Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine > MSK > Flashcards

MSK Flashcards

1
Q

Following microscopic repair of a severed digital nerve, you could expect sensation of the tip of the finger to grow back:

A

1mm/ day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What scan is most sensitive for stress fractures

A

Stress fractures can be confirmed on radionucleotide bone scan several days before changes are evident on a radiograph

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the rule of 2’s for x-rays

A
  • 2 views
  • 2 joints
  • 2 occassions
  • 2 sides (left and right)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is an avulsion fracture

A

An avulsion fracture is an injury to the bone in a location where a tendon or ligament attaches to the bone. When an avulsion fracture occurs, the tendon or ligament pulls off a piece of the bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is a pathological fracture

A

A pathologic fracture is a bone fracture caused by weakness of the bone structure that leads to decrease mechanical resistance to normal mechanical loads.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is a stress fracture

A

A stress fracture is a small crack in a bone, or severe bruising within a bone. Most stress fractures are caused by overuse and repetitive activity, and are common in runners and athletes who participate in running sports, such as soccer and basketball.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What variables influence how well a fracture heals?

A
  1. Would immobilisation
  2. Vascular supply
  3. Presence of infection
  4. Physical stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some common paediatric fractures

A

Paediatric fractures often have distinct fracture patterns due to the unique properties of growing bones.

  • The periosteum in growing bones is thicker and stronger than in adult bones, which is why children are more prone to more incomplete fractures, such as the greenstick fracture or torus fracture
  • In addition, the periosteum is metabolically active, this feature explains why childhood fractures heal faster than fractures in adults

Common paediatric fractures

  • Distal radius fracture
  • Clavicular fracture
  • Supracondylar humerus fracture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a Salter Harris fracture and its classification

A

Definition: Physeal or growth plate fracture

Salter-Harris Fracture Classification

  1. Type I: Transverse fractures of the physis, separating the epiphysis from the metaphysis
  2. Type II: Transverse fractures of the metaphysis and physis. Often involves separation of a triangular section of the metaphysis
  3. Type III: Transverse fractures of the physis and epiphysis. May extend to the joint, affecting the articular surface
  4. Type IV: Fractures through the metaphysis, physis, and epiphysis, entering the joint
  5. Type V:Impaction and disruption of the physis, occurs due to a crush or compression injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Treatment for Salter Harris fractures

A

Salter-Harris Type I and II

  • Closed reduction if displaced and immobilization in a cast with re-evaluation after 7-10 days
  • In case of severe dislocation or concomitant injury: surgical intervention

Salter-Harris Type III and IV

  • Open reduction is required to realign the joint surface because both these types affect the joint
  • Surgical intervention includes open reduction and internal fixation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Complications of Salter-Harris fracture

A
  • Disruption of growth and bone deformity (especially Salter-Harris Types III-V)
  • Leads to discrepancies in limb-length or angular deformities
  • Younger patients are more likely to experience growth arrest
  • Excessive limb growth is rare
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Treatment for open fractures

A
  1. IV antibiotics
  • Start as soon as possible, continue for 24 hours post closure
  • Usually 1st generation cephalosporin e.g. cefazolin
  1. Tetanus
    * If have not had a boost in past 5 years. Initiate in emergency room, toxoid 0.5mL or immunoglobulin
  2. Extremity Stabilization and Dressing
  • Stabilisation – splint, brace or traction for temporary stabilization
  • Dressing –
    • Remove gross debris from wound, do not remove any bone fragments
    • Place sterile saline-soaked dressing on wound
  1. Operative management
  • Urgent irrigation and debridement and antibiotic beads in open dirty wounds
  • Soft tissue coverage is ideal (flap coverage)
  • Reconstruction for bone loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Systematic approach to X-rays

A
  1. Demographics
  • Patient name, DOB, age, sex
  • Previous films (Compare with previous films and compare left to right)
  • Other orientations (Need AP and usually another view e.g. lateral)
  1. Radiograph detail
  • Date
  • Type (AP, lateral, other view)
  • Area of the body (including left or right)
  • Adequacy
  • Area: ideally need joint above and below
  • Rotation
  • Penetration (exposure)
  • Artifact
  1. Interpretation
  2. Alignment
    * Joints and bones – look for dislocation or subluxation
  3. Bones
  • Cortex – trace around looking for fractures
  • Bone fragments
  • Texture of bone between cortex
  1. Cartilage
  • Joint spaces
  • Disruption of joint contours
  • Signs of OA/ RA/ psoriatic gout/ pseudogout
  1. Soft tissue
  • Disruption
  • Swelling
  • Foreign bodies or calcification
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Osteoarthritis and the common joints it affects

A

“Wear and tear” - Progressive functional joint disorder, characterised by altered joint anatomy, especially loss of articular cartilage and is non-inflammatory.

Common joints

  • Knee > hand > hip
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

X-ray findings of osteoarthritis

A
  • Loss of joint space
  • Osteophytes
  • Subchondral sclerosis
  • Sub-articular cysts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Causes of osteoarthritis

A
  • Elderly
  • Family history
  • Pre-existing peculiarities of joint anatomy
  • Obesity
  • Excessive overuse (local inflammation, previous injuries)
  • Trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are heberden and bouchards nodes (Also what joints in the hand does osteoarthritis affect)

A

Heberden’s node - pain and nodular thickening on the dorsal sides of the distal interphalangeal joints

Bouchard’s nodes - pain and nodular thickening on the dorsal sides of the proximal interphalangeal joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

symptoms of osteoarthritis

A
  • Pain on exertion, which is relieved with rest
  • Pain in complete flexion and extension
  • Crepitus on joint movement
  • Joint stiffness and restricted range of motion
  • Morning joint stiffness usually lasting < 30 minutes
  • Gradual onset
  • Large weight bearing joints

In contrast to osteoarthritis, RA does not affect the first metatarsophalangeal or DIP joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Management of OA

A

Initial

  • Non-Pharm - Weight loss, exercise, heat therapy
  • Pharm - Paracetamol, Ibuprofen (NSAIDs), topical capsaicin

Then what else?

  • Duloxetine
  • Corticosteroid injection
  • Joint replacement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Differences between RA and OA

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is RA

A

Rheumatoid arthritis is a chronic inflammatory autoimmune disorder that is characterised by pain, welling, stiffness and destruction of synovial joints. The joints affected are usually peripheral, symmetrical and predominantly small joints (usually hand and feet)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Clinical featues of RA (Inluding extra-articular)

A
  • Pain, hot, swollen, restricted movement
  • Long duration of stiffness in mornings > 30 minutes
  • Systemic, usually small joints of hands and feet
  • Often symmetrical
  • Characteristic deformities: Swan neck, Boutonniere and Hitchhiker thumb deformity

Extra-articular manifestations of RA

  • Rheumatoid nodules
  • Pulmonary disease: Pleuritis, pleural effusion, alveolitis
  • Cardiac: pericarditis, valvular heart disease, pericardial effusion
  • Ocular: feratoconjunctivits sicca, episcleritis, scleritis
  • Neurologic: peripheral neuropathy, nerve entrapment, myelopathy
  • Vasculitis: nailfold, systemic
  • Cutaneous: palmar erythema, pyoderma gangrenosum
  • Haematologic: neutropaenia/ splenomegaly (Fetty’s), hyperviscosity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Investigations for RA

A

Lab tests

  • CRP/ ESR (acute phase reactants) – elevated

Serology

  • ACPA (anti-CCP) Anti-citrulinated peptide – autoimmune antibodies [high specificity]
  • Rheumatoid factor – autoantibodies against the Fc region of IgG [low specificity]
  • Antinuclear antibodies (ANA) – elevated in 30% of cases

