Musculoskeletal System Disorders

Introduction and Learning Outcomes

• Musculoskeletal system includes bones, joints, tendons, ligaments, bursae, and muscles.
• Integrated system where issues in one area can impact others.
• Example: Hip fracture affecting ligaments, tendons, muscles, nerves, and arteries.
• Learning Outcomes:
  • Apply knowledge of pathophysiology to deliver safe, patient-centered care.
  • Discuss and demonstrate systematic assessment, management, and evaluation of care.
  • Assess, plan, implement, and evaluate culturally relevant and age-specific interventions.
  • Use clinical reasoning to identify potential problems and implement appropriate interventions.
  • Discuss pharmacological options and nursing care considerations.
  • Identify interprofessional team members for managing musculoskeletal disorders.

Resources

• Readings:
  • Brown, D. & Edwards, H. (2023). Lewis's Medical-Surgical Nursing (6th edition). Elsevier. Chapter 62: Nursing Management: Musculoskeletal trauma and orthopaedic surgery
  • Craft, J. & Gordon, C. (2022). Understanding Pathophysiology: ANZ edition (4th edition). Elsevier. Chapter 20: The structure and function of the musculoskeletal system; Chapter 21: Alterations of musculoskeletal function across the life span
  • Burchum, J. & Rosenthal, L. (2021) Lehne's Pharmacology for Nursing Care (11th edition). Elsevier. Chapter 31: Opioids Analgesics, Opioid Antagonists, and Nonopioid Centrally Acting Analgesics; Chapter 77: Drug Therapy for Gout
  • Tollefson, J. & Hillman, E. (2025) Clinical Psychomotor Skills (9th edition). Cengage. Chapter 24: Focused musculoskeletal health history and physical assessment and range of motion exercises

Musculoskeletal Facts

• Musculoskeletal disorders place a large burden on society and the healthcare system.
• Nurses have a high incidence of back pain, emphasizing the importance of self-care to prevent injuries.

Revision (Optional)

• Review anatomy and physiology of the musculoskeletal system.
• Musculoskeletal System Overview:
  • Bones: Rigid frame, anchor points for organs (e.g., thoracic cavity for heart and lungs).
  • Bone Marrow: Red marrow produces red blood cells; yellow marrow forms fat reserves.
  • Muscles: Allow movement (articulation) through contraction and relaxation.
  • Tendons: Attach muscles to bones.
  • Ligaments: Attach bones to each other.
  • Cartilage: Smooth surface for bones to glide over each other.

Degenerative Disc Disease

• Back pain is a common health problem in Australia, especially lower back pain.
• Effects of back pain:
  • Mental health impact (anxiety, depression).
  • Leading cause of activity limitation and work absence.
  • Difficult to find the right treatment.
  • Leading cause of health system expenditure.
• Upper Back Pain:
  • Pain from the base of the neck to the thoracic region.
  • Risks: Sedentary lifestyle, prolonged sitting, poor posture, obesity, stress, smoking, pregnancy, prior injuries, frequent heavy lifting.
  • Causes: Herniation of intervertebral discs, ligament sprain, overuse of muscles, osteoarthritis, kyphosis.
• Lower Back Pain (MOST COMMON):
  • Pain in the lumbar region.
  • Risks: Poor muscle tone, sedentary lifestyle.
  • Causes: Lumbosacral sprain, instability of lumbosacral bony mechanisms, osteoarthritis, degenerative disc disease, herniation of intervertebral discs.
• Acute Back Pain:
  • Lasts less than 4 weeks.
  • Causes: Trauma or spinal stress.
  • Symptoms: Muscle ache, spasms, shooting or stabbing pain, poor range of movement, difficulty weight-bearing, difficulty standing straight.
• Chronic (Persistent) Back Pain:
  • Lasts more than 3 months or repeated incapacitating events.
  • Causes: Previous injury, chronic strain, congenital abnormalities, degenerative disorders (arthritis, degenerative disc disease, osteoporosis).
• Degenerative Disc Disease (DDD) is a leading cause of lower back pain.

What is Degenerative Disc Disease?

