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Dermatology and Musculoskeletal > Fractures and Osteomyelitis - Walter > Flashcards

Fractures and Osteomyelitis - Walter Flashcards

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1
Q

What are the three possible etiologies for a fracture?

A

Traumatic - violent force

Non traumatic - pathologic (metabolic, tumors etc)

Stress fracture - repetitive use

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2
Q

What are the three stages of fracture healing?

A
  • Inflammatory phase (1 week)
  • Reparative phase (2-3 weeks)
  • Remodelling phase (1 month)
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3
Q

What is involved in the inflammatory phase 1?

A
  • Immediately after fracture
  • Disruption of blood vessels
  • Fracture hematoma - 1) favors bone healing and removal retards healing 2) Fibrin mesh is formed - seal the the fracture site and provides scaffolding for cells
  • Bone marrow shows hemorrhage and fat necrosis
  • Vascular injury –> ischemia –> bone necrosis
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4
Q

What is involved in inflammatory phase 2

A
  • Inflammatory infiltrate - degranulated plateletss, neutrophils and later macrophages
  • Macrophages - remove red cells, necrotic fat and cell debris. Release cytokines (included are bone morphogenic proteins)
  • Granulation tissue formation
  • Activate osteoblasts and osteoclasts
  • Soft tissue callus (PROCALLUS) is formed
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5
Q

What are the main steps in the reparative stage?

A
  • Primary callus formation - reaches its maximal girth after 2-3 weeks
  • Osteoprogenitor cells deposit trabeculae of woven bone
  • Activated mesenchymal cells also differentiate into chondrocytes - produce fibrocartilage and hyaline
  • Cartilage undergoes endochondrial ossification with organized woven bone
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6
Q

What are the stages involved in the Remodelling phase?

A
  • Secondary callus (mature lamellar bone which gradually replaces the woven bone of primary callus) formation
  • Callus gets reduced to the original size of the bone - osteoclasts resorb and osteoblasts lay down bone. Weight bearing areas that are not physically stressed are resorbed (I think kind of a if you dont need it you lose it kinda way). The medullary cavity is also restored
  • This whole process takes several months, but its more rapid in children
  • Once remodelled, it is impossibl to find the site of fracture
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7
Q

What are the complications of fracture healing?

A

1) Infection
2) Delayed union
3) Non union - pseudoarthrosis

  • Delayed union or non-union are common in:
    • Separation of fractured wounds
    • soft tissue between fractured bone ends
    • Lack of immobilization
    • Pathological fractures
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8
Q

What is Pseudoarthrosis

Etiology?

Therapy?

A
  • If a non-union allows too much motion along the fracture gap, the central portion of the callus undergoes cystic degeneration, and the luminal surface can be lined by synovial-like cells, creating a false joint
  • Etiology:
    • Widespread separation of the fractured ends
    • Interposition of soft tissue between the fracure bone ends
    • Lack of immobilization
    • Pathological fractures eg tumor tissue

Fibrous or fibrocartlogenous connective tissue

Central portion of the callus undergoes cystic degeration - lined by synovial like cells, creating a false joint

Therapy - surgical resection with internal fixation

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9
Q

What is internal callus?

A

Callus that lies within the reparative tissue in the medulla

Internal callus is relatively well vascularized and mechanically more stable contains less cartilage and more woven bone compared to external callus

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10
Q

What is external callus?

A

This is the callus that develops around the fractured bone and is in contact with the surrounding soft tissues, including the muscles

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11
Q

What is the composition of normal callus and what determines this composition?

A

Callus is made up of bone cartilage and fibrous tissue

The composition is dependent on:

  • Stability
  • Vascularity
  • Extent of injury

Poorly vascularized fractures have an abundance of cartilage!!!

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12
Q

Systemic complication of fractures?

