MSK

• Fracture repair - Inflammatory Phase

  1. Immediately at fracture- damaged blood vessels – bleeding in the cortex, marrow, periosteum, and surrounding tissue

  2. Haematoma forms between the medullary canal and beneath the periosteum - fractured end of the bone seals

  3. Damaged blood vessels disrupt O2 supply = bone tissue death immediately adjacent to the fracture

  4. This triggers inflammatory response: vasodilation, increased permeability, exudation of plasma, infiltration of inflammatory mediators such as leukocytes and mast cells

  5. This decalcifies the fractured bone end = procallus
• Fracture repair - Reparative Phase

  1. Capillary network forms within the haematoma from surrounding soft tissue and the marrow cavity into the fractured area - increased blood flow to the area

  2. Phagocytes start 'cleaning up' debris whilst granulation tissue develops

  3. Fibroblasts (collagen-forming cells create fibrocartilaginous callus) and osteoblasts (bone-forming cells create bone matrix) create a bridge of spongy bone between the bone ends

  4. Osteoblasts migrate inwards to mineralise this new bone resulting in a bone callus
• Fracture repair - Remodelling Phase

  1. Gradual spread of the callus with creation of compact and cancellous bone structures (which takes several months, up to 2 years)

  2. Osteoclast cells absorb fragments of dead bone tissue and unnecessary callus

  3. Finally, this 'new bone' has reformed its internal and external structure
• Factors affecting bone healing post-fracture

  • Complexity or type of fracture
  • Genetics, advancing age, lifestyle choices
  • Endogenous factors – Comorbidities, hormones, Inflammation / Infection elsewhere in the body or secondary to fracture, Blood supply to area
  • Immobilisation
  • Internal Fixation Devices
• Clinical manifestations of fractures

  • Immediate localised pain / tenderness
  • Swelling
  • Paraesthesia → damaged nerves
  • Bruising → ecchymosis
  • Deformity (not always present)
  • Muscle spasms → irritation of tissues and protective responses to the injury, can displace the fracture further
  • Loss of function → strength, range of movement, inability to weight-bear
  • Crepitation → crunching and grating together of bony fragments, producing palpable / audible crunching
  • Guarding → a person with a fracture will usually guard the injury against movement, protecting against further injury
• Medical treatment for fractures

  • Surgery – ORIF
  • Reduction - re-establish correct anatomical alignment
  • Closed fracture → non-surgical, manual re-alignment of bone fragments → traction and counter-traction applied under local, procedural, or general anaesthesia → followed by immobilisation with casting after reduction
  • Open fracture →surgical incision
• Immobilisation methods

  • Casting for ADLs, incorporates joints distal and proximal to fracture, limb first covered cotton stockinette, then softban padding, then POP
  • Traction - Application of pulling force to attain re-alignment, Counter-traction pulls in opposite direction, Skin traction (short-term 48-72 hours), Skeletal traction (longer-term)
• Aims of fracture management

  • Managing and relieving pain
  • Identifying mechanism of injury
  • Assessing clinical presentation
  • Improving joint function
  • Correcting deformity and malalignment
  • Increasing functional capacity
  • Reducing the risk of complications
• Nursing management for fractures

  • RICE (Rest, Ice, Compression, Elevation)
  • Open fractures - saturate gauze with normal saline, apply over wound and/or cover with sterile dressing, aseptic technique
  • Do not attempt to reduce fractures
  • Pharmacological management - paracetamol, NSAIDs, opioids
  • Preoperative nursing management
  • Postoperative nursing management
• Preoperative nursing management of fractures

  • Keep patient NBM
  • 1/24 vital signs, pain and neurovascular assessments
  • Fluid balance chart
  • Urinary catheter if clinically required
  • Use pressure relieving mattress
  • VTE risk assessment
  • Pharmacological management as directed
  • Non-pharmacological management - support injured limb with pillows
• Postoperative nursing management of fractures

  • Frequent assessment/observation - vital signs, respiratory, pain, neurovascular, wound
  • DVT prophylaxis
  • Indwelling catheter care
  • Mobilisation
  • FBC, IVC care
  • Hygiene, prevention of constipation
  • Address psychosocial needs
• Postoperative nursing care for hip fractures

  • Commence mobilising, with full weight-bearing as tolerated, the day after surgery
  • Pressure area care
  • Removal of catheter 24/24 after surgery
• Logroll is performed for hygiene needs or pressure area care, with the aim to avoid internal or external rotation of the hip in hip fractures, and analgesics should be administered prior
• Sprains and strains

  • Sprain - tear or stretching of a ligament surrounding a joint, usually from a traumatic event
  • Strain - tear, twist, or excessive stretch of a muscle, its muscle sheath and/or its tendon, usually from overexertion, trauma or repetitive movement
• Risk factors for sprains and strains

  • Advancing age
  • Obesity
  • Poor physical fitness/sedentary lifestyle
  • Smoking
  • Medications - steroids
  • Poor posture
  • Comorbidities that result in muscle fatigue/tightness/imbalance
  • Not warming up before activity
• Complications of sprains and strains

  • Severe sprains can result in a fracture
  • Dislocation
  • Chronic instability
  • Loss of function/strength
  • Chronic pain and swelling
  • Arthritis
  • Muscle atrophy
  • Muscle fibrosis
  • Compartment syndrome
• Prevention of strain

