Musculoskeletal Flashcards
Define Acute Compartment Syndrome
‘an orthopaedic emergency resulting from elevated interstitial pressure within a closed fascial compartment resulting in microvascular compromise, most commonly in the leg, forearm or thigh which could lead to loss of function, limb or life’
Describe the pathology of Acute Compartment Syndrome
Increased Internal Pressure (Bleeding, Swelling)
Increased External Compression (Casts, Bandages)
Pressure within the compartment exceeds the pressure within the capillaries
Muscles become ischaemic and develop oedema through increased endothelial permeability
Necrosis begins in the ischaemic muscles after four hours
Ischaemic nerves become neuropraxic (loss of motor and sensory function)
This may recover if relieved early, however permanent damage may result after only four hours
In the later stages, there is a compromise of the arterial supply
Describe the clinical features of Acute Compartment Syndrome
Pain (out of proportion to that expected from the injury and on passive stretching of the compartment)
Pallor
Paraesthesia
Paralysis
Pulselessness
Swelling
Shiny Skin
Autonomic Response - Sweating, Tachycardia
Reduced Consciousness Level
Describe the management of Acute Compartment Syndrome
Open any constricting dressings/bandages
Surgical Release:
Full length decompression of all compartments
Excise any dead muscles
Leave wounds open
Repeat debridement until pressure is down and all dead muscle has been excised
Later, close the wound and graft the skin if needed
Define Tendinopathy
‘chronic tendon injury of over use due to repetitive loading, characterised by degeneration and disorganisation of collagen fibres, increased cellularity and only little inflammation’
Describe the pathology of Tendinopathy
Tendinopathy is likely not an inflammatory process
Deranged collagen fibres and degeneration with a scarcity of inflammatory cells
Increased vascularity around the tendon
Failed healing response to micro-tears
Inflammatory mediators including IL-1, NO and Prostaglandins are released which cause apoptosis, pain and provoke degeneration through release of Matric Metalloproteinases
Describe the management of Tendinopathy
Pharmacological:
NSAIDs
GTN Patches
PRP Injection
Prolotherapy
Steroid Injection
Non-Pharmacological:
Activity Modification
Physiotherapy
Extracorporeal Shockwave Therapy
Radiofrequency Coblation
Operative Management:
Debridement
Excision of Diseased Tissue
Describe the presentation, diagnosis and management of large vessel vasculitis
- Takayasu’s Arteritis
- Pulseless disease or aortic arch syndrome
- Systemic features include fever, malaise, night sweats, weight loss, myalgia, arthralgia and fatigue
- Late features include bruits, absent/reduced pulses, claudication, ischaemic heart disease, headaches, BP variability
- Diagnosed by CT/MR Angiography
- Managed with Prednisolone for all patients, and further immunosuppression (e.g. methotrexate) in some
- Giant Cell (Temporal) Arteritis
- Presents with scalp tenderness, jaw claudication, fatigue and headache
- Diagnosed by high ESR or biopsy
- Managed with PO Prednisolone
Describe the presentation, diagnosis and management of medium vessel vasculitis
- Polyarteritis Nodosa
- Severe systemic manifestations with fibrinoid necrosis of the vessel wall with microaneurysm formation, thrombosis and infarction
- Systemic features include fever, weight loss, malaise, myalgia and arthralgia
- Associated with infarction and ischaemia of organs including the gut, brain, heart, liver, skin, PNS, limbs and kidneys
- Investigated with CRP/ESR and CT/MR angiography and biopsy
- Treated with PO/IV Prednisolone with or without DMARD
- Kawasaki Disease
- Vasculitis of young children characterised by aneurysm formation in medium to large sized arteries, including the coronary, axillary, iliac and popliteal arteries
- Early features include high fever, mucositis and conjunctivitis
- Late features include (fatal) aneurysms
- Investigated with bloods, USS of testes and gallbladder and lumbar puncture