• Intervertebral discs provide shock absorption, allow movement, and protect joints.
• DDD involves deterioration and herniation of these discs, occurring with aging.
• Locations: Cervical, thoracic, and/or lumbar regions.
• Causes: Structural degeneration.
• Risk Factors:
  • Advancing age.
  • Family history/genetics.
  • Excessive strain (heavy lifting, repetitive movement).
  • Sedentary lifestyle, poor posture.
  • Smoking.
  • Obesity.
• Diagnosis:
  • Past medical/surgical history.
  • Clinical presentation (recent/current clinical manifestations).
  • Focused musculoskeletal system assessment, falls risk, and pressure injury risk assessments.
  • Radiological imaging (X-rays, CT scans, MRI scans).
• Complications:
  • Chronic debilitating pain.
  • Incontinence.
  • Limb weakness.
  • Altered limb sensation.
  • Herniated discs.
  • Osteoarthritis.
  • Bone spurs.
  • Reduced mobility.
  • Spinal canal/cord compression.
  • Spinal stenosis.
• Treatment:
  • Conservative: Supportive care, limiting spinal movement (spinal brace/corset/belts), improving mobility (exercises), pharmacological management (NSAIDs, corticosteroids, analgesia, opioids (short-term only), tricyclic antidepressants, anticonvulsants).
  • Surgery: Microdiscectomy, laminectomy, hemilaminectomy, laminotomy, discectomy, or foraminotomy; considered a last option for severe nerve root and spinal cord damage.

Clinical Manifestations

• Back pain can be classified as:
  • Localized: Pain on palpation.
  • Diffuse: Pain spread over a large area.
  • Radicular: Irritation of the nerve root (e.g., sciatica).
  • Referred: Pain originating in another area (e.g., kidneys, abdomen).
• Clinical manifestations of DDD:
  • Radiculopathy: Altered sensation and motor responses due to nerve pressure.
  • Cervical radiculopathy: Pain in shoulders, arms, hands.
  • Lumbar radiculopathy: Pain in hips, buttocks, posterior legs; can be continuous (mild to moderate) or severe, sharp, sudden, intense, stabbing, or hot; eases with position changes; increases with prolonged sitting, bending, twisting, or heavy lifting.
  • Spinal instability: Sensation of spine 'giving out,' locking up, or 'seizing.'
  • Altered lower limb sensation and decreased motor function.
  • Loss of spinal flexibility, bone spurs, muscle spasms/tension, and spinal deformity.

Osteoporosis

• Metabolic bone disease characterized by decreased bone density and loss of structural integrity.
• Cortical bone becomes weaker, thinner, and more porous.
• Risk Factors:
  • Genetics.
  • Advancing age (>65 years, especially with endocrine disorders or malignancies).
  • Hormonal changes (estrogen, calcitonin, testosterone).
  • Gender (higher risk for women).
  • Poor nutritional status (low calcium and vitamin D intake, excessive sodium, low magnesium, high caffeine intake).
  • Decreased sun exposure.
  • Lifestyle choices (caffeine, smoking, alcohol).
  • Medications (corticosteroids, heparin, thyroid hormone therapy, aluminum-containing antacids).
  • Comorbidities (obesity, anorexia nervosa, hyperthyroidism, kidney failure).
• Types of Osteoporosis:
  • Generalized: Involving major portions of the axial skeleton.
  • Regional: Involving one segment of the appendicular skeleton.
• Diseases Associated with Osteoporosis:
  • Inflammatory Bowel Disease (IBD).
  • Intestinal malabsorption.
  • Kidney disease.
  • Rheumatoid arthritis.
  • Diabetes Mellitus.
  • Cirrhosis of the liver.
  • Hyperthyroidism.
  • Hypogonadism.
• Diagnosis:
  • Past medical history.
  • Clinical presentation.
  • Investigations: Routine radiographs (may be undetected until 25-40% demineralization), Dual-energy X-ray absorptiometry (DEXA) scan, pathology/laboratory results, other X-rays; Bone Mineral Density (BMD) testing.
  • DEXA scan: Results presented as a T-score; fracture risk doubles with each reduction in T-score.
• Complications:
  • Disability.
  • Pathological fractures (especially in the thoracic and lumbar spine, neck, intertrochanteric region of the femur and wrists).
• Prevention:
  • Lifestyle modification: Balanced diet with high calcium and vitamin D, calcium supplements (with vitamin C), regular weight-bearing exercises, avoid excessive alcohol intake, smoking cessation, and adequate sun exposure.
• Treatment:
  • Slow down calcium and bone loss.
  • Prevent further deterioration.
  • Increase dietary calcium (1,500 mg/day).
  • Increase Vitamin D intake with supplements.
  • Increase magnesium intake.
  • Decrease phosphorus intake.
  • Weight-bearing exercises to slow bone loss, reverse demineralization, and increase bone strength.

