1. By
Sherif El-aidy
Assistant lectuerer of Orthopedic Surgery
Faculty of Medicine - Zagazig University

2. •
Osteomyelitis:
1-acute OM
2-subacute OM
3-chronic OM
•
Septic arthritis
•
Tuberculosis bone and joint infection

3. Definition : It is acute
blood born infectious process that involves bone and its medullary
cavity
Incidence: 5
Bacteriology:
% of infections , almost invariably disease of childrens
staph aureus and epidermidis, B hemolytic streptococci , gram-ve bacteria
e.g pseudomonas and E.coli , salamonella(more in sickle cell anaemia),Haemophius influenza
(more in children below 4 years old) and anaerobic bacteria.
predisposing factors :
lowered immunity by disease( sickle cell anaemia , DM) or
drugs (steroids) or debility (malnutrition) and immunosuppression . Trauma may play role
in determining site.
Pathgenesis:
infection is most commonly in the metaphysis of
long bones of the lower limb Blood Flow slowed
and turbulent by terminal branches of Metaphseal
arteries entering growth Plate and forming loops
then irregular sinsuids inAddition linning cells
have no or little phagocytic Activity.

4. Osteomyelitis that starts in the metaphysis
spreads in two directions:
(1) down the medullary cavity
(2) through the relatively thin metaphyseal
cortex .
Fortunately, the cartilaginous growth
plate is a barrier, and the physis and
adjacent epiphysis are typically spared.
When the infectious process penetrates the
metaphyseal cortex, pus elevates the
loosely adherent periosteum, and a
subperiosteal abscess may form and may
lead to concomitant septic arthritis .

5. Pathology:
Clinically :
Fever, anorexia, headache, malaise. Local Pain, Redness, Hotness, Swelling, Tenderness. history
Septic focus. Limb is held still é no or little movement . enlarged LN.
Radiologically:
Plain x ray:
Early soft tissue swelling , bone
demineralisation (10-14 days) ,
Late , Seqestration and
involucrum
•MRI: it shows changes in bone
and bone marrow before plane
films : T1 bone marrow signal
T2 signal relative to normal fat.
•Bones scans:
• 99mTc-HDP uptake in perfusion
& bone phases.
• 111 Indium & 67Gadolinium both
are more specific .
•CT and US: usefull in localizing
abscess and pus

6. Laboratory investigations:
Blood:
• WBC
• ESR >30 mm (late to rise & late to return)
ASOT
•Anemia and Blood culture +ve
• CRP > 6 IU (1st to rise & 1st to return)
Aspirates:
• Cell Count >25.000/mm3 (May be helpful 85%)
• Differential Count ........... >75% PNL
• Gram stain ............................... +ve 25%
• Glucose
P rotein
• PCR and IL6 serum level are newly introduced to diagnostic tools .
Differential diagnosis:
[1]. Acute cellulitis
[4]. Acute rheumatic fever
[2]. Suppurative arthritis
[5]. Sickle crisis
[3]. Necrotizing myocitis
[6]. Gaucher’s crisis
Complications:
[1]. Septicemia
[2]. Suppurative arthritis: especially for intra-capsular metaphysis and infants.
[3]. Spread of infections to near by joints, bones, and soft tissue.
[4]. Chronicity.
[5]. Physeal damage & leg length discrepency.

7. Treatment:
•General supportive ttt: bed rest , fluids and analgesics anti-inflamatory .
•Splintage: skin traction or slab decrease contractures and pain .
•Antibiotic suppression:
1- start immediate broad spectrum antibiotic untill culture and sensitivity appears .
2- for 2 weeks I V and 6 weeks oral antibiotics untill CRP is normal .
3- combinations include :
 flucloxacillin + fucidin
for staph infections
 flucloxacillin + benzyl penicillin for strept infections
 cefotaxime or augmentine for Hemophilus influenza (< 4 years)
 chloramphenicol or co timoxazole for salamonella ( sickle cell anaemia)
 new cephalosporins for immunocompromized patients
•Drainage and debridment :

8. •Etioligy;
• most common orgamisms include staph aureus ,
Pseudomonas , coliforms or polymicrobial agents
•Clinial picture and laboratory tests are similar to
that of acute h. OM
Classification of postoperative infection :
1- Early: superficial or deep or both
2- Late : following early one or covert infection
appeared late or following long period of normality

