Orthopaedics notes - Infection

1. Orthopaedics Notes Infection

2. Outlines • Introduction • Acute hematogenous osteomyelitis • Subacute hematogenous osteomyelitis • Chronic osteomyelitis • Acute suppurative arthritis • Tuberculosis Other: • Post-traumatic osteomyelitis • Garre sclerosing osteomyelitis • Multifocal non-suppurative osteomyelitis

3. Introduction • Infections: A condition where pathogenic organisms multiply and spread within the body tissues. • It will then give rise to inflammatory reaction (acute/ chronic) – the way of the body combating it. • Signs of inflammation: • Redness • Swelling • Heat • Pain • Loss of function • Bone infection vs Soft-tissue infection • Bone consists collection of rigid components  more susceptible to vascular damage & cell-death due to build-up pressure.

4. Factors predisposing to bone infection Immunosuppresive conditions Malnutrition & general debility Diabetes mellitus Corticosteroid administration Immune deficiency Immunosuppresive drugs Poor limbs circulations Venous stasis in the limb Peripheral vascular disease Trauma Loss of sensibility Iatrogenic invasive measures

5. Principles of treatment Analgesia and supportive measures Rest the affected part Identify the infecting organism & administer effective antibiotic treatment or chemotherapy Release pus as soon as possible it is detected Stabilize bone if fractured Eradicate avascular/ necrotic tissue Restore continuity if there is a gap in the bone Maintain soft tissue and skin cover

6. Acute Hematogenous Osteomyelitis

7. Aetiology and Pathogenesis • Mainly a disease of children • If adults are affected – immunosuppressed. • Organism: • Staphylococcus aureus (70%) • Gram +ve cocci • Group A B-haemolytic streptococcus: Strep.pyogene – in chronic infection • Group B streptococcus – in newborns • Alpha-haemolytic diplococcus: S.pneumonia • Hemophilus influenza – in 1-4 year old,osteomyelitis and septic arthritis. But reduced due to vaccination. • Salmonella typhi – Patients with sickle cell disease

8. • Due to invasion of the blood stream, eg: • Minor skin abrasion • Treading on sharp objects • Injection point • A boil • A septic tooth • An infected umbilical cord • Indwelling catheter • Arterial line etc

9. • Infection usually starts in the vascular metaphysis of a long bone: • Proximal tibia • Distal or proximal ends of the femur. • Common at this site due to the peculiar arrangement of the blood vessels in that area. • In children, there are anastomoses  infection can go up to the epiphysis.

10. Non-anastomosing terminal branches of the nutrient artery (metaphyseal artery) twist back in hairpin loops before entering the large network of sinusoidal vein  stasis  bacterial colonization Fine vessels in the hypertrophic zone of the physis allows bacteria more easily to pass through and adhere to type 1 collagen in that area.

11. Inflammation Suppuration Bone necrosis Reactive new bone formation Resolution and healing OR intractable chronicity Characteristic progression of acute hematogenous osteomyelitis:

12. Acute Osteomylitis - Children • 2-6 years old showed classical pictures. Inflammation • At the metaphysis • Vascular congestion Suppuration • Exudation of fluid • Infiltration by polymorphonuclear (PMN) lecukocytes • Increased intraosseous pressure • Intense pain, blood flow obstruction, intravascular thrombosis • 2-3 days, subperiosteal abscess: pus within the bone along the Volkmann canal to the surface Bone necrosis • Rising intraosseous pressure, vascular stasis, small-vessel thrombosis and periosteal stripping  reduced blood supply • Also due to bacterial toxins and leukocytic activity. Reactive new bone formation • Gradual ingrowth of granulation bone • Pieces of dead bone may separate as ‘sequestra’ varying in size Resolution and healing OR intractable chronicity • With time this new bone thickens to form a casement (‘involucrum’) enclosing the sequestrum and infected tissue. • If infection persists, may discharge through perforations (cloacae) in the involucrum and track by sinuses to the skin surface.

