Orthopaedics Flashcards

1
Q

Garden classification

A

1+2 = no displacement (1 = partial fracture, no displacement, 2 = full fracture, no displacement) 3+4 = a degree of displacement (3 = full fracture, partial displacement, 4 = full fracture, full displacement) These groups also help with management - 1+2, use a screw, 3+4, displaced, replace

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2
Q

GRUsome MURder

A

G: Galeazzi R: radius fracture U: ulna dislocation.
M: Monteggia U: ulna fracture R: radial head dislocation.

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3
Q

Osteoarthritis

A

Osteoarthritis is often described as “wear and tear” in the joints. It occurs in the synovial joints and results from genetic factors, overuse and injury. Osteoarthritis is thought to result from an imbalance between cartilage damage and the chondrocyte response, leading to structural issues in the joint. Risk factors include obesity, age, occupation, trauma, being female and family history.

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4
Q

Commonly affected joints in osteoarthritis

A

Hips
Knees
Distal interphalangeal (DIP) joints in the hands
Carpometacarpal (CMC) joint at the base of the thumb
Lumbar spine
Cervical spine (cervical spondylosis)

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5
Q

X-ray changes in osteoarthritis

A

The four key x-ray changes in osteoarthritis can be remembered with the “LOSS” mnemonic:

L – Loss of joint space
O – Osteophytes (bone spurs)
S – Subarticular sclerosis (increased density of the bone along the joint line)
S – Subchondral cysts (fluid-filled holes in the bone)

X-ray reports might describe findings of osteoarthritis as degenerative changes. X-ray changes do not necessarily correlate with symptoms. A patient might have significant signs on an x-ray but minimal symptoms, or the reverse.

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6
Q

Presentation of osteoarthritis

A

Osteoarthritis presents with joint pain and stiffness. The pain and stiffness tend to worsen with activity and at the end of the day. This is the reverse of the pattern in inflammatory arthritis, where symptoms are worse in the morning and improve with activity. Osteoarthritis leads to deformity, instability and reduced function of the joint.

General signs of osteoarthritis are:

Bulky, bony enlargement of the joint
Restricted range of motion
Crepitus on movement
Effusions (fluid) around the joint

Signs in the Hands

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

The carpometacarpal joint at the base of the thumb is a saddle joint, with the metacarpal bone sitting on the trapezius bone, using it like a saddle. It gets a lot of use and is very prone to wear.

TOM TIP: Patients may present with referred pain, particularly in the adjacent joints. For example, consider osteoarthritis in the hip in patients presenting with lower back or knee pain.

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7
Q

Diagnosing osteoarthritis

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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8
Q

Managing osteoarthritis

A

Non-pharmacological management involves patient education and lifestyle changes, such as:

Therapeutic exercise to improve strength and function and reduce pain
Weight loss if overweight, to reduce the load on the joint
Occupational therapy to support activities and function (e.g., walking aids and adaptations to the home)

Pharmacological management recommended by the NICE guidelines (2022) are:

Topical NSAIDs first-line for knee osteoarthritis
Oral NSAIDs where required and suitable (co-prescribed with a proton pump inhibitor for gastroprotection)

Weak opiates and paracetamol are only recommended for short-term, infrequent use. NICE (2022) recommend against using any strong opiates for osteoarthritis.

Intra-articular steroid injections may temporarily improve symptoms (NICE say up to 10 weeks).

Joint replacement may be used in severe cases. The hips and knees are the most commonly replaced joints.

Medication Notes

NSAIDs (e.g., ibuprofen or naproxen) are very effective for musculoskeletal pain. However, they must be used cautiously, particularly in older patients and those on anticoagulants, such as aspirin or DOACs. They are best used intermittently, only for a short time during flares. They have several potential adverse effects, including:

Gastrointestinal side effects, such as gastritis and peptic ulcers (leading to upper gastrointestinal bleeding)
Renal side effects, such as acute kidney injury (e.g., acute tubular necrosis) and chronic kidney disease
Cardiovascular side effects, such as hypertension, heart failure, myocardial infarction and stroke
Exacerbating asthma

There is little evidence that opiates help with chronic pain. They are associated with side effects, risks, tolerance, dependence and withdrawal. They often result in dependence without any objective benefits.