Synovial fluid analysis

  • Synovial fluid is collected by joint aspiration, Findings:
  • Cloudy yellow appearance
  • Sterile specimen with leucocytosis

Imaging

  • X-ray
  • Early – soft tissue swelling, demineralization
  • Late – joint space narrowing, erosions of cartilage and bone, demineralisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Treatment of RA

A

Non-Pharm

  • refer to rheumatologist
  • smoking cessation
  • weight loss and exrcise

Pharm

Acute anti-inflam therapy

  1. Glucocorticoids e.g. methylprednisalone acetate 120mg IM
  2. NSAIDs

DMARDs

  1. Methotrexate 10mg orally, once weekly
  2. Leflunomide 10-20mg orally OD
  3. Sulfasalazine
  4. Hydroxychloroquine

bDMARDs

  • TNF-a inhib (Adalimumab 40 mg OD)
  • Ankinra (Anti-IL6)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do you monitor progress of RA treatment

A

Inflammation is most reliably assessed by the number of swollen or tender joints as well as the inflammatory markers C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR); neither measure should be used alone. Patient-reported outcomes include pain, physical function, psychological health, sleep patterns, relationships, and participation in social and work-related activities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is osteoporosis and osteopenia

A

Osteoporosis is a complex skeletal disease characterised by low bone density and micro-architectural defects in bone tissue, resulting in increased bone fragility and susceptibility to fracture.

Osteopenia – decreased bone strength but less severe than osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Causes of Osteoporosis (Primary and Secondary)

A

Primary Osteoporosis

  • Type I – post-menopausal women
  • Oestrogen stimulates osteoblasts and inhibits osteoclasts the decreased oestrogen levels following menopause leads to increased bone resorption.
  • Type II – gradual loss of bone mass (age > 70)

Secondary Osteoporosis

  • Drug induced – especially long term corticosteroids
  • Endocrine – hyperthyroidism, hypogonadism, hyperparathyroidismrenal disease
  • Immobilization
  • Alcohol abuse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Complications of osteoporosis

A

Pathological fractures – spontaneous fracture following mild physical exertion or minor trauma

  • Localisations – vertebral > femoral neck > distal radius (colles)
  • Vertebral compression fractures are commonly asymptomatic but may cause acute back pain
  • Decreased height (2-3cm with each fracture)
  • Thoracic hyperhyphosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Investigations for osteoporosis

A

DXA (Dual-energy X-ray absorptiometry)

  • Calculates bone mineral density
  • Osteoporosis: T-score <= - 2.5
  • Osteopenia: T-score of -1 to -2.5

Radiography

  • Can be diagnosed if vertebral compression fractures

Other tests

  • Urine – increase cross-links (e.g. deoxypyridinoline), markers of bone turnover
  • Blood tests
    • serum calcium,
    • serum 25-hydroxyvitamin D concentration
    • Alkaline phosphates
    • Serum phosphates
    • Serum TSH concentration
    • Liver biochemistry and kidney function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

treatment of osteoporosis

A

Pharmacological

  • Sufficient calcium and vitamin D intake
    1. Bisphosphonates (Alendronate, Risedronate)
  • Decrease bone resorption (osteoclastic activity)
    1. Denosumab – RANK Ligand Inhibitor
  • Decrease bone resorption (osteoclastic activity). Monoclonal antibody blocks RANKL-RANK interaction
    1. Teripartide
  • Recombinant PTH – increases bone formation – osteoblastic activity
  • Side effects - Increase risk of DVT
  1. Raloxifene
    * Selective oestrogen receptor modulator – decrease bone resorption (osteoclastic activity)
  2. Testosterone
    * Decrease bone resorption

Non- Pharmacological

  • Stop smoking/ drinking
  • Exercise
  • Falls reduction strategies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is gout?

A

Gout is a common inflammatory arthropathy characterised by painful and swollen joint resulting from precipitating uric acid crystals.

Acute gout attacks typically manifest with a severely painful big toe (podagral) and occur most often in men following triggers such as alcohol consumption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Causes of gout

A

Hyperuricaemia predisposes to gout.

  • Uric acid is an end-product of purine metabolism that is removed feom the human body by renal excretion
  • Insufficient excretion or increased production of purines leads to hyperuricaemia, possible triggering a gout attack
  1. Primary hyeruricaemia (aggravated by poor dietary habits)
  2. Secondary hyperuricaemia
  • Decreased uric acid excretion Medications (NSAIDs, loop diuretics, thiazides, pyrazinamide)
  • Chronic renal insufficiency
  • Ketoacidosis, lactic acidosis
  • Increased uric acid production
  • High cell turnover (haemolytic anaemia, psoriasis, chemotherapy, radiation)
  • Enzyme defects
  • High-protein diet
  • Obesity
  • Combined decrease excretion and overproduction
    • Alcohol consumption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

clinical features of gout

A
  • Usually mono-arthritic during first attack
  • Very painful joint with redness, decreased range of motion, swelling and warmth
  • More likely to occur at night, typically waking the patient
  • Symptoms peak after 12-24 hours; regression may take days to weeks
  • Most commonly metatarsophalangeal inflammation of the big toe

Chronic gout

  • Tophi formation – multiple painless hard nodules with possible joint deformities, usually on extensor surface
  • Renal manifestations with uric acid nephrolithiasis and uric acid nephropathy
  • Progressive joint destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Investigations for gout

A
  1. Arthrocentesis
  • Polarized light microscopy findings – negatively birefringent monosodium urate crystals
  • Synovial fluid findings: WBC > 2000/uL with > 50% neutrophils
  1. Laboratory tests
  • Increased serum uric acid levels
  • Typical in acute attacks – raised WBC and ESR
  1. Imaging
  • Normal in early disease
  • MRI – detect tophi formation
  • CT – bone erosion and tophi
  • X-ray – in acute gout isn’t useful, in chronic gout detects punched-out lytic bone lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Treatment in acute and chronic gout

A

*Do not start urate-lowering until 2-4 weeks after attack resolved

Treat as it is super painful and high uric acid levels is risk factor for CVD, stroke and kidney disease

Acute gout

  1. NSAIDs
  2. Glucocorticoids (prednisolone 15-30mg orally)
  3. Intra-articular corticosteroids
  4. Colchicine 1mg orally initially, then 500mcg 1 hour later, as a single one-day course (total 1.5mg)
  • Bind tubulin which stops microtubule assembly to affect cell division, neutrophil motility, decrease chemokine production, overall it stops inflammatory cell recruitment
  • Side effects – vomiting, diarrhoea

Chronic gout

  1. Allopurinol 50mg orally, daily for 4 weeks; then increase by 50mg every 2 to 4 weeks or by 100mg every 4 weeks to achieve the target serum uric acid concentration
  • Inhibits Xanthine oxidase to decrease uric acid synthesis
  • Side effects – GI, stevens-Johnson syndrome
  • Allopurinol increases the effects of mercaptopurine and azathipprine
  1. Febuxostat
    * Non-purine selective inhibitor of XO
  2. Uricase agent – Rasburicase
    * Catalyses conversion of uric acid to allantoin
  3. Uricosuric agent – Probenicid 250mg BD and titrated up, Benzbromarone
    * Blocks urate reuptake in the proximal tubules, acting on URAT 1

*Add on prophylactic colchicine to prevent flare up with urate lowering therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is Pseudogout (Calcium Pyrophosphate Deposition Disease) and what are the clinical features, investigations and treatment