Pathophysiology

• Bone remodeling involves bone formation by osteoblasts and bone resorption by osteoclasts in a balanced state.
• Bone formation = osteoblasts (building cells), controlled by hormones, cytokines, and chemical messengers.
• Bone resorption = osteoclasts (destroying cells)
• Peak bone mass is reached between 20-40 years; age-related bone loss starts thereafter.
• Step-by-step pathophysiology:
  • Cytokine binds to osteoclast precursor cell receptors.
  • Osteoclast precursor cells multiply and become activated.
  • Bone matrix creates a decoy receptor for the cytokine.
  • Homeostatic balance is required between cytokines, decoy receptors, and osteoclast precursor receptors.
  • Imbalance leads to increased bone resorption over bone formation, resulting in weak, brittle, fragile, and porous bones.

Clinical Manifestations

• Onset is insidious, often occurring once the disease has advanced.
• Common clinical manifestations:
  • Joint and bone pain.
  • Bone deformities.
  • Fractures (long bones, distal radius, ribs, vertebrae, neck of femur).
  • Kyphosis.
  • Diminished height.
  • Low energy, fatigue.
• Rare clinical manifestations:
  • Fat embolism.
  • Pulmonary embolism.
  • Pneumonia.
  • Haemorrhage.

Arthritis

• Inflammatory joint disease affecting over 15% of the population; rates increase with age, mainly in women over 75.
• Over 100 different types exist, including osteoarthritis, rheumatoid arthritis, and gout.
• Risk Factors:
  • Non-modifiable: Advanced age, genetics, existing endocrine disorders.
  • Modifiable: Occupation (load-bearing), obesity, smoking, excessive alcohol intake, poor diet, sedentary lifestyle.
• Types of Arthritis Based on Causes:
  • Infectious: Joint invasion by bacteria, mycoplasma, viruses, fungi, protozoa through traumatic wounds invasive procedures, or bloodstream transfer.
  • Non-Infectious:
  • Inappropriate immune response (rheumatoid arthritis, psoriatic arthritis).
  • Deposition of urate crystals in the synovial fluid (gout).

Osteoarthritis

• Disease process rather than a specific illness; most prevalent and disabling joint disorder.
• Leading cause of pain and disability in the elderly.
• Degenerative joint changes occur in 90% of the population by age 40.
• Affects more women than men.
• Classifications:
  • Primary/secondary, localized/generalized, early/moderate/advanced
• Causes:
  • Post-inflammation disorders (rheumatoid arthritis, septic joint).
  • Trauma (fracture, dislocation, ligament/meniscus injury).
  • Cumulative occupation or recreational trauma/mechanical stress.
  • Anatomical or bony disorders (hip dysplasia, avascular necrosis, Paget's disease).
  • Metabolic disorders (calcium crystal deposition, acromegaly, Wilson's disease).
  • Menopause (due to estrogen reduction).
• Risk Factors:
  • Obesity. Previous joint damage/trauma. Anatomical deformity. Genetic predisposition.
• Pathophysiology:
  • Articular cartilage degradation, bone stiffening, and reactive inflammation of the synovium.
  • Collagen matrix becomes disorganized and proteoglycan content is lost.
  • Progressive loss of articular cartilage.
  • Osteophytosis (new bone formation of the joint margin) leads to subchondral bone changes with a variable degree of synovitis.
  • Clinical manifestations develop due to contact between exposed bony joint surfaces.
• Clinical Manifestations:
  • Usually manifest after age 50.
  • Pain (mild discomfort to severe disability).
  • Joint stiffness (most commonly experienced in the morning for less than 30 minutes and worse after periods of inactivity / static inactivity)
  • Crepitus with movement.
  • Asymmetry of joints.
  • Joint effusions and deformity.
  • Functional impairment.

Rheumatoid Arthritis

• A chronic systemic, autoimmune disease where there is inflammation of the connective tissue in synovial joints.

• Affects multiple joints, usually bilaterally (e.g., both hands or both knees).

