A comprehensive yet complete presentation about the causes, types, manifestattions and treatment of acute and chronic osteomyelitis

2. OSTEOMYELITIS
DR M. TAHIR KARIM
PGR
ORTHOPAEDIC SURGERY UNIT-I
JHL

3. OUTCOMES
 Epidemiology
 Risk factors
 Pathophysiology
 Clinical features
 Diagnosis
 Management
 Complications

4. OSTEOMYELITIS
 Osteomyelitis is the
inflammation or swelling of
bone that is usually the result
of infection
 It may be localized or may
spread through the bone to
involve the marrow, cortex,
periosteum, and soft tissue
around the bone.

5. EPIDEMIOLOGY
 Bimodal age distribution
 Under 20
 Over 50
 Pediatrics:
 boys>girls
 Usually no identifiable risk factors
 Adults:
 Usually have risk factors
 Incidence of infection increases with increase in grade of
compounding (Guistilo Anderson): 2% for type I and II,
approx.10-50% for type III

6. HOW DO YOU GET OSTEOMYELITIS
1.Exogenous 2. Contiguous focus 3. Haematogenous spread
• Most common
• Direct inoculation of bone
after trauma, surgery,
insertion of hardware
• Can occur at any age and
with any bone
• Second most common
• Related to diseases such as
Diabetes mellitus, peripheral
vascular disease
• Almost always begins with a
soft tissue infection that
spreads to bone
• Least common
• Seeded from other source
• Seen most commonly in
adolescent children
(metaphysis of long bones)
and elderly (vertebrae)
• Occurs in metaphysis
• Examples: IV drug abusers,
sickle cell disease

7. RISK FACTORS
 Diabetes mellitus
 Sickle cell disease
 AIDS
 Alcoholism
 IV drug abuse
 Chronic corticosteroid use
 Preexisting joint disease
 Other immunosuppressed states
 Postsurgical patients—especially those with prosthetic devices

8. Organisms isolated in Bacterial Osteomyelitis
Organisms Comments
Staphylococcus aureus Most common in all types
Coagulase-negative staphylococci
Propionibacterium species
Foreign body associated infection
Enterobacteriaceae species
Pseudomonas aeruginosa
Nosocomial infections and punctured wounds
Streptococci or anaerobic bacteria With bites/fist injuries with other person,
diabetic foot lesions, decubitus ulcers
Salmonella species Sickle cell disease

9. OTHER PATHOGENS
 Viruses and fungi may also be involved
 Gram negative bacteria (in elderly patients)
 Mycobacterium (in immunosuppressed, alcoholic, IV drug abusers or
residents of endemic areas)
 MRSA, MRSE, and VRE have emerged as a significant microbiologic
problem in the past decade
 Polymicrobial (36 to 50%) more likely in diabetic foot osteomyelitis,
posttraumatic osteomyelitis and chronic osteomyelitis

10. Based on duration and type of symptoms
Acute <2 weeks
Subacute 2-6 weeks
Chronic >6 weeks,
Involves relapses

11. PRESENTATION
SYMPTOMS
 Bone pain
 Fever (High grade in case of blood infection)
 Systemic complaints (general discomfort, fatigue, malaise)
 Difficulty bearing weight or walking (in lower limbs)
 Stiff back (in vertebral involvement)
 Discharging sinus (in chronic osteomyelitis)
SIGNS
 Swelling, redness on inspection
 Severe tenderness, warmth on palpation
 Difficulty in moving joints around the affected area

12. SUBACUTE OSTEOMYELITIS
 More insidious onset and lack of severity of symptoms
 Diagnosis typically is delayed for more than 2 weeks
 Pathogen is identified only 60% of the time
 S. aureus and S. epidermis are usually involved
 The diagnosis is often established by an open biopsy or
culture

13. CHRONIC OSTEOMYELITIS
 Sequestrum, Involucrum, abscess or sinus (cloaca) is present
 Sinus usually has a purulent or seropurulent discharge
 May remain dormant for months or years with acute or
subacute flares.
 X-ray shows signs of bone destruction
 Tuberculosis, Fungal infection and Brodie’s abscess usually
leads to chronic osteomyelitis
 Muscle wasting contractures, atrophy may occur