13. Acute Osteomyelitis - Infants • The early features of acute osteomyelitis in infants are much the same as those in older children. • Difference: During the first year of life • Frequency with which the metaphyseal infection spreads to the epiphysis & adjacent joint. • The physeal anlage may be irreparably damaged, further growth at that site is severely retarded and the joint will be permanently deformed.

14. Acute Osteomyelitis- Adults • Usually follows an open injury, an operation or spread from a contiguous focus of infection (e.g. a neuropathic ulcer or an infected diabetic foot). • If a long bone is infected, the abscess is likely to spread within the medullary cavity  eroding the cortex  extending into the surrounding soft tissues.

15. Clinical Features Age groups Features Infants • <1 y/o • Constitutional disturbance - irritable • Failure to thrive • History of birth difficulty, umbilical artery catheterization, site of infection • Metaphyseal tenderness • Resistance to joint movements Children • >4 y/o • Severe pain • Malaise • Fever • Toxaemia • Refused to use limb/ touched • + recent history of infection: septic toe, boil, sore throat, ear discharge • Ill and feverish • PR >100 bpm • Tenderness over the limb • ‘pseudoparalysis’ • Local redness, swelling, warmth and oedema are later signs and signify that pus has escaped from the interior of the bone. Adults • Commonest site: Thoracolumbar spine • Mild fever • Backache • Local tenderness might not be marked Cardinal features in children: • Pain • Fever • Refusal to bear weight • Elevated white cell count • Elevated ESR • Elevated CRP

16. Diagnostic Imaging Imaging Features Plain x-ray • 1st week of the onset of symptoms: • May be normal. • Soft-tissue swelling: Displacement of the fat planes • >2nd week: • Periosteal new bone formation: Faint extracortical outlines (sign of early acute pyogenic osteomyelitis) • Regional osteoporosis with a localized segment of apparently increased density. Ultrasonography • Subperiosteal collection of fluid (but could not distinguish between pus vs hematoma) Radionuclide scanning • Radioscintigraphy with 99mTc-HDP: increased activity in both the perfusion phase and the bone phase • Other inflammatory changes may show the same MRI • In doubtful cases, esp axial skelton. • Best method to show bone marrow inflammation • Very sensitive (even in early phase): Able to distinguish between soft-tissue infection vs osteomyelitis.

17. Investigations • Pus/ fluid aspiration from the metaphyseal subperiosteal abscess (tissue aspiration) • Gram stain • C+S • Blood culture • C-reactive protein (CRP): Elevated 12-24 hrs • Erythrocyte sedimentation rate (ESR): 24-48 hrs • WBC • Antistaphylococcal antibody titres raise: Done in atypical cases

18. Differential Diagnoses • Cellulitis • Acute suppurative arthritis • Streptococcal necrotizing myositis • Acute rheumatism • Sickle-cell crisis • Gaucher’s disease

19. Management • Supportive treatment for pain and dehydration. • Splintage of the affected part. • Appropriate antimicrobial therapy. • Surgical drainage.

20. Age Relevance Choice of antibiotics <6 months • Should be effective against penicillin- resistant Staphylococcus aureus + Group B streptococcus + Gram- negative organisms • Flucloxacillin + 3rd generation cephalosporin (eg cefotaxime) OR • Flucloxacillin (for penicillin-resistant) + benzylpenicillin (for GBS) + gentamycin (for gram –ve) 6 mo – 6yo • Should cover Hemophilus influenza • Flucloxacillin + cefotaxime/ cefuroxime Older children, fit adults • Majority are due to Staphylococcal infection • Flucloxacillin + fusidic acid • Fusidic acid is preferred compared to benzylpenicillin d/t penicillin- resistance prevalence. • If allergic to penicillin, treat with second/ third generation of cephalosporin Sickle cell • Chloramphenicol – be aware of the complication of aplastic anaemia • Third generation cephalosporin or fluoroquinolone (eg ciprofloxacin) Meticillin-resistant Staphyloccous aureus (MRSA) • History of MRSA • MRSA-endemic ward • Vancomycin + 3rd generation cephalosporin Duration of treatment: • IV abx 2-4 weeks: until CRP normalized + patient fits • Oral abx 3-6 weeks: after completing IV abx