A

Clinical features

  • Usually monoarthritis, mostly affecting the knees and other large joints
  • May become chronic (osteoarthritis with CPPD most common symptomatic CPPD)
  • Progressive joint degeneration with episodes of acute inflammatory arthritis

Investigations

  1. Arthrocentesis
  • Polarized light microscopy findings – rhomboid-shaped, positively birefringent CPPD crystals
  • Synovial fluid findings: WBC between 10,000-50,000/uL with > 90% neutrophils
  1. Laboratory tests
  • Hypercalcaemia
  • Serum uric acid levels are normal
  • Typical in acute attacks – raised WBC and ESR
  1. Imaging (X-ray)
  • Cartilage calcification of the affected joint
  • Fibrocartilage and hyaline cartilage may be affected

Treatment

  1. Asymptomatic cases do not require treatment unless there is an underlying condition (hyperparathyroidism)
  2. NSAIDs
  3. Colchicine or intra-articular corticosteroids
  4. Arthroscopic lavage
  5. Joint replacement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

pathophysiology and pathogens in osteomyelitis

A
  1. Haematogenous osteomyelitis
  • Most commonly due to a single pathogen
  • Bodily infection à enters bloodstream à infiltrates bone marrow
  1. Exogenous osteomyelitis
    * Usually multiple pathogens
  2. Post-traumatic – infection following deep injury
  3. Contiguous – spread of infection from adjacent tissue (e.g. secondary to infected foot ulcer)

Pathogens

  • most common –> Staphylococcus aureus
  • staph epidermidis (Diabetic0
  • Pseudomonas aeruginnosa (IVDU)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Clinical feature of osteomyelitis

A

Acute

  • Pain at site of infection, possibly related to movement
  • Point tenderness, swelling, redness, warmth
  • Malaise, fever, chills

Chronic

  • Recurrent pain
  • Swelling, redness
  • Local sinus tract formation, perhaps draining pus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Investigations in osteomyelitis

A

Lab tests

  1. Inflammatory markers (raised CRP and ESR)
  2. Leukocytosis
  3. Blood cultures

Imaging

  1. X-ray – in later stages can see bone destruction, sequestrum formation, periosteal reactions
  2. MRI – shows signs of inflammation < 5 days after infection onset
  3. Skeletal scintigraphy – visualises areas of increased bone turnover
  4. Sonography – assess soft tissue involvement
  5. Radionuclide-labelled leukocyte scintigraphy

Biopsy – confirmatory test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Treatment for osteomyelitis

A
  1. Bed rest and immobilization of affected extremity
  2. Antibiotics
  • IV vancomycin + cefeprime/ ciprofloxacin
    1. Surgical
  • Debridement of necrotic bone or tissue
  • Abscess drainage
  • Infected prosthetic removal
  • Revascularisation in case of poor wound healing due to peripheral artery disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Common pathogens and variants of septic arthritis

A

Pathogens

  • Staphylococcus aureus
  • Streptococci
  • Staphylococcus epidermidis
  • H. influenzae
  • Neisseria gonorrhoea

Variants

  1. Prosthetic joint infection
  2. Bacterial coxitis
  3. Gonococcal arthritis
  4. Lyme disease arthritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Clinical features of septic arthritis

A
  • Acute onset
  • Usually monoarticular (knee, hip, wrist, shoulder)
  • Triad of:
  • Fever
  • Joint pain
  • Restricted range of motion
  • Join may be swollen, red, warm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Investigations for septic arthritis

A
  1. U/S guided arthrocentesis (definitive diagnosis requires detection of bacteria in synovial fluid)
  • Synovial fluid gram stain and culture
  • Increased synovial fluid WBC (above 50,000 per high-powered field) and dominance of polymorphonuclear (neutrophil > 90% à bacterial) cells
  • Fluid appears yellowish-green and turbid
  • Also alleviates pain by decreasing intraarticular pressure
  1. Lab tests
  • Raised CRP/ ESR
  • Blood culture – at least 2 sets of blood cultures to rule out a bacteraemic origin
  1. Imaging
  • Look for signs of underlying osteomyelitis and concurrent joint disease
  • U/S – effusion, oedema of the surrounding soft tissue, possible empyema
  • X-ray – unremarkable early; osteolysis usually visible after 2-3 weeks
  • MRI or scintigraphy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Treatment for septic arthritis

A
  1. Following arthrocentesis and culture, simultaneous empiric antibiotic therapy (based on gram stain) and evacuation of purulent material
  • Gram positive cocci à Vancomycin
  • Gram negative cocci à ceftriaxone
  • Grame negative bacilli à ceftriaxone
  • Pseudomonas infection à Gentamicin
  • Tailor antibiotics to gram stain and culture
    1. Immobilisation and NSAIDs for pain relied and reduce inflammation

Physiotherapy to prevent contracture of both joint and capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Clinical features (exam findings) of a lipoma

A
  • Slow-growing round, soft ‘rubbery’ tumour
  • Non-tender
  • Localization: almost any subcutaneous region
  • Mobile, superficial, soft, <5cm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is bursitis and where are some common locations

A

Bursitis is an cute or chronic inflammatory condition of a bursa. A bursa is a jelly-like space that usually contains a small amount of synovial fluid. A bursa lies between a tendon and either bone or skin to act as a friction buffer and facilitate movement of adjacent structures. In primary care, bursitis is most commonly present in the knee, subacromial, trochanteric, retro calcaneal and olecranon bursae.

  1. Olecranon bursitis – inflammation of the bursa of the elbow joint that is often caused by leaning on the elbow for long periods of time
  2. Subacromial bursitis – inflammation of the bursa located between the acromion and the supraspinatus muscle that is often caused by repetitive overhead motion
  3. Prepatellar bursitis – inflammation of the bursa between the skin and the patella that is often caused by chronic strain on flexed knee joints or after falls on the knee
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is compartment syndrome

A

Compartment syndrome is a condition in which increased pressure within a muscle compartment (containing nerves and vasculature, enclosed by unyielding fascia) leads to impaired tissue perfusion. It most commonly affects the lower legs, but can also occur in other parts of the extremities or the abdomen.

Compartment syndrome may be acute (e.g. after trauma) or chronic (e.g. collectively excessive training in athletes).

Acute compartment syndrome is a surgical emergency which initially presents with rapidly progressive pain, paraesthesia, and pallor. Pronounced neurological symptoms with motor deficits, absent pulses and poikilothermic (cool limb) occur later on and indicated irreversible damage.

This diagnosis should be suspected on the basis of clinical findings and then confirmed via measurement of compartment pressures.

48
Q

causes of compartment syndrome

A

Trauma-related

  • External compressing forces
  • Constrictive bandage/ cast
  • Burn eschars - A skin lesion characterized by dried, necrotic, skin tissue. Etiologies include burns, infection, gangrene, and pressure ulcers.
  • Internal expanding forces
  • Fracture haematoma
  • Blood vessel injury with haermorrhage
  • Repetitive muscle use
  • Crush injury
  • Penetrating injury (gunshot, stab wound)
  • Burn oedema
  • Reperfusion syndrome with ischaemia-reperfusion oedema

Non-traumatic

  • External compressing forces
  • Incorrect positioning limbs (e.g. immobile patient)
  • Internal expanding forces
  • Increased capillary permeability e.g. shock
  • Coagulopathies
49
Q

clinical features of compartment syndrome

A

Most common sites are the lower legs and arms. Less common sites include the feet, hands, thighs and gluteal region.

