MSK Flashcards
What is Osteoarthritis?
Osteoarthritis is often described as “wear and tear” in the joints. It occurs in the synovial joints and results from genetic factors, overuse and injury. Osteoarthritis is thought to result from an imbalance between cartilage damage and the chondrocyte response, leading to structural issues in the joint.
Commonly affected joints in osteoarthritis?
Hips
Knees
Distal interphalangeal (DIP) joints in the hands
Carpometacarpal (CMC) joint at the base of the thumb
Lumbar spine
Cervical spine (cervical spondylosis)
X ray changes seen in osteoarthritis
The four key x-ray changes in osteoarthritis can be remembered with the “LOSS” mnemonic:
L – Loss of joint space
O – Osteophytes (bone spurs)
S – Subarticular sclerosis (increased density of the bone along the joint line)
S – Subchondral cysts (fluid-filled holes in the bone)
X-ray reports might describe findings of osteoarthritis as degenerative changes. X-ray changes do not necessarily correlate with symptoms. A patient might have significant signs on an x-ray but minimal symptoms, or the reverse.
Presentation of osteoarthritis
Osteoarthritis presents with joint pain and stiffness. The pain and stiffness tend to worsen with activity and at the end of the day. This is the reverse of the pattern in inflammatory arthritis, where symptoms are worse in the morning and improve with activity. Osteoarthritis leads to deformity, instability and reduced function of the joint.
General signs of osteoarthritis are:
Bulky, bony enlargement of the joint
Restricted range of motion
Crepitus on movement
Effusions (fluid) around the joint
Signs of osteoarthritis in the hands
Heberden’s nodes (in the DIP joints)
Bouchard’s nodes (in the PIP joints)
Squaring at the base of the thumb (CMC joint)
Weak grip
Reduced range of motion The carpometacarpal joint at the base of the thumb is a saddle joint, with the metacarpal bone sitting on the trapezius bone, using it like a saddle. It gets a lot of use and is very prone to wear.
Dx of osteoarthritis
The NICE guidelines (2022) suggest that a diagnosis can be made without any investigations if the patient is over 45, has typical pain associated with activity and has no morning stiffness (or stiffness lasting under 30 minutes).
First line managament for osteoarthritis
Conservative management: Education and advice about their condition
Exercise: both muscle strengthening and general aerobic fitness
Weight loss (if overweight or obese)
Medical management
Non-pharmacological managament of osteoarthritis
Non-pharmacological management involves patient education and lifestyle changes, such as:
Therapeutic exercise to improve strength and function and reduce pain
Weight loss if overweight, to reduce the load on the joint
Occupational therapy to support activities and function (e.g., walking aids and adaptations to the home)
Stepwise management of osteoarthritis
First-line: topical non-steroidal anti-inflammatory drugs (NSAIDs)
Second-line: paracetamol and topical analgesia
Third-line: NSAID, paracetamol and topical capsaicin
Fourth-line: opioid, NSAID, paracetamol and topical capsaicin
Pharmacological management of osteoarthritis
Pharmacological management recommended by the NICE guidelines (2022) are:
Topical NSAIDs first-line for knee osteoarthritis
Oral NSAIDs where required and suitable (co-prescribed with a proton pump inhibitor for gastroprotection)
Weak opiates and paracetamol are only recommended for short-term, infrequent use. NICE (2022) recommend against using any strong opiates for osteoarthritis.
Intra-articular steroid injections may temporarily improve symptoms (NICE say up to 10 weeks).
Joint replacement may be used in severe cases. The hips and knees are the most commonly replaced joints.
Why do you have to be careful with NSAIDs with osteoarthritis tx?
NSAIDs (e.g., ibuprofen or naproxen) are very effective for musculoskeletal pain. However, they must be used cautiously, particularly in older patients and those on anticoagulants, such as aspirin or DOACs. They are best used intermittently, only for a short time during flares. They have several potential adverse effects, including:
Gastrointestinal side effects, such as gastritis and peptic ulcers (leading to upper gastrointestinal bleeding)
Renal side effects, such as acute kidney injury (e.g., acute tubular necrosis) and chronic kidney disease
Cardiovascular side effects, such as hypertension, heart failure, myocardial infarction and stroke
Exacerbating asthma
There is little evidence that opiates help with chronic pain. They are associated with side effects, risks, tolerance, dependence and withdrawal. They often result in dependence without any objective benefits.
Differentials for Osteoarthritis
Any joint: fracture, inflammatory arthropathies (such as rheumatoid arthritis), crystal arthropathies (such as gout), septic arthritis or malignancy
Knee: meniscal or ligamentous tears
Hip: bursitis, avascular necrosis
Hand: De Quervain’s tenosynovitis
What can be offered for the acute exacerbation of pain in osteoarthritis?
