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MSK Flashcards

Don't you wanna come with me? Don't you wanna feel my boneson your bones? It's only natural

1
Q

What are the X-ray changes in OA?

A

LOSS

Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts

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2
Q

What are some hand signs of OA?

A

Heberden’s nodes (DIP)
Bouchard’s nodes (PIP)
Squaring at the base of the thumb (CMC)
Weak grip
Reduced range of motion

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3
Q

How can OA be diagnosed clinically according to NICE guidelines?

A

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).

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4
Q

Management for OA

A
  1. Non-pharm: exercise, weight loss, OT
  2. Pharm: topical NSAIDs, then oral NSAIDs
    :::::::::::::weak opiates and paracetamol only for short-term, strong opiates not recommended::::::::::::::
  3. Intra-articular steroid injections may temporarily improve symptoms
  4. Joint replacement
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5
Q

What is the most common associated gene with RA?

A

HLA DR4

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6
Q

What antibodies are associated with RA? What are the sensitivities?

A

RF and anti-CCP (anti-cyclic citrullinated peptide)

RF present in 70% of RA pts
anti-CCP present in 80% of RA pts, more sensitive and specific

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7
Q

What are the hand signs in RA?

A

Z-shaped deformity to the thumb
Swan neck deformity (hyperextended PIP and flexed DIP)
Boutonniere deformity (hyperextended DIP and flexed PIP)
Ulnar deviation of the fingers at the MCP joints

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8
Q

How can RA affect the cervical spine?

A

Atlantoaxial subluxation => SCC (emergency)
risk of this during GA and intubation

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9
Q

What are some extra-articular manifestations of RA?

A

Pulmonary fibrosis
Felty’s syndrome (a triad of rheumatoid arthritis, neutropenia and splenomegaly)
Sjögren’s syndrome (with dry eyes and dry mouth)
Anaemia of chronic disease
Cardiovascular disease
Eye manifestations:
:::::::::Dry eye syndrome (keratoconjunctivitis sicca)
Episcleritis
Scleritis
Keratitis
Cataracts (secondary to steroids)
Retinopathy (secondary to hydroxychloroquine):::::::::::::::
Rheumatoid nodules (firm, painless lumps under the skin, typically on the elbows and fingers)
Lymphadenopathy
Carpel tunnel syndrome
Amyloidosis
Bronchiolitis obliterans (small airway destruction and airflow obstruction in the lungs)
Caplan syndrome (pulmonary nodules in patients with rheumatoid arthritis exposed to coal, silica or asbestos dust)

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10
Q

How is RA diagnosed?

A

urgent rheum referral (within 3w) for persistent synovitis
Bloods:
- RF
- anti-CCP Ab’s
- inflam markers: CRP, ESR
- X-rays of hands and feet
- USS/MRI to detect synovitis

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11
Q

What are the X-ray findings in RA?

A

LESS
Loss of joint space
Erosions
Soft tissue swellings
Soft bones (periarticular osteopenia)

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12
Q

What are some scoring systems for RA?

A

Health Assessment Questionnaire (HAQ) - functional ability

Disease Activity Score 28 Joints (DAS28) - monitor disease activity and response to treatment

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13
Q

What is the management of RA and how do you monitor response to treatment?

A

Short-term steroids while initiating treatment and during flares

conventional disease-modifying anti-rheumatic drugs (cDMARDs) and biologic DMARDs e.g.
1. monotherapy: methotrexate, leflunomide or sulfasalazine
2. combination treatment with multiple cDMARDs
3. biologic therapies alongside methotrexate

hydroxychloroquine - in mild disease, mildest DMARD, safe in pregnancy

cDMARDs - azathioprine, ciclosporin, cyclophosphamide, mycophenolate

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14
Q

What DMARDs are safe in pregnancy?

A

Hydroxychloroquine - mildest DMARD

Sulfasalazine - needs extra folic acid

Methotrexate and leflunomides are VERY BAD AND TERATOGENIC!!!

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15
Q

What are some different biologic therapies for RA?

A

Tumour necrosis factor (TNF) inhibitors (e.g., adalimumab, infliximab, etanercept, golimumab and certolizumab)

Anti-CD20 on B cells (e.g., rituximab)

Anti-interleukin-6 inhibitors (e.g., sarilumab and tocilizumab)

JAK inhibitors (e.g., upadacitinib, tofacitinib and baricitinib)

T-cell co-stimulation inhibitors (e.g., abatacept)

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16
Q

Which autoantibody is most associated with SLE? How do they function?

