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Tufts OpenCourseware
Author: Debra D. Poutsiaka, M.D.,Ph.D.
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1. General Introduction

1.1. Case 1

A 9 year old girl with a recent history of a sty of her eyelid developed fever and right hip pain. Initial radiographs of the hip showed evidence of infection of the right hip space (increase in the joint space). Four weeks later, repeat radiograph shows progressive destruction of the joint with the loss of joint space, bony lesions and destruction of cartilage. The process involves the proximal femur, ileum and ischium. This case illustrates both septic arthritis and osteomyelitis.

Initial radiograph – widening of the joint space, a subtle finding of an infected joint.

Radiograph 1

Second radiograph – 4 weeks later – progressive destruction of the joint with loss of joint space, bony lesions, destruction of cartilage. Process involves the proximal femur, ileum, ischium.

Radiograph 2

1.2. What is this process?

Differential diagnosis includes

  • Osteomyelitis
  • Cancer

2. Osteomyelitis

Definition -
Infectious process involving the various components of bone characterized by progressive inflammatory destruction of bone, necrosis and new bone formation.
Acute osteomyelitis -
usually evolves over several weeks
Chronic osteomyelitis -
usually evolves over months. Long-standing infection characterized by the persistence of microorganisms, low-grade inflammation, presence of dead bone ("sequestrum") and/or foreign material, and fistulous tracts

2.1. How did the infection develop?

2.1.1. Pathophysiology - Three modes of development of acute and chronic osteomyelitis Hematogenous spread

an infection at another site disseminates to the blood (bacteremia), which then carries the bacteria to the site in the bone

Location is age dependent:

  • children - distal femur and proximal tibia are favored sites
    • Case 2: 12 year old girl with 18 months of ankle pain but no fever or chills. Eventually a radiograph was done that demonstrated a Brodie's abscess – a chronic localized bone abscess, usually found in the distal tibia.

    Brodie's Abscess

  • adults - most common sites – vertebrae, sternoclavicular joint, sacroiliac joint, symphysis pubis Contiguous spread

  • Implies an initial infection that by continuity gains access to bone In association with vascular insufficiency

  • Associated with poor wound healing and chronic ulcers
  • Seen in diabetics or others with peripheral vascular disease
  • Most often affects lower extremities

3. Who gets Osteomyelitis?

3.1. Risk Factors:

  • Presence of foreign materials (PMN defect, adhesion of microorganisms)
  • Diabetes (microvascular disease, poor wound healing, neuropathy)
  • Surgery
  • Adjacent soft tissue infection
  • Peripheral vascular disease
  • Sickle cell disease (devitalized bone)
  • Congenital defects in phagocyte function

4. How is the diagnosis of Osteomyelitis made?

4.1. History and physical examination

  1. presence of risk factors
  2. fever, local pain and tenderness, swelling, decreased range of motion of a joint, erythema, warmth, drainage, sinus tracts, ulceration

4.2. Radiographic diagnosis

  1. Routine radiographs ("plain films")
    • fairly specific but appearance of abnormalities might be delayed (up to 15 days after symptoms appear)
    • Cortical destruction with periosteal new bone formation

    Ex. 1. Salmonella osteomyelitis of the tibia, began in shaft. See cortical destruction, new bone formation and fissure in cortical bone

    Radiographic findings of osteomyelitis

  2. Bone scan
    • intravenously injected radioisotope localizes to the areas of increased bone activity that occur at the site of a bone infection
    • very sensitive but has low specificity
  3. Computed tomography (CT scan)
    • 3-dimensional view of affected area - visualizes bone, surrounding soft tissue and sequestra (islands of dead bone)
  4. Magnetic resonance imaging (MRI)
    • visualizes bone and surrounding soft tissue in a 3-dimensional fashion
    • the appearance of the bone marrow changes due to the inflammation associated with the bone infection
    • test of choice for vertebral osteomyelitis

    Diagnosis of Diagnosis of Osteomyelitis: Radiograph 1

    Diagnosis of Osteomyelitis: Radiograph 2

4.3. Bone biopsy – the "Gold Standard"

abundant PMN's, bony necrosis, positive gram stain
positive culture confirms diagnosis

5. What are the major pathogens causing Osteomyelitis?

Pathogens are age specific

  1. neonates
    • S. aureus, group B streptococci
  2. infants
    • S. aureus, H. influenzae
  3. later in life
    • S. aureus predominates
  4. adults
    • Usually S. aureus
    • "Mixed infection" (gram positive organisms, gram negative aerobes, anaerobes) - in the setting of peripheral vascular disease and/or diabetes

6. How is Osteomyelistis treated?

  • An individualized treatment plan is often necessary
  • Treatment often involves medical and surgical modalities. Treatment "failures" are frequently due to the need for more surgical treatment as opposed to more or different antibiotics.

6.1. Medical modalities

  • antibiotics
    • ex. methicillin-sensitive S. aureus osteomyelitis - optimal antibiotics are oxacillin +/- an aminoglycoside for synergy
    • treatment is frequently long-term (for example, 4-6 weeks)
  • optimization of the management of underlying conditions such as diabetes

6.2. Surgical modalities

  • debridement – removal of nonviable material, including pus, dead tissue and bone, and foreign material. This removes the nidus of persistent infection.
  • revascularization - improving blood flow to the affected areas in persons with underlying peripheral vascular disease. This improves wound healing and delivery of antibiotics to the site.

Ablation or amputation might be necessary to eradicate or control the infection

7. Septic Arthritis

Case 3:

  • A 53 year old woman presents to the emergency room with a 2 to 3 day history of fever and chills, followed by the abrupt onset earlier in the day of wrist pain, swelling and redness.

    Case three: picture 1

7.1. What is this process?

The differential diagnosis includes noninfectious inflammatory arthritis such as rheumatoid arthritis and infectious or "septic" arthritis

Definition of septic arthritis
infection of the joint space (monoarticular – 90%, polyarticular, suppurative, nonsuppurative)

7.2. How did the infection develop?

The pathogenesis of septic arthritis can occur through three pathways:

  • hematogenous spread
    • from a blood borne infection (Remember case 1?)
    • Synovial tissue is very vascular and thus susceptible to hematogenous seeding
  • direct inoculation
    • such as a sharp contaminated object (ex. cat's claw) penetrating the synovial space
  • from a contiguous infection (i.e., via direct extension)
  • within hours of a joint becoming infected, an inflammatory and destructive process of the joint begins

7.3. Who gets Septic Arthritis?

Risk factors for and/or comorbidities associated with septic arthritis are:

immunosuppression injection drug use
intravenous catheterization potential acquisition of sexually transmitted diseases
geographic location joint prosthesis
joint disease (RA) trauma (including joint injection)
diabetes advanced age
malignancy corticosteroid use

8. How is the diagnosis of Septic Arthitis made?

8.1. History

  • elicit pertinent features such as a history of joint disease or trauma and other risk factors/comorbidities, symptoms suggesting bacteremia
  • fairly sudden articular or peri-articular pain, especially if at rest, should not be ignored

8.2. Physical Examination

  • key joint findings - limited range of motion, tenderness, swelling, warmth, erythema
  • knee>hip> shoulder = ankle = wrist
  • associated physical findings looking for a potential source of infection or portals of entry (Remember the sty from case 1?)

8.3. Radiography

  • plain radiographs might be useful
  • CT scan and MRI are very useful for defining joints and complex surrounding structures

Ex. Tuberculous septic arthritis of the hip – extensive destruction of the femoral head and neck (Protrusio Acetabula) due to bony resorption, soft tissue abscess.

