be a sequel to
pyogenic septicemia from which the pt has recovered
but stayed dormant for years or may be found in a pt
which is known to have had osteomyelitis affecting a
bone other than in which Brodie’s abscess is discovered
Chronic osteomyelitis
• Clinical Features:
It may remain quiescent for months or years with acute and
subacute attacks (flares) i.e.
– recurring pain
• local
• Transitory effusion
– Pyrexia and tenderness
– Discharging sinus (seropurulent)
– In long standing cases, tissues may be puckered in where a
scar or sinus is attached
Chronic osteomyelitis
• Investigations:
– ↑ESR & TWBCs during acute flares
– ↑ASO titre
– C&S
Chronic osteomyelitis
– Radiography is diagnostic:
• The classical picture of bone resorption (as
patchy loss of density or frank excavation)
with thickening and sclerosis of the
surrounding bone. However there is marked
variations (no more than localized
trabeculation, or an area of osteoporosis, or
periosteal thickening)
Chronic osteomyelitis
• Bone scan: increased activity
• CT and MRI:
– extent of bone destruction
– Reactive edema
– Hidden abscesses and sequestra
Chronic osteomyelitis
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Treatment:
1. Antibiotics
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Exacerbations are treated by immobilization and antibiotics but
only to recur again
It is also used to stop spread of infection to healthy bone
2. Local treatment:
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Sinus: dressing
Abscess: drainage
Chronic osteomyelitis
3. Operation:
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Waiting policy.
The objective is removal of dead bone and
elimination of dead space
Under antibiotic cover, all infected soft tissue and all
dead bone must be excised
Dead material can be identified by pre-op injection of
sulphan blue or probing a sinus or by radiograph
Access to the bone is usually through a previous scar
Chronic osteomyelitis
• Double-lumen tubes are laid in the resulting cavity and
the tissues are closed with the tubes emerging through
separate stab wounds. an appropriate antibiotic
solution is instilled 4-hourrly and cleared shortly before
the next procedure by low pressure suction. Cavity
injection and drainage should be cont. until the effluent
is sterile (usually 3-4 weeks). The tubes are then
gradually withdrawn as the cavity diminishes in size.
• Gentamicin –impregnated beads
Chronic osteomyelitis
• Driange tube
• (double lumen tube)
Chronic osteomyelitis
• Dead space is obliterated by packing the cavity with
cancellous bone chips or local muscle flap.
• Amyloid disease is taken into consideration when copious
amount of pus has persisted for years
• Amputation: if exacerbations are frequent and prolonged.
• Brodie’s abscess should be treated by evacuation and
curettage of the cavity under antibiotic cover. If the cavity is of
moderate size, packing with cancellous bone chips is used.
Chronic osteomyelitis
• Aftercare: Success is difficult.
• prognosis should always be guarded
• The watchword is cautious optimism and after all, probable
cure is better than no cure.
Chronic osteomyelitis
Definition
• Inflammation of a synovial membrane with
purulent effusion into the joint capsule, often
due to bacterial infection
Synonyms
• Bacterial, suppurative, purulent or infectious
arthritis, gonococcal or nongonococcal
A Big Problem
• Despite advances in diagnostic studies,
powerful antibiotics, and early drainage,
significant joint destruction commonly occurs
• Why?
– Lack of clinical suspicion
– Delay in definitive diagnostic needle aspiration
– Failure to adequately drain the joint
Frequency
• 2-10 cases per 100,000 in the general
population
• 30-70 cases per 100,000 in patients with
immunological disorders or deficiencies, and
joint replacements
• Gonococcal: women 3x > men
Etiology
• Staph aureus
• Streptococci
• In all age groups, 80% due to gram-positive aerobes,
20% due to gram-negative anaerobes
• Neonates and infants < 6mos S aureus and gramnegative anaerobes
– Incidence of H. influenzae has decreased due to the
vaccine
Pathophysiology
• Adults
– Knee 40-50 %
– Hip 20-25 %
– Infants and young children
• Hip 95 %
Infection Sources
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Trauma: direct
Hematogenous: IV drug injection
Osteomyelitis adjacent to joint capsule
Soft tissue infections: cellulitis, abscess,
bursitis, tenosynovitis
Clinical Presentation: “red,
hot, painful joint”
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Fever
Erythema
Edema
Heat
Pain
Markedly decreased passive and active ROM
Age Related Presentation
• Young sexually active pts: + fever,
tenosynovitis, migratory polyarthralgia and
dermatitis ( papular rash over trunk and distal
extremity extensor surfaces that may turn
hemorrhagic ) = Suspect N gonorrheae
• IVDU = Pseudomonas
• Infants and young children = difficult
Pediatric Presentation
• Fever, decreased appetite and irritability without
obvious joint involvement is common
• Differentiation from transient synovitis important: 4
independent variables
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History of fever
Non-weight-bearing
ESR > 40mm/h
WBC > 12,000/uL
Diagnosis
• Needle aspiration, open drainage and lavage
(arthroscopically or arthrotomy)
Contraindications to arthrocentesis:
1. avoid aspirating from an area that has
overlying soft tissue infection
2. Bleeding disorders
3. Anticoagulation therapy
Lab Studies
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CBC with diff: leukocytosis and left shift
ESR: monitor treatment
CRP: monitor treatment
Blood cultures: may be + in 50% S aureus
Urethral, cervical , pharyngeal and rectal swabs: N
gonorrheae
• Synovial fluid analysis: Gram stain, culture, cell
count, and crystal analysis
Treatment
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Supportive.
Splintage.
Drainage of pus.
Antibiotics.
physiotherapy.