Intra-articular corticosteroid injection can be offered for acute exacerbation of pain despite regular use of the above analgesia. Typically, these are performed in an outpatient clinic environment. The injection consists of both a steroid and local anaesthetic, the latter providing immediate symptomatic relief to the patient for the first few hours. Patients may experience a worsening of symptoms for the first few days after administration, this is known as the ‘steroid flare’.
What is osteoporosis?
Osteoporosis involves a significant reduction in bone density.
What is osteopenia?
Osteopenia refers to a less severe decrease in bone density. Reduced bone density makes the bones weaker and prone to fractures.
What is the T score?
The World Health Organization (WHO) provide definitions based on the T-score of the femoral neck, measured on a DEXA scan. The T-score is the number of standard deviations the patient is from an average healthy young adult. A T-score of -1 means the bone mineral density is 1 standard deviation below the average for healthy young adults.
T score >-1
Normal
T score -1 to -2.5
Osteopenia.
T score < -2.5
Osteoporosis.
T score < -2.5 + fracture
Severe osteroporosis
How is Bone Mineral Density measured
Bone mineral density (BMD) is measured using a DEXA scan (dual-energy x-ray absorptiometry). DEXA scans are a type of x-ray that measures how much radiation is absorbed by the bones, indicating how dense the bone is. The bone mineral density can be measured anywhere on the skeleton, but the femoral neck reading is most important.
Bone density can be represented as a Z-score or T-score.
What is the Z score
The Z-score is the number of standard deviations the patient is from the average for their age, sex and ethnicity
Risk factors for osteoporosis
Older age
Post-menopausal women
Reduced mobility and activity
Low BMI (under 19 kg/m2)
Low calcium or vitamin D intake
Alcohol and smoking
Personal or family history of fractures
Chronic diseases (e.g., chronic kidney disease, hyperthyroidism and rheumatoid arthritis)
Long-term corticosteroids (e.g., 7.5mg or more of prednisolone daily for longer than 3 months)
Certain medications (e.g., SSRIs, PPIs, anti-epileptics and anti-oestrogens)
The NICE clinical knowledge summaries (April 2023) recommend assessing for osteoporosis in who?
Anyone on long-term oral corticosteroids or with a previous fragility fracture
Anyone 50 and over with risk factors
All women 65 and over
All men 75 and over
The 10-year risk of a major osteoporotic fracture and a hip fracture can be calculated using either:
QFracture tool (preferred by NICE)
FRAX tool (NICE say this may underestimate the risk in some patients)
Management of osteoporosis (without jumping to medications)
The first step is to address reversible risk factors. For example, increase physical activity, maintain a healthy weight, stop smoking and reduce alcohol consumption.
The second step is to address insufficient intake of calcium (less than 700mg per day) and inadequate vitamin D (e.g., limited sun exposure) with additional:
Calcium (at least 1000mg)
Vitamin D (400-800 IU)
What is the first line pharmacological tx for osteoporosis
Bisphosphonates are the first-line treatment for osteoporosis. They are recommended for patients with osteoporosis based on a DEXA scan. They are considered in patients on long-term steroids. They work by interfering with the way osteoclasts attach to bone, reducing their activity and the reabsorption of bone.
SE of bisphosphonates
Reflux and oesophageal erosions
Atypical fractures (e.g., atypical femoral fractures)
Osteonecrosis of the jaw (regular dental checkups are recommended before and during treatment)
Osteonecrosis of the external auditory canal
What’s the way to take bisphosponates?
Oral bisphosphonates are taken on an empty stomach with a full glass of water. Afterwards, the patient should sit upright for 30 minutes before moving or eating to reduce the risk of reflux and oesophageal erosions.
Give some examples (+doses) of bisphosphonates
Alendronate 70 mg once weekly (oral)
Risedronate 35 mg once weekly (oral)
Zoledronic acid 5 mg once yearly (intravenous)
What is the follow-up management for osteoporosis?
The NICE CKS (2023) recommend reassessing treatment with bisphosphonates after 3-5 years. They suggest a repeat DEXA scan and stopping treatment if the T-score is more than -2.5. Treatment is continued in high-risk patients.
Other specialist options for treating osteoporosis (where bisphosphonates are not suitable) include:
Denosumab (a monoclonal antibody that targets osteoclasts)
Romosozumab (a monoclonal antibody that targets sclerostin – a protein in osteocytes that inhibits bone formation)
Teriparatide (acts as parathyroid hormone)
Hormone replacement therapy (particularly in women with early menopause)
Raloxifene (a selective oestrogen receptor modulator)
Strontium ranelate (a similar element to calcium that stimulates osteoblasts and blocks osteoclasts)
Strontium ranelate increases the risk of ______ and _____.
venous thromboembolism ; myocardial infarction.