TOM TIP: The WHO pain ladder is not helpful in chronic pain. Paracetamol and opiates are not recommended for regular use in osteoarthritis. Remember that NSAIDs cause hypertension by blocking prostaglandins (prostaglandins cause vasodilation) and should be used very cautiously with a history of high blood pressure.

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9
Q

Elective joint replacement

A

The most common joints replaced electively are the hip, knee and shoulder. The most common indication is osteoarthritis. Most patients that have joint replacements are over 60.

The artificial joints are built to last more than 10-15 years. However, they may be affected by loosening, wear and dislocation. Some patients may require further surgery and replacement of the artificial joint at some point.

Joint replacement is major surgery. Patients need to have the alternatives discussed before deciding to undergo surgery. The other options usually include analgesia, steroid injections and physiotherapy.

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10
Q

Indications for joint replacement

A

Osteoarthritis is the most common indication for an elective joint replacement. It is not usually performed until symptoms are severe and not manageable with conservative treatments.

Joints may also require replacement for:

Fractures
Septic arthritis
Osteonecrosis
Bone tumours
Rheumatoid arthritis

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11
Q

Joint replacement options

A

There are several options for elective joint replacement surgery:

Total joint replacement – replacing both articular surfaces of the joint
Hemiarthroplasty – replacing half of the joint (e.g., the head of the femur in the hip joint)
Partial joint resurfacing – replacing part of the joint surfaces (e.g., only the medial joint surfaces of the knee)

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12
Q

Total hip replacement

A

Usually, a lateral incision over the outer aspect of the hip is used. The hip joint is dislocated (separated) to give access to both articular surfaces.

The head of the femur is removed. A metal or ceramic replacement head of femur, on a metal stem, is used to replace it. The stem can either be cemented into the shaft of the femur or carefully pushed into the shaft to make a tight enough fit to hold it securely in place. Uncemented stems have a rough surface that holds them tightly in place.

The acetabulum (socket) of the pelvis is hollowed out and replaced by a metal socket, which is cemented or screwed into place. A spacer is used between the new head and socket to complete the new artificial joint.

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13
Q

Total Knee Replacement

A

Usually, a vertical, anterior incision is made down the front of the knee. The patella is rotated out of the way to allow access to the knee joint.

The articular surfaces (the cartilage and some of the bone) of the femur and tibia are removed. A new metal surface replaces these. They can be either cemented or pushed tightly into place.

A spacer is added between the new articular surfaces of the femur and tibia to complete the new artificial joint.

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14
Q

Total Shoulder Replacement

A

Usually, an anterior incision is made down the front of the shoulder, along the deltoid. The shoulder joint is dislocated (separated) to give access to both articular surfaces.

The head of the humerus is removed and replaced with a metal or ceramic ball. This replacement head is attached to the humerus either by a metal stem or screws (stemless).

The glenoid (socket) is hollowed out and replaced by a metal socket. This completes the artificial shoulder joint.

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15
Q

Reverse Total Shoulder Replacement

A

A reverse total shoulder replacement involves adding a sphere in place of the glenoid (socket) and a spacer with a cup to replace the head of the humerus. This reverses the normal ball-in-cup structure of the shoulder joint, but the joint function remains the same.

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16
Q

Joint replacement surgery

A

Before Surgery

Planning for joint replacement surgery will involve:

X-rays
CT or MRI scans may be required for a more detailed assessment
Pre-operative assessment (pre-op)
Consent for surgery
Bloods (including group and save and crossmatching of blood)
Medication changes if needed (e.g., temporarily stopping anticoagulation)
Venous thromboembolism assessment
Fasting immediately before surgery
The limb will be marked with the patient awake to ensure the operation is performed on the correct joint

During Surgery

Joint replacement surgery requires a general anaesthetic. Alternatively, a spinal anaesthetic may be used for lower limb surgery.

Prophylactic antibiotics are given before the procedure to reduce the risk of infection.

Tranexamic acid may be used to minimise blood loss during the procedure.