A

anti-nuclear antibodies (ANA) - positive in 85% of pts
autoantibodies against protein within cell nucleus
generate chronic inflammatory response

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17
Q

Name some associated symptoms/signs of SLE

A

Photosensitive malar rash “butterfly” shape

Arthralgia (joint pain), Non-erosive arthritis
Myalgia (muscle pain)

Fatigue, Weight loss, Fever
Shortness of breath, Pleuritic chest pain

Lymphadenopathy, Splenomegaly

Mouth ulcers
Hair loss
Raynaud’s phenomenon
Oedema (due to nephritis)

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18
Q

What lab findings are seen in SLE?

A

Autoantibodies - ANA in 85% of pts
anti-dsDNA (anti-double stranded DNA) - highly specific to SLE
anti-Sm, anti-centromere, anti-Ro, anti-La, anti-Scl-70, anti-Jo-1

FBC:
::::::::: anaemia of chronic disease, low WCC, low plt

Chem: CRP and ESR may be raised

C3 and C4 (reminder: compliment cascade in immune response, low levels indicate autoimmune disease)

Urinalysis: urine Pr:Cr shows proteinuria and lupus nephritis

Renal biopsy: lupus nephritis

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19
Q

What autoantibodies can be present in SLE?

A

⭐⭐anti-nuclear antibodies (ANA) - positive in 85% of pts

⭐Anti-double stranded DNA (anti-dsDNA) antibodies - highly specific, can be used to monitor disease activity

  • Anti-Sm (highly specific to SLE but not very sensitive)
  • Anti-centromere antibodies (most associated with limited cutaneous systemic sclerosis)
  • Anti-Ro and anti-La (most associated with Sjögren’s syndrome)
  • Anti-Scl-70 (most associated with systemic sclerosis)
  • Anti-Jo-1 (most associated with dermatomyositis)
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20
Q

What can be used as diagnostic criteria for SLE?

A

European League Against Rheumatism (EULAR) / American College of Rheumatology (ACR) criteria (2019)

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21
Q

What are some complications of SLE?

A
  • Cardiovascular disease - leading cause of death
  • Infection
  • Anaemia - anaemia of chronic disease, autoimmune haemolytic anaemia, bone marrow suppression by medications or kidney disease
  • Pericarditis
  • Pleuritis
  • Interstitial lung disease => pulmonary fibrosis
  • Lupus nephritis
  • Neuropsychiatric SLE - optic neuritis, transverse myelitis, psychosis
  • Recurrent miscarriage, IUGR, pre-eclampsia, pre-term labour
  • VTE (assoc w antiphospholipid syndrome)
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22
Q

What is the management of SLE?

A

1st line:
::::::::: hydroxychloroquine ⭐
NSAIDS
steroids e.g. pred

2nd line:
::::::::::::DMARDs e.g. methotrexate, mycophenolate mofetil, cyclophosphamide
:::::::::::::Biologics - rituximab (targets CD20 protein on the surface of B cells), belimumab (targets B-cell activating factor)

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23
Q

What biologics can be used in SLE and what do they target?

A

rituximab (targets CD20 protein on the surface of B cells)

belimumab (targets B-cell activating factor)

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24
Q

Which genetic factors are most associated with SLE?

A

major histocompatibility complex (MHC) region, notably HLA-DR2 and HLA-DR

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25
Q

What is the pathophysiology of gout?

A

crystal arthropathy
high blood uric acid
urate crystals deposited in joint

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26
Q

What is a critical differential for gout?

A

Septic arthritis

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27
Q

What investigations and findings are found in gout?

A

Bloods: high serum uric acid

Joint aspiration - monosodium urate crystals, needle-shaped 🪡 negatively birefringent of polarised light 🌈 and NO bacterial growth

X-ray;
- Maintained joint space (no loss of joint space)
- Lytic lesions in the bone
- Punched out erosions
- Erosions can have sclerotic borders with overhanding edges

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28
Q

What is the finding on joint aspiration in pseudogout?

A

calcium pyrophosphate crystals of pseudogout are rhomboid-shaped and➕ positively birefringent.

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29
Q

What are the X-ray findings in gout?

A

Maintained joint space (no loss of joint space)
Lytic lesions in the bone
Punched out erosions
Erosions can have sclerotic borders with overhanding edges

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30
Q

What is the management of gout? Prophylaxis?

A

Acute flares: NSAIDs e.g. naproxen +PPI
2nd line - colchicine (renal impairment or sig heart disease)
3rd line - oral steroids e.g. pred

Prophylaxis - xanthine oxidase inhibitors
::: allopurinol ::: febuxostat :::

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31
Q

Which signs may indicate cervical myelopathy in patients with neck pain?

A

Paresis, sensory changes, altered muscle tone, clumsy or weak hands, gait disturbance, Babinski’s sign, Hoffman’s sign, Lhermitte’s sign, profound hand weakness, bowel or bladder dysfunction, and severe gait ataxia.

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32
Q

What is Babinski’s sign?

A

up-going plantar reflex, hyper-reflexia, clonus, spasticity.

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33
Q

What is Hoffman’s sign

A

involuntary flexion and adduction of the thumb and flexion of the index finger when the nail of the middle finger is flicked downwards. (Not reliable in isolation as may be present normally).

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34
Q

What is Lhermitte’s sign?

A

flexion of the neck causes an electric shock-type sensation that radiates down the spine and into the limbs.

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35
Q

What are the main causes of neck pain?

A

Muscle or ligament strain, torticollis, whiplash, and cervical spondylosis.

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36
Q

What are the main causes of sciatica?

A

Herniated disc, spondylolisthesis, and spinal stenosis.

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37
Q

What is a red flag for cauda equina syndrome in a patient with sciatica?

A

Bilateral sciatica.

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38
Q

What cancers commonly metastasise to the bones, potentially causing back pain?

A

Prostate, Renal, Thyroid, Breast, and Lung (PoRTaBLe mnemonic)

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39
Q

What tool is used to stratify the risk of a patient with acute back pain developing chronic back pain?

A

The STarT Back Screening Tool.

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40
Q

What medications should be avoided in the treatment of non-specific low back pain according to NICE guidelines?

A

Opioids, antidepressants, amitriptyline, gabapentin, and pregabalin.

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41
Q

What medications are NOT recommended for sciatica according to NICE guidelines?

A

Gabapentin, pregabalin, diazepam, oral corticosteroids, and opioids for chronic sciatica.

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42
Q

What specialist treatments may be considered for chronic sciatica?

A

Epidural corticosteroid injections, local anaesthetic injections, and radiofrequency denervation.

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43
Q

Where does the cauda equina begin in the spinal column?

A

The cauda equina begins after the spinal cord terminates at the conus medullaris around L2/L3.

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44
Q

What functions do the nerves of the cauda equina supply?

A
  • Sensation to the lower limbs, perineum, bladder, and rectum
  • Motor innervation to the lower limbs and sphincters
  • Parasympathetic innervation of the bladder and rectum
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45
Q

What is the most common cause of cauda equina syndrome? Name three other causes of cauda equina syndrome

A

Herniated disc.

Tumours (especially metastasis)
Spondylolisthesis
Abscesses or infection
Trauma

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46
Q

What are the key red flags for cauda equina syndrome?

A

Saddle anaesthesia
Urinary retention or incontinence
Faecal incontinence
Bilateral sciatica
Severe motor weakness in the legs
Reduced anal tone on PR examination

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47
Q

What are the sensory and motor symptoms of CES?

A

Sensory: Numbness in the perineum, bladder, or rectum.

Motor: Weakness or paralysis in the legs, loss of control over bladder and bowel function.

48
Q

What is the initial management of suspected cauda equina syndrome?

A

Immediate hospital admission
Emergency MRI scan to confirm diagnosis
Neurosurgical input for potential lumbar decompression surgery

49
Q

What are the possible outcomes even after surgery for cauda equina syndrome?

A

Even with early surgery, patients may have persistent issues like bladder, bowel, or sexual dysfunction, as well as leg weakness and sensory impairment.

50
Q

How does metastatic spinal cord compression (MSCC) differ from cauda equina syndrome?

A

MSCC involves compression of the spinal cord higher up than CES, leading to upper motor neuron signs like increased tone, brisk reflexes, and upgoing plantar responses, while CES causes lower motor neuron signs (reduced tone, reduced reflexes).

51
Q

What are common treatments for metastatic spinal cord compression (MSCC)?

A

High-dose dexamethasone
Analgesia
Surgery, radiotherapy, or chemotherapy depending on individual factors.

52
Q

What is spinal stenosis?

A

The narrowing of part of the spinal canal, leading to compression of the spinal cord or nerve roots, typically affecting the cervical or lumbar spine.