14. CHRONIC OSTEOMYELITIS
 Sequestrum is the necrotic
bone embedded in the
pus/infected granulation
tissue
 Involucrum is the new bone
laid down by the
periosteum that surrounds
the sequestra.
 Cloaca is the opening in the
involucrum through which
pus & sequestra make their
way out

15. CHRONIC OSTEOMYELITIS
 Brodie’s abscess:
 Sequela of subacute or chronic osteomyelitis
 Bone abscess containing pus or jelly like granulation tissue
surrounded by a zone of sclerosis
 11-20yrs, metaphyseal area, usually upper tibia or lower
femur.
 Deep pain, worst at night, relieved by rest.
 On radiograph, circular or oval lucency surrounded by
zone of sclerosis

16. Bacteria invades
bone and proliferate
Alerts macrophages
that release enzymes
Bone breakdown,
local destruction
Acute
Immune system
eventually destroys all
bacteria
Resolution, osteoblasts
and osteoclasts repair
the damage
Chronic
Bone becomes necrotic
due to impaired blood
flow and separates
(Sequestrum)
Osteoblasts form new
bone around
sequestrum
(Involucrum)
Pathophysiology

17. Cierny-Mader Classification System
Anatomical type
I Medullary osteomyelitis
II Superficial osteomyelitis
III Localized osteomyelitis
IV Diffuse osteomyelitis
Physiological class
A Good immune system
B Compromised locally(BL) or systemically
(BS)
C Requires suppressive or no treatment,
minimal disability,
treatment worse than disease,
not a surgical candidate

18. DIAGNOSIS
 WBC
 Neither sensitive nor specific
 Usually elevated with leftward shift
 Values commonly range from normal to 15,000/mm3
 ESR
 Usually elevated
 Very sensitivity but very nonspecific
 Can be used to follow treatment
 CRP
 yet another nonspecific marker of inflammation
 Elevated earlier than ESR

19. DIAGNOSIS
 Plain films:
 Low sensitivity early in the disease
 3-5 days: may detect soft tissue edema
 7-10 days: >66% still have normal x-rays
 By 28 days, >90% of plain films will be positive
 By the time there is X-ray evidence of bone destruction(30-
50% reduction of bone density), the patient has entered he
chronic phase of the disease
 Characteristic finding: lytic lesions of cortical bone
destruction
 Advanced disease: lytic lesions are surrounded by dense,
sclerotic bone, and sequestrum may be noted

20. Blue arrow: Area of bone
destruction on the great toe.
Mottled appearance and
irregularities at the edge of the
bone.
Red arrow: Notice the normal
bone of first metatarsal

21. Plain film radiograph
showing osteomyelitis of
second metacarpal.
Periosteal elevation,
cortical disruption and
medullary involvement are
present

22. Involucrum
Sequestrum

23. DIAGNOSIS
 Ultrasound
 Can not directly access bone marrow abnormalities
present in osteomyelitis
 Can document osteomyelitis indirectly by identifying
periosseous soft tissue abnormalities
 Allows for ultrasound guided aspiration
 The very first sonographic sign is edematous swelling of
the deep soft tissues

24. DIAGNOSIS
 Bone Scan:
 More useful early on than plain radiographs
 Can detect osteomyelitis within 48 to 72 hours of disease
onset
 Sensitivity 90% with technetium-99 scan
 False positive rate is high (trauma, surgery, tumors, soft
tissue infection)

25. DIAGNOSIS
 In 111 -labeled leucocyte scan
 Can distinguish infected bone from bone that has
increased turnover from other reasons
 Usually reserved for equivocal or normal bone scans in
patients where osteomyelitis is still a consideration

26. Bone scan showing accumulation of tracer in right ankle.

27. DIAGNOSIS
 CT
 Used for infection in bones that are difficult to visualize on
plain radiographs and bone scans: sternum, vertebrae,
pelvic bones, and calcaneus
 Appears as rarefaction or lucent areas, on the CT scan
images
 Gas may also be visible in bony abscess cavities
 Limitation: disease must be present for > 1 week

28. Left femoral head fluffiness and distortion due to acute osteomyelitis (arrow)

29. DIAGNOSIS
 MRI
 Highly sensitive and specific (>90%)
 Good for early detection and surgical localization
 Useful in differentiating bone and soft tissue infection
 Limitation: A metallic implant in the region may produce
focal artifacts and can cause a safety hazard.

