Orthopaedics - general principles

Question 1

What is an open fracture?

Answer 1

Open fracture: a direct communication between the fracture site & the external environment
Most often through skin but also pelvic fracture may be internally open, having penetrated in to the vagina/rectum

Question 2

What is the difference of an ‘in-to-out’ and ‘out-to-in’ injury?

Answer 2

‘in-to-out’ = sharp bone ends penetrate the skin from beneath
‘out-to-in’ = a high energy injury penetrates the skin, traumatising the subtending soft tissues and bone

Question 3

List the most common fractures that can become open

Answer 3

Tibial
Phalangeal
Forearm
Ankle
Metacarpal

Question 4

Describe the different outcomes of an open fracture

Answer 4

1) Skin: very small wound to significant tissue loss
2) Soft tissues: range from very little tissue devitalisation to significant muscle/tendon/ligament loss requiring reconstructive surgery
3) Neurovascular injury
4) Infection

Question 5

Describe the clinical features of an open fracture

Answer 5

Pain, swelling and deformity with an overlying wound or punctum
Examination – check neurovascular status & overlying skin for any skin or tissue loss

Question 6

What is the classification of open fractures?

Answer 6

Gustilo-Anderson classification can be used to classify open fractures:
-type 1: <1cm wound and clean
-type 2: 1-10cm wound and clean
-type 3A: >10cm wound and high-energy, but with adequate soft tissue coverage
-type 3B: >10cm wound and high-energy, but with inadequate soft tissue coverage
-type 3C: all injuries with vascular injury
3A = ortho alone, 3B = requires plastic input, 3C = vascular input

Question 7

Which investigations will patients with a suspected open fracture have?

Answer 7

Basic blood tests – including a clotting screen and a group & save
Plain film radiograph
CT-scan for very comminuted/complex fracture patterns

Question 8

Describe the management of open fractures

Answer 8

Suitable resus and stabilisation
Urgent realignment and splinting of the limb
Broad-spectrum antibiotic cover, a tetanus vaccination is required
Photograph the wound & remove any gross debris
Definitive surgical management – requires debridement of the wound & fracture site
Ensure the wound is washed out with copious volumes of saline & definitive skeletal stabilisation within 72 hours

Question 9

Define compartment syndrome

Answer 9

Compartment syndrome is defined as a critical pressure increase within a confined compartmental space
Most common sites affected are in the leg, thigh, forearm, foot, hand and buttock

Question 10

Describe the pathophysiology of compartment syndrome

Answer 10

Fascial compartments cannot be distended & any fluid that is deposited there will cause an increase in the intra-compartmental pressure
Increase in pressure, the veins will be compressed -> increases the hydrostatic pressure within them and causes fluid to move out of the veins in the compartment
Next, the traversing nerves are compressed – causes a sensory +/- motor deficit in the distal distribution (paraesthesia is common)
Leg becomes ischaemic when the intra-compartmental pressure reaches the diastolic blood pressure

Question 11

Describe the clinical features of compartment syndrome

Answer 11

Severe pain, disproportionate to the injury, which is not readily improved with initial measures
-pain made worse by passively stretching the muscle bellies traversing the affected fascial compartment
Paraesthesia (presence of evolving neurology)
Affected compartment may feel tense but not generally swollen
If disease progresses, the features of acute limb ischaemia will subsequently develop (5 P’s)

Question 12

List investigations for compartment syndrome

Answer 12

A clinical diagnosis, based on symptoms and risk factors present
Most reliable diagnostic test – an intra-compartmental pressure monitor
CK may aid diagnosis

Question 13

Describe the management of compartment syndrome

Answer 13

Immediate surgical treatment via urgent fasciotomies
Prior to definitive intervention, additional management steps should include:
-keep the limb at a neutral level with the patient
-improve oxygen delivery with high flow oxygen
-augment BP with bolus of intravenous crystalloid fluids
-remove all dressings/splints/casts down to the skin
-treat symptomatically with opioid analgesia
Once fasciotomies have been performed – skin incisions are left open & re-look is planned for 24-48 hours where assess for any dead tissue that needs to be debrided
Monitor renal function – potential effects of rhabdomyolysis/reperfusion injury

Question 14

OA pathophysiology

Answer 14

Degradation of cartilage and remodelling of bone due to an active response of chondrocytes in the articular cartilage & inflammatory cells in the surrounding tissues
Release of enzymes from these cells -> break down collagen & proteoglycans, destroying the articular cartilage
Exposure of underlying subchondral bone results in sclerosis -> reactive remodelling changes that lead to the formation of osteophytes & subchondral bone cysts
Joint space is progressively lost over time

Question 15

OA risk factors

Answer 15

Obesity
Advancing age
Female gender
Manual labour occupations

Question 16

OA clinical features

Answer 16

Most common joints – small joints of hands & feet, hip joint, knee joint
Symptoms are insidious, chronic and gradually worsening
Pain and stiffness in joints, worsened with activity, relieved by rest
Prolonged OA results in deformity & reduced range of movement
Examination – inspect for deformity, crepitus