- Managed with IV immunoglobulin or methylprednisolone plus aspirin
Describe Henoch-Schonlein Purpura
An immune complex mediated small vessel vasculitis
Most common vasculitis in childhood
Characterised by deposition of IgA
Diagnostic triad of palpable purpura, abdominal pain and arthritis
Investigations include urinalysis, IgA levels, U&Es
Treated with analgesics only if simple
If renal involvement, add corticosteroids and/or immunosuppressants
Describe ANCA associated small vessel vasculitis
cANCA or pANCA
Granulomatous Polyangiitis (classically involves the upper and lower respiratory tracts and kidneys)
Eosinophilic Granulomatous Polyangiitis - Churg-Strauss (Associated with eosinophilia, asthma, eosinophil-rich granulomata, peripheral neuropathy, pulmonary infiltrates)
Microscopic Polyangiitis (common manifestations are glomerulonephritis, weight loss, skin lesions, peripheral neuropathy, fever)
Investigations include ANCA, CT Chest, biopsy, bloods and urinalysis
Corticosteroid and Cyclophosphamide/Methotrexate
Describe the presentation and investigations of secondary bone tumours
Found in up to 60% of patients dying from cancer
Most often from the bronchus, breast, prostate, kidney and thyroid
Bones with a good blood supply are most often affected, including the long bones and vertebrae
Effects include bone pain, destruction and hypercalcaemia
May result in pathological fractures in the long bones
In the vertebrae there may be vertebral collapse, spinal cord/nerve root compression and back pain
Investigated with MRI and/or PET-CT
Describe the difference between lytic and sclerotic metastatic bone lesions
- Lytic
- Most common
- Tumour replaces bone marrow
- Tumour cells produce cytokines which activate bone resorbing osteoclasts
- These patients are therefore more prone to pathological fracture
- Bisphosphonates inhibit bone resorption so can be used to treat this
- Sclerotic
- Thickening of the bone
- Most common cause is Prostate CA but also seen in breast carcinoma
- Tumour cells promote deposition of immature woven bone by osteoblasts
- Appears sclerotic (thickened and white) on x-ray
Describe myeloma, its presentation and management
Most common malignant primary bone tumours
Monoclonal proliferation of plasma cells
Effects include:
Bone Lesions (generalised osteopenia and punched out lytic foci)
Marrow Replacement (anaemia, leukopenia, thrombocytopenia and pancytopenia)
Diagnosed by Immunoglobulin Excess (ESR >100, Serum Electrophoresis and Urine Bence Jones Protein), Biopsy and Pepper Pot Skull on X-Ray
High dose chemotherapy with a bortezomib regimen and autologous SCT
Describe benign tumours of the bone
Osteoid Osteoma
Small, benign osteoblastic proliferation
Common in any age, especially adolescents
Can affect any bone, including long bones and spine
C/F include pain (worse at night, relieved by aspirin) and may cause scoliosis
Managed with analgesia and surgical resection
Describe malignant tumours of the bone
Osteosarcoma; a malignant tumour with cells arising from osteoid or bone and a peak age of 10-25yrs. Highly malignant with early lung metastases
Chondrosarcoma; central, within the medullary canal or peripheral on the bone surface. Predominantly affects middle-aged and elderly, more commonly men
Ewing’s Sarcoma; Peaks at 5-15yrs, usually in the diaphysis/metaphysis of the long bones or flat bones of the limb girdles. Early metastases to lung, bone marrow and bone
Describe septic arthritis, its presentation, investigation and management
‘inflammation of the synovium due to pathogenic inflammation of the joint’
Common organisms include Staph. Aureus, Neisseria Gonorrhoea and Haemophilus Influenzae
Presents with a hot, red, swollen and painful joint
Investigations include joint aspirate, blood cultures and FBC
Manage with IV antibiotics for 1-2 weeks (Flucloxacillin or Erythromycin)
Describe reactive arthritis, its presentation and management
‘sterile inflammatory synovitis occurring following an infection’
Trigger organisms include salmonella, shigella, yersinia and chlamydia trachomatis
Preceding illnesses include gastroenteritis, urethritis and chlamydia infection