53
Q

What are the possible causes of spinal stenosis?

A

Congenital spinal stenosis
Degenerative changes (facet joint changes, disc disease, bone spurs)
Herniated discs
Thickening of ligamenta flava or posterior longitudinal ligament
Spinal fractures
Spondylolisthesis
Tumours

54
Q

What are the key symptoms of intermittent neurogenic claudication, associated with lumbar spinal stenosis?

A

Lower back pain
Buttock and leg pain
Leg weakness

55
Q

What is Osgood-Schlatter disease?

A

It is a condition caused by inflammation at the tibial tuberosity where the patella ligament inserts, leading to anterior knee pain in adolescents. Usually unilateral, sometimes bilateral.

56
Q

What age group is most commonly affected by Osgood-Schlatter disease?

A

Adolescents aged 10–15 years old. More common in boys.

57
Q

Describe the pathophysiology of Osgood-Schlatter disease.

A

The patella tendon inserts into the tibial tuberosity, and repetitive stress can cause minor avulsion fractures. The patella ligament pulls away tiny pieces of bone, causing the tibial tuberosity to grow, which leads to a visible and initially tender lump.

58
Q

What happens to the lump at the tibial tuberosity over time in Osgood-Schlatter disease?

A

Initially, the lump is tender due to inflammation, but as it heals, it becomes a hard, non-tender, permanent lump.

59
Q

What are the typical symptoms of Osgood-Schlatter disease?

A

A hard and tender lump at the tibial tuberosity, anterior knee pain, and pain that worsens with physical activity, kneeling, or knee extension.

60
Q

What initial management steps are recommended for Osgood-Schlatter disease?

A

Reducing physical activity, applying ice, and taking NSAIDs (e.g., ibuprofen) to relieve pain and inflammation.

61
Q

What additional treatments are suggested once symptoms of Osgood-Schlatter disease begin to settle?

A

Stretching and physiotherapy to strengthen the joint and improve function.

62
Q

What is the long-term prognosis for patients with Osgood-Schlatter disease?

A

Symptoms typically resolve over time, but patients are usually left with a hard, bony lump on their knee.

63
Q

What rare complication can occur with Osgood-Schlatter disease, and what does it require?

A

A complete avulsion fracture, where the tibial tuberosity is separated from the tibia, requiring surgical intervention.

64
Q

What is the function of the menisci in the knee?

A

The menisci help the femur and tibia fit together, act as shock absorbers, distribute weight, and stabilize the knee joint.

65
Q

Where is the patella located, and what is its function?

A

The patella sits in the trochlea (groove on the femur) and helps with knee extension by transferring force from the quadriceps tendon to the tibia via the patellar ligament.

66
Q

What are the four main ligaments in the knee?

A

The anterior cruciate ligament, posterior cruciate ligament, lateral collateral ligament, and medial collateral ligament.

67
Q

How do meniscal tears commonly occur in young vs. older patients?

A

In young patients, they often occur from sports-related twisting; in older patients, they can occur with minor twists, such as standing up with an awkward knee twist.

68
Q

What are common symptoms of a meniscal tear?

A

Symptoms include pain, swelling, stiffness, restricted range of motion, knee locking, and instability or giving way.

69
Q

What are the two key physical tests traditionally used for meniscal tears?

A

McMurray’s test and Apley grind test.

70
Q

Describe McMurray’s Test for meniscal tears.

A

The patient lies supine with knee flexed, and the examiner rotates the tibia while applying varus or valgus pressure. Pain or restriction (locking) indicates meniscal damage.

71
Q

Describe the Apley Grind Test for meniscal tears.

A

The patient lies prone with the knee at 90 degrees, and the examiner applies downward pressure while rotating the tibia. Pain indicates meniscal damage.

72
Q

What are the Ottawa Knee Rules?

A

They determine if a knee x-ray is needed after an injury if the patient is 55+, has patella or fibular head tenderness, cannot flex the knee to 90 degrees, or cannot bear weight for 4 steps.

73
Q

What is the first-line imaging investigation for diagnosing a meniscal tear?

A

MRI

74
Q

What is the gold-standard investigation for diagnosing and treating meniscal tears?

A

Arthroscopy, which allows direct visualization and potential repair or removal of the meniscus.

75
Q

What are the main components of the RICE mnemonic for managing acute meniscal tears?