Question 17

OA investigations

Answer 17

Plain radiographs
- L: loss of joint space
- O: osteophytes
- S: subchondral cysts
- S: subchondral sclerosis

Question 18

OA management

Answer 18

Conservative – education, weight loss, local heat/ice packs, PT
Medical – simple analgesics & topical NSAIDs, intra-articular steroid injections
Surgical – arthroplasty, other options: osteotomy & arthrodesis

Question 19

Acutely swollen joint investigations

Answer 19

Routine bloods – FBC, CRP, ESR, serum urate
Plain film radiographs of affected joint
Joint aspiration – can be sent for WCC, microscopy, culture & sensitivity, light microscopy (for crystals)

Question 20

Gout

Answer 20

Inflammatory arthritis caused by the collection of monosodium urate crystals in a joint
Caused by hyperuricaemia leading to crystallisation of the urate in the joint space
Classically affects the 1st MTPJ
Often episodic, diagnosis is made by joint aspiration and microscopy
Acute gout – NSAIDs, prophylactic agents – allopurinol for prevention

Question 21

Pseudogout

Answer 21

Inflammatory arthritis caused by deposits of calcium pyrophosphate crystals within the joint
More likely to affect proximal joints – elbow and knee
Present with acute onset joint swelling
Risk factors: advanced age, hyperparathyroidism and hypophosphatemia
Diagnosis made via joint aspiration and microscopy and treated acutely with NSAIDs

Question 22

Spondyloarthropathies

Answer 22

Group of conditions comprising of psoriatic arthritis, ankylosing spondylitis, reactive arthritis & enteropathic arthropathy
Classified as being seronegative conditions and are associated with HLA-B27
All can present with ‘axial arthritis’ or affecting any joint in the body as oligoarthritis/monoarthritis, also can cause enthesitis and dactylitis
Most diagnoses are made clinically

Question 23

Haemarthrosis

Answer 23

Bleeding into a joint cavity, most common cause is a joint injury
Initial investigations – routine bloods, plain film radiographs, joint aspiration can be performed (can make a definitive diagnosis)
Initial management – RICE and sufficient analgesia, majority of cases are managed conservatively, including the correction of any underlying coagulopathies

Question 24

Metastatic bone cancer

Answer 24

Most common cause of bone cancer, most common primary sites are renal, thyroid, lung, prostate and breast
Most common site for a bony metastases is the spine
Rarely treated surgically, with mainstay of disease management via systemic therapies and is palliative
Prophylactic nailing of certain long bones can be performed in certain individuals at high risk of pathological fractures

Question 25

Bone cancer risk factors

Answer 25

Genetic association Previous exposure to radiation/alkylating agents in chemotherapy Benign bone conditions eg. Paget’s disease and fibrous dysplasia

Question 26

Bone cancer clinical features

Answer 26

Pain – not associated with movement and is worse at night Mass may be palpable & fracture without a history of trauma (pathological fracture)

Question 27

Benign bone tumours

Answer 27

Osteoid osteoma Osteochondromas Chondroma Giant cell tumour

Question 28

Malignant bone tumours

Answer 28

Osteosarcoma Ewing’s sarcoma Chondrosarcoma

Question 29

Osteoid osteoma

Answer 29

Arise from osteoblasts, often around the second decade of life, more common in males Typically small tumours located usually around the metaphysis of long bones Present with localised progressive pain, worse at night, made better with NSAIDs Radiologically show a small mass, comprised of a radiolucent nidus with a rim of reactive bone Most can be managed conservatively, severe pain = may warrant surgical resection

Question 30

Osteochondroma

Answer 30

Benign bony tumours forming as an outgrowth from the metaphysis of long bones covered with a cartilaginous cap Develop in the second decade of life and more common in males Most are detected incidentally Most can be managed conservatively (serial radiological imaging every 4-6 months), however those with significant deformity/neurological symptoms = surgical resection

Question 31

Chondroma

Answer 31

Arise from chondroblasts within the medullary cavity of the bones/from the cortical surface Present in patients 20-50 years old, most commonly affecting the long bones Most are asymptomatic, but can present as a pathological fracture Plain film radiograph -> well circumscribed oval lucency with intact cortex Most can be observed but if large/symptomatic = require removal with curettage and bone grafting

Question 32

Giant cell tumour

Answer 32

Arise from multinucleated giant cells and stromal cells Occur in patients 20-30 years old, usually affecting the epiphysis of long bones Patients will typically present with pain, swelling or joint movement limitation Plain radiograph – eccentric lytic area, giving a ‘soap bubble’ appearance Surgical resection is treatment of choice