How does Raloxifene work?
Raloxifene stimulates oestrogen receptors in the bone but not in the uterus or breast. It increases the risk of venous thromboembolism.
Complications of osteoporosis
fragility fractures (hip, rib, wrist, vertebral), chronic pain, atypical fractures, osteonecrosis of the jaw, venous thromboembolism.
Mneumonic for causes of osteoporosis
SHATTERED FAMILY:
- S - steroid use (Other medications: SSRIs, PPIs, anti-epileptics and anti-oestrogens)
- H - hyperthyroidism, hyperparathyroidism, hypercalciuria
- A - alcohol & smoking - Smoking affects the body’s ability to absorb calcium
- T - thin (BMI<22)
- T - testosterone deficiency
- E - early menopause / post-menopause
- R - renal failure (e.g. CKD- causes long-term Vitamin D deficiency) or liver failure
- E - erosive/inflammatory bone disease (Myeloma, rheumatoid arthritis)
- D - diabetes, malabsorption (IBD, Coeliac)
- FAMILY History
What is Fibromyalgia?
Fibromyalgia syndrome (FMS) is a chronic disorder characterised by widespread musculoskeletal pain, often accompanied by fatigue, sleep disturbances, cognitive dysfunction, and mood disturbances
What is the type of pain in Fibromyalgia ?
The pain in FMS is described as nociplastic, which refers to pain that is “more widespread or intense, or both, than would be expected given the amount of identifiable tissue or nerve damage”. This type of pain is often associated with additional symptoms such as fatigue, sleep problems, and mood or memory disturbances.
Who does Fibromyalgia affect?
Fibromyalgia affects approximately 2% of the global population, with prevalence increasing during middle age (50-59 years) and declining in older adults (80+ years).
The average age of onset is between 30 and 50 years, with a female-to-male ratio of approximately 3:1 in studies that do not use tender points as a criterion
Causes of Fibromyalgia?
The physiological hallmark of FMS is central sensitisation, a phenomenon in which the central nervous system (CNS) exhibits an amplified response to sensory input. Clinically, this can be identified through diffuse tenderness to palpation.
Central sensitisation is an umbrella term encompassing various dysfunctions in ascending and descending neural pathways, resulting in heightened sensitivity to mechanical stimulation.
This amplified CNS signalling underpins many symptoms associated with FMS, including widespread pain and sensitivity to touch
Risk factors for fibromyalgia
Family history of chronic pain: the first-degree relatives of FM patients are 8 times as likely to have this condition
Environmental factors (stressors): early lifetime adverse events, medical illnesses (including infections), trauma, psychosocial stressors
Fibromyalgia is also commonly seen as a comorbidity in other chronic pain conditions such as osteoarthritis, rheumatoid arthritis, and systemic lupus erythematosus.
Typical symptoms of fibromyalgia
Widespread pain: the defining symptom, typically described as a persistent, dull ache affecting both sides of the body, above and below the waist
Tender points: 18 specific areas sensitive to touch or pressure, historically used in diagnosis, though modern criteria are less reliant on this
Fatigue and sleep disturbances: difficulty falling or staying asleep, often accompanied by non-restorative sleep, leaving patients feeling unrefreshed
Musculoskeletal stiffness: predominantly in the morning, improving throughout the day and unresponsive to corticosteroids (unlike other conditions)
Cognitive difficulties: issues with memory, concentration, and cognitive tasks
Irritable bowel syndrome (IBS): symptoms such as bloating, constipation, diarrhoea, and abdominal discomfort frequently co-occur
Environmental sensitivity: heightened intolerance to bright lights, loud noises, strong odours, and cold, possibly linked to central sensitisation
Differential Dx for fibromyalgia
Rheumatoid arthritis (RA): an autoimmune disease causing joint stiffness, pain, and swelling. Unlike fibromyalgia, RA pain is typically localised to specific joints and is associated with inflammation, visible on clinical examination and confirmed by blood tests (e.g. elevated inflammatory markers or rheumatoid factor).
Systemic lupus erythematosus (SLE): another autoimmune condition that can cause widespread pain, fatigue, and cognitive issues. However, SLE often involves additional systemic features such as skin rashes (e.g. butterfly rash), kidney involvement, and respiratory symptoms, which are not seen in fibromyalgia.
Multiple sclerosis (MS): a neurological disorder with many symptoms, including muscle weakness, coordination problems, and sensory disturbances (e.g. numbness or tingling). While MS can share fatigue and pain with fibromyalgia, distinctive features like visual disturbances (optic neuritis) and objective neurological findings on imaging (e.g. MRI) help distinguish it.