A

R - Rest
I - Ice
C - Compression
E - Elevation

76
Q

What is the first-line medication for pain relief in musculoskeletal injuries like meniscal tears?

A

NSAIDs

77
Q

When is surgery indicated for a meniscal tear?

A

Surgery is considered if symptoms persist despite conservative management and may involve meniscal repair or resection.

78
Q

What are the risks of meniscal resection surgery?

A

Meniscal resection often leads to osteoarthritis in the affected knee due to loss of cartilage.

79
Q

Where do the ACL and PCL attach on the tibia?

A

The ACL attaches to the anterior intercondylar area of the tibia, and the PCL attaches to the posterior intercondylar area of the tibia.

80
Q

What is the primary function of the ACL? What is the primary function of the PCL?

A

The ACL prevents the tibia from sliding forward in relation to the femur. The PCL prevents the tibia from sliding backward in relation to the femur.

81
Q

How does an ACL injury typically occur?

A

An ACL injury usually occurs during a twisting movement of the knee, often resulting in a “pop” sound or sensation, pain, and swelling.

82
Q

What are the common symptoms of an ACL tear?

A

Symptoms include pain, swelling, instability, a “pop” sound or sensation, and potential knee buckling.

83
Q

What is the Lachman test, and how does it differ from the anterior draw test?

A

The Lachman test assesses ACL integrity with the knee flexed at around 20-30 degrees, as opposed to 90 degrees in the anterior draw test.

84
Q

When might arthroscopic surgery be recommended for an ACL injury?

A

Surgery is often recommended for young or active patients, especially athletes, to reconstruct the ACL for knee stability.

85
Q

What types of grafts are used to reconstruct the ACL during surgery?

A
  • Hamstring tendon graft
  • Quadriceps tendon graft
  • Bone-patellar tendon-bone graft
86
Q

What are the signs suggesting an acute ACL tear that require urgent referral?

A

A “pop” sound, rapid swelling, instability, or knee giving way.

87
Q

What is another name for a Baker’s cyst?

A

A popliteal cyst.

88
Q

What anatomical structures form the boundaries of the popliteal fossa?

A
  • Superior and Medial - Semimembranosus and Semitendinosus tendons
  • Superior and Lateral - Biceps femoris tendon
  • Inferior and Medial - Medial head of the gastrocnemius
  • Inferior and Lateral - Lateral head of the gastrocnemius
89
Q

What are common conditions associated with Baker’s cysts in adults?

A

Meniscal tears, osteoarthritis, knee injuries, and inflammatory arthritis (e.g., rheumatoid arthritis).

90
Q

How does a Baker’s cyst form?

A

Synovial fluid leaks from the knee joint into the popliteal fossa, creating a fluid-filled sac.

91
Q

What are the common symptoms of a Baker’s cyst?

A

Pain, discomfort, a feeling of fullness or pressure, a palpable lump, and sometimes restricted knee motion.

92
Q

What is Foucher’s sign in Baker’s cysts?

A

The lump appears more prominent when the knee is extended and smaller or disappears when flexed to 45 degrees.

93
Q

What can a ruptured Baker’s cyst cause?

A

Pain, swelling, erythema, and it can mimic the presentation of a deep vein thrombosis (DVT).

94
Q

What are some differential diagnoses for a popliteal fossa lump?

A
  • Deep vein thrombosis
  • Abscess
  • Popliteal artery aneurysm
  • Ganglion cyst
  • Lipoma
  • Varicose veins
  • Tumor
95
Q

What is the first-line imaging technique for diagnosing a Baker’s cyst?

A

Ultrasound, which also helps to rule out DVT.

96
Q

What non-surgical treatments are available for symptomatic Baker’s cysts?

A

Modified activity, NSAIDs for pain relief, physiotherapy, ultrasound-guided aspiration, and steroid injections.

97
Q

What are typical symptoms of plantar fasciitis?

A

Gradual onset of pain on the heel’s plantar aspect, especially with prolonged standing or walking, and tenderness on palpation.

98
Q

What are common treatments for plantar fasciitis?

A

Rest, ice, NSAIDs, physiotherapy, and possibly steroid injections (though rare due to risk of rupture or fat pad atrophy)

99
Q

What advanced therapies may be required for severe plantar fasciitis cases?

A

Extracorporeal shockwave therapy or surgery.

100
Q

What is fat pad atrophy, and where does it occur? How does fat pad atrophy present? How is fat pad atrophy managed?