After Surgery

Post-operative management after joint replacement surgery involves:

Analgesia
Physiotherapy to guide when and how to mobilise
VTE prophylaxis
Post-operative x-rays
Post-operative full blood count (to check for anaemia)
Monitoring for complications (e.g., deep vein thrombosis or infection)

VTE prophylaxis usually involves low molecular weight heparin (LMWH). The 2018 NICE guidelines on VTE prophylaxis have specific recommendations on potential regimes that can be used after joint replacement surgery (see full national and local guidelines when treating patients). This involves the option of LMWH for:

28 days post elective hip replacement
14 days post elective knee replacement

Other measures that may be used for VTE prophylaxis after joint replacement surgery are:

Aspirin
DOACs (e.g., rivaroxaban)
Anti-embolism stockings

Risks

The generic risks of joint replacement surgery are:

Risks of the anaesthetic
Pain
Bleeding
Infection – infection of the prosthesis can be highly problematic (see below)
Damage to nearby structures (e.g., nerves or arteries)
Stiffness or restricted range of motion in the joint
Joint dislocation
Loosening
Fracture during the procedure
Venous thromboembolism (DVT or PE)

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17
Q

Prosthetic Joint Infections

A

Infection in a prosthetic joint is a big problem. This occurs in around 1% of joint replacements and extensive measures are taken to prevent it, such as perioperative prophylactic antibiotics. It is more likely to occur in revision surgery rather than during the initial joint replacement. The most common organism is Staphylococcus aureus (a common skin organism).

Risk factors for prosthetic joint infection are:

Prolonged operative time
Obesity
Diabetes

Symptoms include:

Fever
Pain
Swelling
Erythema
Increased warmth

Diagnosis involves a combination of clinical findings, x-rays, blood tests (raised inflammatory markers), cultures (e.g., blood or synovial fluid) and findings during further operations.

Management involves repeat surgery and prolonged antibiotics (over months). Surgery may involve joint irrigation, debridement or complete replacement.

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18
Q

Types of fractures

A

A compound fracture is when the skin is broken and the broken bone is exposed to the air. The broken bone can puncture through the skin.

A stable fracture refers to when the sections of bone remain in alignment at the fracture.

A pathological fracture refers to when a bone breaks due to an abnormality within the bone (see below).

There are terms used to describe in what way a bone breaks:

Transverse
Oblique
Spiral
Segmental
Comminuted (breaking into multiple fragments)
Compression fractures (affecting the vertebrae in the spine)
Greenstick
Buckle (torus)
Salter-Harris (growth plate fracture)

Greenstick and buckle fractures typically occur in children rather than adults. Salter-Harris fractures only occur in children (adults do not have growth plates).

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19
Q

Wrist fractures

A

A Colle’s fracture refers to a transverse fracture of the distal radius near the wrist, causing the distal portion to displace posteriorly (upwards), causing a “dinner fork deformity”. This is usually the result of a fall onto an outstretched hand (FOOSH).

A scaphoid fracture is often caused by a FOOSH. The scaphoid is one of the carpal bones and is located below the base of the thumb. A key sign of a scaphoid fracture is tenderness in the anatomical snuffbox (the groove between the tendons when extending the thumb). It is worth noting that the scaphoid has a retrograde blood supply, with blood vessels supplying the bone from only one direction. This means a fracture can cut off the blood supply, resulting in avascular necrosis and non-union.

TOM TIP: Some key bones have vulnerable blood supplies, where a fracture can lead to avascular necrosis, impaired healing, and non-union. These are the scaphoid bone, the femoral head, the humeral head and the talus, navicular and fifth metatarsal in the foot.

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20
Q

Ankle fractures

A

Ankle fractures involve the lateral malleolus (distal fibula) or the medial malleolus (distal tibia).

The Weber classification can be used to describe fractures of the lateral malleolus (distal fibula). The fracture is described in relation to the distal syndesmosis (fibrous join) between the tibia and fibula. This tibiofibular syndesmosis is very important for the stability and function of the ankle joint. If the fracture disrupts the syndesmosis, surgery is more likely to be required in order to regain good stability and function of the joint.