Presents with acute, asymmetrical lower limb arthritis, days to weeks after the initial infection
Also associated with enthesitis, sacroiliitis, spondylitis, anterior uveitis, conjunctivitis, keratoderma blemorrhagica
Managed with analgesia (NSAIDs or intra-articular steroids)
Usually self-limiting with occasional chronic progression or cardiac complications
Describe gout, its presentation and management
Excess levels of uric acid leads to deposition of urate crystals in joints or soft tissue
Commonly affects the big toe
Risk factors include obesity, diabetes, high alcohol consumption and high protein diet
Severely painful, red, hot, swollen joint
Investigate with aspirate or serum urate levels
Manage with NSAIDs, colchicine, corticosteroids or allopurinol
State indications for allopurinol in the prophylaxis of gout
Urate-lowering drug
Recommended for gout prophylaxis after one attack
Usually lifelong treatment
NSAID/Colchicine may need to be taken in conjunction for the first 4-6 weeks
Describe the investigation of a patient presenting with acute joint pain and swelling, as per BSR guidelines
All patients presenting with a hot, red, swollen, tender and restricted joint should be regarded as having septic arthritis until proven otherwise (even in the absence of fever)
Synovial fluid should be aspirated, gram-stained and cultured prior to antibiotics
Infected prosthetic joints should be referred to an orthopaedic surgeon
Blood cultures should be taken
ESR, WCC and CRP should all be measured
X-Ray should be conducted as a baseline
Describe the pathophysiology of osteoporosis
- Osteoporosis results from a cellular process imbalance, i.e. an increase in bone resorption by osteoclasts and decrease in bone formation by osteoblasts
- In younger patients, it is usually a decrease in bone formation, while in post-menopausal women, it is usually increased bone resorption
- Oestrogen Deficiency
- Oestrogen levels decrease greatly in females during the menopause
- This can cause increased osteoclast recruitment, differentiation and prolonged osteoclast survival
- This is achieved by increased activity of Interleukin-1 (increases production of osteoclasts) and Interleukin-6 (normally inhibited by oestrogen and secreted by osteoblasts to induce osteoclast formation)
- The RANK receptor is normally expressed on pre-osteoclasts, where binding of the RANK-Ligand causes differentiation to mature osteoclasts, while Osteoprotegerin (OPG) inhibits the RANK receptor
- Oestrogen deficiency causes increased RANK expression and decreased OPG secretion, resulting in increased osteoclast formation (i.e. increased bone resorption)
- Age Related
- The efficiency of calcium absorption in the intestines diminishes with age, meaning many elderly people are at risk of hypocalcaemia
- This can be worsened by a vitamin D deficiency, which reduces the amount of calcium that can be absorbed
- The efficiency of calcium absorption in the intestines diminishes with age, meaning many elderly people are at risk of hypocalcaemia
- The above factors cause low bone density and quality, leading to an increased fracture risk
State the role of DEXA scanning in osteoporosis and indications for its use
Measurement of bone mineral density
DXA scan should be offered to patients over the age of 50 with a history of fragility fracture, or to those under 50 with a major risk factor for fragility fracture
Major risk factors include frequent oral corticosteroid use, low BMI, premature menopause, hypogonadism, COPD, CKD, excess alcohol intake
T-Score (number of standard deviations below average BMD for a young female):
≥ -1 = Normal
-1 to -2.4 = Osteopenia
≤ -2.5 = Osteoporosis
Describe the mechanism of action of bisphosphonates
PO - Alendronate, Risedronate
IV - Zalendronate (Zoledronic Acid)
Bisphosphonates are absorbed into hydroxyapatite crystals on bone, thereby slowing their rate of growth and dissolution to reduce the rate of bone turnover
Alendronic Acid is given once weekly PO
Zoledronic Acid is given by a 6-monthly IV infusion