A
  • Shock syndrome- due to blood loss.
  • Myoglobinuria, the latter occurring when there is significant muscle injury.
  • Fat embolization - through the damaged venous system by disrupting the bone marrow which contains adipose tissue. Fat embolization becomes a clinical problem in severe multiple fractures and extensive orthopedic surgery.
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13
Q

What are the determinants of fracture healing?

A
  • Age
  • Fracture type
  • Fracture site
  • Extent of soft tissue
  • Local factors - vascular supply, mechanical factors
  • Overal health and nutrition status of patient - diabetis, calcium, phosphorous, vitamins, infections
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14
Q

What is osteomyelitis?

*What does it imply

A

This is inflammation of bone and/or marrow

It implies that there is an infection

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15
Q

What are the possible routes of infection of the bone or the marrow

A
  • Blood
  • Direct spread from neighbors
  • Penetrating injury
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16
Q

What is pyogenic osteomyelitis?

A

This is osteomyelitis that is usually of bacterial etiology

No organism isolated in 50%.
• S. aureus (80-90%)
• Gram- rods (E. coli, Klebsiella, Pseudomonas)
o GU infection, IV drug abuse
• Mixed bacterial (direct inoculation)
• H. influenza (neonates)
• Group B Streptococcus (neonates)
• Salmonella (sickle cell disease)

17
Q

Acute hematogenous osteomyelitis

Epidimiology:

Age affected?

Gender?

Location

Predisposing factors?

A
  • Young, growing children
  • Adults (> 50 years)
  • Gender M:F = 2:1
  • Location - Long tubular bones (femur, tibia, humerus), vertebral bodies
  • Predisposing factors - catheter, trauma, infection, underlying disease, IV drug abuse
18
Q

Where does hematogeous osteomyelitis usually begin?

A

Hematogenous osteomyletis usually begins in the metaphysis of a bone.

Thought to be initial site of infection for anatomic reasons:
• Nutrient arteries terminate in venous sinusoids (ideal lakes for bacterial seeding) rather than forming anastomosis with veins through capillaries.
• These vascular loops and terminal branches have low oxygen tension and inhibited phagocytosis, conducive to bacterial growth.

19
Q

Acute hematogenous starts of inthe metaphysis of the bone. Describe how the it continues to spread and its effects.

A
  • After the metaphysis the infection spreads to adjacent trabecular and cancellous bone.
  • Continuing infection results in the formation of abscesses within the medulla and beneath the periosteum.
  • Inflammatory swelling leads to the loss of both endosseal and periosseal blood supply and necrosis of nearby bony trabeculae including a segment of cortex.This necrotic bone is called sequestrum.
  • After infection reaches periosseum, it is elevated, becomes reactive and starts forming new bone.
  • Similar sleeve of new bone (involucrum) develops around the necrotic cortex and medulla
  • Subperiosseal abscess eventually ruptures into soft tissue, forming soft tissue abscess and ultimately draining sinuses opening onto the skin surface - fistula.
20
Q

What is the clinical presentation of pyogenic osteomyelitis?

Symptoms?

Physical Exam

Lab findings?

A

Symptoms - chills, fever, malaise, irritability and pain at the site of infection

Physical exam - erythema, swelling, tenderness and restricked range of motion

Lab findings - leukocytosis with a left shift elevated sedimentation rate

On imaging, the changes are seen late. They have a lag time of at least two weeks before anything can be seen and the changes are also non-specific. MRI is more sensitive

21
Q

Vertebral Pyogenic Osteomyelitis

Where does it commonly arise?

What are the predisposing factors

Where does it begin and continue to?

A

Commonly arises in the lumbar spine, less frequently thoracic and cervical spine

Predisposing factors include UTIs, diabetes, and IV drug abuse

Begins in vertebral body and spread to involve the disc (discitis) —> disc destruction is more common in pyogenic than non-pyogenic infections of the spine

22
Q

Complications of vertebral pyogenic osteomyelitis?