• Characterized by periods of remission with exacerbations.

• Prevalence increases with age and is more common in women; worse in colder climates.

• Can also affect other tissues in the body such as lungs, heart, and eyes.

• Classifications:

  • Number of joints involved, serology inflammatory markers, duration of symptoms.

• Causes:

  • Likely linked with genetics and environmental triggers interactive with inflammatory mediators.

• Risk Factors:

  • Advancing age, smoking, gender (females), history of live births, obesity, stress, genetics, infection, surgery.

• Pathophysiology:

  • Affects the synovial membrane first, before spreading to articular cartilage, fibrous joint capsule, and surrounding ligaments and tendons.
  • Inflammatory Phase:
  • Initial immune response triggers formation of abnormal immunoglobulin G (IgG).
  • Autoantibodies called rheumatoid factor (RF) develop and combine with IgG to form immune complexes.
  • Inflammatory response initiates phagocytes to ingest these immune complexes.
  • Release of enzymes causes cartilage breakdown and thickening of synovial lining.
  • T-helper cells are activated which produces more RF.
  • Synovium continues digesting nearby cartilage which further stimulates the inflammatory response
  • Secondary Phase:
  • Synovial membrane thickens increasing pressure on vessels and compromising blood supply.
  • Hypoxaemia and metabolic acidosis result which stimulates the release of enzymes from synovial cells into surrounding tissue.
  • Tissues breakdown, articular cartilage erodes, ligaments / tendons are inflamed.
  • Haemorrhage and coagulation of the synovial membrane, fibrin deposits on synovial membrane, and in synovial fluid.
  • Granulation and scar tissue formation, leading to immobilisation and joint stiffness.

• Clinical Manifestations:

  • Insidious, gradual onset with generalized, systemic clinical manifestations:
  • Fever, fatigue, malaise, rash, anorexia, weight loss, generalized aching and stiffness.
  • Later onset of localized clinical manifestations:
  • Joint pain and tenderness (increases with movement).
  • Joint stiffness (especially following activity).
  • Joints become warm-to-touch, swell and deform.
  • Loss of dexterity, disability.
  • Elevated serum leukocyte levels and serum fibrinogen levels.

• Complications:

  • Osteoporosis (OA), Rheumatoid nodules, Dry eyes/mouth, Infections, Carpal Tunnel Syndrome, Lung Diseases, Cardiac Diseases such as premature heart disease.

Gout

• Gout is a complex, recurring, inflammatory arthritis.
• Disruption of the body's control of uric acid production or excretion.
• Affects men more than women, with a peak affected age between 40 - 60 years for men, but later years for women
• Classifications of Gout:
  • Primary (90% of Gout cases): Hereditary origin, dysfunction of purine metabolism.
  • Secondary: Gout develops as a result of other risks factors.
  • Acute: Sudden onset of symptoms, usually in the peripheral joints.
  • Chronic: Multiple joints involved, visible deposits of sodium urate crystals called tophi.
• Causes:
  • Increase in uric acid production
  • Decrease in uric acid excretion
  • Increase in consumption of food / drinks containing high levels of purine e.g., seafood, shellfish, alcohol, sugary drinks.
• Risk Factors:
  • Medications: Those that increase cell death e.g., chemotherapy, Thiazide diuretics, Aspirin, Immunosuppressants.
  • Obesity, trauma, post-menopausal women
  • Comorbidities: Particularly hypertension, Diabetes Mellitus, hyperlipidaemia, sickle cell anaemia, renal disorders, atherosclerosis, cancer.
• Pathophysiology:
  • Closely related to purine metabolism and kidney function.
  • Purines are natural chemical compounds found in food and produced in the body. Examples include adenine and guanine, Used for the production of ATP and nucleic acids.
    • Uric acid is the major end produce of purine metabolism → excreted by the kidneys Urate is filtered at the glomerulus → reabsorbed or excreted in urine
  • Those with a history of gout will have either: Accelerated purine synthesis OR Breakdown or poor uric acid secretion in the kidneys
  • One or more of the aforementioned causes in conjunction with increased urate reabsorption OR sluggish urate excretion by the kidneys means monosodium urate crystals are deposited in renal interstitial tissues.
• Aggravating Mechanisms for Crystal Deposition
  • Low body temperature Decreased albumin or glycosaminoglycan levels
  • Changes in ion concentration
  • Changes to pH
  • Trauma
• Stages of Crystal Deposition
  • Asymptomatic hyperuricaemia: serum urate is elevated but arthritic symptoms, tophi, and renal complications are not present
  • Acute gouty arthritis: exacerbation of symptoms with elevated serum urate concentration, occurs with sudden or sustained increase in urate levels, can also occur with medications, alcohol, or trauma
  • Tophaceous gout: chronic stage; tophi appear in cartilage, synovial membranes, tendons, and soft tissue
• Clinical Manifestations:
  • Acute:
  • Joint changes: Dusky / erythematous appearance, Sudden swelling, Excruciating pain, Hot-to-touch, Decreased range of movement, Difficulty weight-bearing
  • Systemic signs of inflammation:
    • Low-grade fever, Lymphadenopathy → enlarged, swollen lymph nodes.
  • Chronic:
  • Lingering joint discomfort, Limited range of movement, Slowly progressive disability Chronic joint inflammation
• Complications:
  • Kidney dysfunction, Acute Kidney Injury (AKI), Kidney stones, Pyelonephritis.
  • Tophi (see image below) = grotesque deformities, usually painless, but can lead to additional complications:
  • Large clumps may perforate through the overlying skin causing wound infections.
  • Progressive stiffness and movement limitations Persistent aching Nerve compressions → carpal tunnel