Chronic fatigue syndrome (CFS): characterised by profound, unrelenting fatigue not alleviated by rest. Shared symptoms with fibromyalgia include cognitive dysfunction, muscle pain, and headaches, but CFS often lacks the widespread pain and tender points typical of fibromyalgia
Ix for Fibromyalgia
Full blood count
Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)
Creatine kinase (CK)
Liver function tests (LFT)
Thyroid-stimulating hormone (TSH)
HbA1c
Urea and electrolytes (U&Es)
Rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP)
Autoimmune screen
Dx for Fibromyalgia
The diagnosis of fibromyalgia can take more than 2 years, with patients seeing an average of 3.7 different doctors during that time.
FMS is not a diagnosis of exclusion. The symptoms can also appear in other conditions and coexist with other medical conditions (e.g. rheumatoid arthritis).
The American College of Rheumatologists (ACR) 2016 diagnostic criteria can help clinicians decide more accurately whether to diagnose fibromyalgia
ACR diagnostic criteria for fibromyalgia
Generalised pain, defined as pain in at least 4 of 5 regions
Symptoms have been present at a similar level for at least 3 months
Widespread pain index (WPI) ≥ 7 and symptom severity scale (SSS) score ≥ 5
OR WPI of 4-6 and SSS score ≥ 9
The Royal College of Physicians has a diagnostic worksheet for calculating the widespread pain index (WPI) and symptom severity scale (SSS).
Managment of Fibromyalgia - Non-pharmacological
Self-management advice
Structured exercise programmes
Signposting to websites (e.g. British Pain Society, Pain Tool Kit, Live well with pain)
Keeping a pain diary and thinking of ways to manage flares of pain
Health promotion
Promoting a healthy, balanced diet
Advice about alcohol and drug use
Smoking cessation advice
Physiotherapy
Massage therapy, myofascial release
Acupuncture
Transcutaneous electrical nerve stimulation (TENS)
Exercises
Psychological interventions
Cognitive behavioural therapy (CBT)
Acceptance and commitment therapy (ACT)
Support groups
Sleep management
Sleep hygiene advice
Pain management programmes can also be helpful. Patients may require referral to secondary care pain specialist teams.
Managment of Fibromyalgia - Pharmacological
The European Medicines Agency has not approved any specific medications for the treatment of fibromyalgia.
In adults aged 18 and over, antidepressants such as amitriptyline, citalopram, duloxetine, fluoxetine, paroxetine, or sertraline may be prescribed “off-label.” This should follow a thorough discussion with the patient about potential side effects, risks, benefits, and interactions with other medications.
Antidepressants can help manage fibromyalgia-related pain and psychological distress and may also improve sleep quality.
There is limited evidence supporting the use of NSAIDs, opioids, or other pain medications in chronic primary pain, including fibromyalgia.
It is essential to review these treatments and assess their continued use. If a benefit is reported, a plan for ongoing use can be made. However, if the benefit is minimal, reducing and discontinuing these medications should be considered
Complications of Fibromyalgia
Cognitive difficulties: patients may experience trouble concentrating, memory issues, and mental cloudiness (“brain fog”)
Mental health conditions: depression and anxiety are common and can significantly reduce quality of life
Dermatological symptoms: skin conditions such as rashes and itching are frequently reported in fibromyalgia patients
Reduced physical activity: chronic pain and fatigue may lead to decreased physical activity, potentially contributing to secondary health problems and increased cardiovascular risk
Chronic headaches: recurrent headaches, including migraines, are prevalent
Gastrointestinal problems: conditions such as irritable bowel syndrome (IBS) and acid reflux are often associated with fibromyalgia
What is PMR ?
Polymyalgia rheumatica (PMR) is an inflammatory condition that causes pain and stiffness in the shoulders, pelvic girdle and neck. There is a strong association with giant cell arteritis, and the two conditions often occur together.
The cause is not fully understood. There are no relevant antibodies. It is more common in older white patients.
Presentation of PMR
Patients may have a relatively rapid onset of symptoms over days to weeks. Symptoms should be present for two weeks before a diagnosis is considered. The core symptoms are pain and stiffness of the:
Shoulders, potentially radiating to the upper arm and elbow
Pelvic girdle (around the hips), potentially radiating to the thighs
Neck
In PMR, the characteristic features of the pain and stiffness are:
Worse in the morning
Worse after rest or inactivity
Interfere with sleep
Take at least 45 minutes to ease in the morning
Somewhat improve with activity
Associated features of PMR
Systemic symptoms (e.g., weight loss, fatigue and low-grade fever)
Muscle tenderness
Carpel tunnel syndrome
Peripheral oedema
Differential Dx for PMR
The presenting symptoms are not specific to PMR, and there is a long list of differentials, including:
Osteoarthritis
Rheumatoid arthritis
Systemic lupus erythematosus
Statin-induced myopathy
Myositis (e.g., polymyositis)
Cervical spondylosis
Adhesive capsulitis (frozen shoulder)
Hyperthyroidism or hypothyroidism
Osteomalacia
Fibromyalgia
Lymphoma or leukaemia
Myeloma
Dx of PMR
Diagnosis is based on clinical presentation, response to steroids and excluding differentials.
