osteomyelitis

Lecturer : Dr Nwukor
 Introduction

 Osteomyelitis is an infection of the bone caused by bacteria, fungi, or mycobacteria.

 The infection can spread in the bone through hematogenous, contiguous spread from
adjacent soft tissues, or direct inoculation during trauma, or even surgery.

 The disease process is characterized by the progressive destruction of bone at the center of
infection and new appositional bone growth around it
Anatomy of bone
Osteomyelitis

 Inflammatory disease of the bone and marrow secondary to infection

 Often manifests as a solitary focus of disease

 All types of organisms can produce osteomyelitis but mostly due to

-Pyogenic bacterial osteomyelitis

-Tuberculous osteomyelitis
 Pyogenic Osteomyelitis

 Usually of bacterial cause

 Haematogenous spread resulting from bacteremia

 Direct implantation by penetrating trauma

 Contiguous spread
 Risk factors
 HIV/AIDs
 Sickle cell disorder
 Tuberculosis
 Diabetes
 Immunosupression
 Trauma
 Prosthetic orthopaedic implants
 Chronic steroid use
 Intravenous drug abuse
 Peripheral vascular disease, etc
aetiology

 Haematogenuous in origin

 Develops in the long bones

 Bacteremia stem from trivial mucosal injuries, such as may occur

during defecation or vigorous chewing of hard foods
Structure and function of the metaphysis
 Infection

 Staph aureous (most common, 80 – 90%)

 Neonates –Haemophilus influenza type b and Group B Streptococci

 SCD patients – Salmonella infection

 During surgery and in open fractures

 In patients with genitourinary tract infections and IV drug abusers …

E. coli, pseudomonas and klebsiella
Location

 Neonate and infants younger than one year – metaphysis, epiphysis

or both

 In Older Children – metaphysis

 Pathophysiology

 Metaphysis of the long bones are highly vascularized zones

 From the diaphysis the medullary arteries get to the growth plate

 Growth plate is the area of the greatest activity and branch into
capillaries with sluggish flow of blood, hence enlogdement of bacteria
therein

 The venous systems in this area drains towards diaphysis

In summary
 Osteomyelitis in children occurs most commonly in the metaphysis of the femur or tibia due
to hematogenous seeding that is circulating bacteria in the bloodstream land in the bone.

 In children over the age of 18 months, the metaphyseal region has straight, narrow
capillaries coursing to, but not across, the growth plate.

 These vessels then turn back at a 180-degree angle to drain into the veins.

 This “hair pin” turn decelerates the blood and allows any bacteria within the bloodstream to
escape and lodge within the bone
Consequent event of osteomyelitis
 (a) initial metaphyseal focus
 (b) lateral spread to the cortex
 (c) cortical penetration and periosteal elevation
 (d) formation of a thick involucrum
 (e) further expansion of the metaphyseal focus with extensive involucrum.
 Acute stage
 Bacteria usually proliferate and induce neutrophilic inflammatory reaction and cause
cell death.
 The inflammatory spread and may percolate throughout the haversian systems, then
eventually reach the periosteum.

 Bone undergoes necrosis within the 1st 48hrs with resultant subperiosteal abscess.

 This is followed by lifting of periosteum, segmental bone necrosis, sequestrum (dead

piece of bone)

 Rupture of periosteum leads to a soft tissue abscess in the surrounding soft tissue and
the formation of draining sinuses.
 Among the infants , the epiphyseal infection spread the articular surface or along capsular
and tendoligamentous insertions into a joint , producing septic or suppurative arthritis

 In children, periosteum is loosely attached to the cortex and subperiosteal abscesses may
dissect for long distances along the bone surfaces
Chronic stage

 After 1st week, chronic inflammatory cells become more numerous

and cyokines from leukocytes stimulate

- Osteoclastic bone resorption

- Ingrowth of fibrous tissue
- Deposition of reactive bone in the periphery

 Reactive woven or lamellar bone which forms sleeve of living tissue

surrounding dead bone is called involucrum (living piece of bone)
 Morphologic variants

 Brodie abscess: An intraosseous abscess that frequently involves the cortex and is walled off
by reactive bone.

