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Osteomyelitis

Osteomyelitis

OSTEO : bone
MYELO : marrow
ITIS : Inflammation / Infection

Types
Pyogenic: Streptococcus & Staphylococcus

Specific organisms
TB, Syphilitic, Salmonella
Osteomyelitis
Spread of infection
 Haematogenous spread
 Direct spread
 Neighboring focus
 Iatrogenic causes

Haematogenous
from a distant site in the body : throat infection, skin
infection, dental carries etc.

Direct
open fracture
Osteomyelitis

Spread of infection
Neighboring focus
 Mastoiditis from middle ear infection
 Dental root infection producing osteomyelitis
of the mandible or maxilla
Iatrogenic
Following surgery for some other reason : ORIF
Osteomyelitis
Clinical types of OM
 Acute osteomyelitis
 Chronic osteomyelitis
 Primary subacute osteomyelitis
 Acute flare up of chronic osteomyelitis
Osteomyelitis
Pyogenic osteomyelitis
 Common organisms
Staphylococcus aureus
Streptococcus pyogenes
 In children < 4 years
Haemophilus influenzae
 Unusual organisms
 Seen in drug addicts
 Sickle cell anemia
Osteomyelitis

Acute pyogenic osteomyelitis


 Haematogenous osteomyelitis
 Common
 Focus of infection usually from infections:
impetigo, septic tooth, throat infection,
infected umbilical cord
Osteomyelitis

Acute pyogenic osteomyelitis


Pathogenesis
 Infection starts in the metaphysis of bone
 Peculiar anatomy in metaphysis of long bones

predisposes to lodging of infection in this region


 Arteries loop around
 Vascular stasis favors colonization
 Less phagocytosis in the metaphysis
Osteomyelitis

Pathogenesis
Inflammation in reaction to organisms

Phagocytic reaction, exudation of fluid,


vascular congestion

Intraosseous pressure increases

Pain, obstruction to blood flow, Vascular


thrombosis

Pus forms in bone and pushed out


through Volkman’s canal when
Intraosseous pressure increases
Osteomyelitis - Pathogenesis
Subperiosteal abscess

Bursts through Strips periosteum :


periosteum into soft periosteal blood supply
tissue through sinus or lost : Sequestrum
tracks along soft tissue
to reach joint

(When metaphysis is
intra-capsular : infection
directly seeps into joint) Intramedullary extension of pus cuts
the Intraosseous blood :
Sequestrum
Osteomyelitis
Pathogenesis
Healing takes place at any stage
 Antibiotics
 Natural resistance

Walled off area of infection may flare up again later


: chronic osteomyelitis
Osteomyelitis

Clinical features
 Antecedent infection
 Irritable,restless,vomiting,high grade fever with chills
 Peudoparalysis of the limb
 At first : no swelling : later +, indicates subperiosteal
abscess formation
 Affected metaphysis is tender
Osteomyelitis
Clinical features
 Fluctuation + : after abscess in soft tissue
 Effusion : adjacent joint : sympathetic effusion
 If infection continues : septicemia: fatal
Laboratory findings
 Haemoglobin : low
 Total WBC : as high as 30,000 with leukocytosis
 ESR : high
 Blood culture : demonstrates bacteremia
Osteomyelitis
Radiology
Initially : upto 10 days - normal
Later :
 Localised areas of destruction in
metaphysis extending to diaphysis :
moth-eaten appearance
 Periosteal elevation : multiple
laminations of bone deposition
parallel to bone : appears like
onion-peel appearance seen in
Ewing’s sarcoma
Osteomyelitis
Other investigations
 CT Scan : Diagnosis & needle aided
drainage of pus for c/s from
inaccessible parts : vertebra
 MRI : Useful in early detection of
osteomyelitis & soft tissue extension
 Radio nuclide examination

Differential diagnosis
• Rheumatic fever
• Ewings sarcoma
• Acute septic arthritis
Osteomyelitis
Treatment
 Early diagnosis with a high degree of suspicion is
beneficial and necessary
 Blood for investigations are collected and high doses
of antibiotics are started as early as possible
 Antibiotics are changed later if necessary as per
culture and sensitivity reports
 Immediate drainage is of paramount importance:
cortical window at suspected site
 Prolonged antibiotics as per c/s report for minimum
period of 6 wks with initial 2 weeks of parenteral
antibiotics
Osteomyelitis

Complications
 Acute osteomyelitis ends up as chronic osteomyelitis
 Septicemia and fatal end
 Multi-focal osteomyelitis - debilitated individuals - rare
Chronic osteomyelitis
After an attack of acute osteomyelitis recurrence
of infection is a rule : the interval may vary:
Once an osteomyelitis
Always an osteomyelitis
Causes
 Acute osteomyelitis leading to chronic OM
 Haematogenous infection with a low virulence

organism may be chronic from the beginning


 Infection from an external wound usually ends up as

chronic osteomyelitis
Osteomyelitis
Pathogenesis
Dead infected bone (sequestrum)

Small Large
gradually separated from
absorbed by granulation
living bone destroyed /
tissue and osteoclastic
extruded
activity
When sequestrum has formed : exudation continues till it
is absorbed or extruded
Chronic Osteomyelitis

Pathology
 The surrounding tissue attemps to wall off infection :
forms thick bony wall : called the involucrum
 Involucrum has multiple openings called cloacae :
openings for exudate, debris and sequestra to drain
through the sinus
 Once sequestrum is extruded : infection is better
controlled and settles down
Chronic Osteomyelitis