A

It’s the thinning of the protective fat pad beneath the heel (under the calcaneus), often due to aging or repetitive impact activities.

Sx: Pain and tenderness in the heel, worsened by walking, especially on hard surfaces or barefoot.

Mx: Supportive shoes, custom insoles, activity modifications, and weight loss if appropriate.

101
Q

What is Morton’s neuroma?
What symptoms are associated with Morton’s neuroma?

A

Dysfunction of a nerve, usually between the third and fourth metatarsals, often due to foot biomechanics and exacerbated by tight or high-heeled shoes.

Pain in the front of the foot, a sensation of a lump in the shoe, and burning or numbness in the distal toes.

102
Q

What tests can help diagnose Morton’s neuroma?
What imaging techniques confirm Morton’s neuroma?

A

Deep pressure on the intermetatarsal space, metatarsal squeeze test, and Mulder’s sign (painful click with manipulation of the metatarsals).

Ultrasound or MRI.

103
Q

What are the management options for Morton’s neuroma?

A

Activity modification, NSAIDs, insoles, weight loss, steroid injections, radiofrequency ablation, or surgery.

104
Q

What does the Achilles tendon connect, and what movement does it facilitate?

A

The Achilles tendon connects the calf muscles (gastrocnemius and soleus) to the heel bone (calcaneus). It enables plantar flexion of the ankle when the calf muscles contract.

105
Q

What is Achilles tendinopathy?

A

Achilles tendinopathy is a condition involving damage, swelling, inflammation, and reduced function in the Achilles tendon.

106
Q

What are the two types of Achilles tendinopathy, and where are they located?

A
  1. Insertion tendinopathy: Located within 2 cm of the tendon’s insertion on the calcaneus.
  2. Mid-portion tendinopathy: Located 2–6 cm above the insertion point.
107
Q

List some risk factors for Achilles tendinopathy.

A
  • Sports that stress the Achilles (e.g., basketball, tennis, track athletics)
  • Inflammatory conditions (e.g., rheumatoid arthritis, ankylosing spondylitis)
  • Diabetes
  • Raised cholesterol
  • Fluoroquinolone antibiotics (e.g., ciprofloxacin, levofloxacin)
108
Q

What are the common symptoms of Achilles tendinopathy?

A

Symptoms include gradual onset of pain or aching in the Achilles tendon or heel with activity, stiffness, tenderness, swelling, and nodularity on palpation of the tendon.

109
Q

How is Achilles tendinopathy diagnosed, and what is an essential condition to rule out?

A

Achilles tendinopathy is primarily diagnosed clinically. It is important to rule out an Achilles tendon rupture, often using Simmonds’ calf squeeze test, with ultrasound used to confirm tendon ruptures.

110
Q

List some risk factors for Achilles tendon rupture.

A
  • Sports stressing the Achilles (e.g., basketball, tennis)
  • Increasing age
  • Existing Achilles tendinopathy
  • Family history
  • Fluoroquinolone antibiotics (e.g., ciprofloxacin) sometimes within 48hrs of starting abx
  • Systemic steroid use
111
Q

Describe the typical presentation of an Achilles tendon rupture.

A
  • Sudden onset of pain in the Achilles or calf
  • A snapping sound or sensation
  • Feeling as if something has hit the back of the leg
112
Q

What are key signs of Achilles tendon rupture on physical examination?

A
  • Affected ankle rests in a more dorsiflexed position
  • Tenderness in the Achilles area
  • Palpable gap in the tendon (may be obscured by swelling)
  • Weakness of plantar flexion
  • Inability to stand on tiptoes on the affected leg
  • Positive Simmonds’ calf squeeze test
113
Q

Which imaging method is used to confirm Achilles tendon rupture?

A

Ultrasound is the preferred method to confirm Achilles tendon rupture

114
Q

How should a suspected Achilles tendon rupture be initially managed?

A

Immediate management includes rest and immobilisation, ice, elevation, and analgesia. Venous thromboembolism prophylaxis may be necessary during ankle immobilisation.

115
Q

What are the main differences between non-surgical and surgical management of an Achilles tendon rupture?

A

Non-surgical: Involves immobilisation in a boot, gradually moving the ankle from full plantar flexion to neutral. Lower re-rupture risk but avoids surgery risks (e.g., anaesthetic, infection).

Surgical: Involves reattaching the tendon, followed by immobilisation in a similar boot sequence. Both methods require extensive rehabilitation for full recovery.

MSRA (18 decks)

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