Septic Arthritis

• Septic arthritis is an infectious arthritis caused by the invasion of a bacteria into the joint cavity.
• Bacteria travels throughout the body in the bloodstream and deposits in any joint cavity This process is referred to as haematogenous seeding
• Usually monoarthritic (affecting one joint only)
• Considered a medical emergency due to the high risk of serious complications
• Causes
  • Active infection elsewhere in the body → bacteraemia (bacteria in the bloodstream) e.g) Cellulitis, urinary tract infection (UTI), Upper or Lower respiratory tract infection (URTI, LRTI), osteomyelitis, Sexually Transmitted Infection (STI)
  • Trauma
  • Surgical incisions and procedures: Arthrocentesis, joint injections
  • IV drug use
• Bacteria Causes Septic Arthritis
  • Staphylococcus aureus (most common: 50% of cases, especially if the line of infection came from IV drug use)
  • Streptococcus haemolyticus
  • Neisseria gonorrhoeae (especially if the line of infection came from an STI)
  • Salmonella
• Risk Factors
  • ImmunocompromiseRecent Infection: Cellulitis, skin ulcers, bacteraemia
  • Medications: Corticosteroids, immunosuppressants
  • Pre-existing joint disease, especially RA Previous joint replacement or prosthesis
• Pathophysiology
  • The pathophysiology of septic arthritis is multifactorial and is directly related to the cause, the pathogen, and the patient's immune response
• Clinical Manifestations:
  • Single joint with severe pain, worse with movement Poor range of movement Effusion
  • Symptoms of inflammation → erythematous and swollen joint, hot-to-touch
  • Symptoms of infection → fevers, rigours, lethargy, myalgia, tachycardia, weight loss
• Complications
  • Septic arthritis can cause irreversible cartilage destruction within 8 hours.
  • If left untreated, septic arthritis can progress from a localised infection → septicaemia → sepsis → death (10 - 20% mortality rate). Avascular necrosis

Psoriatic & Inflammatory

• A chronic, immune-mediated inflammatory joint disorder.
• 1 in 5 affected will have a history of psoriasis Part of a group of joint disorders called seronegative spondyloarthropathy
• Can be an oligoarthritis → a chronic, inflammatory arthritis of unknown origin affective <5 joints, with an onset that occurs <6 years of age and lasts for approximately 6 weeks
• What is Psoriasis?
  • Psoriasis is also a chronic autoimmune disorder characterised by the rapid build up of skin cells that form patches of scaly, itchy, dry skin. These patches will be red or silvery
• Types of Psoriatic Arthritis:
  • Symmetric, Asymmetric, Distal, spondylitic, Arthritis mutilans
• Causes
  • While the main cause is unknown, there is a strong genetic link combined with immune and environmental factors e.g) trauma and frequent / certain bacterial infections.
• Clinical Manifestations:
  • Insidious, gradual onset with generalised, systemic clinical manifestations:
  • Joint inflammation → swollen, stiff, painful, erythema, joints are hot-to-touch
  • Skin changes → from psoriasis, skin can develop plaques.
  • Lower back pain Onycholysis → separation of the nail
  • Dactylitis → inflammation and swelling of full digits / fingers
  • Enthesitis → inflammation and pain of point where tendon joins to bone e.g) heel
• Complications
  • Pencil-in-a-cup' deformity of the distal joints in fingers.
  • PsA-Associated Comorbidities: Psoriasis, Systemic Lupus Erythematosus (SLE), Crohn's Disease and ulcerative colitis, Coronary heart disease, Depression.
• Inflammatory Arthritis:
  • Is a group of diseases that results in joint inflammation, swelling, stiffness, decreased range of movement with potentially disabling clinical manifestations.