Acute compartment syndrome

Typically present with a rapid progression of symptoms

Early presentation

  • Pain
  • Often out of proportion to the extent of injury
  • Worse with passive stretching or extension of muscles
  • Very tight, wood-like muscles that are extremely tender to touch
  • Paraesthesia (pins and needles)
  • Soft tissue swelling
  • Initially, peripheral circulation and distal pulses are maintained

Late presentation

  • Muscle weakness to paralysis
  • Absent (or weak) distal pulses
  • Cold peripheries
  • Pallor or cyanosis
  • Worsened pain and swelling

6 P’s of acute limb ischaemia: Pain, Pallor, Paraesthesia, Perishingly Cold Peripheries, Pulsenessless, Paralysis

50
Q

Investigations for compartment syndrome

A
  1. Compartment pressures (initial and confirmatory test)
  • Measurement of tissue pressure with a manometer and calculation of delta pressures
    (delta pressure = diastolic – tissue pressure = less than 30mmHg
  1. Lab tests for rhabdomyolysis
  • Blood
    • CK increased
    • Myoglobin increased
    • Lactate dehydrogenase increased
    • Raised potassium and phosphate, reduced calcium
  • Urine – myoglobinuria
  1. X-ray
  2. Pulse oximetry – help to identify limb hypoperfusion
51
Q

treatment of compartment

A

Surgical treatment

Is required for all cases of acute compartment syndrome. Also indicated if conservative treatment fails in chronic compartment syndrome.

  1. Fasciotomy (tissue and fascia incisions) to relieve pressure, thus restoring perfusion
  • Should be conducted within 6 hours after the onset of the condition to prevent necrosis
  • If fasciotomy fails à may need fibulectomy
  1. Escharotomy – in cases of circumfrential compression by burn eschar
  2. Last resort is amputation

Supportive measures

Indicated as perioperative care

  • Eliminate any underlying cause e.g. remove restrictive cast/ dressing
  • Cooling and positioning of the limb at heart level to relieve pressure
    • Note – elevated psotiioning may worsen ischaemia by reducing blood flow
  • Close monitoring
  • Correct any fluid imbalances
  • Supplemental oxygen
  • Analgesia

Most common type is anterior compartment syndrome of lower leg. Presents with:

  • Sensory – loss of sensation/ paraesthesia in the nerve territory
  • Motor – toe dorsiflexion weakness
52
Q

Causes of spinal cord compression

A
  • Acute onset (within minutes to hour):
  • Vertebral fracture
  • Acute disc herniation
  • Spondylolisthesis
  • Haematoma
  • Trauma – vertebral fracture of facet joint dislocation
  • Insidious onset
  • Abscess
  • Primary tumour, metastasis
  • Degenerative spine changes – spondylosis
  • Stenosis
  • Osteophytes
53
Q

Clinical features of spinal cord compression

A

Depends on the location of the spinal compression

Common features

Neurological deficits below the level of the lesion (first sensory abnormalities, followed by motor and/ or bladder/ bowel dysfunction)

  • Sensation and proprioception will often be impaired at dermatome levels below the cord compression
  • Back pain or radicular pain
    • Pain often aggravated by straining such as coughing or sneezing
  • Bilateral or unilateral weakness in most cases
  • Upper motor neurone signs present (as opposed to the lower sign seen in peripheral nerve compression or cauda equina syndrome)
    • Hypertonia, hyperreflexia, Babinski sign, clonus
    • Reflexes tend to be absent at the level of the lesion, as the lower motor neurone within the ventral horn is compressed, so producing a lower motor neurone deficit
  • Any autonomic involvement is a late stage and therefore carries a worse prognosis. Clinical features include bowel incontinence or constipation or urinary retention
54
Q

Management of spinal cord compression/ spinal cord injury

A

Acute

  • Intensive medical care and analgesia
  • Insert urinary catheter
  • VTE prophylaxis (Heparin)
  • IV corticosteroids to reduce swelling and inflammation of spinal cord

Definitive

  • Bracing or surgical repair (decompression and stabilization of spine fracture)
  • C1-4 tetraplegia: phrenic nerve pacemakers may be indicated; a tracheostomy and/ or ventilator may be needed

Rehabilitation

  • Making aids
  • Physical, occupational, psychotherapy
  • Pressure ulcer prophylaxis, osteoporosis prophylaxis, treatment of pneumonia and UTIs
55
Q

What is degenerative disc disease (Disc protrusion, disc herniation, disc sequestration)

A

DDD refers to a variety of pathologies with displacement of disc material into the spinal canal, such as protrusion, herniation and sequestration. DDD results in mechanical compression on either the spinal cord or a nerve root.

  1. Disc protrusion: Pressure on the vertebra causes the gelatinous core, called the nucleus pulposus, to move and press against the annulus fibrosis. This bulge compresses a spinal nerve and thus causes paint
  2. Disc herniation (Disc extrusion or prolapse): A tear in the annulus fibrosis results in extrusion of then nucleus pulposus and potential compression of the spinal nerve
  3. Disc sequestration: Extrusion of the nucleus pulposus and separation of a fragment that enters the spinal canal and may cause compression of the spinal nerve
56
Q

clinical features of degenerative disc disease

A
  • Acute onset of severe back pain
  • Stabbing or resembling electric shock
  • Radiates to the legs (sciatic pain) or the arms
  • Paraesthesia of affected dermatome
  • Muscle weakness and atrophy
  • Loss of deep tendon reflexes in the indicator muscles
  • Pain increases with pressure (coughing, sneezing)
  • Short walks and changing position reduces the pain
57
Q

Investigations and physical examinations for suspected disc herniation

A
  1. Physical examination (reflexes, motor strength, sensory deficits)
  2. Straight leg-raising manoeuvres
  • Straight leg is raised à increased pain in the ipsilateral leg with radiation to the motor or sensory area of the affected nerve root
  • Crossed straight leg raise test: opposite straight leg of patient raised à increased pain in contralateral leg with radiation into the motor/ sensory area of the affected nerve root
  1. Spurling’s manoeuvre
  • Used for cervical spine radiculopathy
  • Forward flexion, tilting, and rotation of the neck towards the affected side and application of downward pressure to the head à reproduction of pain or paraesthesia
  1. MRI
  2. CT-myelogram
  3. Plain radiographs (Won’t show herniated disc, but can show spondylolisthesis, osteophytes, stenosis)
58
Q

treatment for disc herniation

A

Conservative

  • Physiotherapy with exercises strengthening the back
  • No bed rest, but continuation of activities
  • Local heat
  • Analgesics (NSAIDs)
  • Periradicular therapy: CT-navigated injection of a local anaesthetic (e.g. ropivacaine) and glucocorticoids at the intervertebral foramen

Surgical

  • Emergency indications:
  • Significant progressive neurological deficits
  • Bladder or bowel incontinence
  • Cauda equina syndrome/ conus medullaris syndrome
59
Q

What is radiculopathy

A

Radiculopathy is a conduction block in the axons of a spinal nerve or its roots, with impact on motor axons causing weakness and on sensory axons causing paraesthesia and or anaesthesia

The distinction between radiculopathy and radicular pain

  1. Radiculopathy is a state of neurological loss and may or may not be associated with radicular pain
  2. Radicular pain is pain deriving from damage or irritation of the spinal nerve tissue particularly the dorsal root ganglion
60
Q

causes of radiculopathy

A

Radiculopathy is most commonly a result of nerve compression, which can be caused by:

  • Intervertebral disc prolapse
    • The lumbar spine is predominantly affected by repeated minor stresses that predispose to rupture of the annulus fibrosus and sequestration of disc material (the nucleus pulposus)
  • Degenerative diseases of the spine – leading to neuroforaminal or spinal canal stenosis
    • The cervical spine is the most mobile segment of the spine and degenerative change is a normal part of ageing process; 80% of the population over 55 years old have degenerative changes between C5/6 and C6/7
  • Fracture – either trauma or pathological
  • Malignancy – most commonly metastatic
  • Infection – such as extradural abscesses, osteomyelitis (most commonly tuberculosis (‘Pott’s disease’)), or Herpes Zoster
61
Q

Management for radiculopathies

A

Definitive long-term management depends on the underlying cause. In general, the only condition that requires emergency surgical treatment is cauda equina syndrome.