  • Balanced nutrition
  • Maintain a healthy weight
  • Regular exercise
  • Avoid playing sports / exercising when fatigued or in pain
  • Avoid traumatic injuries → be aware of falling hazards
  • Maintain strength
  • Warm up and stretch before exercise / sports
  • Wear good fitting and good quality shoes
  • Wear protective braces / equipment during sports
• Medical management of sprains and strains

  1. Conservative management and little intervention

  2. Severe injuries may require surgical intervention if: poor recovery from conservative management and clinical manifestations persist, severely torn ligament with an unstable joint, a complete tear in the muscle and it has become unattached from the bone
• Grade I sprain

  Mild stretching of the ligament (only a few fibres torn) without joint instability
• Grade II sprain

  Partial tear (rupture) of the ligament but without joint instability (or with mild instability)
• Grade III sprain

  A severe sprain: complete rupture of the ligament with instability of the joint
• Pathophysiology of sprain

  Torn tendon or ligament → inflammatory process triggered → inflammatory fluids accumulate at the ends of the damaged tissue → inflammatory cells such as macrophages, fibroblasts, capillary buds and prostaglandins grow inwards from surrounding tissue to begin repair process → 4-5 days later, new collagen has formed → new collagen begins to be organised and associate with existing tendon fibres new and surrounding tissue fuse into single mass → 4-5 weeks post injury, healing tendon or ligament will have adequate enough strength to withstand strong pull
• Signs and symptoms of sprains and strains

  • Pain / tenderness
  • Swelling / oedema
  • Ecchymosis (bruising)
  • Loss of function → limited / decreased range of movement, loss of strength
  • Difficulty weight bearing
  • Antalgic gait
  • Contusion
  • Altered sensation with severe oedema
  • Muscle spasms
• Nursing management of sprains and strains

  • Pharmacological: Simple analgesia including NSAIDs: Paracetamol, Ibuprofen
  • Non-pharmacological: RICE (Rest, Ice, Compression, Elevation), avoid HARM (Heat, Alcohol, Running, Massage) for first 72 hours, education on home management
• The 6 P's (Pain, Pallor, Paralysis, Pulses, Appearance, Capillary Refill Time) are assessed bilaterally to evaluate neurovascular status
• Pathophysiology of DDD

  Nucleus pulposus dries out and shrinks, pressure load transferred to disc annulus which progressively deteriorates, nucleus pulposus herniates through damaged annulus and puts pressure on nearby nerves
• Types of back pain

  • Localised - pain where area palpated
  • Diffused - pain spread from a large area, generate in deep tissues
  • Radicular - irritated caused from nerve root
  • Referred - pain occurs in one area but originates in another
• Management of DDD

  1. Supportive care - limit spinal movement, exercise, pharmacological, improve mobility

  2. Surgery - last option, when conservative management has failed
• Complications of DDD


  • Incontinence
  • Chronic pain
  • Limb weakness
  • Osteoarthritis
  • Reduced mobility
• Osteoporosis


  Metabolic bone disease characterised by abnormal bone structure - loss structural integrity of trabecular bone, decreased bone density, cortical bone becomes weak, thin and more porous
• Pathophysiology of osteoporosis


  Cytokine binds to osteoclast precursor cell receptors, osteoclast precursor cells activate and become osteoclasts, bone matrix creates a decoy receptor for cytokine, imbalance between cytokines, decoy receptors and osteoclast precursor receptors results in bone loss
• Types of osteoporosis

  • Generalised - involves major proportions of axial skeleton
  • Regional - involves one segment of appendicular skeleton
• Risk factors for osteoporosis

  • Genetics
  • Advancing age - 65 years
  • Gender - increased risk for women
  • Nutritional status - poor intake calcium and essential vitamins
  • Physical exercise - bones need a level of stress for maintenance
  • Decreased sun exposure - VD
• Investigations for osteoporosis

  1. Dual-energy x-ray absorptiometry - DEXA scan

  2. Pathology/lab results - Ca, phosphate, VD, thyroid function, haematocrit, erythrocyte sedimentation rate (ESR), sex hormones

  3. Other x-rays - rule out other possible dx

  4. BMD - risk of fracture by comparing persons current degree of loss of bone density to typical density of a young adult
• Clinical manifestations of osteoporosis

  • Joint and bone pain
  • Bone deformities
  • Fractures
• Treatment of osteoporosis

  1. Slow down rate of calcium and bone loss

  2. Prevent further deterioration - increase Ca intake to 1,500mg/day, VD supplement to enable absorption of Ca, magnesium, weight-bearing exercise to slow bone loss, reverse demineralisation, decrease risk of falls
• Gout

  Complex, recurring, inflammatory arthritis - metabolic disorder characterised by acute exacerbation with long periods of remission, can progress to chronic gout
• Purine

  Natural chemical compounds found in food and produced in body, used for production of ATP and nucleic acids, uric acid major end product of purine metabolism - excreted by kidneys
• Classifications of gout

  • Primary - 90% cases, hereditary origin, dysfunction purine metabolism
  • Secondary - develops as result of other risk factors
  • Acute - sudden onset symptoms usually in peripheral joints, usually occurs at night - resolving in 2-10 days, 1-4 joints involved, exacerbation of big toe most common
  • Chronic - multiple joints, visible deposits of sodium urate crystals called tophi
• Pathophysiology of gout

  1. Accelerated purine synthesis or breakdown of poor uric acid secretion in kidneys

  2. Monosodium crystals deposited in renal interstitial tissues

  3. Crystals impair urine flow and accumulate in CT and cause IR

  4. Neutrophils die and release additional crystals, further damaging tissue and inflammation occurs