Inflammatory markers (e.g., ESR and CRP) are usually raised (but may be normal).
Ix for PMR
The NICE clinical knowledge summaries (updated January 2023) advise investigations before initiating steroids:
Full blood count
Renal profile (U&E)
Liver function tests
Calcium (abnormal in hyperparathyroidism, cancer and osteomalacia)
Serum protein electrophoresis for myeloma
Thyroid-stimulating hormone for thyroid function
Creatine kinase for myositis
Rheumatoid factor for rheumatoid arthritis
Urine dipstick
Additional investigations to consider:
Anti-nuclear antibodies (ANA) for systemic lupus erythematosus
Anti-cyclic citrullinated peptide (anti-CCP) for rheumatoid arthritis
Urine Bence Jones protein for myeloma
Chest x-ray for lung and mediastinal abnormalities (e.g., lung cancer or lymphoma)
Tx for PMR
Treatment of PMR is with steroids. The NICE clinical knowledge summaries (updated January 2023) recommend:
15mg prednisolone daily initially
Follow up after 1 week
Treatment with steroids typically lasts 1-2 years. NICE suggest the following reducing regime of prednisolone:
15mg until the symptoms are fully controlled, then
12.5mg for 3 weeks, then
10mg for 4-6 weeks, then
Reducing by 1mg every 4-8 weeks
Prognosis of PMR
Patients with PMR have a dramatic improvement in symptoms (at least 70%) within one week. Inflammatory markers return to normal within one month. A poor response to steroids suggests an alternative diagnosis.
Additional management for patients on long-term steroids can be remembered with the “Don’t STOP” mnemonic:
Don’t – steroid dependence occurs after 3 weeks of treatment, and abruptly stopping risks adrenal crisis
S – Sick day rules (steroid doses may need to be increased if the patient becomes unwell)
T – Treatment card – patients should carry a steroid treatment card to alert others that they are steroid-dependent
O – Osteoporosis prevention may be required (e.g., bisphosphonates and calcium and vitamin D)
P – Proton pump inhibitors are considered for gastro-protection (e.g., omeprazole)
SE of glucocorticoid use
Diabetes: glucocorticoids cause hyperglycaemia and can precipitate a hyperglycaemic hyperosmolar state (HHS) in patients with co-morbid diabetes
Gastro-oesophageal reflux disease (GORD)/peptic ulcer disease: glucocorticoids can worsen acid reflux, so the addition of a proton-pump inhibitor (PPI) may be indicated
Osteoporosis: given that elderly women have lower bone density and are the main demographic of PMR, glucocorticoids can further increase fracture risk. This group may benefit from bone prophylaxis like denosumab (RANKL antagonist), calcium and vitamin D supplements.
What is olecranon bursitis ?
Olecranon bursitis refers to inflammation and swelling of the bursa over the elbow. The olecranon is the bony lump at the elbow, which is part of the ulna bone.
What are bursae?
Bursae are sacs created by synovial membrane filled with a small amount of synovial fluid. They are found at bony prominences (e.g., at the greater trochanter, knee, shoulder and elbow). They act to reduce the friction between the bones and soft tissues during movement.
What is bursitis?
Bursitis is inflammation of a bursa. This causes thickening of the synovial membrane and increased fluid production, causing swelling.
Causes of bursitis
Friction from repetitive movements or leaning on the elbow
Trauma
Inflammatory conditions (e.g., rheumatoid arthritis or gout)
Infection – referred to as septic bursitis Repetitive trauma (29%) - writers and students leaning on elbows, plumbers, miners
Direct trauma (17%)
Infection (33%) - 50% of cases occur in immunosuppressed patients (alcohol abuse, diabetes, taking steroids, renal failure, malignancy). 90% of cases due to Staphylococcus aureus.
Gout (7%)
Rheumatoid arthritis (5%)
Idiopathic (5%)
Why is olecranon bursitis sometimes called “student’s elbow”?
Olecranon bursitis is sometimes called “student’s elbow”, as students may lean on their elbow for prolonged periods while studying, resulting in friction and mild trauma leading to bursitis. It can also occur with people with occupations that require leaning on the elbow, such as plumbers or drivers.
The typical presentation of olecranon bursitis is a young/middle-aged man with an elbow that is:
Swollen
Warm
Tender
Fluctuant (fluid-filled)
It is important to identify where bursitis is caused by infection. Features of infection are:
Hot to touch
More tender
Erythema spreading to the surrounding skin
Fever
Features of sepsis (e.g., tachycardia, hypotension and confusion)
An important differential diagnosis is septic arthritis. Consider septic arthritis if there is:
Swelling in the joint (rather than the bursa)
Painful and reduced range of motion in the elbow
When is aspiration of fluid needed in bursitis?
The NICE clinical knowledge summaries (updated January 2021) recommend aspiration of fluid from the bursa when an infection is suspected. They advise that the appearance can give an indication of the underlying cause:
Pus indicates infection
Straw-coloured fluid indicates infection is less likely
Blood-stained fluid may indicate trauma, infection or inflammatory causes
Milky fluid indicates gout or pseudogout
Aspiration should ideally be performed before starting antibiotics. The fluid is sent to the lab for microscopy and culture. During microscopy, they will examine for crystals (gout and pseudogout) and gram-staining for bacteria.
Management of olecranon bursitis
Rest
Ice
Compression
Analgesia (e.g., paracetamol or NSAIDs)
Protecting the elbow from pressure or trauma
Aspiration of fluid may be used to relieve pressure
Steroid injections may be used in problematic cases where infection has been excluded
When infection is suspected or cannot be excluded, management of olecranon bursitis involves:
Aspiration of the fluid for microscopy and culture
Antibiotics : The NICE CKS recommend flucloxacillin first-line, with clarithromycin as an alternative.
When does a patient with olecranon bursitis require hospital admission?
Bloods (including lactate)
Blood cultures
IV antibiotics
IV fluids
What is a soft tissue injury of the lower limb?
A soft tissue injury refers to damage to muscles, ligaments, or tendons in the lower limb due to trauma, overuse, or strain.
What are common causes of lower limb soft tissue injuries?
Causes include direct trauma (e.g., falls, sports injuries), overuse (e.g., running, repetitive strain), and sudden movements (e.g., twisting injuries).
Fill in the blank: The most commonly injured ligament in an ankle sprain is the __________.
anterior talofibular ligament (ATFL)
What is the most common mechanism of injury in an ankle sprain?
Inversion of the foot, leading to strain on the lateral ligaments.
A __________ occurs when a muscle or tendon is overstretched or torn.
strain.
What are the stages of soft tissue healing?
Inflammatory phase (0-5 days): Increased blood flow, swelling, and recruitment of immune cells.
Proliferation phase (5-21 days): Fibroblast activity leads to collagen deposition.
Remodelling phase (21+ days): Collagen strengthens, and tissue regains function.
Tendon injuries heal more slowly than muscle injuries due to their __________ blood supply.
limited
What are the common symptoms of a lower limb soft tissue injury?
Pain, swelling, bruising, reduced range of motion, and difficulty bearing weight.
How can a clinician differentiate between a ligamentous and muscular injury?
Ligament injuries typically involve joint instability and pain on passive movement, while muscular injuries cause pain on active contraction.
What are the Ottawa Ankle Rules, and why are they used?
The Ottawa Ankle Rules help determine if an X-ray is needed for an ankle injury. An X-ray is required if there is pain in the malleolar zone plus either:
Tenderness at the posterior edge/tip of the lateral or medial malleolus, or
Inability to bear weight for 4 steps.
What imaging modality is best for assessing ligament or tendon injuries?
MRI is the gold standard for assessing soft tissue damage, particularly for ligament and tendon injuries.
What does the PRICE protocol stand for in soft tissue injury management?
Protection
Rest
Ice
Compression
Elevation
The POLICE approach modifies PRICE by emphasizing __________ instead of complete rest.
optimal loading
When are NSAIDs recommended for soft tissue injuries?
NSAIDs (e.g., ibuprofen) can be used after the first 48 hours to reduce pain and inflammation but should be avoided early to prevent delayed healing.
What are the indications for physiotherapy in soft tissue injuries?
Indications include persistent pain, reduced range of motion, muscle weakness, or difficulty returning to normal activities.
What are potential complications of a lower limb soft tissue injury?
Chronic instability (e.g., recurrent ankle sprains)
Tendon rupture (e.g., Achilles tendon)
Persistent pain and stiffness (e.g., fibrosis)
Deep vein thrombosis (DVT) due to immobility
Fill in the blank: Achilles tendon rupture is often associated with a sudden “pop” sensation and inability to perform a __________.
calf raise
What is a soft tissue injury of the upper limb?
A soft tissue injury refers to damage to muscles, tendons, or ligaments in the upper limb due to trauma, overuse, or strain.
What are common causes of upper limb soft tissue injuries?
Causes include falls onto an outstretched hand (FOOSH), direct trauma, repetitive strain (e.g., tennis elbow), and excessive loading (e.g., weightlifting injuries).
A rotator cuff tear most commonly affects the __________ muscle.
supraspinatus
What is the most common mechanism of injury for an acromioclavicular (AC) joint sprain?