21. Complications • Epiphyseal damaged and altered bone growth • Suppurative arthritis • In very young infants • In where the metaphysis is intracapsular – eg upper femur • In metastatic infection • Metastatic infection • Pathological fracture • Chronic osteomyelitis

22. Subacute Hematogenous Osteomyelitis

23. Pathogenesis • Relatively mild – due to less virulence or patient’s resistance. • Sites: • Variable • Distal femur • Proximal and distal tibia • Sometimes epiphysis and vertebral bodies • Usually there is a well-defined cavity in cancellous bone (usually tibial metaphysis) • Contains glairy seropurulent fluid (rarely pus) • Lined by granulation tissue with acute and chronic inflammatory cells • Surrounding bone trabeculae usually thickened • Lesion sometimes erodes the bone cortex

24. Clinical Features Patient is a child or adolescent + hx of big joint pain several weeks or months ago. Limping Slight swelling Muscle wastingLocal tenderness Normal temperature WBC might be normal, ESR might be elevated

25. Imaging Circumscribed, round/oval radioluscent cavity 1-2cm diameter Sometimes the cavity is surrounded by a halo of sclerosis (‘Brodie’s abscess) Or less well-defined, extending to the diaphysis Metaphyseal lesions: • less or no periosteal reaction Diaphysis lesion: • periosteal new bone formation, marked cortical thickening Radioisotope scan: Increased activity

26. Treatment • Conservative: if the diagnosis is not in doubt • Immobilization • Antibiotics: Flucloxacillin + fusidic acid • IV 4-5 days • Oral 6 weeks • Biopsy and curettage: If diagnosis is in doubt

27. Chronic Osteomyelitis

28. • Organisms: • Staphylococcus aureus • Escherichia coli • Streptococcus pyogenes • Proteus mirabilis • Pseudomonas aeruginosa • Staphylococcus epidermidis (if there’s implant) • Predisposing factors: • Untreated/ inadequately treated acute hematogenous osteomyelitis • Immunosuppresive conditions • Local trauma – open fracture, prolonged bone operation, implants

29. Pathogenesis • Sequestra/ implants act as substrates for bacterial adhesion  persistence of infection until they are removed or discharged through perforation  bone destruction  pathological fractures • Sinus may seal off  appearance of healing  tissue tension increases  reopen/ or appear at somewhere else.

30. Clinical Features • Pain • Pyrexia • Redness and tenderness recurred • Discharging sinus • Thickened tissues with puckered (scar or sinus adhere to the underlying bone) • Post-traumatic OM: non-union, deformity

31. Imaging Imaging modality Features X-ray • Bone resorption – patchy loss of density or implant excavation + thickening/ sclerosis of the surrounding bone. • Localized loss of trabeculation • Area of osteoporosis • Periosteal thickening • Sequestra shows up as unnaturally dense with surrounding osteopaenic bone • Bone crudely thickened and misshapen – resembles tumour Radioisotope scintigraphy • Sensitive but not specific • 99mTc-HDP scans: Increased activity both perfusion and bone scan • 67Ga-citrate or 111In-labelled leucocytes is said to be more specific for osteomyelitis – for hidden foci of infection CT scan/ MRI • For operative treatment planning – the extent of bone destruction, reactive edema, hidden abscess and sequestra.