9. •Prevention of postoperative infection:
Pre-operative :All septic lesions must be identified & treated
Intra-operative : careful tissue handling & haemostasis , wound lavage , antibiotic
prophylaxis , ab loaded cement , Body Exhaust Suit ,Weaved Gortex and vertical laminar air
flow
Post-operative: AB cover
•Treatment:
 post-traumatic infection:
prevented and treated by cleaning ,
debridement of the wound , leave wound open
,immobilize fracture and antibiotics
( broad spectum cephalosporins and metronidazole)
wound closure is delayed untill infection subsides
Posoperative infection :
 Operations without implants : the same as post traumatic infection
 After internal fixaion of fracture : first , appropriate AB , if pus formed , drainage and
excision of all dead infected tissues up to implant removal and external fixation
 Infection following arthroplasty: options include( antibotic suppression , drainage and
debridement , arthrodesis , resection arthroplasty , revision arthroplasty)

10. •Discovered radiologically in Patient with
painfull limp with no systemic manifestations
•WBC and blood culture may be normal but
ESR is elevated
•Patient is usually child or adolescent
•Common sites are tibia and femur
•Treatment:
conservative : if diagnosis is not in doubt by
immobilization and antibiotics for 6 weeks
healing takes 6-12 months
 curretage and open biopsy : if tumor is
suspected

11. Comparison between: subacute OM , Garré's sclerosing OM, subacute recurrent multifocal
OM(SRMO) , sternocostoclavicular hyperostosis (SCCH) ,Caffey's

12. Garré's sclerosing OM

13. Sternocostoclavicular
hyperostosis (SCCH)
Subacute recurrent
multifocal OM(SRMO)

14. •Etiology; inapproriate ttt of acute OM ,trauma or soft tissue spraed , DM and
immunosuppressed pt
•Orgamisms : staph aureus and epidermidis ,psudomonas aeruginosa or mixed
•Clinical picture : periods of quiescence followed by acute exacerbations , skin and soft tissue
are involved with sinus formation
•Imaging:
Xray :bone resorption , patchy loss of density ,Periosteal
thickening , sequestration and sinogram localizes site
 Bone scan , CT and MRI
•Investigaions : ESR and WBC increase during flares

15. •Classification :
Cierney & Mader
•Treatment :
 antibiotics : stop spread and control acute flares
Local treatment : sinus care by dressing or colostomy patch to prevent skin excoriation
Operation : indicated in significant symptoms , clear sequestrum and abscess formation
Under antibiotic cover all devitalized or infected soft tissue and bone are removed
Further treatment options include : double lumen tube irrigation , addition of antibiotic
beads or sheets , Papineau technique ( packing cavity with bone graft , AB and fibrin sealant
muscle flap transfer)
In refractory cases: excision of the devitalized segment then closure of gap by bone
transport by ilizarov

16. Route of infection :

Direct invasion : penetrating wound, intra
articular inj , arthroscopy

Eruption of bone abscess

Haematogenous
•Causative organism: staphylococus aureus , haemophilus influenzae
streptococcus pyogenes , escherishae coli
•
Pathology :
acute synovitis with purulent joint effusion
articular cartilage attacked by bacterial toxin
and cellular enzyme
complete destruction of the articular cartilage.
•
Sequelae:
complete recovery
partial loss of the articular cartilage
fibrous or bony ankylosis
osteonecrosis
•

17. •Clinical picture:
1. Neonate:
Picture of Septicemia , irritability
resistance to movement
2. Child:
i. Acute pain in single large joint
ii. reluctant to move the joint
iii. increase temp. and pulse
iv. Increasing tenderness
3. Adult : often involve superficial
joint (knee, ankle, wrist)
•Laboratory investigation:
•WBC, ESR CRP ,blood culture
•X ray
•Ultrasound
•Aspiration

18. •Differential Diagnosis:
 acute osteomyelitis






trauma
irritable joint
hemophilia
rheumatic fever
gout
Gaucher disease
•Treatment:
confirm diagnosis by aspiration
Followed by:

general supportive measures

antibiotics

surgical drainage

19. •Incidence:

Showed a steady decline in its prevalence in developed countries during the 1960s and
1970s, due to the effectiveness of public health programs and advances in chemotherapy.
 In the past two decades, however, the annual incidence has risen again which may be
attributed to changes in population movements, the spread of intravenous drug abuse
and the emergence of AIDS.