Most IV disc prolapses can be managed non-operatively, but indications for surgical treatment include unremitting pain despite comprehensive non-surgical management, progressive weakness, and new or progressive myelopathy (compression of the spinal cord).

Symptomatic management

Analgesia is an important aspect of management in these patients. The WHO analgesic ladder can be utilised in the first instance, however neuropathic pain medications are frequently utilised.

Amitriptyline is usually first line, which may then be added to GABA antagonists (such as pregabalin or gabapentin). The patients may also suffer from muscle spasms and these can be managed with benzodiazepines (often diazepam) and/or baclofen.

Physiotherapy remains an important part of management in this patient group.

62
Q

What is sciatica

A

The pain from sciatica is felt along the path of the sciatic nerve and can be felt deep in the buttock, with pain that travels down the back of the leg, sometimes to the foot. The pain can be accompanied by tingling, ‘pins and needles’, or numbness, and sometimes by muscular weakness in the leg.

Sciatica is usually felt in only one leg at a time. Sometimes, a sensation like an electric shock can be felt along the nerve. The nerve pain can range from a mild ache to incapacitating pain. Sciatic nerve pain is often felt when you sneeze, cough, go to the toilet, or when you’re sitting, and may be accompanied by lower back pain.

63
Q

What is cauda equina syndrome and its features

A

The Cauda Equina is a bundle of nerves situated inferior to the spinal cord.

The spinal cord tapers to an end (known as the conus medularis), approximately at the first lumbar vertebra, with nerve roots L1-S5 leaving from at this region to pass down the spinal canal (as the cauda equina) to exit at their respective foramaina.

Consequently, the cauda equina is formed by lower motor neurons, containing motor and sensory impulses to the lower limbs, motor innervation to the anal sphincters and parasympathetic innervation to the bladder.

Features:

  • Lower motor signs and symptoms
  • Reduced lower limb sensation (often bilateral)
  • Bladder or bowel dysfunction
    • E.g. bladder retention
  • Impotence
  • Lower limb motor weakness
  • Severe back pain

Phyisical

  • Perianal or lower limb anesthesia, loss of anal tone, urinary retention
  • Lower limb weakness
  • Hyporeflexia
64
Q

causes of cauda equina syndrome

A
  1. Disc herniation (most common at L5/S2 and L4/5 level)
  2. Trauma – including vertebral frature and subluxation
  3. Neoplasm
  4. Infection e.g. Discitis or Potts disease
  5. Chronic spinal inflammation e.g. ankylosing spondylitis
  6. Iatrogenic – haematoma secondary to spinal anesthesia
65
Q

treatment of cauda equina

A
  1. High dose steroids e.g. dexamethasone to reduce localized swelling
  2. In case of trauma à immobilization
  3. Surgical decompression
66
Q

what is spinal shock

A

Complete spinal cord injury is the complete sensory and motor loss below the site of spinal cord injury following acute or chronic destruction, compression or ischaemia of the spinal cord.

Initially it may present as spinal shock, which is an acute physiological loss or depression of spinal cord function. It presents as a flaccid areflexic paralysis below the level of the injury with autonomic features (e.g. hypotension and bradycardia)

After some days to weeks the spinal shock wears off and a complete spinal cord injury may remain. It presents with spastic paresis, hyperreflexia, and continues sensory loss.

67
Q

What are the rotator cuff muscles and there function

A

Rotator cuff is a group of 4 muscles that support and rotate the gleno-humeral joint

  • Supraspinatus – abduction
  • Infraspinatus – external rotation
  • Teres minor – external rotation
  • Subscapularis – internal rotation
68
Q

Special tests of the shoulder for rotator cuff pathology

A
  1. Empty Can test – tests the supraspinatus
    * Positive test present if there is weakness on resistance
  2. Lift-off test – tests subscapularis
    * Positive test is weakness in actively lifting the hand away from back
  3. External rotation test
    * Positive test is weakness on resistance when externally rotating arm with elbow flexed at 90 degrees
69
Q

treatment of rotator cuff tear

A

Conservative

Preferred if not limited by pain

  1. Analgesia
  2. Physiotherapy
  3. Corticosteroid injections into the sub-acromial space

Surgical

For those remaining symptomatic despite conservative management OR large tear

70
Q

What is adhesive capsulitis and the clinical features

A

Adhesive capsulitis is a chronic fibrosing condition characterized by insidious and progressive severe restriction of both active and passive shoulder range of motion in the absence of a known intrinsic disorder of the shoulder. It is generally regarded as a self-limiting condition that usually resolves within 18 to 24 months.

The glenohumeral join capsule becomes contracted and adherent to the humeral head.

Clinical features

  • Shoulder stiffness
  • Decreased range of active and passive motion
  • Generalized deep and constant pain of the shoulder, that often disturbs sleep
71
Q

what are some risk factors for developing adhesive capsulitis

A
  • Rotator tendinopathy
  • Sub-acromial impingement syndrome
  • Biceps tendinopathy
  • Previous surgery
  • Diabetes mellitus
  • Inflammatory conditions
72
Q

treatment for adhesive capsulitis

A

Conservative

  • Self-limiting condition, however recurrence is not uncommon
    • Usually occurs over months to a few years
  • Initial management involves education and reassurance
  • All patients should receive physiotherapy
  • Analgesia with paracetamol or NSAIDs, glunohumeral joint infections may be considered if patient fails to improve

If not improvement following three months of conservative treatment or symptoms significantly affecting quality of life may benefit from surgical intervention

73
Q

What are the types of shoulder dislocations

A
  1. Antero-inferior dislocation (95%)
    Anterior dislocation is classically caused by force being applied to an extended, abducted and externally rotated humerus
  2. Inferior dislocation
  3. Posterior dislocation
74
Q

associated injuries in shoulder dislocations

A

Shoulder dislocations have many commonly associated injuries, which can be divided into bony or labral and ligamentous problems:

  • Bony:
    • Bony Bankart lesions are fractures of the anterior inferior glenoid bone, most commonly present in those with recurrent dislocations
    • Hill-Sachs defects are impaction injuries to the chondral surface of the posterior and superior portions of the humeral head, present in approximately 80% of traumatic dislocations
    • Fractures of the greater tuberosity and the surgical neck of humerus can also occur
  • Labral, ligamentous, and rotator cuff:
    • (Soft) Bankart lesions are avulsions of the anterior labrum and inferior glenohumeral ligament
    • Glenohumeral ligament avulsion
    • Rotator cuff injuries occur frequently in anterior dislocations; in younger patients, around a third have at least one tear
  • Arterial and neuro
    • Injury to the axilla à consequent paralysis of the deltoid muscle, with a small area of anaesthesia at the lateral aspect of the arm
    • Fracture of greater tuberosity of the humerus
    • Occasionally – axillary artery damage and damage to posterior brachial plexus
75
Q

Management of shoulder dislocation

A
  1. Reduction
  • Closed reduction using the Hippocratic method
  • Assess the neurovascular status both pre and post reduction
  • Any failed closed reduction may warrant attempted manipulation under anesthesia in theatres
  1. Immobilization
  • Once reduced, the arm should be placed in to a broad-arm sling
  • Typically for 2-3 weeks, apply ice
  1. Rehabilitation
    * All dislocations require physiotherapy aiming to restore range of movement, functionality and to strengthen the rotator cuff and pericapsular muscular

*Don’t drive, play sports, lift arm above head

76
Q

What is subacromial impingement syndrome

A

SAIS refers to the inflammation and irritation of the rotator cuff tendons as they pass through the subacromial space, resulting in pain, weakness and reduced range of motion within the shoulder.