A direct blow to the shoulder or a fall onto the shoulder.
__________ is a common overuse injury of the extensor tendons at the lateral epicondyle of the humerus.
Tennis elbow (lateral epicondylitis)
What are the typical signs and symptoms of an upper limb soft tissue injury?
Pain, swelling, bruising, reduced range of motion, weakness, and difficulty performing specific movements.
How can a rotator cuff tear be differentiated from shoulder impingement syndrome?
A full-thickness rotator cuff tear often causes weakness in shoulder abduction, while impingement presents with pain but preserved strength.
The __________ test is used to assess for rotator cuff tears.
empty can test
What imaging is most useful for diagnosing soft tissue injuries of the upper limb?
X-ray: Rules out fractures or dislocations.
Ultrasound: Assesses tendon and ligament integrity (e.g., rotator cuff tears).
MRI: Gold standard for detailed soft tissue assessment.
The __________ test is used to assess for biceps tendinopathy
Speed’s test
What is the recommended first-line management for most upper limb soft tissue injuries?
The POLICE approach:
Protection
Optimal Loading
Ice
Compression
Elevation
NSAIDs should generally be avoided in the first __________ hours after injury to prevent delayed healing.
48
When is physiotherapy recommended for upper limb soft tissue injuries?
When there is persistent pain, reduced range of motion, muscle weakness, or difficulty returning to normal activities.
What are the indications for surgical intervention in an upper limb soft tissue injury?
Full-thickness rotator cuff tears
Chronic tendon rupture (e.g., distal biceps rupture)
Severe AC joint dislocations
Recurrent shoulder instability
What are the potential complications of an upper limb soft tissue injury?
Chronic pain and stiffness (e.g., frozen shoulder)
Tendon rupture (e.g., chronic rotator cuff tear)
Muscle atrophy due to disuse
Joint instability (e.g., recurrent shoulder dislocations)
Frozen shoulder (adhesive capsulitis) is characterised by progressive __________ and __________ of the glenohumeral joint.
pain, stiffness
What is Gout ?
Gout is a type of crystal arthropathy associated with chronically high blood uric acid levels. Urate crystals are deposited in the joint, causing it to become inflamed.
What are Gouty Tophi?
Gouty tophi are subcutaneous uric acid deposits typically seen on the hands, elbows and ears.
Typical presentation of gout
Gout typically presents with a single acute hot, swollen and painful joint
What is the critical differential dx for gout?
Septic arthritis
Risk factors for gout
Male
Family history
Obesity
High purine diet (e.g., meat and seafood)
Alcohol
Diuretics
Cardiovascular disease
Kidney disease
Typical joints affected in gout
The most commonly affected joints are:
The base of the big toe – the metatarsophalangeal joint (MTP joint)
The base of the thumb – the carpometacarpal joint (CMC joint)
Wrist Gout can also affect larger joints (e.g., knee and ankle).
Dx of Gout
Diagnosis is usually made clinically, supported by a raised serum urate level on a blood test.
It is essential to exclude septic arthritis, a potentially life-threatening differential diagnosis. Any suspicion of septic arthritis requires emergency management with joint aspiration and antibiotics.
What does aspirated joint fluid show for Gout?
Aspirated joint fluid shows monosodium urate crystals. These are needle-shaped and negatively birefringent of polarised light. There should be no bacterial growth.
X ray signs of Gout
Maintained joint space (no loss of joint space)
Lytic lesions in the bone
Punched out erosions
Erosions can have sclerotic borders with overhanging edges
Acute flares of gout are treated with ….
NSAIDs (e.g., naproxen) first-line (co-prescribed with a proton pump inhibitor for gastroprotection)
Colchicine second-line
Oral steroids (e.g., prednisolone) third-line
Why may NSAIDs be contraindicated?
Patients with renal impairement or significant heart disease
Why is Colchicine a dangerous drug?
Abdominal symptoms and diarrhoea are common side effects. These may be mild and resolve with a reduced dose. However, more severe symptoms may indicate toxicity. Colchicine is very dangerous in overdose and can cause multiple organ failure. It is only prescribed for a short course (up to 6mg per course).
Prophylaxis of gout
Prophylaxis is with xanthine oxidase inhibitors, which lower the uric acid level. The options are:
Allopurinol
Febuxostat
Prophylaxis is not started until weeks after the acute attack has resolved.
Lifestyle changes for patients who have gout
Lifestyle changes can reduce the risk of gout. This involves losing weight, staying hydrated and minimising the consumption of alcohol and purine-based food (e.g., meat and seafood).
Decreased excretion of uric acid
drugs*: diuretics
chronic kidney disease
lead toxicity
Increased production of uric acid
myeloproliferative/lymphoproliferative disorder
cytotoxic drugs
severe psoriasis
What is Pseudogout?