20. •Predisposing factors:
Chronic debilitating disorders,
Drug abuse,
Prolonged corticosteroid medication,
AIDS and other disorders resulting in reduced
defense mechanisms.
•Pathology:
Mycobacterium tuberculosis ( usually human, sometimes bovine ) enters the body via the
lung ( droplet infection ) or the gut ( swallowing infected milk products ) or, rarely through
the skin.
Primary complex:The initial lesion in lung, pharynx or gut
Secondary spread mayo ccur, giving rise to miliary tuberculosis or meningitis. More
often, blood spread occurs months or years later and bacilli are deposited in extrapulmonary
tissues.
Tertiary lesion. Bones or joints are affected in about 5 of patients with tuberculosis. There
is a predilection for the vertebral bodies and the large synovial joints.

21. •The characteristic microscopic lesion is the tuberculous granuloma – a collection of
epithelioid and multinucleated giant cells surrounding an area of necrosis, with round cells
( mainly lymphocytes ) around the periphery.
•Bone lesions tend to spread quite rapidly.
epiphyseal cartilage is no barrier to invasion
and soon the infection reaches the joint.
only in the vertebral bodies, and more
rarely in the greater trochanter of the femur
or small bones of the hands or feet, does
the infection persist as a pure chronic
osteomyelitis.
•Caseation and infection may extend into the surrounding soft tissues to produce a cold
abscess. This may burst through the skin, forming a sinus, or it may track along the tissue
planes to point at some distant site. Secondary infection by pyogenic organisms is common.

22. •Clinical picture:
There may be a history of previous infection or recent contact with tuberculosis.
The patient is usually a child or young adult.
Pain and (in a superficial joint) swelling.
In advanced cases there may be attacks of fever or lassitude and loss of weight.
Relatives tell of “ night cries “ .
Muscle wasting is characteristic.
Synovial thickening is often striking.
Movements are limited in all directions.
As articular erosion progresses the joint becomes stiff and deformed.

23. In tuberculosis of the spine, pain may be deceptively slight- often no more than an
ache when the spine is jarred. Consequently the patient may not present until there
is a visible abcess ( usually in the groin or the lumber region to one side of the
midline ) or until collapse causes a localized kyphosis. Occasionally the presenting
feature is weakness or loss of sensibility in the lower limbs.

24. •Radiology:
X-ray and MRI are helpfull
Soft - tissue swelling and periarticular osteoporosis are characteristic (early).
The bone ends take on a “ washed-out “ appearance and the articular space is
narrowed.
Later on there is erosion of the subarticular bone, characteristically seen on both
sides of the joint.
Cystic lesions may appear in the adjacent bone ends but there is little or no
periosteal reaction.
In the spine: bone erosion and collapse around an intervertebral disc space; the
soft tissue shadows may define a paravertebral abscess.

25. •Investigations
The ESR: is increased.
CBC: relative lymphocytosis.
The mantoux or Heaf test: will be positive, these are sensitive but not specific
tests.
If synovial fluid is aspirated, it may be cloudy, the protein concentration is
increased and the white cell count is elevated.
Acid-fast bacilli are identified in synovial fluid in 10-20 of cases, and cultures
are positive in over half.
A synovial biopsy is more reliable; sections will show the characteristic
histological features, and acid fast bacilli may be identified; cultures are positive in
over 80 of cases.

26. •Diagnosis:
Features that should trigger more active investigation are:

A long history

Involvement of only one joint

Marked synovial thickening

Marked muscle wasting

Periarticular osteoporosis

A positive Mantoux test

Synovial biopsy for histological examination and culture is often necessary.
•Differential diagnosis:
Transient synovitis
Monoarticular rheumatoid arthritis
Subacute arthritis
Haemorrhagic arthritis
Pyogenic arthritis (in long standing cases).

27. •Treatment :
Rest :
This often involved splintage of the joint and traction to overcome muscle spasm
and prevent collapse of the articular surfaces. With modern chemotherapy this is
no longer mandatory; rest and splintage are varied according to the needs of the
individual patient.
Chemotherapy :
The most effective treatment is a combination of antituberculous drugs, which
should always include rifampicin and isoniazid. A recommended regimen is
rifampicin, isoniazide and ethambutol ( or pyrazinamide ) for 8 weeks, and
thereafter rifampicin and isoniazide for a further 6-12 months.

28. Operation :
Operative drainage or clearance of a tuberculous focus is seldom necessary nowadays.
However, a cold abscess may need immediate draining.
Once the condition is controlled and arthritis has completely subsided, normal activity
can be resumed, though the patient must report any renewed symptoms.
If , however, the joint is painful and the articular surface is destroyed, arthrodesis or
replacement arthroplasty may be considered. The longer the period of inactivity, the
less the risk of reactivation of the disease; there is always some risk and it is essential to
give chemotherapy before and after the operation.