The Weber classification defines fractures of the lateral malleolus as:

Type A – below the ankle joint – will leave the syndesmosis intact
Type B – at the level of the ankle joint – the syndesmosis will be intact or partially torn
Type C – above the ankle joint – the syndesmosis will be disrupted

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21
Q

Pelvic ring fractures

A

The pelvis forms a ring. When one part of the pelvic ring fractures, another part will also fracture (similar to fracturing a polo mint).

Pelvic fractures often lead to significant intra-abdominal bleeding, either due to vascular injury or from the cancellous bone of the pelvis. This can lead to shock and death, so needs emergency resuscitation and trauma management.

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22
Q

Pathological fractures

A

Pathological fractures occur due to an underlying disease of the bone, such as a tumour, osteoporosis or Paget’s disease of the bone. They may occur with minor trauma or even spontaneously without any history of trauma. Common sites are the femur and the vertebral bodies.

The main cancers that metastasise to the bones are (mnemonic: PoRTaBLe):

Po – Prostate
R – Renal
Ta – Thyroid
B – Breast
Le – Lung

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23
Q

Fragility fractures

A

Fragility fractures occur due to weakness in the bone, usually due to osteoporosis. They often occur without the appropriate trauma that is typically required to break a bone. For example, a patient may present with a fractured femur after a minor fall.

A patient’s risk of a fragility fracture over the next 10 years can be predicted using the FRAX tool.

Bone mineral density can be measured using a DEXA scan.

The WHO criteria for osteopenia and osteoporosis are:

T Score at the Hip
Bone Mineral Density

More than -1
Normal

-1 to -2.5
Osteopenia

Less than -2.5
Osteoporosis

Less than -2.5 plus a fracture
Severe Osteoporosis

The NOGG guidelines can be used to guide the medical treatments appropriate for an individual based on their FRAX score. The first-line medical treatments for reducing the risk of fragility fractures are:

Calcium and vitamin D
Bisphosphonates (e.g., alendronic acid)

Bisphosphonates work by interfering with osteoclasts and reducing their activity, preventing the reabsorption of bone. There are a few key side effects to remember:

Reflux and oesophageal erosions (oral bisphosphonates are taken on an empty stomach sitting upright for 30 minutes before moving or eating to prevent this)
Atypical fractures (e.g. atypical femoral fractures)
Osteonecrosis of the jaw
Osteonecrosis of the external auditory canal

Denosumab is a monoclonal antibody that works by blocking the activity of osteoclasts. It is an alternative to bisphosphonates where they are contraindicated, not tolerated or not effective.

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24
Q

Imaging fractures

A

X-rays are the initial imaging investigation when a bone fracture is suspected. Two views (two x-rays taken from different angles) are always required, as a single view may miss a fraction.

CT scans give a more detailed view of the bones when the x-rays are inconclusive or further information is needed.

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25
Q

Principles of fracture management

A

The first principle is to achieve mechanical alignment of the fracture by:

Closed reduction via manipulation of the limb
Open reduction via surgery

The second principle is to provide relative stability for some time to allow healing to occur. This can be done by fixing the bone in the correct position while it heals. There are various ways the bone can be fixed in position:

External casts (e.g., plaster cast)
K wires
Intramedullary wires
Intramedullary nails
Screws
Plate and screws

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26
Q

Managing fractures

A

Patients presenting to A&E will be investigated with x-rays to establish the diagnosis.

Patients with fractures require appropriate pain management.

Straightforward fractures may be managed in A&E (e.g., a Colle’s fracture in a young adult). They may require closed reduction if the bones are out of alignment. A plaster cast may be applied, and the patient can be discharged with a follow-up appointment in the fracture clinic.

Complex fractures and those requiring surgery (e.g., hip fractures) are referred to the on-call trauma and orthopaedics team. They are admitted and made nil by mouth if they may need an operation. They are discussed at the trauma meeting the following day (typically, this starts at 7.45 am), then seen on the morning ward round. A plan will be made for further management at this stage.

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27
Q

Complications of fractures

A

The complications will depend on the location and nature of the fracture.

