ACEM Primary
Orthopaedic Pathology
Fractures
Classification:
- Complete/ incomplete
- Closed (overlying tissue intact)/ compound (fracture site communicates with skin)
- Comminuted (splintered bone)
- Displaced (ends of bone are not aligned)
- Pathologic (bone altered by disease process)
- Stress (slowly developing when bone is subject to repetitive loads)
Healing process:
| Week 1 Haematoma | Immediately after fracture, rupture of blood vessels leads to haematoma Fills the fracture gap Provides fibrin mesh framework for influx of inflammatory cells and fibroblasts Platelets release PDGF, TGF-b, FGF and interleukins -> activate osteoprogenitor cells Forms Pro callous |
| Week 2-3 Bony callous | Activated osteoprogenitor cells deposit subperiosteal trabeculae of woven bone Oriented perpendicular to cortical axis within medullary cavity Chondroblasts make fibro/ hyaline cartilage Fractured ends of bone are bridged by bony callous Increases in strength as mineralises Excess fibrous tissues, cartilage and bone is produced |
| Week 5-6 Remodelling | As subjected to weight bearing forces, callous undergoes remodelling Altered activity of osteoblasts and osteoclasts – parts of bone that are not physically stressed are reabsorbed Reduced size of callous until original outline of bone established |
| Factors which impede fracture healing: Inadequate immobilisation Non-union or malunion Infection Diabetes Immunosuppression |
Osteomyelitis
= Inflammation of bone and marrow in setting of infection
- Pyogenic (bacterial infection)
- Organisms reach bone via haematogenous spread, extension from contiguous site or direct implantation
- Staphylococcus aureus in 80-90% of cases, express receptors for bony matrix
- Also E Coli, Klebsiella, Pseudomonas common in IVDU
- In neonates, GBS or H influenzae
- In 50% cases, no organism can be isolated
- Morphology:
- Depend on stage (acute/ subacute/ chronic)
- Initial inflammatory response
- Subperiosteal abscess
- Bone necrosis (sequestrum = dead piece of bone)
- Involucrum = newly deposited bone forms sleeve of living tissue around segment of devitalised bone
- Brodie abscess = intraosseous abscess
- Sclerosing osteomyelitis of Garre = involves jaw
- Clinical course:
- May manifest as acute systemic illness (fevers, malaise, leukocytosis, marked pain of affected area)
- Radiographic findings of lytic bony destruction surrounded by zones of sclerosis
- Positive blood cultures
- Treatment is antibiotics +/- surgical drainage
- Complications: sepsis, pathologic fracture, endocarditis, sarcoma
- Tuberculous osteomyelitis (tuberculosis)
- Skeletal syphilis (T pallidum or T pertenue)
Arthritis
| Osteoarthritis (OA) | Rheumatoid Arthritis (RA) | Gout | Pseudogout | |
| Description | Progressive erosion of articular cartilage -Can affect knees, hands and hips. -Associated with previous joint injury or congenital deformity (oligoarticular), diabetes, obesity (secondary OA) | Chronic inflammatory arthritis -> destruction of articular cartilage and ankylosis of joints -Women 3-5 times more commonly affected than men -Aged 40-70 years old | Transient attacks of acute arthritis due to crystallisation of urate crystals within joint | Calcium pyrophosphate crystal deposition disease (CPPD) -Patients > 50 yo -Women and men equally affected |
| Pathogenesis | Multifactorial -Genetic -Environmental = ageing, biomechanical stress | -Genetic susceptibility (HLA-DRB1 allele) -Autoimmune reaction (80% have auto antibodies to IgG rheumatoid factors or citrullinated proteins) -Environmental arthritogen (EBV, mycobacteria, retrovirus) | Primary gout = 90% idiopathic cases (diet, enzyme deficiency) Associated with increasing age, genetic predisposition, ETOH consumption, obesity, drugs (thiazides) and lead toxicity. Secondary gout = 10%, cause of hyperuricaemia is known (cancer, psoriasis, leukaemia, tumour lysis syndrome) Deposition of monosodium urate crystals into joints -> inflammatory response. | Idiopathic Hereditary Secondary (due to joint damage, hyperparathyroidism, hemochromatosis, diabetes) Exact basis for crystal formation is unknown. |
| Morphology | Subchondral cysts Joint mice (dislodged pieces of cartilage/bone) Bone eburnation (polished ivory appearance due to friction) Sclerosis | Inflammatory infiltrate Increased vascularity Pannus formation (mass of synovium consisting of inflammatory cells growing over articular cartilage) Rheumatoid nodules on skin (elbows, occiput) Rheumatoid vasculitis | Acute arthritis Chronic tophaceous arthritis Tophi in various sites (aggregation of urate crystals surrounded by intense inflammatory reaction) Gouty nephropathy | Inflammatory reaction Crystals are weakly birefringent Rare tophi formation |
| Clinical course | -Asymptomatic -Joint pain that worsens with use, morning stiffness and limited ROM -Impingement on spinal foramina by osteophytes = cervical/ lumbar radiculopathy -Heberden nodes (osteophytes at DIPJ) | -Variable -Malaise, fatigue, generalised MSK pain -Symmetrical, small joints affected before larger ones = hands (MCPJ/PIPJ), feet, wrists, elbows and knees -Joints are warm, swollen and painful -Improves with use -20% patients have periods of partial/ complete remission then relapse -XR hallmarks = joint effusions, juxta-articular osteopenia, narrowing of joint space and loss of articular cartilage -Deformities = radial deviation of the wrist, ulnar deviation of fingers, flexion-hyperextension abnormalities of fingers (Boutonniere/ Swan neck) -Treatment is analgesia, corticosteroids, immune modulating drugs | Four stages: -Asymptomatic -Acute gouty arthritis (sudden onset excruciating joint pain – most are monoarticular, 50% occur in first MTP) -Intercritical gout (asymptomatic) -Chronic tophaceous gout | Asymptomatic Can produce acute, subacute or chronic arthritis Supportive therapy |
Last Updated on September 24, 2021 by Andrew Crofton
Andrew Crofton
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