A comparative review of osteomyelitis for MBBS final professional examination.

1. OSTEOMYELITIS
through the student glasses
RISHABHA MEHTA
VIMS PAWAPURI, 2K13 BATCH

2. OSTEOMYELITIS - A severe persistent and
incapacitating infection of bone & bone marrow.
SEQUESTRUM – A dead piece of bone lying in a
pool of pus, surrounded by infected granulation
tissue trying to eat the sequestrum away.
INVOLUCRUM- It is the dense sclerotic bone
overlying the sequestrum, having holes called
CLOACAE.

3. ACUTE
HEMATOGENOUS
SUBACUTE CHRONIC GARRE’S
SCLEROSING
EPIDEMIOLOGY Infants & children
mainly, Adults-
(20%)lowered
resistance,
immunodeficient,
drug addicts
Between 11 to 20
years
Same as Acute;
incidence is
and is more in
developing countries
Adolescents and
young adults
ETIOLOGY Infant - H/O Birth
difficulty, umbilical
artery
inflamed IV site
Child - H/O sore
throat, boil, ear
discharge
Adult - H/O f
urological procedure
Less virulent organism,
More resistant host
Sequel to Acute OM(
>3 months),
open
fracture/operation,
presence of foreign
implants
CAUSATIVE
ORGANISM
Staphylococcus aureus, Streptococcus pyogens(grpA), Grp B
Streptococcus( Neonate), alpha haemolytic S.pneumoniae, Kingella
kingae/H. influenza, Salmonella typhi(sickle cell disease)
Viral, Fungal
Staphylococcus

4. Pathogenesis of Acute Hematogenous OM
Haematogenous seeding of metaphysis due to hairpin loop arrangement, abnormally permeable BVs at the physis
Resultant relative vascular stasis , lowered O2 tension favours bacterial colonization
Activation of local and systemic immune component

5.  Exuberant bony destruction and pus formation
 Pus finds its way through the Volkmann canals to form sub-periosteal abscess- periosteal
stripping - ISCHAEMIA
 Increased Bone death and sequestrum formed by the end of 1st week
 Fine streaks of sub – periosteal new bone formed- Typical of pyogenic infection- involucrum
Vascular congestion, exudation, local edema, infiltration of neutrophils
RAPID RISE IN INTRAOSSEOUS PRESSURE & INTRA VASCULAR THROMBOSIS( ISCHAEMIA)
Escape route for pus and bony spicules-
1. Discharging sinus through the adjacent skin and soft tissue
2. Travels proximally or distally to another site intra medullary
3. Crosses physis to involve Epiphysis and Joints

6.  Special points-
 1. In Infants: Infection more often spreads to adjacent joints through epiphysis due to persistence of
anastomosis between Epi & Metaphysis- leads to irreversible damage of the physeal cartilage – Lifelong
joint deformity
 2. In Adults: Direct Infection by trauma, open fracture & sx than haematogenous spread- Vertebrae and
calcaneus m/cly involved
 Also , Adults are more prone to fractures due less obvious periosteal new bone formation.
 3. Osteomyelitis can also accur secondary to septic arthritis in joints with INTRACAPSULAR METAPHYSIS
e.g.- hip, shoulder & elbow joints
 Fate Of Acute OM infection :
 1. Infection is controlled – Residual thickening of Bone , +/- Deformity
 2. If Infection persists – Chronic Osteomyelitis follows
Common sites of involvement in Acute & Chronic OM:
1. Proximal and distal ends of femur and Tibia
2. Adults: Thoracolumbar spine , calcaneus

7.  Pathogenesis of Chronic OM
 The foci of infection is locked in side a non-collapsing cavity, surrounded by scar tissue, dead and dying
bone without any access to new BVs --- Antibiotics and immune cells cant reach the foci.
 Sequestra and foreign implants are subtrates of bacterial adhesion- glycocalx helps in adhesion &
from antibiotics.
 Bone destruction and increasingly brittle sclerosis result in pathological fracture.
Pathogenesis of Garre’s Sclerosing Osteomyelitis
1. No abscess formed.
2. Characterised by marked sclerosis and cortical thickening.
3. Diaphysis of tubular bones & mandible are involved.
Pathogenesis of Sub-acute OM ( Brodie’s Abscess)
1. Lesion: well defines cavity, lined by granulation tissue containing GLAIRY SEROPURULENT FLUID ( Pus i
rare) ; mix of acute and chronic inflammatory cells ;
2. Ususlly in Tibial Metaphysis, sometime in epiphysis & cortex