Sequestrum : dead infected bone in situ

Types Causes / site


Cortical Pyogenic OM : adults
Diaphyseal Pyogenic OM : children
Sandy Tubercular OM : vertebra
Tubular Tubercular OM:long bone
Ivory Syphylitic osteomyelitis
Ring Stump / skeletal traction
Black Prolonged exposure of
bone
Chronic Osteomyelitis
Clinical features
 In the period of inactivity no symptoms
 Fever, pain, swelling and tenderness of bone
 Sinuses discharging pus and bony spicules :
sequestrum
 Bone is thick, irregular or may
be deformed
 Skin dusky ,thin and scarred
 Muscles are scarred and
contracted : produce
deformities of adjoining joints
Chronic Osteomyelitis
Radiology
 Moth-eaten appearance
 Osteoporotic bone
 Sequestrum
 Involucrum
 Bone thick and irregular
 Bone may be deformed
 Pathological fracture

Sinogram
 Traces the sinus tract & helps planning of surgery
& removal of entire tract to prevent recurrence
Chronic Osteomyelitis
Treatment
 Sequestrectomy & saucerisation
 Secondary healing of wound
 Prolonged antibiotics- minimum of 6 wks to 3 months
according to c/s report with initial parenteral
antibiotics
Chronic Osteomyelitis
Complications
 Acute flare up of chronic osteomyelitis
 Squamous cell carcinoma: chronic discharging sinus
 Contracture of muscle : deformity of joints
 Stimulation /destruction of growth plate leading to
discrepancy of limb length or deformities
 Pathological fracture
 Septic arthritis of adjacent joint- deformity & ankylosis
 Amyloidosis
Brodie’s abscess

 Described by Brodie in the tibial metaphysis in 1832


 Subacute pyogenic osteomyelitis - staphylococcal
 Commonly seen in children : boys
 Commonly affects the ends of the tibia
 Abscess varies from 1- 4cm in diameter
 Radiology : cavity surrounded by dense ring of bone
Brodie’s abscess

 Appropriate antibiotics may decrease


size of lesion
 If pain persists : may require surgical
decompression of abscess
Septic arthritis
Septic Arthritis

Syn: Acute Suppurative arthritis


Joint becomes infected
 Direct invasion
 Penetrating wound
 Injection and arthroscopy
 Eruption of bone abscess
 Blood spread from a distant site

Hip joint is most commonly affected due to the fact that :


1. Infection is common in metaphysis
2. Metaphysis of proximal femur is intracapsular
Septic Arthritis

Predisposing factors
 Pre existing arthritis
 Trauma
 Diabetes mellitus
 Immune suppression
 Bacteremia / systemic infection
 Sickle cell anemia
 Prosthesis
Septic Arthritis

Usual organisms
 Staphylococcus aureus
 Haemophilus influenzae
 Neonates : E.Coli, H.Influenzae
 Child : H.Influenzae
 Elderly : Gram negative enteric bacteria
 Prosthetic : S.Epidermidis
 Fit adult : N.Gonorrhea
Osteomyelitis
Infection to the joint
 In infants and adults
 vascularity pattern
 intracapsular infected
metaphysis / epiphysis
 Penetrates periosteum :
tracks along soft tissue :
penetrates capsule
 Disruption of cartilage & spread
 Pathological fracture
Septic Arthritis

Pathology Infection reaches joint

Seats in synovial membrane: Inflammatory reaction

Seropurulent exudate and increase in synovial fluid

Articular cartilage eroded


Epiphysis destroyed-infants
In children - avascular necrosis of epiphysis

When left untreated - may spread to adjacent bone


or burst out of joint - abscess and sinus
Septic Arthritis

Healing
 Complete : normal joint
 Partial loss of articular cartilage : fibrous ankylosis
 Complete loss of articular cartilage : bony ankylosis
 Bone destruction : permanent deformity of the joint
Septic Arthritis
Clinical features

 Infection elsewhere : septicemia : knee & hip


 Irritable, febrile
 Pseudoparesis
 Local warmth, tenderness
 Decreased range of movement
Septic Arthritis
Clinical features
Adults
 Superficial joints : knee wrist and ankle
 Febrile
 Local warmth, tender
 Decreased range of movement
 Gonococcal infection and drug abuse to be ruled out
Septic Arthritis
Investigations
Blood
 Increased WBC & ESR
 Blood culture may be positive

Synovial fluid
 Turbid, purulent fluid
 Gram staining & culture
 Cell count / sugar / protein
Septic Arthritis
Investigations - X rays
Early stage
 Normal
 Increase in joint space
 Subluxation of joint
 Changes in proximal femur indicating OM
Later
 Osteoporosis
 Narrowing of joint space
 Destruction of bone
Septic Arthritis

Differential diagnosis
 Acute osteomyelitis
 Trauma
 Transient synovitis
 Haemophilic bleed
 Rheumatic fever
 Gout / pseudogout
Septic Arthritis
Treatment
 General supportive care

 Splintage
 Antibiotics : duration
 Drainage : surgical emergency
 Aftercare
Complications
 Injury or destruction of epiphysis

 Avascular necrosis of epiphysis


 Subluxation and dislocation of joint
 Destruction of articular cartilage: ankylosis & deformity

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