Nursing Assessment and Management of MSK Conditions

• Can be similarities in the nursing assessment and management of patients with Musculoskeletal disorders.
• Patient comes in perform primary assessment secondary assessment and vital signs.
• Important to note that there may be limited variation in the vital signs due to these MSK disorders, regardless of what the patient has presented with
• Focused Musculoskeletal System Assessment.
  • Inspection - general build, muscle configuration and symmetry of joints. Any swelling, nodules, masses, deformity and bilateral discrepancies.
  • Palpation - with care. Assessing for skin temperature, tenderness, swelling and crepitation.
  • Motion - Range of movement - passive or active
  • Strength - flexion and extension, comparing bilaterally.
  • Measurement - assessing discrepancies in length and/or circumference.
  • Other - posture and gait, use of mobility aids, e.g, straight leg raise test and leg raise test.
• Focused Neurovascular System Assessment: peripheral pulses, capillary refill and colour, warmth, movement and sensation (CWMS)
• Additional Focused System Assessments:
  • Pain assessment, Falls Risk assessment (), Pressure injury risk assessment ()
  • Integumentary assessment, Dermatome assessment, Assessing for any paraesthesia e.g., weight loss, smoking cessation. Minimize alcohol consumption Pain management strategies, dietary advise and education
• Nursing Management aims to conserve mobility and pain management. Conserving mobility enhances an individual's quality of life.
  • Non-pharmacological Management: Reposition patient, Distraction techniques, Heat, ice packs, Assistance with Activities of Daily Living (ADLs) and light physical activity.
  • Explanation of condition and management plan
• Falls Prevention - Practical implications of preventing fractures is limiting the risk of falls when the patient is admitted to hospital

MSK Injuries - Fractures

• A fracture is a break in the continuity of a bone when force exceeds bone's capacity to absorb.
• Severity depends on location and fracture subtype.
• Average person experiences two fractures in their lifetime.
• In medical notes, a fracture is often written as '#' eg) Left Femur #

Classification and Types

• Classification system aims to organize knowledge, guide treatment, estimate prognosis, and improve communication.
• Fractures are classified by:
  • Location eg) femur fracture
  • Displacement of fracture lines Appearance of the limb eg) dinner fork deformity
  • Which part of the bone is fractured Fracture pattern eg) anatomical alignment of bone fragments
  • Severity of overall injury eg) stable vs unstable
• Main Fracture Categories:
  • Displaced: Bone breaks in two or more parts and shifts so that the ends do not align anymore
  • Non-displaced: Bone breaks either part or all of the way through but does not move and maintains proper alignment
  • Open: Bone breaks through the skin
  • Closed: No break/ puncture would through the skin
• Subtype Fracture Categories:
  • Paediatric Nursing ONLY🚸: Greenstick, Buckle
  • Comminuted, Oblique, Spiral, Transverse, Compression, Impacted, Pathological, Stress, Avulsion
    -Hip Fracture:
  • A break occurring at the upper third (proximal) of the femur, which extends 5 cm below the lesser trochanter.
  • Commonly referred to as a ''fractured NOF'' or #NOF where NOF stands for ''Neck of Femur''
  • Patient frequently has comorbidities exacerbated by age-related factors.
• Causes of Fractures
  • Trauma, Overuse, Pathological where there are underlying diseases processes
• Risk Factors:
  • Younger population = sustain more trauma-related injuries
  • Older population have muscle deterioration and general frailty
  • Conditions that produce decreased cerebral arterial perfusion, osteoporosis, diabetes mellitus, rheumatoid arthritis, coeliac disease, inflammatory bowel disease
• Complications
  • Direct: Osteomyelitis, Delayed, non-union, or malunion of the fracture, Permanent disability
  • Indirect:
    • Soft tissue injury, Adverse reaction to internal fixation devices Complex Regional Pain Syndrome (CRPS)
    • Compartment Syndrome, Rhabdomyolysis, Amputation Deep Vein Thrombosis (DVT) Pulmonary embolism Fat embolism Sarcoma
• Prevention Consume adequate amounts of Calcium and Vitamin D, healthy amounts of exercise, Minimize alcohol intake, Cease smoking and Avoid misadventure and avoid falls

