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Osteomyelitis: Pathophysiology & Treatment Decisions

Osteomyelitis: Pathophysiology & Treatment Decisions. Clifford B. Jones, MD Associate Clinical Professor, Michigan State University Grand Rapids Orthopaedic Residency Program Orthopaedic Associates of Grand Rapids, Grand Rapids, MI Created March 2004; Revised February 2007.

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Osteomyelitis: Pathophysiology & Treatment Decisions

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  1. Osteomyelitis:Pathophysiology & Treatment Decisions Clifford B. Jones, MD Associate Clinical Professor, Michigan State University Grand Rapids Orthopaedic Residency Program Orthopaedic Associates of Grand Rapids, Grand Rapids, MICreated March 2004; Revised February 2007

  2. “One Should Especially Avoid Such Cases if One has a Respectable Excuse, for the Favorable Chances are Few and the Risks are Many….

  3. ….Besides, if a Man does not Reduce the Fracture, He will be Thought Unskillful. If He does Reduce It, He will bring the Patient Nearer to Death than Recovery.” Hippocratic Writings, New York, Pelican Books, 1978

  4. Fracture Management Goals • Osseous Union • Restore Limb Function • Avoid Complications

  5. Osteomyelitis Results in: • Reduction in limb function • Psychological & Social dysfunction • Increased cost

  6. Hansen’s 7 DsConcerning Prolonged Orthopaedic Problems Despair Divorce Destitute Depression Delinquency Default Death Sigvard Ted Hansen, 1997

  7. Introduction • 350,000 long bone fxs/yr • Infection risk varies: • Type I open – 10/1,000 infections • Type III open – up to 25%

  8. Gustilo Open Fx ClassJBJS, 72A: 299-303, 1990 2% 7% 7% 10-50% 25-50%

  9. Open Fractures Type II Type IIIA Type IIIB Type IIIB

  10. Negative Biology of Open Fx Contamination Crushing Stripping Devascularization Comminution

  11. Blood SupplyRhinelander, CORR, 1974

  12. Blood SupplyRhinelander, CORR, 1974 Normal - endosteal/medullary 2/3-3/4 internal external Fracture - periosteal/external majority internal external Periosteal Blood Supply Important

  13. Centripetal FlowRhinelander, CORR, 1974

  14. Initial Emergent Treatment dT Antibiotics, IV Reduce Stabilize Cover wound

  15. Why infection risk high? Infection risk ≈ Fracture type (soft tissue) Open fx = Contamination (70% cx +) Open fx = Infected fx > 8 hours

  16. Cost Analysis Infection • Increase cost 16-21%/pt • Increase hosp stay 36-50%/pt Total Cost  $ 271 million/yr

  17. Definition • Group of conditions • “…presence of bacteria & an inflammatory response causing progressive destruction of bone.” • Fears, RL, et al, 1998 • “…suppurative process in bone caused by a pyogenic organism” • Pelligrini, VD, et al, 1996

  18. Why destruction of bone matrix? Proteolytic enzymes Hyperemia Osteoclasts

  19. Do Not Delay Tx & Dx

  20. Classification • Waldvogel, 1971 • Classification based on pathogenesis • May, 1989 • 5 parts, post-traumatic tibial osteomyelitis • Cierny & Mader, 1985 • 4 factors affecting outcome • Host, site, extent of necrosis, degree of impairment

  21. PathogenesisWaldvogel, 1971 • Hematogenous • Contiguous focus of infection • Direct inoculation

  22. AnatomicClassification (Cierny-Mader) 1985 I: II: III: IV:

  23. Classification Break-Down • Medullary Endosteal nidus, min soft tissue involvement, ? Sinus tract • Superficial Surface of bone, usu 2° to soft tissue defect • Localized Localized sequestra, usu sinus tract, Usu stables/p excision • Diffuse Permeative process, combination of I/II/III, Usu Unstable s/p excision

  24. Physiologic Classification(Cierny-Mader, 1985) A-Host: Good immune system & delivery B-Host: Compromised host BL: locally compromised BS: systemically compromised BC: combined C-Host: Requires suppressive or no Tx Minimal disability Tx worse than dz, not a surgical candidate

  25. Clinical Staging(Cierny-Mader, 1985) Anatomic Type +Clinical Stage Physiologic Class Example: IV BS tibial osteomyelitis = diffuse tibial lesion in a systemically compromised host