Tuberculous Arthritis of the Hip

8.4. Laboratory examination

  • Blood culture – detection of bacteremia in septic arthritis varies (10-50%)
  • synovial fluid examination
    • elevated WBC count – usually >50,000
    • Gram stain generally positive in 1/3 of cases
    • cultures positive in 25-80%

8.5. Microbiology

  • Causative organism identified in 2/3 of cases
  • Gram positive bacteria account for 70-80% of cases in university-based studies. S. aureus accounts for half of these (35-40% of all cases). Streptococcus species - most common is group A beta-hemolytic streptococci.
  • Gram negative aerobic rods - 9-20% of cases in teaching hospitals, especially among the immunocompromised
  • Gonococcal septic arthritis – due to Neisseria gonorrhoeae, agent causing gonorrhea - 3-7.5% of cases in most series implies dissemination from a mucosal port of entry in a sexually active person (Remember Case 3? This patient had sexual intercourse with a new partner 7 days earlier.)
    • Monoarticular septic arthritis
      • one joint involved, organism recovered from synovial fluid
    • Dermatitis-septic arthritis syndrome
      • classic triad of dermatitis, migratory polyarthralgias or polyarthritis, tenosynovitis
      • Fever, skin lesions, polyarticular involvement, bacteremia

      Case three: picture 2

9. How is Septic Arthritis treated?

  • An individualized treatment plan is often necessary.
  • Treatment often involves medical and surgical modalities. Treatment "failures" are frequently due to the need for more surgical treatment as opposed to more or different antibiotics.
  • Outcome of treatment is related to the rapidity of institution of therapy

9.1. Medical modalities:

9.1.1. Antibiotics

  • example 1: Methicillin-sensitive S. aureus septic arthrithis - optimal antibiotics are oxacillin +/- an aminoglycoside for synergy
  • example 2: N. gonorrhoeae septic arthritis – ceftriaxone is a good choice
  • treatment is frequently long-term (for example, 4 or more weeks)

9.1.2. Percutaneous arthrocentesis

9.2. "Surgical" modality:

9.2.1. Arthroscopic or open surgical drainage

  • Infection of the hip joint and other poorly accessible joints
  • Joints that are difficult to monitor (shoulder)
  • Suspected soft tissue extension (ex. an abscess erupting from the joint capsule)
  • Inadequate clinical response after a few days of antibiotics
  • Should also be considered for those with rheumatoid arthritis or other previously damaged joints since outcome after medical therapy is poor

10. Ancillary Material

10.1. Readings

10.1.1. Required

  • Schaecter, Chapter 62, pages 582-588.

10.1.2. Suggested

  • Smith JW, Peircy EA. Infectious Arthritis, in Principles and Practice of Infectious Disease, Mandell GL, et al, ed. Churchill Livingstone, New York, 1995, fourth edition, pp. 1032-1039.
  • Mader JT, Calhoun J. Osteomyelitis, in Principles and Practice of Infectious Disease, Mandell GL, et al, ed. Churchill Livingstone, New York, 1995, fourth edition, pp. 1039-1051
  • Deely DM, Schweitzer. MR imaging of bone marrow disorders. Radiol Clin N America, 1997;35:193-212. .
  • Haas DW, McAndrew MP. Bacterial osteomyelitis in adults: Evolving considerations in diagnosis and treatment. Am J Med, 1996;101:550-561. 5
  • Liu NY, Giansiracusa DF. Septic arthritis, in Infectious Diseases, Gorbach SL, et al, ed., W.B. Suanders Company, Philadelphia, 1998, second edition, pp.1344-135.
  • Mader JT, Mohan D, Calhoun J. A practical guide to the diagnosis and management of bone and joint infections. Drugs, 1997;54:253-264. .
  • Musher DM, et al. The current spectrum of Staphylococcus aureus infection in a tertiary care hospital. Medicine, 1994;73:186-208.
  • Kaandorp CJE, et al. Risk factors for septic arthritis in patients with joint disease. Arthritis Rheumatism, 1995;38:1819-1825.
  • Ryan MJ, et al. Bacterial joint infections in England and Wales: Analysis of bacterial isolates over a four year period. Br J Rheum, 1997;36:370-373.
  • Pioro MH, Mandell BF. Septic arthritis. Rheum Dis Clin of N America, 1997, 23:239-258.
  • Waldvogel FA. Osteomyelitis, in Infectious Diseases. Gorbach SL, et al, eds. WB Saunders Company, Philadelpia, 1998, second edition. pp. 1339-1344.