8. Clinical Features:
ACUTE HAEMATOGENOUS CHRONIC OM SUB-
ACUTE/BRODIE’s
Abscess
GARRE’S
SCLEROSING
Child: Fever, malaise, severe bone
pain near larger joints, toxaemia,
refuses to use limb and doesn’t
touch, restricted joint
local inflammatory signs,
lymphadenopathy
Cachectic
Alternate spells of “Flare-ups” &
quiescence.
FLARE –UP- pain, pyrexia,
tenderness and DISCHARGING
SINUS.(pus and bony spicules)
Un-united bone on examination.
Limb lengthening
Pain near larger
joint, limping, local
tenderness and
swelling.
Tenderness on deep
palpation.
No discharging sinus
or abscess
Local inflammatory
signs
Infants: failure to thrive, cries
inconsolably, irritable, multiple
sites common
Scar and sinus are adherent to
underlying bone
Seropurulent discharge and
excoriation of the skin

9. Investigations:
1. Complete blood count- leucocytosis, C-reactive protein raised, ESR raised
2. Sub-periosteal or joint pus or fluid ASPIRATION & culture with sensitivity is diagnostic.
3. Gram staining, tissue aspiration and blood culture
4. Radiograph- ACUTE: PERIOSTEAL REACTION, i.e.; periosteal new bone deposition at metaphysis
5. CHONIC: Thickening and irregularity of the cortex
patchy sclerosis
Bone resorption: patchy loss of density or as a frank excavation around
the implants
Sequestrum: denser than surroundings
5. Sinogram- track the sinus to the site of infection using radio opaque dye.
6. CT & MRI- together they show the extent of bone destruction, reactive edema & hidden abscess.
7. Radioisotope Scintigraphy using 99mTc , 67Ga-citrate or 111In labelled leucocytes - shows increased
activity in both in perfusion phase and bone phase. IMPORTANT IN INFANTS.

10. TREATMENT OF ACUTE OM:
1. Supportive measures- analgesics, adequate hydration
2. Splintage- for comfort , to prevent joint contracture
3. Antimicrobial therapy- ALWAYS INTRAVENOUS – for minimum 2 weeks duration
 Neonates and infants upto 6 months- Flucloxacillin(Staph.), Cefotaxime, Benzyl Pn, Gentamicin.
 from 6 months to 6 yrs- Fluclox, Cefotaxime.
 Older children- Fluclox , Fusidic acid ( more bone penetrating)
 Elderly and previously unfit patients- same
 Patients with sickle cell Disease- Salmonella typhi- fluoroquinolones & 3rd Gen Cephalosporins
 Heroin addicts and immune deficient – FQs & 3rd Gen Cephalosporins
4. Surgical drainage-
 open operation with anaesthesia – indications: no improvement after antibiotics within 36 hrs, signs of
deep pus( swelling, edema & fluctuation) , and aspiration of pus.
 Intramedullary drilling in diff directions : during open procedure – if no pus is found.
 Cutting a small window in the cortex : if extensive intramedullary abscess is formed.

11.  Wound is then closed without a drain & splint is reapplied.
 Full weight bearing possible after 3-4 weeks.
TREATMENT of CHRONIC OM:
Mainly Surgical, antibiotics during flare ups & post operative period.
AIM of Sx: 1. Removal of dead bone, 2. elimination of dead space & cavities, 3. Remove infected
granulation tissues & sinuses.
STEPS of Surgery:
1. Sequestrectomy & Debridement
2. Alternatively, Saucerization- conversion of cavity into a saucer by removing its wall.
3. Currettage- Scraping off the granulation tissue until normal looking bone is seen.
4. Dealing with dead space:
 Gentamycin impregnated cement beads- replaced by cancellous bone grafts after 2-3 weeks.
 Papineau Technique : small cancellous chips+ antibiotic+ fibrin sealing agent----- are used to fill the
cavity

12.  Muscle flap transfer in the cavity
 Free vascularized bone graft.
 Continuous suction and irrigation system-
 developed by Launtenbach , South Africa
 Done after excision of all the dead & avascular tissues
 Done until new vascular granulation tissue is formed
 Procedure: inlet tube is put into medullary cavity and slight suction is applied at the outlet tube bringing the
irrigation fluid out.
 Irrigation fluid m/o- normal saline, antibiotics & detergents for 4-7 days .
5. Excision of infected bone & reconstruction by Ilizarov method
6. amputation- rare- when sinus undergoes malignant change.

13.  DIFFERENTIAL DIAGNOSIS
ACUTE OM:
1. Cellulitis
2.Acute septic arthritis
3. Acute rheumatic arthritis
4. Acute Poliomyelitis
5. Scurvy
6. Sickle cell crisis
7. Gaucher’s disease
CHRONIC OM :
1. Tubercular OM
2. Ewing’s sarcoma
3. Osteoid Osteoma

14.  COMPLICATIONS:
 Septicaemia & pyaemia
 Acute pyogenic arthritis
 Pathological fracture
 Growth plate destruction & deformity
 Joint Stiffness
 Sinus tract Malignancy
 Amyloidosis

15. Reference:
 Apley’s system of Orthopaedics and fractures, 9th edition
 Essential Orthopaedics – Maheshwari & Mhaskar

16. END OF SLIDE
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