A
  • More than one vertebral segment may be involved.
  • May breach the anterior cortex and ligamentous structures to form paravertebral soft tissue abscesses (retropharyngeal abscess, psoas abscess extending to groin and politeal fossa).
  • May spread posteriorly to involve the posterior arch and the neural canal, resulting in meningitis.
23
Q

What is the pathogenesis of Pyogenic Osteomyelitis?

Long version as a FYI

A
  • The initial response to infection with pyogenic organisms is acute inflammation, resulting in fluid exudate containing neutrophils and fibrin.
  • Continuing exudation raises the tissue pressure, which comprises the vascular space, leading to bone death (bone unable to expand to relieve the pressure on vascular space, no swelling as in soft tissue).
  • Major problem in treating patients with OM is the extent of osteonecrosis, which interferes with the access of antibiotics.
  • After infection reaches periosseum, it is elevated, becomes reactive and starts forming new bone.
  • A sleeve of new bone (involucrum) develops around the necrotic cortex.
  • This involucrum is initially composed of reactive woven bone trabeculae, but later, may become organized into a neocortex of compact bone.
24
Q

Summarize the pathology of acute osteomyelitis

A
  • Acute inflammation
  • Bone necrosis
  • Subperiosteal abscess
  • Progressive ischemia leads to segmental bone necrosis (sequestrum) surrounded by viable new bone (involucrum) formation
  • Draining sinus tracts
  • Extension into joint space (acute septic arthritis)
25
Q

What is the treatment of osteromyelitis?

A
  • Treat early
  • IV antibiotics 4-6 weeks
  • Exception: Children with hematogenous spread
  • Oral therapy if organism is susceptible
  • Good compliance
  • Rapid response
  • Consider surgical debridement
26
Q

What can cause the evolution fo acute osteomyelitis into chronic osteomyelitis?

A
  • Delay in diagnosis
  • Inappropriate antibiotics
  • Abbreviated therapy
  • Extensive necrosis
  • Inadequate surgical debridement
  • Underlying medical condition
  • 5-25% of acute osteomyelitis do not resolve → chronic osteomyelitis
27
Q

Characteristics of Chronic Osteomyelitis

Clinical

Pathology

A
  • Clinical
    • Malaise, Leukocytosis, Fever
  • Pathology
    • Chronic inflammation (lymphocytes, plasma cells)
    • Marrow fibrosis
    • Resorption of dead bone
    • deposition of woven bone
    • Brodie absecc: intracortical abscess
    • Sclerosing OM of Garre: jaw extensive new bone foramtion osbscuring much of the underlying bone structure
28
Q

What are the complications of chronic osteomyelitis?

A
  • Recurrent acute exacerbations
  • Pathologic fracture
  • Secondary amyloidosis
  • Endocarditis
  • Sepsis
  • Septic Arthritis
  • Rarely, malignant complications. Like:

Squamous cell carcinoma of fistula tract

Sarcoma of infected bone

29
Q

What is an example of non-pyogenic osteomyelitis?

A

Tuberculosis Osteomyelitis

30
Q

Tuberculosis ostemyelitis

What group of patient does it most common affect?

Common location?

A
  • 1-3% of patients with pulmonary TB
  • Immunocompetent or compromised
  • Location - Spine > knees > hips
  • Because the initial lesion is most often seen in the lower thoracic spine, the psoas muscle sheath is frequently involved. Therefore, patients may present with a fluctuant swelling (cold abcess) in the groin as the result of tracking of infected material from the paraspinal area
31
Q

Describe skeletal tuberculosis

A
  • Usually starts at vertebral bodies and extends to involve intervertebral disc and the bodies of adjacent vertebrae.
  • Very destructive lesion.
  • Spreads through medullary cavity causing extensive necrosis
  • Bone destruction results in anterior angulation of the spine (kyphosis).
  • Extends through intervertebral discs involving multiple bones
  • Difficult to control

Dermatology and Musculoskeletal (10 decks)

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