Possible early complications include:

Damage to local structures (e.g., tendons, muscles, arteries, nerves, skin and lung)
Haemorrhage leading to shock and potentially death
Compartment syndrome
Fat embolism (see below)
Venous thromboembolism (DVTs and PEs) due to immobility

Possible longer-term complications include:

Delayed union (slow healing)
Malunion (misaligned healing)
Non-union (failure to heal)
Avascular necrosis (death of the bone)
Infection (osteomyelitis)
Joint instability
Joint stiffness
Contractures (tightening of the soft tissues)
Arthritis
Chronic pain
Complex regional pain syndrome

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28
Q

Fat embolism

A

Fat embolism can occur following the fracture of long bones (e.g., femur). Fat globules are released into the circulation following a fracture (possibly from the bone marrow). These globules may become lodged in blood vessels (e.g., pulmonary arteries) and cause blood flow obstruction.

Fat embolisation can cause a systemic inflammatory response, resulting in fat embolism syndrome.

It typically presents around 24-72 hours after the fracture. Gurd’s criteria can be for the diagnosis.

Gurd’s major criteria:

Respiratory distress
Petechial rash
Cerebral involvement

There is a long list of Gurd’s minor criteria, including:

Jaundice
Thrombocytopenia
Fever
Tachycardia

Operating early to fix the fracture reduces the risk of fat embolism syndrome.

It can lead to multiple organ failure. Management is supportive while the condition improves. The mortality rate is around 10%.

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29
Q

Hip fractures

A

Hip fractures are an important topic in trauma and orthopaedics. They are common and lead to significant morbidity and mortality. The 30-day mortality is 5-10%. Half of patients become less independent after a hip fracture.

Increasing age and osteoporosis are major risk factors for hip fractures. Females are affected more often than males.

Due to the morbidity and mortality with hip fractures, they are generally prioritised on the trauma list with the aim to perform surgery within 48 hours. There is also a specialty called orthogeriatrics, who focus on identifying and optimising the medical co-morbidities and complications of inpatients on the orthopaedic ward, particularly elderly patients with hip fractures.

Hip fractures can be categorised into:

Intra-capsular fractures
Extra-capsular fractures

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30
Q

Anatomy of the hip

A

There are some basic structures of the top of the femur:

Head
Neck
Greater trochanter (lateral)
Lesser trochanter (medial)
Intertrochanteric line
Shaft (body)

The capsule of the hip joint is a strong fibrous structure. It attaches to the rim of the acetabulum on the pelvis and the intertrochanteric line on the femur. It surrounds the neck and head of the femur.

The head of the femur has a retrograde blood supply. The medial and lateral circumflex femoral arteries join the femoral neck just proximal to the intertrochanteric line. Branches of this artery run along the surface of the femoral neck, within the capsule, towards the femoral head. They provide the only blood supply to the femoral head. A fracture of the intra-capsular neck of the femur can damage these blood vessels, removing the blood supply to the femoral head, leading to avascular necrosis. Therefore, patients with a displaced intra-capsular fracture need to have the femoral head replaced with a hemiarthroplasty or total hip replacement.

TOM TIP: It is worth understanding and remembering the concept of the retrograde blood supply to the head of the femur and how this determines the choice of operation (explained below). When I did an FY1 job in trauma and orthopaedics, the juniors were questioned on this concept almost every time a patient with a hip fracture was admitted. Being able to identify the type of hip fracture on an x-ray (intra-capsular or extra-capsular) and justify the choice of operation made trauma meetings much less stressful.

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31
Q

Intra-capsular hip fractures

A

Intra-capsular fractures involve a break in the femoral neck, within the capsule of the hip joint. This affects the area proximal to the intertrochanteric line.

The Garden classification is used for intra-capsular neck of femur fractures:

Grade I – incomplete fracture and non-displaced
Grade II – complete fracture and non-displaced
Grade III – partial displacement (trabeculae are at an angle)
Grade IV – full displacement (trabeculae are parallel)

Non-displaced intra-capsular fractures may have an intact blood supply to the femoral head, meaning it may be possible to preserve the femoral health without avascular necrosis occurring. They can be treated with internal fixation (e.g., with screws) to hold the femoral head in place while the fracture heals.