Pseudogout is a crystal arthropathy caused by calcium pyrophosphate crystals collecting in the joints. It is formally known as calcium pyrophosphate deposition disease (CPPD). It may also be called chondrocalcinosis.
Presentation of pseudogout?
The presentation varies. Many patients are asymptomatic, and it is picked up incidentally on an x-ray. Others may present with chronic pain and stiffness in multiple joints. It can present acutely with a rapid onset of symptoms.
A typical acute presentation of pseudogout is a patient over 65 years old with a rapid-onset hot, swollen, stiff and painful knee. Other commonly affected joints are the shoulders, hips and wrists.
Dx of Pseudogout
In any patient presenting with a hot, painful and swollen joint, septic arthritis must be excluded as it is a medical emergency. Symptoms of pseudogout tend to be milder than gout or septic arthritis.
Joint aspiration for pseudogout
Joint aspiration is used to confirm the diagnosis. Aspirated joint fluid shows calcium pyrophosphate crystals. These are rhomboid-shaped and positively birefringent of polarised light. There should be no bacterial growth.
Classic X ray findings for pseudogout
Chondrocalcinosis is the classic x-ray change in pseudogout. The calcium deposits in the joint cartilage show up in a thin white line in the middle of the joint space.
Other X-rays changes for pseudogout
Other joint x-ray changes are similar to osteoarthritis, which can be remembered with the “LOSS” mnemonic:
L – Loss of joint space
O – Osteophytes (bone spurs)
S – Subarticular sclerosis (increased density of the bone along the joint line)
S – Subchondral cysts (fluid-filled holes in the bone)
Management of asymptomatic pseudogout
Treatment of pseudogout is targeted at symptoms. There are no proven disease-modifying drugs, prophylactic treatments or dietary modifications. Asymptomatic changes on an x-ray do not require any treatment.
Management of symptomatic pseudogout
Symptomatic management options include:
NSAIDs (e.g., naproxen) first-line (co-prescribed with a proton pump inhibitor for gastroprotection)
Colchicine
Intra-articular steroid injections (septic arthritis must be excluded first)
Oral steroids
Risk factors for pseudogout
Pseudogout is strongly associated with increasing age. Patients who develop pseudogout at a younger age (e.g. < 60 years) usually have some underlying risk factor, such as:
haemochromatosis
hyperparathyroidism
low magnesium, low phosphate
acromegaly, Wilson’s disease
What is reactive arthritis ?
Reactive arthritis involves synovitis in one or more joints in response to an infective trigger. Typically it causes acute monoarthritis, affecting a single joint (most often the knee), presenting with a warm, swollen and painful joint. Reactive arthritis is a seronegative spondyloarthropathy. There is a link with the HLA B27 gene. It is more common in patients with HIV (HIV needs to be excluded in patients with reactive arthritis).
Common triggers of reactive arthritis ?
The most common triggers of reactive arthritis are gastroenteritis or sexually transmitted infections. Chlamydia may cause reactive arthritis. Gonorrhoea typically causes septic arthritis rather than reactive arthritis.
Associations of reactive arthritis
Bilateral conjunctivitis (non-infective)
Anterior uveitis
Urethritis (non-gonococcal)
Circinate balanitis (dermatitis of the head of the penis)
What is the classic triad of symtoms of reactive arthritis?
The classic triad of conjunctivitis, urethritis and arthritis are remembered with the mnemonic, “can’t see, pee or climb a tree”.
Management of suspected reactive arthritis
Patients presenting with an acute warm, swollen, painful joint need to be treated according to the local hot joint policy. Septic arthritis needs to be excluded. Antibiotics may be given until septic arthritis is excluded.
Joint aspiration is required. Synovial fluid is sent for microscopy, culture and sensitivity testing for infection, and crystal examination for gout and pseudogout.
Management of reactive arthritis (after septic arthritis is excluded) involves:
Treatment of the triggering infection (e.g., chlamydia)
NSAIDs
Steroid injection into the affected joints
Systemic steroids may be required, particularly where multiple joints are affected
Prognosis of reactive arthritis
Most cases resolve within 6 months and do not recur.
Recurrent cases of reactive arthritis are tx with ….
Recurrent cases may require DMARDs or anti-TNF medications.
Features of reactiv arthritis
time course
typically develops within 4 weeks of initial infection - symptoms generally last around 4-6 months
around 25% of patients have recurrent episodes whilst 10% of patients develop chronic disease
arthritis is typically an asymmetrical oligoarthritis of lower limbs
dactylitis
symptoms of urethritis
eye
conjunctivitis (seen in 10-30%)
anterior uveitis
skin
circinate balanitis (painless vesicles on the coronal margin of the prepuce)
keratoderma blenorrhagica (waxy yellow/brown papules on palms and soles)