Question 33

Osteosarcoma

Answer 33

Most common malignant primary bone tumour Bimodal age of onset – 10-14 years or in those aged > 65 years, most commonly found at the metaphysis of the distal femur or proximal tibia Localised constant pain and tender soft tissue mass may be palpable Tissue biopsy is needed for diagnosis Aggressive resection with systemic chemotherapy

Question 34

Ewing’s sarcoma

Answer 34

Paediatric malignancies, more common in males & arise from primitive poorly differentiated neuroectodermal cells, commonly affect the diaphysis of long bones Present with a painful and enlarging mass with tenderness and warmth Plain film radiographs – lytic lesion with periosteal reactions (‘onion skin’) Management – neoadjuvant chemotherapy following by surgical excision

Question 35

Chondrosarcoma

Answer 35

Malignant tumours of the cartilage, age of onset is 40-60 years, typically affecting the axial skeleton Typically present with a painful and enlarging mass, plain film radiographs demonstrate lytic lesions with calcification, cortical remodelling & endosteal scalloping Low grade lesions – intralesional curettage Intermediate and high grade lesions – wide en-bloc local excision

Question 36

Bone tumours investigations

Answer 36

Vary depending on suspected tumour type Most will obtain initial plain film radiographs MRI imaging & CT imaging can be useful in determining cortical involvement Bone biopsy may be required for a definitive diagnosis

Question 37

Radiological features of bone tumours

Answer 37

Benign lesions – sharp and well-defined, lacking soft tissue involvement and no cortical destruction Malignant lesions – often poorly defined with rough borders, involving soft tissues and have cortical destruction

Question 38

Osteomyelitis

Answer 38

Infection of the bone Most cases are acute and bacterial in origin Common causative organisms – staph aureus, streptococci, H. influenza, P. aeruginosa

Question 39

Osteomyelitis pathophysiology

Answer 39

Bacteria enter the bone tissue -> express adhesins to bind to the host tissue proteins & produce an extracellular matrix -> pathogens are able to propagate, spread and seed further Chronic causes -> devascularisation of the affected bone, subsequent necrosis & resorption of the surrounding bone (‘floating’ piece of dead bone = sequestrum – not penetrated by abx as avascular) Involucrum can form, whereby the region becomes encased in a thick sheath of periosteal new bone

Question 40

Osteomyelitis risk factors

Answer 40

Diabetes mellitus Immunosuppression Alcohol excess IV drug use

Question 41

Osteomyelitis clinical features

Answer 41

Severe pain in the affected region & associated low grade pyrexia Constant pain & can be worse at night Examination – tender, overlying swelling and erythema, patient may be unable to weight bear if lower limb

Question 42

Potts disease

Answer 42

Infection of the vertebral body and the intervertebral disc by M. TB Patients will present with back pain +/- neurological features, low grade fever MRI is gold-standard investigation Most cases will require a prolonged course of anti-TB medication, however surgical intervention may be required for abscess drainage

Question 43

Osteomyelitis investigations

Answer 43

Routine blood tests, blood cultures Plain film radiographs Definitive diagnosis can be achieved through MRI but gold standard diagnosis is from culture from bone biopsy at debridement

Question 44

Osteomyelitis management

Answer 44

Patient is clinically well -> patients will require long-term IV abx therapy Patient clinically deteriorates -> surgical management may be required to prevent chronic osteomyelitis developing: curettage of the area

Question 45

Osteomyelitis complications

Answer 45

Overwhelming sepsis Mortality Growth disturbances Recurrence of infection Chronic osteomyelitis

Question 46

Chronic osteomyelitis

Answer 46

Present with localised ongoing bone pain and non-specific infection symptoms Surgical management involves local bone and soft tissue debridement for definitive source control, alongside extensive long-term abx therapy Likely need complex staged reconstruction with prolonged rehab, if not, amputation can be considered

Question 47

Septic arthritis

Answer 47

Infection of a joint Main causative organisms – staph aureus (adults), gonorrhoea (most common in sexually active patients) and salmonella (especially in those with sickle cell disease)

Question 48

Septic arthritis risk factors

Answer 48

Increasing age Pre-existing joint disease Diabetes mellitus Immunosuppression CKD Hip/knee joint prosthesis IV drug use

Question 49

Septic arthritis clinical features

Answer 49

Single swollen joint causing severe pain Pyrexia Examination – joint is red, swollen and warm, pain on active and passive movements Unable to weight bear

Question 50

Septic arthritis investigations

Answer 50

Routine bloods, blood cultures Joint aspiration should be performed before abx are given Imaging – plain radiograph, USS can be useful to guide joint aspiration and for drainage, CT/MRI can be useful in specific joint infections

Question 51

Septic arthritis management

Answer 51

Empirical abx treatment Infective native joints require surgical irrigation and debridement in theatre to aid in source control If in prosthetic joint -> revision surgery is typically needed

Question 52

Septic arthritis complications

Answer 52

Osteoarthritis Osteomyelitis