SAIS encompasses a range of pathology including:

  • Rotator cuff tendinosis
  • Subacromial bursitis
  • Calcific tendinitis

All these conditions result in an attrition between the coracoacromial arch (Acromion, coracoacromial ligament and coracoid process) and above the humeral head and greater tuberosity of the humerus.

77
Q

clinical features and physical examination forsubacromial impingement syndrome

A
  • Progressive pain in the anterior superior shoulder
  • Pain is classically exacerbated by abduction and relieved by rest
  • May be associated with weakness and stiffness secondary to the pain

Physical Examination

  1. Neers impingement test
    * The arm is placed by the patients side, fully internally rotated and then passively flexed, and is positive if there is pain in the anterolateral aspect of the shoulder
  2. Hawkins test
    * The shoulder and elbow are flexed to 90 degrees, with the examiner then stabilizing the humerus and passively internally rotates the arm, and the test is positive if pain is in the anterolateral aspect of the should
78
Q

management of subacromial impingement

A

Conservative for most cases

  1. Analgesia - NSAIDs
  2. Regular physiotherapy
  3. Corticosteroid injections if require further treatment
  • 40mg methylprednisolone + local anaesthetic, anterior lateral approach, US guided

Surgical intervention

If SAIS persists beyond 6 months without response to conservative management surgical intervention is recommended

  • Surgical repair of muscular tears
  • Surgical removal of the subacromial bursa
  • Surgical removal of a section of the acromion – subacromial decompression
79
Q

Classification of clavicle fracture

A
  • Type I – fracture of the middle third of the clavicle, constituting 75% clavicular fractures (as the middle third is the weakest segment)
    • They are generally stable, although significant deformity is usually present
  • Type II – fractures involving the lateral third of the clavicle and constituting around 20% of all clavicular fractures
    • When displaced, these type are often unstable
  • Type III – remaining 5% occur in the medial third of the clavicle, commonly associated with multi-system polytrauma
    • As the mediastinum sits directly behind the medial aspect of the clavicle, they can be associated with neurovascular compromise, pneumothorax, or haemothorax
80
Q

Complications of clavicle fractures

A
  • Due to the subcutaneous location of the clavicle, it is important to specifically look for open injuries or threatened skin (appearing as tended, tethered, white and non-blanching skin)
  • Ensure to check neurovascular status of the upper limb, given the propensity for brachial plexus injuries
  • Haemorthorax, pneumothorax
  • Non-union is a major complication of clavicle fractures, most associated with a distal third clavicular fractures
  • Healing time for most clavicular fractures in adults is 4-6 weeks
81
Q

management of clavicle fracture

A

Most can be treated conservatively

  • Over 90% of displaced fractures will unite
  • Metal work is often prominent and therefore requires removal after fracture union

Conservative management

  1. Sling - elbow supported and improves the deformity. Keep sling until the patient regains pain-free movement of the shoulder.
  2. Early movement of the shoulder joint recommended, to prevent development of frozen shoulder

*However proximal fractures may need more management in case of traumatic lung injury

Surgical management

  • Indication: open fractures, very comminuted fractures , bilateral or those that are very shortened
82
Q

What is tendinitis, tendinosis and tenosynovitis

A

Tendinitis – inflammation of the tendon (Where mucle inserts to bone) and results from micro-tears that happen when the musculotendinous unit is acutely overloaded with a tensile force that is too heavy and/ or too sudden

Tendinosis – degeneration of the tendon’s collagen in response to chronic overuse; when overuse is continued without giving the tendon time to heal and rest, such as with repatative strain injury

Tenosynovitis - An inflammation of a tendon and its synovial sheath. Most commonly affects the hands and wrists. Often due to tendon overuse (e.g., texting, typing)

83
Q

Lateral Epicondylitis (Tennis Elbow) clinical features

A

Epicondylitis is a chronic symptomatic inflammation of the forearm tendons at the elbow. It is an overuse syndrome in the elbow, caused by micro tears in the tendons attaching to the epicondyles of the elbow following repetitive injury.

Clinical features

  • Pain affecting the elbow and radiating down the forearm
  • The pain typically worsens over weeks to months, most often affecting the dominant arm
84
Q

physical examination tests for tennis elbow

A
  • Local tenderness on palpation over the lateral epicondyle and common extensor tendon
  • Due to the pain there may be reduced grip strength, despite full range of movements at the wrist and elbow

Special tests for lateral epicondylitis – both tests being positive if pain is felt during the respective manoeuvres

  1. Cozen’s test
  • The patients elbow is help flexed at 90 degrees, with one examiners hand held over the lateral epicondyle, whilst the other hand holds the patients hand in a radially deviated position with the forearm pronated
  • The patient is then asked to extend their wrist against resistance from the doctor
  1. Mill’s test
    * The patients lateral epicondyle is palpated by the examiner, whilst also pronating the patients forearm, flexing the wrist, and extending the elbow
85
Q

Management of tennis elbow (lateral epidondylitis)

A

Conservative

  1. Modify activities, reducing the repetitive actions causing the condition
  2. Simple analgesics alongside topical NSAIDs
  3. If symptoms persist, corticosteroid injections can be administered
  4. Physiotherapy can provide longer term relief via stretching and strengthening exercises
  5. Orthoses (a wrist or elbow brace) can be used in conjunction with physiotherapy for potential longer term symptom relief

Surgical

  1. Referrals to an orthopaedic surgeon may be warranted if symptoms are not controlled through conservative measures
  2. Open or arthroscopic debridement of tendinosis and/ or release or repair of any damage tendon insertions may be required. If the tendon has more than 50% damage, tendon transfer may be required to ensure function is retained.
86
Q

Treatment of radial head fracture

A
  • Mason type 1 - non-displaced or minimally displaced fracture (<2mm)
  • Mason type 2 –particular articular fracture with displacement > 2mm or angulation
  • Mason type 3 – comminuted fracture and displacement
  • Mason type 1 injuries – treated non-operatively, with a short period of immobilization with sling (less than 1 week) followed by early mobilization
    • A plaster is applying with the elbow at a right angle and with the forearm midway between pronation and supination (Long arm cast). The plaster is worn for 3 weeks, after which active mobilizing exercises are arranged.
  • Mason Type 2 injuries – if no mechanical block then can be treated as per a type 1 injury, whilst if a mechanical block is present then these may need surgery (typically an open reduction internal fixation (ORIF))
  • Mason Type 3 injuries – will nearly always warrant surgical intervention, either via ORIF or radial head excision or replacement (especially in highly comminuted fractures)
87
Q

What is a Monteggia Fracture

A

A Monteggia fracture is a displaced fracture of the ulnar accompanied by a dislocation of the radial head.

It is usually caused by a fall associated with forced pronation of the forearm. The unla is angles forwards and the head of the radius is dislocated forwards.

Can be reduced with closed methods. Should then be plastered with elbow at a right angle and forearm supinated.