32. Investigations • Acute flare: • Elevated CSR, ESR, WBC • Discharging sinus culture and sensitivity • Staging of chronic osteomyelitis in long bones • Assess risk benefit • Predictive value in treatment outcome

33. Staging for Adult Chronic Osteomyelitis LESION TYPE Stage I Stage II Stage III Stage IV Medullary Superficial Localized Diffuse HOST CATEGORY Type A Type B Type C Normal Compromised by by local/systemic conditions Severely compromised by local/systemic conditions

34. Treatment • Antibiotics & bactericidal drugs • Fusidic acid, clindamycin and the cephalosporins • Vancomycin and teicoplanin (MRSA) • Local treatment • Dressings for the sinus • Operation • Debridement • Dealing with dead space – porous antibiotics-impregnated beads 2-3 weeks then replace with cancellous bone graft

35. Acute Suppurative Arthritis

36. Pathogenesis • A joint can become infected by: • Direct invasion – penetrating wound, intra-articular wound, arthroscopy • Direct spread – from adjacent bone abscess • Blood spread from distant site • Organisms: • Staph.aureus • H.influenza (1-4 yo, reduced d/t vaccination) • Streptococcus • E.coli • Proteus mirabilis

37. • Haematogenous infection which settles in the synovial membrane  acute inflammatory reaction with a serous or seropurulent exudate  increase in synovial fluid. • Pus appears in the joint  articular cartilage is eroded and destroyed (by bacterial enzymes and proteolytic enzymes)

38. Clinical Features New-born infants: • Septicaemia • Irritable • Refused to feed • Rapid pulse • Fever • Check for umbilical cord infection, site of infection Children • Single joint pain (commonly hip or knee) with local tenderness • Pseudoparesis • Rapid pulse • Swinging fever Adults • Superficial joint pain (knee, wrist, finger, ankle, toe) + inflammed • Patients with rheumatoid arthritis, and especially those on corticosteroid treatment, may develop a ‘silent’ joint infection.

39. Treatment • Aspirate joint fluid and examine • Analgesics • Splintage – for resting and prevent dislocation • Antibiotics – same as acute OM • Drainage under anaesthesia • Young infants • When hip joint is involved • If the aspirated pus is very thick • When no improvement within 48 hrs

40. Complications Under 6 years old has higher incidence for complications Subluxation and dislocation of the hip Knee instability Damage to the cartilaginous physis/ epiphysis in growing child • Retarded growth • Partial/ complete epiphysis destruction • Joint deformity • Osteonecrosis • Acetabular dysplasia • Pseudoarthrosis of the hip Articular cartilage erosion Joint ankylosis

41. Tuberculosis

42. Pathogenesis • Primary complex • Pulmonary, pharynx, guts • Regional lymphatic nodes spread • Secondary complex • Extrapulmonary: Miliary tuberculosis, meningitis, multiple tuberculous lesion • Tertiary complex • Bones and joints • Chronic inflammatory reactions – tuberculous granuloma, collection of epitheloid & multinucleated giant cells surrounding an area of necrosis, round cells at periphery (mainly lymphocyte)

43. Clinical Features • History of previous infection/ contact with tuberculosis • Joint pain • Fever, night sweats, loss of weight • Muscle wasting • Synovial thickening • Enlargement & tenderness of of regional lymph nodes • Limited movements • TB spine – pain, localized kyphosis, weakness/ instability of the lower limbs

44. Imaging X-ray • Soft-tissue swelling • Periarticular osteoporosis • ‘Washed-out’ bone ends • Reduced joint space • Enlarged epiphysis – children • Subarticular bone erosion • Little or no periosteal reaction

45. Investigations • Elevated ESR • Lymphocytosis • Positive Mantoux/ Heaf test – sensitive but not specific • Synovial fluid – cloudy, increased protein concentration, increased white cells, AFB

46. Treatment • Rest – joint splintage to overcome muscle spasm and collapse of articular surface • Chemotherapy – antituberculous medications (rifampicin, isoniazid) • Intensive phase treatment (5-6 months) • Isoniazid 300-400mg • Rifampicin 450-600mg • Fluoroquinolones 400-600mg • Continuation phase treatment • Isoniazid + pyrazinamide 1500 mg/d (4.5 months) • Isoniazide + rifampicin (4.5 months) • Prophylaxis phase treatment • Isoniazide + ethambutol 1200 mg/d • Operation • Operative drainage