introduction , types , clinical manifestation , diagnosis , management of osteomyelitis

1. OSTEOMYELITIS
Dr. Sunil pahari
2nd Year Resident
Department of Orthopedics
Yangtze University

2. OSTEOMYELITIS
 Nelaton coined
osteomyelitis in 1834
It includes three root words
 osteon (bone)
 myelo (marrow)
 Combination: itis
(inflammation)
to define the clinical state in
which bone is infected with
microorganisms.

3.  Infection of bone and marrow is known as osteomyelitis.
 It may remain localized, or it may spread through the
bone to involve the marrow, cortex, periosteum, and soft
tissue surrounding the bone.

4. CLASSIFICATION
Duration
 Acute / Subacute / Chronic
Mechanism
 Heamatogenous (tonsil , lungs , ear/ GIT)
 Exogenous (injection , open fractures)
Host response
 Pyogenic / Granulomatous

5. Osteomyelitis is divided into 3 forms as per duration:
1. 1. Acute osteomyelitis
2. 2. Subacute osteomyelitis
3. 3. Chronic osteomyelitis

6. OSTEOMYELITIS
BASED ON THE DURATION AND TYPE OF SYMPTOMS
Acute: <2weeks Early acute
Late acute(4-
5days)
Subacute
:
2weeks
—
3months
Less virulent –
more immune
Chronic: >3month
s

7. Three basic mechanisms allow an infection to reach the
bone;
1. Haematogenous spread
2. Contagious source
of infection
3. Direct implantation

8. - Primary haematogenous osteomyelitis is characterized by an
acute infection of bone caused by seeding of bacteria within
the bone from a remote source
- Haematogenous osteomyelitis usually occurs during period of
growth and thus occur primarily in children. However, all ages
may be affected and cases are even found in old age.
HAEMATOGENOUS OSTEOMYELITIS

9. CAUSES: OSTEOMYELITIS
 General factors
 Anaemia
 Debility
 Infection
 Poor nutrition
 Poor immune status
 Local factors
 Hair pin bend vessels
 Metaphyseal haemorrhage
 Defective Phagocytosis
 Rapid growth at metaphysis
 Vasospasm

10. TYPE OF ORGANISMS
 Bacteria, viruses and fungi can all infect bone, soft
tissues and joints. Generally, bacterial infections
are more destructive and move rapidly.
 Fungi tend to produce slow and chronic infections.
 Tuberculosis and brucellosis range from aggressive
to reparative

11. PATHOPHYSIOLOGY:
 Metaphysis of the long bones are
highly vascularized zones.
 From the diaphysis the medullary
arteries reach upto the growth
plate—the area of greatest activity
and branch into capillaries. The
venous systems in this area
drains towards diaphysis
 Thus, the vessel in this zone are
arranged in the form of loop (hair
pin arrangement) resulting in
“sluggish flow” of blood, leading to
bacterial enlodgement and thus
haematogenous osteomyelitis.

12. CLINICAL FEATURES
Early Acute •Febrile illness
•Limping to walk
•Avoidance of using the extremity
Late Acute
• Swelling
• pain
Sub acute
Cannot pinpoint onset
Fever/swelling-mild
Chronic purulent drainage

13.  Fever
 Fatigue
 Irritability
 Malaise
 Restriction of movement of limb
 Local edema, erythema and tenderness
GENERAL SYMPTOMS OF OSTEOMYELITIS ARE :-

14. DEVELOPMENT OF OSTEOMYELITIS

15. RISK FACTORS
 Trauma (orthopaedic surgery or open fracture)
 Prosthetic orthopaedic device
 Diabetes
 Peripheral vascular disease
 Intravenous drug abuse
 Chronic steroid use
 Immunosuppression
 Tuberculosis
 HIV and AIDS
 Sickle cell disease

16. DIAGNOSIS
 Early diagnosis of acute osteomyelitis is critical
because prompt antibiotic therapy may prevent
necrosis of bone.
 Osteomyelitis is primarily a clinical diagnosis,
although the clinical picture may be confusing.
 An inadequate or late diagnosis significantly
diminishes the cure rate and increases the degree
of complications and morbidity.