88
Q

What is a Galeazzi fracture

A

A Galeazzi fracture occurs when the radius is fractured in the shaft and there is a dislocation of the lower end of the ulna. Usually requires operative reduction.

89
Q

What are the common humeral fractures in the elderly and children

A
  1. Proximal humerus fractures commonly occur in the elderly
  2. Distal supracondylar fractures are the most common type of fracture in the paediatric population
90
Q

Complications of proximal, shaft and distal fractures of humerus

A

Proximal fracture

  • Adhesive capsulitis/ joint stiffness
  • axillary nerve damage
  • Avascular necrosis of humeral head (axillary artery injury)
  • Heterotopic bone formation
  • dislocation of shoulder

Humeral shaft fracture

  • Radial nerve palsy (common)

Distal humeral fracture

  • Malunion and varus deformity of elbow
  • Brachial artery injury (common)
    • Absent radial pulses suggest brachial artery entrapment (especially following reduction) and compartment syndrome
  • -> Volkmann’s ischaemic contracture (late complication)
    • median nerve, ulnar nerve or radial nerve palsy
    • Median nerve and brachial artery injuries, which both cross the elbow, are common complications of supracondylar fractures
91
Q

Treatment of humeral factures

A

Conservative

  • Indication: nondisplaced, closed fracture
  • Hanging-arm cast or coaptation splint and sling for approximately one to two weeks; subsequent follow-up X-ray and brace

*The shoulder is prone to become stiff if it is immobilised for a long time, especially in old persons

  • Early physical therapy to restore function

Surgical

  • Indication: open fractures, displaced fractures that cannot be reduced, associated injuries (nerves, blood vessels), floating elbow (simultaneous humerus and forearm fracture), pseudarthrosis
  • Procedures
    • Internal fixation using plates and screws, or intramedullary implants
    • External fixation (e.g. open fracture, polytrauma)
    • Arthroplasty of humeral head or elbow (complex fractures or poor quality bone), especially in elderly

Proximal (neck)

  • Impacted à immobilization is unnecessary. Active and assisted shoulder movements should be begun immediately and continued daily, can use sling intermittently
  • Unimpacted à immediate shoulder exercises impractical because of pain. Arm should be supported in a sling. Elbow, hand and wrist exercises started promptly, shoulder exercises started in 3 weeks.
  • Good results of function for elderly with displaced fracture (may not bother). With younger patients, try reduce. Then place in abduction in a plaster shoulder spica

Shaft #

  • Reduction
  • Most surgeons rely upon a plaster cylinder encircling only the upper arm from the axilla to the elbow
  • Some prefer to extend the plaster down to the forearm, with the elbow fixed at 90 degrees
  • In either case further support with a sling

Epidoncondylar fracture

  • Undisplaced fractures à 3 weeks in hanging cast
  • If brachial artery damage
    • Remove any splint or bandage as could be constricting circulation
    • Displacement of the fragments corrected with gentle manipulation
    • Hot bottles applied over the other three limbs to promote general vasodilation
    • If these three steps don’t bring about adequate circulation in 30 mins then à
    • surgery
92
Q

Management of elbow dislocation

A
  1. Closed reduction
  2. Ensure sufficient analgesia +/- sedation if appropriate
  3. Plain film radiography to confirm reduction
  4. Apply elbow backslab once reduced to keep the elbow at 90 degrees for 3 weeks before physio
93
Q

What is cubital tunnel syndrome and how does it present

A

Compression of the ulnar nerve at the wrist.

  • Muscle weakness and atrophy
  • Claw hand deformity: little and ring finer loss of extension at PIP and loss of flexion at MCP
  • Wartenberg sign – little finger in persistent abduction due to weak third palmar interosseous mucle
  • Froment sign – the thumb flexes at the interphalangeal joint while pinching a piece of paper to compensate for a weak adductor pollicis muscle
  • Sensory loss
  • Loss of sensation over the hypothenar eminence, ulnar 1 ½ fingers
  • Lesions at the elbow: positive Tinel test
    • Marked paresthesias can be reproduced in the ulnar portion of the hand by tapping on the medial epicondyle of the humerus
  • Lesions at the wrist – sensory symptoms may or may not be present
  • Pain – elbow lesions typically present with referred pain in the forearm

*Proximal as well as distal lesions leas to claw hand deformity

94
Q

Investigations for cubital tunnel syndrome

A
  1. EMG (electomyography) – main confirmatory test, identifies level of nerve compression
  2. U/S and MRI – cause of compression?
95
Q

Treatment for cubital tunnel syndrome

A

Conservative

  • Analgesia (NSAIDs)
  • Modify behaviour (avoid prolonged resting on or repeated flexion of elbow)
  • Bracing at night

Surgical decompression

  • Indicated if clinical features severe, persistent (>6-12 weeks) or progressively worsening despite conservative therapy
96
Q

Clinical features and physical examination for carpel tunnel syndrome

A

Clinical features

  • Pain, numbness and/ or paraesthesia throughout the median nerve sensory distribution
  • The palm is often spared, due to the palmar cutaneous branch of the median nerve branching proximal to the flexor retinaculum and passing over the carpal tunnel
  • Symptoms typically worse at night, symptoms can often be temporarily relieved by hanging the affected arm over the side of the bed or by shaking it back and forth

Physical examination

  • No visible findings during early stages
  • Sensory symptoms can be produced by either percussing over the median nerve (Tinel’s Test) or holding the wrist in full flexion for one minute (Phalen’s test)
  • In later stages may have weakness of thumb abdusction (due to denervation atrophy of the thenar muscles) and/ or wasting of the thenar eminence
97
Q

Treatment for carpal tunnel syndrome

A

Initially can be treated conservatively

  • Wrist splint, preventing wrist flexion and holds the wrist as to not exacerbate the tingling and pain
  • Physiotherapy and various training exercises
  • Corticosteroid injections can be trialed or NSAIDs to reduce swelling however limited evidence for this

Surgical treatment

  • Carpal tunnel release surgery – decompresses the carpal tunnel – involves cutting through the flexor retinaculum. This can be done under local anesthetic and is performed as a day case.
98
Q

What are the three types of distal radial fractures

A
  1. Colles’ Fracture
  • Extra-articular fracture of the distal radius with dorsal angulation and dorsal displacement, within 2cm of the articular surface
  • Colle’s fracture also usually includes an avulsion fracture of the ulnar styloid
  • Caused typically in osteoporotic bone with a fall on dorsiflexed wrist
  1. Smith’s Fracture
  • Volar angulation of the distal fragment of an extra-articular fracture of the distal radius, with or without volar displacement
  • Caused by landing on the dorsal surface of the wrist and are less common
  1. Barton’s Fracture
    * This is an intra-articular fracture of the distal radius with associated dislocation of the radio-carpal joint
99
Q

Treatment of Collies fracture

A
  1. Closed reduction
  • Can be performed under conscious sedation with a Bier’s block or haematoma block
  • Important the position of the fragments be checked by radiography a week after initial reduction and another week after as redisplacement is common
  1. Restriction
  • Stable and successfully reduced fractures can typically be placed in a below-elbow back-slab case, then radiographs repeated after 1 week to check for displacement
  • Plaster retained for 6 weeks

Significantly displaced or unstable fractures can require surgical intervention, as they have a risk of otherwise displacing overtime

  • Options of surgical management include open reduction and internal fixation, K-wire fixation or external fixation
    1. Rehabilitation
  • Once sufficient bone healing has occurred, rehab via physiotherapy
100
Q

What is tenosynovitis, and what is De Quervain’s tenosynovitis

A

Tenosynovitis is the inflammation of a tendon (tendinitis) and its synovial sheath (synovitis). This inflammation is often due to tendon overuse (e.g. texting, typing), but can also be due to systemic disease (RA, sarcoidosis) or infection following penetrating injury. The tendons of the hand and wrist are most commonly affected.