Pathophysiology

• Pathophysiology is determined according to bone strength and the frequency and effects of injuries.
• Force exceeds what bone can absorb.
• Regardless of the cause, fracture pathophysiology disrupts periosteum, cortex, blood vessels, marrow, and surrounding soft tissue.
• Bleeding occurs from damaged ends of the bone and surrounding soft tissue; blood loss can be extreme and life-threatening.
• Approximate blood loss:
  • Humerus #: 200 - 300 mLs blood loss
  • Femur #: 500 - 1000 mLs blood loss
  • Pelvis #: 1000 - 1500 mLs blood loss
• Bone healing commences in three phases:
  • Inflammatory phase (0 - 2 weeks): Bleeding occurs and a fracture hematoma forms.
  • Reparative phase (2 - 6 weeks): Capillary network forms, granulation tissue develops, and bone callus is created.
  • Remodeling phase (>6 weeks, several months): Gradual spread of callus and creation of compact and cancellous bone structures.
• Factors Affecting Bone Healing
  • Complexity or type of fracture
  • Displacement
  • Comminuted Compound
  • Genetics
  • Advancing age
  • High alcohol consumption, Smoking , Illicit drug use
  • Medication -Comorbidities
  • Hormones, Inflammation / Infection elsewhere in the body or secondary to fracture
  • Blood supply to area
• Complications of fracture healing:
  • Delayed union, Non-union, Malunion, Angulation, Pseudoarthrosis, Re-fracture, Myositis

Clinical Manifestations

• Clinical manifestations vary from mild to severe.
• Immediate localized pain/tenderness.
• Swelling Paraesthesia Bruising
• Deformity (not always present).
• Muscle spasms Loss of function Crepitation Guarding
• Hip Fractures:
• Pain: Hip and groin or in the medial side of the knee, Abducted with external rotation

Medical Management

MEDICAL TREATMENT: Surgery on fractured bone

• Reduction of the fracture
  • Closed #: non-surgical
  • Open #:surgical incision with either
• Immobilisation
  • Casting
• Traction
  • Skin: short-term
  • Skeletal:longer-term
• Open fractures require additional treatment to prevent infection

Musculoskeletal Injuries- Sprains & Strains

• Injury types include sprains, strains, tendonitis, contusions, bursitis
• Sprains: occur in response to a tear or the stretching of a ligament surrounding a joint
• Strains: occurs in reaction to a tear, twist, or excessive stretch of a muscle, its muscle sheath and / or its tendon

Pathophysiology

• Grade I - mild stretching of the ligament (only a few fibres torn) without joint instability.
• Grade II - partial tear (rupture) of the ligament but without joint instability (or with mild instability).
• Grade III - a severe sprain: complete rupture of the ligament with instability of the joint.

Clinical Manifestions

- similar signs and symptoms for both sprains and strains
- pain / tenderness, swelling / oedema, ecchymosis ,contusion, altered sensation with severe oedema

Musculosketal Injuries- Nursing Assessment and Management

• Patients with musculoskeletal injuries can either be managed by their GP, or at the Emergency Department
  • obtain a thorough history and completion of assessments and observations, prior to implementing nursing interventions.
• Secondary Assessment
  • general appearance - Looks well vs unwell, comfortable vs any discomfort, skin colour: pale / pallor or redness / flushed face, sometimes patient's can be described as 'grey-looking' (very unwell)
  • Full set of vital signs,
• Focused Neurovascular Assessment
  • The 6 P's Observations to be performed on BILATERALLY to consider what is 'normal' for the patient
    • Pain, Pallor, Paralysis, Pulses, Capillary Refill Time (CRT), Swelling / Oedema