  26. Types of Pathophysiology Acute/Hematogenous Chronic/Nonhematogenous

  27. Acute/Hematogenous • Anatomy (Hobo) • Sharp twist in metaphyseal capillaries • Stasis (Trueta) • Decreased flow in capillaries & veins • Combination (Morrissy) • Trauma & Bacteria

  28. Acute/HematogenousProgression of Dz • Cell death 2° to bacterial exotoxins • bacterial culture medium • worsens condition •  Vascularity, leukocytosis, edema • Pressure w/in rigid osseous container • Pain, swelling, erythema • Potential for septic arthritis (knee, hip, shoulder)

  29. Chronic/Nonhematogenous S. aureus ↑ Pseudomonas aureginosa ↑ Enterobacter > 30% Polymicrobial

  30. Erythema Swelling Sinus Tract Drainage Limp Fluctuence None Pain Tenderness Fever HA Nausea/Vomiting Clinical Findings (varied)

  31. Clinical Findings • Must have high index of suspicion • Inappropriate use of Abx – obscure Sx • Must obtain Dx quickly • If Tx started < 72°: • Decrease incidence of chronic osteomyelitis • Decrease destruction of bone

  32. Laboratory Data Acute (Morrey, BF, OCNA, 1975) •  WBC (25% of time) • Abnormal differential, Left Shift (65%) • Blood Cx – 50% positive Chronic • Mild anemia, WESR, C-reactive protein • Possible leukocytosis with L shift • Blood Cx – usually negative

  33. Radiographs Early – usu negative Changes – delayed (10-21 days)

  34. Radiographs Soft Tissue • Swelling, obscured soft tissue planes, haziness Osseous • Hyperemia, demineralization • Lysis (when > 40% resorbed) • Periosteal reaction • Sclerosis (late)

  35. Radionucleotide Imaging 99M Tc 67Ga 111In WBC

  36. 99M Tc • Action • binds to hydroxyapetite crystals • Osteoblastic activity • Demineralized bone • Immature collagen

  37. 99M Tc • 3 Phase Bone Scan • Radionucleotide angiogram • Immediate post injection blood pool • Three hour:  soft tissue, urinary excretion • Diagnosis • Cellulitis:  Phases 1 &2, no change 3 • Osteomyelitis:  Phases 1 & 2, focal  3 • Results: 94% sensitivity, 95% specificity • Rosenthal 1992, Schauwecker 1992

  38. Cellulitis

  39. Osteomyelitis

  40. 99M Tc: False Positive DM foot d/o Septic arthritis Inflammatory bone dz Adjacent to pressure sores

  41. 99M Tc 4 Phase Bone Scan • New development • Action: • Mature bone: uptake stops at 4 hr • Immature woven bone: cont’d uptake at 24 hr • Problem: needs f/u imaging at 24 hr (compliance) • Gupta 1988, Israel 1987, Schauwecker 1992

  42. 67Ga • Exudation of in vivo labeled serum protein • Transferrin, haptoglobin, albumin • Results • 81% sensitivity, 69% specificity • Schauwecker, 1992 • Combination with Tc •  sensitivity, but  specificity

  43. 111In WBC • Used in combination (Seabold, 1989) • In/Tc: 88% accurate • Ga/Tc: 39% accurate • Preparation problem •  rad dose to spleen, 18-24hr delay • Spine (Whalen, Spine 1991) • 83% false negative  use MRI

  44. MRI No radiation Good soft tissue imaging Imaging: • T1 Dark • T2 Bright/Mixed

  45. T1 bright T2 dark

  46. T1 bright T2 dark

  47. MRI • Acute: •  marrow fat •  granulation tissue H2O • Chronic: thickened cortex • Low signal on all scans • Cellulitis: no marrow changes

  48. MRI ResultsSchauwecker, 1992 • Sensitivity 92-100% • Specificity 89-100% • Excellent for Spine (Modic, RCNA, 1986) • Sens 96%, Spec 92%, Accuracy 94% • Soft tissue extension • Sinus tract formation • Bright Tx from skin to bone

  49. CT Imaging Image cortical and cancellous bone Evaluate osseous adequacy of debridement

  50. Aspiration Biopsy Acute • Good, only 10-15% false negative Chronic • Sinus tract cx: 76% sens, 80% spec • 70% with S aureus & Enterococcus • 30% Pseudomonas • Does not determine correct Abx

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