 Sclerosing osteomyelitis of Garre: It typically develops in jaw and is associated with

extensive new bone formation that obscures much of the underlying osseous structures
Clinical manifestation

 Sudden onset is a classical presentation

 Usual symptoms include : fever, malaise, irritability, fatigue, localized

warmth, pain, localized oedema, erythema and tenderness over the
area of infection

 Ulceration, drainage and localized pain are the typical signs and
symptoms
Diagnosis

 Prompt and early diagnosis is critical as timely initiation of antibiotics

will prevent bone necrosis and progression to chronic form

 Osteomyelitis is a clinical diagnosis though picture may be

ambiguous

 Misdiagosis predisposes to decrease poor cure rate and high degree

of complications and morbidity
Laboratory Findings

 Aspirate pus or fluid smeared to examine for cells and organisms xtic
of a type of infection
 WBC counts are elevated with increased PMNL count
 CRP is elevated
 ESR elevated up 90%
 Blood culture is positive in pxs with haematogenous osteomyelitis 40
– 45% yield of the causative organisms.
Radiological findings

 The earliest radiographic signs of bone infection are soft tissue

swelling and loss of fascial planes, ususally seen within 24 -48hrs of
infection
 1st 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 – 10 days: destructive lytic lesion
 3 – 6 weeks: elevation of periosteum and layed new bone formation
 3 – 8 weeks: the dead bone (sequestrum formation) occurs
The focal area of increased opacity represents
necrotic bone or sequestrum (blue arrow) in a
plain radiograph of femur
(Left) Plain radiograph of osteomyelitis of the
tibia demonstrating a lytic lesion in the
metaphysis (red arrow) with periosteal
reaction (green arrow)
Other investigations

 Ultrasound, CT scan and MRI

Differential diagnosis

 Cellulitis
 Acute suppurative arthritis
 Streptococcal necrotising myositis
 Sickle cell crisis
 Tuberculosis
 Ewing sarcoma
 Gaucher’s disease
Treatment

 Multidisciplinary
 General treatment: Nutritional therapy or general supportive
treatment by taking of enough calorie, protein, vits,etc
 Antiobiotics – a broadspectrum esp cephalosporins eg cefotaxime is
useful in neonates , but in areas of MRSA ,vancomycin is a drug of
choice until sensitivity results confirms or exclude MRSA
 Surgical treatment including incision and drainage
 Immobilization
- Splintage of affected part
Complications

 Chronic osteomyelitis
 Septic arthritis
 Growth disturbance (growth plate affectation)
 Septicaemia
 DVT
 Pulmonary embolism
 Pathological fracture
 Metastatic infection
 Prevention

 Individuals with sickle cell anemia can be immunized against salmonella, haemophilus
influenza type b.

 Patients with diabetic neuropathy should perform daily foot exams and complete early
treatment of minor foot injuries to prevent potentially devastating complications of
osteomyelitis.

 Avoid other risk factors where possible

 Patient education
SEPTIC ARTHRITIS
 Introduction
 An inflammation of the synovial membrane with purulent effusion into the joint capsule
secondary to infection

 It is also referred to as infectious arthritis

 A medical emergency and can lead to septic shock which can be fatal

 Antibiotic therapy must be commenced within 24 – 48 hrs to forestall subchondrial bone

loss and permanent joint deformity
 Epidemiology
 All age groups are affected , but commoner among the age group 1 – 5yrs
 50% < 3 yrs
 M=F
 The knee is the most commonly affected joint and single joint involvement is seen in
94% of cases
 Infants – hip
 Older children – knee
 Aetiology
 The infection can originate any where in the body

 May also begin as the result of an open wound, trauma, surgery or unsterile injection

 Septic arthritis occurs when the infective organism travels through the blood stream to the
joint