17. LAB FINDINGS:
 Aspirate pus or fluid, a smear is examined for cells
and organisms(to identify a type of infection)
 WBC counts are elevated with increased
polymorphoneuclear leukocyte count.
 C-reactive proteins – level is elevated
 ESR usually elevate up to 90%.
 Blood culture results are positive in patients with
haematogenous osteomyelitis.

18. RADIOLOGICAL FINDINGS
 Plain X-ray
 The earliest radiographic signs of bone infection are soft
tissue swelling and loss of fascial planes.
 These are usually encountered with in 24 to 48 hours of
infection.
 Plain radiographs shows:
 Ist week: No abnormality of bone
 2nd week : Faint extra cortical outline due to periosteal new
bone formation ( a classic x-ray sign of early pyogenic
osteomyelitis.)
 7 to 10 days : destructive lytic lesion, usually occurs.
 3 to 6 weeks : elevation of periosteum and layered new bone
formation .
 3-8 weeks :The dead bone (i.e. sequestrum formation) occurs.

19. INFECTION AT THE FRACTURE SITE HAS
DELAYED UNION IN THE HUMERUS. NOTE
THE EXTENSIVE PERIOSTEAL REACTION.

20.  Sequestra surrounded
by involucrum

21. ULTRASOUND
 Ultrasound may detect a sub periosteal collection
of fluid in the early stage of osteomyelitis but it
cannot distinguish between hematoma and pus.

22. CT SCANNING
 CT is useful method to detect early osseous erosion and
to document the presence of sequestrum, foreign body, or
gas formation
 Though of less value in diagnosis, CT demonstrates
changes in subacute or chronic osteomyelitis well.
 Sequestra, as on conventional films is shown as area of
dense or high attenuation spicules of bone lying in areas
of osteolysis.

23. M.R.I. FINDINGS
 MRI can be helpful in case of doubtful diagnosis
 It is highly sensitive for detecting osteomyelitis as early
as 3 to 5 days after the onset of infection
 It is best method of demonstrating bone marrow
inflammation.
 It helps to differentiate between soft tissue infection and
osteomyelitis.

24. DIFFERENTIAL DIAGNOSIS:
 Cellulitis
 Acute suppurative arthritis
 Streptococcal necrotising myositis
 Sickle –cell crisis
 Gaucher’s Disease
 Tuberculosis –
 Ewing sarcoma

25. TREATMENT
1. General treatment: nutritional therapy or
general supportive treatment by intaking
enough caloric, protein, vitamin etc.
2. Antibiotic therapy
3. Surgical treatment
 I&D
4. Immobilization
 Splintage of affected part

26. COMPLICATIONS
 Chronic osteomyelitis
 Septic arthritis
 Growth disturbance
 Septicemia
 DVT
 Pulmonary embolism
 Pathological fracture
 Metastatic infection

27. MANAGEMENT OF ACUTE OSTEOMYELITIS.
ACUTE
OSTEOMYELITIS

28. SUB ACUTE OM TREATMENT
Conservative :
a) Immobilization
b) Antibiotics (flucloxacillin + fusidic acid) for 6weeks
Surgical (if the diagnosis is in doubt / failed conservative
treatment) :
a) Open biopsy
b) Perform curettage on the lesion
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29. CHRONIC OSTEOMYELITIS
“ A severe, persistent and incapacitating infection of
bone and bone marrow ”
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CHRONIC OSTEOMYELITIS

30. CHRONIC OSTEOMYELITIS

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32. SEQUESTRUM
PERIOSTEAL NEW BONE
FORMATION
INVOLUCRUM
CHRONIC OSTEOMYELITIS

33. INVOLUCRUM (the new bone)
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CHRONIC OSTEOMYELITIS

34. STAGING OF OSTEOMYELITIS:
 The Cierny-Mader staging system.
 It is determined by the status of the disease
process.
 It takes into account the state of the bone, the
patient's overall condition and factors affecting the
development of osteomyelitis.
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CHRONIC OSTEOMYELITIS

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CHRONIC OSTEOMYELITIS

36. THE CIERNY-MADER CLASSIFICATION
 Stage 1: Medullary Osteomyelitis -
Infection confined to medullary
cavity.
 Stage 2: Superficial Osteomyelitis
Contiguous type of infection. Confined
to surface of bone.
 Stage 3: Localized Osteomyelitis -
Full-thickness cortical sequestration
which can easily be removed
surgically.
 Stage 4: Diffuse Osteomyelitis -Loss
of bone stability, even after surgical
debridement.
CHRONIC OSTEOMYELITIS

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CHRONIC OSTEOMYELITIS

38. TREATMENT - ANTIBIOTICS
- Chronic infection is seldom eradicated by
antibiotics alone.
- Bactericidal drugs are important to:
a) Stop the spread of infection to healthy bone
b) Control acute flares
- Antibiotics used in treating chronic osteomyelitis
(Fusidic acid, Clindamycin, Vancomycin,
Cefazolin)
CHRONIC OSTEOMYELITIS

39. ANTIBIOTIC CHOICE
 Guided by microbiology department
 Clindamycin and vancomycin have good bone
penetration
 Minimum length 6 weeks with 3 months being the
standard treatment course
 May need to treat for 6-12 months
 Antibiotic (IV route) is given for 10 days prior to
surgery.
 After the major debridement surgery, antibiotic is
continued for another 6 weeks (min) but usually
>3months.
[treat until inflammatory parameters (ESR) are
normal]
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CHRONIC OSTEOMYELITIS

40. SURGICAL TREATMENT
- After 10 days of
antibiotic
administration,
debridement is
done to remove:
a) All the infected
tissue
b) Dead /
devitalised bone
(Sequestrectomy
)
c) Sinus tract
CHRONIC OSTEOMYELITIS
Sequestrectomy and curettage. A, Affected
bone is exposed, and sequestrum is
removed. B, All infected matter is
removed. C, Wound is either packed open
or closed loosely over drains.

41. Closure of dead space
- After debridement is done, a large dead
space is left in the bone
- Among the methods of managing dead
space:
Open cancellous grafting – Papineau
technique
 Useful for bone deficiencies of less than
4cm
 (preferably autogenous) mixed with an
antibiotic and fibrin sealant
Vascularised bone graft
 Heals as a segmental fracture
 Indicated when defect is > 6cm
 Iliac crest for defects > 8cm
 Fibula 6-35cm can be bridged
Bypass graft
 Involves the establishment of a cross union
between the fibula and tibia proximally and
distally to the defect which has been
debrided and bone grafted
CHRONIC OSTEOMYELITIS

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CHRONIC OSTEOMYELITIS

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CHRONIC OSTEOMYELITIS

45.  M.C.Q:-
1) involucrum is found
A. underneath the sequestrum B.metaphysis
C. around the sequestrum D.beneath the
periostium
2) acute haematogenous osteomyelitis is treated with
all except :
A.antibiotics B.splinting
C.anelgesics D. surgery

46.  3)Chronic osteomyelitis is diagnosed mainly by:
A.Sequestrum B. Bone fracture
C. Deformity C.Brodie’ abscess
4) Osteomyelitis of spine most common organism
is:
A.Staphylococcus aureus B. pseudomonas
C.Tuberculosis C. Streptococcus

47.  6)When does the boney lesion of osteomyelitis
appear on x-ray:
A.2week B.24hours
C.1week D.2hours
7)Osteomyelitis most commonly starts at:
A.Metaphysis B.Epiphysis
C.Diaphysis D. None
8)The most common causing osteomyelitis in drug
abusers is:
A.Pseudomonas B.staphylococcus Aureus
C. E.coli D. Kiebsiella.

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