30. MRI showing osteomyelitis of 5th metatarsal (A) and L4-5 vertebral
bodies and intervertebral disc (B)

31. DIAGNOSIS
 Microbiologic Diagnosis:
 Needle aspiration or surgical specimen is best
 Swab of draining wound or sinus is not adequate
 Blood cultures in untreated patients are positive ~50% of
the time

33. Differential Diagnosis
 Tumor:
 Osteoid osteoma, chondroblastoma, Ewing’s sarcoma, metastases,
lymphoma
 Trauma
 Myositis ossificans
 Erythema nodosum
 Cellulitis
 Eosinophilic granuloma

34. Treatment
 Goals of treatment
 Complete removal of necrotic bone and affected
soft tissue
 Control of infection and elimination of dead space
(after removal of dead bone)
 Pain management

35. Treatment
 Surgery and Antibiotics are complimentary to each other.
 General measures include IV fluids, proper analgesia and
comfortable positioning of the limb
 Patient should be treated with appropriate antimicrobial
therapy for 4-6 weeks, dating from the initiation of
therapy or last major surgical debridement

36. Indications of Surgery
 The presence of abscess requiring drainage
 Failure of clinical improvement despite appropriate
intravenous antibiotics (Occult abscesses must be sought)
Surgery may range from minor debridement to amputation of
infected bone.

37. Sequestrectomy:
 Well formed involucrum surrounding the discretely visible
sequestrum (at least 2/3rd diameter of bone) and symptomatic
patient with pus discharge or chronic disabling pain are pre-
requisites of sequestrectomy.
 It is critical to preserve Involucrum to minimize the risk of
fracture, deformity & segment loss.
 Preferable to wait 3-6 months before performing
sequestrectomy

38. Management of dead space
 Adequate debridement may leave a large bone defect,
termed as dead space.
 The goal is to replace dead bone and scar tissue with
durable vascularized tissue.
 Free vascularized bone graft, local tissue flaps or free flaps,
cancellous bone grafts or open cancellous grafts can be
used accordingly for this purpose.
 Antibiotic beads may be used to sterilize and temporarily
maintain a dead space, usually removed within 2-4 weeks
and replaced with a cancellous bone graft.

40. After Surgery:
 Skin is closed over drains
 Limb is splinted
 Once wound is healed, protected weight bearing is
begun
 Limb protected for a few weeks to prevent
pathological fracture
 Patient is followed for one year

41. Nade’s Principles
1. Antibiotics are effective before pus forms.
2. Antibiotics can not sterilize avascular tissue or abscess
3. Antibiotics prevent reformation of pus once removed,
therefore primary closure should be safe
4. Pus removal restores periosteum, restores blood flow
5. Antibiotics should be continued after surgery

42. SPECIAL CONSIDERATIONS
 Infection of an orthopaedic prosthesis may need to be
removed along with the infected tissue around it.
 If the patient is diabetic, needs to have well controlled.
 If the patient has some vascular disease, surgery to improve
blood flow may also be needed.
 In patients with vertebral osteomyelitis, there is risk of
paralysis and epidural abscess.
 Patients with sickle cell disease have increased risk of
developing osteomyelitis due to salmonella.

43. COMPLICATIONS
 Acute exacerbations - most common
 Septicemia
 Growth abnormalities
 Deformities
 Pathological Fractures
 Joint stiffness
 Thrombophlebitis
 Amyloidosis
 Malignancy(0.25%) – sq. cell carcinoma, fibrosarcoma, reticulum cell
carcinoma
 Septic arthritis