 The infection can be caused by bacterium, virus or fungus

 Aetiology

 <3months – staph aureus, streptococcus sp, g-ve bacilli, Neisseria gonorrhea

 Infants – staph aureus, kingella kingae, H. influenza type b

 Older children – staph aureus , salmonella

 Adolescent – staph aureus and Neisseria gonorrhoea

 Iv drug users – pseudomonas and atypical organisms

 Routes of infection
 Haematogenous spread
–most frequent
-bacterial associated with urti, skin or GIT infections or invasive procedures

 Direct innoculations eg joint contamination by foreign body

 Contiguous spread osteomyelitis due to several factors in infants

pathogenesis: Acute septic arthritis
Bacteria deposits in synovium producing inflammation
↓
Spreads to synovial fluid and multiplies
↓
Products of inflammation destroys joint components
(swollen, painful joint)
↓
Sequelae
1.infants: epiphyseal destruction,
2. older children: epiphyseal bone necrosis due to vascular occlusion
 Pathogenesis

 In the early stage, there is an acute synovitis with a purulent effusion

 Soon the articular cartilage is attacked by bacterial and cellular

enzyme

 If infection is not arrested, the cartilage may be completely destroyed

 In summary sequelae includes necrosis, subluxation,

dislocation and ankylosis
Clinical features

 Infants
-more septicaemic that localized joint symptoms and signs
- Irritable
- Refusal to feed
- Fever with tachycardia
- Inflammed joints/Pseudoparalysis
Older Children

 Acute pain in a single large joint

 Pseudoparesis
 Fever
 Tachycardia
 Swollen and inflamed overlying skin
 Warm and tender joint
 Restricted movt in the affected joint
 Healing process

 Complete resolution

 Partial loss of cartilage and fibrosis of joint

 Loss of articular cartilage and bony ankylosis

 Bone destruction and permanent deformity of the joint

Management of septic arthritis

 Hx
-onset
-progression
-joint trauma
-falls, cuts, bites
-skin lesions
-immunization
-family hx of rheumatological dx
 Physical examination
 Lower limb – Anthalgic limp/cannot walk

 Upper limb- affected part is closely guarded

 Marked tenderness , active and passive range of motion are greatly limited

 Examine for synovial fluid effusions, erythema , heat and tenderness

 Spasm of muscles around the joint may be marked

 Patient may hold the joint in a position to reduce the intra-articular pressure to minimize
pain
 Investigations

 FBC - ↑WBC greater than 12,000mm3

 ESR >40mm/hr

 CRP >20mg/dl

 Blood culture may be positive

 XRAY

 Early stage could be normal finding

 Later on – Joint space widening may be present and

subluxation of the joint may be present

 In late stages- irregularities of the joint

 Differential diagnosis

 Trauma
 Transient synovitis
 Acute osteomyelitis
 Rheumatic fever
 Haemophilic joint
 Gout and pseudogout
Treatment
 Hospitalize all paediatric patients presumed to have septic arthritis for empiric
intravenous antibiotic therapy
 Antibiotics Broadspectrum like ampicillin, cefotaxime, ceftriaxone, are usually given
intravenously (IV) at first, and then switched to oral antibiotics depending on age and
suspected organism involved

 Antibiotics are typically taken for two to six weeks

 Other antibiotics include vancomycin, gentamycin, clindamycin, penicillin G depending on

organism and sensitive pattern

 Antituberculous for tuberculous arthritis

 Amphotericin B and fluconazole are used for candida arthritis while NASIDs are indicated for
reactive arthritis
Other treatment options

 Orthopaedic surgeon consults for

- Aspiration of Joint for fluid drainage which is both diagnostic and
therapeutic
- Arthrotomy
-Arthroplasty, or Joint replacement surgery
 Physical therapy
 complications
 Coxa magna

 Joint destruction leading to limb shortening or lengthening

 Decreased range of movement

 Abnormal gait

 Unstable joint articulation

 Pathological dislocation

 Acute osteomyelitis

 Septicaemia

 Secondary osteoarthritis

 Avascular necrosis