De Quervain’s tenosynovitis

  • Inflammation of the abductor pollicis longus and extensor pollicis brevis
  • Female > male, 30-50yo
  • Causes: repetitive abduction and extension of the thumb, RA
  • Clinically: Pain with or without swelling of the radial styloid; pain may radiate to thumb or elbow, exacerbation on movement

Positive Finkelstein test: patient makes a fist while cupping the thumb, then abducts the wrist towards the ulnar side –> pain

101
Q

What is trigger finger

A

Stenosing tenosynovitis (trigger finger)

  • Females > males (6:1), age > 40
  • Trigger finger: painful locking of a finger in flexed position; releases suddenly with a snap/ pop on extension
  • Often associated with tenderness and a palpable nodule at the base of the metacarpophalangeal joint
  • Mostly affects thumb and ring finger
102
Q

Investigations and treatment of tenosynovitis

A

Tenosynovitis is a clinical diagnosis with specific tests used to establish the aetiology

  1. Lab test
  • Leukocytosis, CRP, ESR elevated
  • Aspiration and analysis of synovial fluid (WBC count, gram stain, culture)
  1. Imaging (X-ray)
    * Assessment of possible bone involvement, detection of a foreign body causing penetrating trauma

Treatment

  1. Conservative
  • NSAIDs
  • Splinting (immobilisation) of affected finger
  1. Glucocorticoid injection into the tendon sheath
  2. Treatment of infectious tenosynovitis
  • Analgesics and broad spectrum IV antibiotics
  • Surgery – incision and drainage, debridement of infectious tissue
103
Q

What is a gangion cyst and how is it managed

A
  • Subcutaneous wrist mass
  • Dorsal, typically 1-4cm
  • Non-tender
  • Increase in size after activity
  • Typical glow of fluid filled cyst when penlight held next to it

Wrist pain – aching discomfort secondary to compression

Treatment

  1. Analgesia – NSAIDs, compressive wraps
  2. Cyst aspiration – cyst puncture and drainage, with or without corticosteroid infection
  3. Surgical excision
104
Q

Complication of scaphoid fracture

A

It is important to appreciate the blood supply to the scaphoid, which is supplied by branches of the radial artery. The dorsal branch of the radial artery, which supplies 80% of the blood, enters in the distal pole and travels in a retrograde fashion towards the proximal pole.

Consequently, fractures can comprise the blood supply, leading to avascular necrosis and subsequent degenerative wrist disease

105
Q

treatment of dupytren contractures

A

Patients who present early with no functional disability can be monitored and treated with conservative management

Conservative

  • Patients are advised to undergo hand therapy, keeping the hand active with stretching exercises
  • Injectable collagenase clostridium histolyticum is used by some clinicians

Surgical management

  • Excision of diseased fascia (fasciectomy)
  • Indicated for those with functional impairment, MCP joint contracture > 30 degrees, any PIP contracture or rapidly progressive disease.
106
Q

What is Perthes disease, its clinical features and treatment for it

A

Legg-Calvé-Perthes disease (LCPD, or Perthes disease) refers to an idiopathic, avascular necrosis of the femoral head. It may occur unilaterally or bilaterally and typically manifests between the ages of four and ten (the younger the patient at the time of diagnosis, the better the prognosis).

Clinical features

  • Analgesic gait (on weight-bearing leg)
  • Pain in the hip or the upper leg, sometimes projecting to the knee
    • Insidious onset, pain may fluctuate depending on physical activity
    • Often exacerbated by internal rotation
    • Flexion, Abduction, external rotation elicits pain
    • Groin tender on palpation
  • Restricted range of movement is always present, especially regarding internal rotation and abduction
  • Hinge abduction: refers to the lateral femoral head bumping into the venterolateral acetabulum when the leg is abducted, possibly involving pain, a palpable clunk and restricted range of movement
  • Contralateral involvement in 15% of cases

Treatment

Conservative treatment

  • Limited weight bearing, physical therapy
  • Indicated for lateral pillar A classification and young children < 6yo
  • Femoral head mostly undamaged
  • Consider casting and bracing before surgery if femoral head deformity develops or range of motion worsens

Surgical – femoral osteotomy

  • Indicated for older children >8yo or lateral pillar B/C classification
  • Extensive damage of the femoral head
107
Q

Risk factors for hip dyslplasia

A
  • Breech Position
  • Female
  • inadequate intrauterine space
    • Oligohydramnios
    • Twins
    • Large birth weight
    • oligohydramnios
108
Q

What is barlow sign (Examining hips of newborn)

A

Barlow sign - a palpable clunk caused by hip dislocation when the hip is flexed and adducted while applying downward force

109
Q

What is slipped capital femoral epiphysis

A

SCFE refers to the posterior and inferior displacement of the femoral head in relation to the femoral neck at the proximal femoral growth plate.

presents with acute or chronic dull pain in medial thigh, knee, groin or hip. A sudden limp, restricted ROM. Bilateral in 40% of cases.

110
Q

What is avascular necrosis of the femoral head, its aetiology and its presentation

A

Necrosis due to insufficient vascular supply to the femoral head

Causes

ASEPTIC

  • Alcohol
  • Sickle cell Disease/ SLE
  • Exogenous Steroids
  • Pancreatitis
  • Trauma (Lateral or medial femoral neck fractures, particularly with dislocation + femoral head fractures)
  • Infection
  • Caisson disease (Decompression sickness)

Clinical - slowly progressing groin pain

111
Q

ACL clinical features and tests

A
  • Rapid joint swelling and significant pain (highly vascular) - haemarthrosis in 15-30 minute
    1. Lachman test
  • Knee at 30 degrees’ flexion and, with one hand stabilising the femur, pulling the tibia forward to assess the amount of anterior movement
    1. Anterior Draw test
  • Knee flexed at 90 degrees, placing the thumbs on the joint line and their index fingers on the hamstring tendons posteriorly. Force applied to demonstrate tibial excursion
    1. Pivot test
  • Tests rotary sublaxation of the tibia
112
Q

MCL clinical features

A
  • Typically occurs after trauma to the lateral aspect of the knee
  • The patient may report hearing a ‘pop’ with immediate medial joint line pain
  • Swelling tends to follow after a few hours (Unless there is an associated haemarthrosis, in which case it will occur within minutes)

*MCL tear in isolation usually heals conservatively

à MCL + ACL injuries – treat ACL after MCL has healed (~6 weeks)

113
Q

Clinical features and tests for meniscals tears

A
  • Patients often report ‘tearing sensation’ in their knee
  • Intense sudden-onset pain
  • Knee swells slowly subsequently over a period of 6-12 hours
  • In cases where the meniscal tear results in a free body within the knee (typically the bucket-handle type), it may be locked in flexion and unable to extend

Tests

  • McMurrays + Apleys Grind Tests
114
Q

Treatment of achilles tendinitis

A

Tendinitis

Acute tendinitis can be treated with supportive measures.

  • Patients are encouraged to stop precipitating exercise
  • Ice the area
  • Use anti-inflammatory medications

If chronic

  • Rehabilitation and physiotherapy
115
Q

what is the most common cause of heel pain (80%)

A

Plantar fasciitis refers to inflammation of the plantar fascia of the foot. It is a common condition and can be unilateral or bilateral (however, any bilateral presentation suggests a systemic cause)

116
Q
A

Medicine (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions