Acute and sub-acute Osteomyelitis

Acute and subacute osteomyelitis
Dr Kuldeep singh
Resident doctor
Aiims Bhopal

1. ACUTE AND SUBACUTE OSTEOMYELITIS Dr. Kuldeep Singh Resident doctor Department of orthopaedics Aiims Bhopal

2. Introduction Osteomyelitis is defined as infection of bone or bone marrow by an infecting organism. It may remain localized, or it may spread through the bone to involve the marrow, cortex, periosteum , and soft tissue surrounding the bone.

3. C lassification Classification is based on Timing of the onset Method of spread.

4. Timing of onset Acute OM : <2week of duration Subacute OM: 2weeks—6weeks of duration Chronic OM: >6 weeks of duration

5. Method of spreads 1.Exogenously : - trauma surgery (iatrogenic) contiguous infection 2. Hematogenous ( bacteremia )

6. Hematogenous osteomyelitis: occurs in children < 15 years of age occurs in the metaphysis of the long bones- Decreased activity of macrophages Frequent trauma Precarious blood supply

7. Diaphyseal osteomyelitis : Begins in metaphysis, but due to growth becomes diaphyseal - Mostly in children. Or direct trauma to diaphysis Tubercular

8. Pathophysiology: Metaphysis - highly vascularized zones. Vessels are arranged in hair pin arrangement resulting in “sluggish flow” of blood, leading to bacterial enlodgement

9. Pathogenesis M/c route- hematogenous Appendicular skeleton > Axial skeleton Most common bone involved in OM- Overall- metaphysis of distal femur > tibia Infant/children- metaphysis of distal femur Adults- vertebral body

10. Development of osteomyelitis

11. Most common cause of Acute Hematogenous OM - Adult :- S.aureus is the commonest cause SCA(sickle cell anemia) patient:- Salmonella is the usual cause Intravenous drug abusers :- Pseudomonas aeruginosa and S.epidermidis .

12. Why staphylococcus most common? S.aureus and S.epidermis ----- elements of normal skin flora S.aureus ----- increased affinity for host proteins ( traumatised bone) Enzymes ( coagulase , surface factor A) ----- hosts immune response .

13. Why staphylococcus most common Inactive “L” forms ------ dormant for years “ Biofilm ” (polysaccharide “slime” layer) ---- increases bacterial adherence to any substrate Large variety of adhesive proteins and glycoproteins ----- mediate binding with bone components.

14. Causes General factors Anemia Infection Poor nutrition Poor immune status Local factors Hair pin bend vessels Metaphyseal haemorrhage Defective Phagocytosis Vasospasm

15. Pathogenesis Host factors Chronic steroid use Diabetes Peripheral vascular disease Intravenous drug abuse Immunosuppression (HIV and AIDS) Tuberculosis Sickle cell disease

16. Acute Osteomyelitis Clinical findings Rapid presentation of pain, Raised temperature, Redness

17. Diagnosis of acute osteomyelitis • PELTOLA AND VAHVANEN’S CRITERIA (if 2/4 are found) 1. Purulent material on aspiration of the affected bone 2. Positive findings of bone tissue or blood culture 3. Localised classic physical findings a. bonny tenderness b. overlying soft tissue edema , erythema 4 Positive radiological imaging Principles And Practice Of Pediatrics Infectious Disease( 5 th edition) by  Sarah S. Long MD  ,  Charles G. Prober MD  ,  Marc Fischer MD

18. Acute Osteomyelitis lab reports- Inflammatory markers will be raised CRP- most sensitive marker short half-life decreases about a week after effective treatment.

19. Plain radiographs shows Ist week : soft tissue shadow/ lucency appear within 48hrs- first/ earliest x-ray sign (but not appreciable). 2nd week : Faint extra cortical outline due to periosteal new bone formation ( classic x-ray sign of early pyogenic osteomyelitis- first appreciable sign )

20. Plain radiographs shows 3 to 6 weeks : elevation of periosteum and layered new bone formation . 3-8 weeks :The dead bone (i.e . sequestrum formation) occurs

21. ULTRASOUND Sub periosteal collection of fluid in the early stage of osteomyelitis But cannot distinguish between hematoma and pus.

22. CT To detect early osseous erosion To document the presence of sequestrum , foreign body, or gas formation

23. M.R.I. It is highly sensitive for detecting osteomyelitis as early as 3 to 5 days after the onset of infection [ Marrow edema within 24hr ]. It is best method of demonstrating bone marrow inflammation. It helps to differentiate between soft tissue infection and osteomyelitis .

24. Three phase bone scan 99mTc-MDP Components of a three-phase technetium bone scan- (A) Initial dynamic [ angiographic ] phase (B) Blood pool phase (c) Delayed [ bone] phase

25. Bone scan I) Three phase bone scan 99mTc-MDP i ) Increased uptake in all 3 phases of scan ii) Highly sensitive(95%) in acute infection. II) Gallium scan and indium-111 labelled leukocyte scan used in conjugation with technetium scanning

26. Differential Diagnosis Cellulitis Acute suppurative arthritis Tuberculosis Sickle cell crisis Streptococcal necrotising myositis

27. Treatment 1.General treatment : Analgesics, nutrition general supportive treatment by intaking enough caloric, protein, vitamin etc. 2. Antibiotic therapy 3. Surgical treatment 4. Immobilization Splintage of affected part

28. Nade’s principles of treatment of acute OM. 1)An appropriate antibiotic is effective before pus formation. 2)Antibiotics do not sterilize avascular tissues or abscesses, such areas require surgical removal. 3)If such removal is effective antibiotics should prevent their reformation and primary wound closure should be safe. General Principles Of Orthopedics And Trauma[ K. Mohan Iyer ]-2 nd edition

29. Nade’s principles of treatment of acute OM. 4)Surgery should not damage further already ischemic bone and soft tissues 5)Antibiotics to be continued after surgery. General Principles Of Orthopedics And Trauma[ K. Mohan Iyer ]-2 nd edition

30. Prerequisites for Antibiotics Drug which penetrates infected tissues and attains sufficient levels in bone and pus. If abscess not found, IV antibiotics to be started based on gram stain. The antibiotic dosage for OM is usually 2x to 3x the standard dose to ensure a peak serum bactericidal titer of 1:8 or greater Parenteral antibiotic continued till appropriate clinical/lab response has occurred.

31. Antibiotics Under most circumstances most appropriate antibiotic is semi synthetic penicillin( oxacillin / naficilllin ) or 1 st gen.cephalosporins . If allergic, clindamycin because of good intra osseous penetration

32. End point of treatment

33. Nade’s indications for surgery Abscess 2. Severely ill & moribund child with features of acute osteomyelitis 3. Failure to respond to IV antibiotics for >48 hrs General principles of orthopedics and trauma[ K. Mohan Iyer ]- 2 nd edition

34. Technique for drainage of acute OM TIBIA Tourniquet applied whenever possible, don’t exsanguinate if infection present. Make antero -medial incision 5-7.5cms over affected part of tibia. Periosteum elevated, any compressed pus will escape. Drill several holes 4mm through cortex into medullary canal, if pus escapes drill to outline cortical window and cortex removed with osteotome .

35. Technique for drainage of acute OM TIBIA Evacuate any intra medullary pus and necrotic tissue. Irrigate cavity with 3L saline with pulsatile lavage system with antibiotics. Skin closed loosely over drains, do not close wound if it produces excessive tension on skin

36. Technique for drainage of acute OM TIBIA

37. After treatment Long leg posterior slab is applied with foot in neutral position, ankle at 90 degrees, knee at 20 degree flexion. Antibiotics continued based on culture sensitivities 2 week coarse of IV antibiotics given if culture is grown positive.

38. Complications of acute OM Early: 1) Septic arthritis. 2) Thrombophlebitis 3) deep vein thrombosis 4) Multiple pyogenic abscess. 5) Adverse reactions of antibiotics

39. Complications of acute OM Late 1) Chronic osteomyelitis 2) Pathological fracture 3) Local growth disturbances over growth-due to prolonged hyperemia 4) Premature closure of epiphysis 5) Deformity

40. Neonatal OM Occurs in 2 distinct varieties 1)Seen in 2-8 weeks of age S.aureus : MC Manifests by lack of movement, visible swelling of extremity. Fever and irritability not present, inflammatory response not mounted, so diagnosis difficult. High index of suspicion, aspiration done and antibiotics to be started. 2) Second form encountered in NICU units - Typically seen in LBW infants, neonates requiring endotracheal intubation & IV lines.

41. Features in neonatal OM In children < 2 years, transphyseal blood vessels cross the physis , allow the spread of infection into the epiphysis. Cortex is porous, pus collects in sub-periosteal space. Susceptible to shortening and angular deformity. Even joint is also involved, hip joint being common.

42. Features in neonatal OM -Pelvis of 1yr old girl who had osteomyelitis of proximal femur and septic arthritis of hip. -These infections resulted in destruction of physis and epiphysis

43. Sub-Acute Osteomyelitis

44. Subacute Osteomyelitis Subacute osteomyelitis is a consequence of an altered host-pathogen relationship characterized by decreased bacterial virulence , Increased host resistance, or a combination of these factors Microbes get entrapped in fibrous tissue proliferation.

45. Subacute Osteomyelitis Incidental finding on radiographs- localized radiolucency surrounded by sclerotic margin ( Brodie’s abscess ).

46. Sub acute OM Features- • Insidious onset, indolent course • Mild pain , temp • Blood culture –Negative • Aspiration , biopsy – Positive in 60% cases

47. Sub-acute OM Plain radiographs show poorly permeative lytic changes in the left proximal femur.

48. Sub acute osteomyelitis CT scan shows permeative cortical erosions with periosteal reaction. MRI shows diffuse femoral marrow signal changes with a fluid collection adjacent to bone suggestive of abscess rather than liquefied tumor necrosis. Biopsy and culture confirm the diagnosis of subacute OM

49. Gledhill Classification for subacute OM This classification system is based on Anatomic location, Response of the surrounding tissue to infection Similarity to benign or malignant tumors 1.Central metaphyseal (1a,1b) 2.Eccentric metaphyseal 3.Diaphyseal cortical 4.Diaphyseal with periosteal new bone 5.Epiphyseal 6. Vertebral lesion

50. Brodie Abscess • Localised subacute osteomyelitis. • Long bones lower limb. • In Adults Metaphyseal-epiphyseal area • Intermittent pain, local tenderness. • X ray- lytic lesion ,sclerotic rim. • S. aureus in 50% , negative culture in 20% .

51. Differential diagnosis of Sub-Acute OM When lesion is metaphyseal Ewing sarcoma Osteoid osteoma Osteogenic sarcoma Langerhens cell histiocytosis When lesion is epiphyseal Chondroblastoma Fungal osteomyelitis Tuberculous osteomyelitis Aneurysmal bone cyst  Giant cell tumor

52. Treatment Immobilization surgical drainage - Open biopsy Curettage of the lesion Bone grafting intravenous antibiotics followed by 6 weeks of oral antibiotics once the levels of inflammatory markers have decreased.

53. Special Situations Garre’s sclerosing OM Long standing chronic OM. Common in children. Mandible > Tibia. Excessive periosteal reaction by an extremely sensitive periosteum in response to low grade anaerobes. Swelling+ but pain-/sinus-/ sequestrum -/pus- . Treatment- antibiotics plus NSAIDS .

54. Special Situations Vertebral Osteomyelitis commonly stems from a disc-space infection seeded through hematogenous dissemination or surgery. Usually a/w severe pain and limited ability to function. MRI is an important imaging modality to detect.

55. Vertebral Osteomyelitis Usually cured without surgery, even though there may be extensive bone involvement. A six-week course of antibiotic therapy is commonly recommended

56. Chronic recurrent multifocal osteomyelitis (CRMO) Inflammatory bone condition. Mainly affect the metaphysis of long bone, in addition to the spine. Initially osteolytic, later hyper- osteotic and sclerotic lesson. Associated with other inflammatory condition like Psoriasis and IBD.

57. Chronic recurrent multifocal osteomyelitis (CRMO) Arthritis of adjacent and distal joint is frequent. NSAIDS are effective. In children with spinal lesions, Infliximab +/- bisphosphonate & bisphosphonate alone showed favourable outcomes In children with persistently active symptoms and abnormal MRI findings, additional treatments including DMARDs, TNF inhibitors, and/or bisphosphonates are necessary to induce remission and reduce skeletal damage . Antibiotics are ineffective.