Displaced intra-capsular fractures (grade III and IV) disrupt the blood supply to the head of the femur. Therefore, the head of the femur needs to be removed and replaced.

Hemiarthroplasty involves replacing the head of the femur but leaving the acetabulum (socket) in place. Cement is used to hold the stem of the prosthesis in the shaft of the femur. This is generally offered to patients who have limited mobility or significant co-morbidities.

Total hip replacement involves replacing both the head of the femur and the socket. This is generally offered to patients who can walk independently and are fit for surgery.

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32
Q

Extra-capsular hip fractures

A

Extra-capsular fractures leave the blood supply to the head of the femur intact. Therefore, the head of the femur does not need to be replaced.

Intertrochanteric fractures occur between the greater and lesser trochanter. These are treated with a dynamic hip screw (AKA sliding hip screw). A screw goes through the neck and into the head of the femur. A plate with a barrel that holds the screw is screwed to the outside of the femoral shaft. The screw that goes through the femur to the head allows some controlled compression at the fracture site, whilst still holding it in the correct alignment. Adding some controlled compression across the fracture improves healing.

Subtrochanteric fractures occur distal to the lesser trochanter (although within 5cm). The fracture occurs to the proximal shaft of the femur. These may be treated with an intramedullary nail (a metal pole inserted through the greater trochanter into the central cavity of the shaft of the femur).

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33
Q

Hip Fracture Presentation

A

The typical scenario is an older patient (over 60) who has fallen, presenting with:

Pain in the groin or hip, which may radiate to the knee
Not able to weight bear
Shortened, abducted and externally rotated leg

An essential part of assessing patients with a new hip fracture is to determine any other acute illnesses. There is often a good reason for them to fall and break a hip. They may also be suffering with:

Anaemia
Electrolyte imbalances
Arrhythmias
Heart failure
Myocardial infarction
Stroke
Urinary or chest infection

These conditions need to be identified as early as possible so that the patient can be optimised and surgery can proceed with minimal delays.

TOM TIP: The term “mechanical fall” is often used to imply a simple explanation for why the patient fell, such as tripping over an object or being knocked over. It is worth exploring the fall in more detail. In many cases, there may be a correctable underlying medical cause for the fall, such as anaemia, arrhythmia or even underlying Parkinson’s disease. There may also be social contributors to the fall, such as dehydration, incorrect eyewear, poor footwear or obstacles in the home. If you identify an underlying reversible cause, you could make a big difference to that patient and impress your orthogeriatric colleagues.

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34
Q

Imaging hip fractures

A

X-rays are the initial investigation of choice. Two views are essential, as a single view can miss the fracture. Anterior-to-posterior (AP) and lateral views are standard.

Shenton’s line can be seen on an AP x-ray of the hip. It is one continuous curving line formed by the medial border of the femoral neck and continues to the inferior border of the superior pubic ramus. Disruption of Shenton’s line is a key sign of a fractured neck of femur (NOF).

MRI or CT scanning may be used where the x-ray is negative, but a fracture is still suspected.

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35
Q

Managing hip fractures

A

On admission, patients will have:

Appropriate analgesia
Investigations to establish the diagnosis (e.g., x-rays)
Venous thromboembolism risk assessment and prophylaxis (e.g., low molecular weight heparin)
Pre-operative assessment (including bloods and an ECG) to ensure they are fit and optimised for surgery
Orthogeriatrics input

The NICE guidelines (updated 2017) say that surgery should be carried out either the same day or the day after the patient is admitted (within 48 hours).

The operation should allow the patient to weight bear straight away. This allows the physiotherapists to start mobilisation and rehabilitation as soon as possible after the operation. Post-operative analgesia is important to encourage the patient to mobilise as quickly as possible.

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36
Q

Compartment syndrome

A

Compartment syndrome is where the pressure within a fascial compartment is abnormally elevated, cutting off the blood flow to the contents of that compartment.

Fascial compartments involve muscles, nerves and blood vessels surrounded by fascia. Fascia is a sheet of strong, fibrous connective tissue that encases the contents of the compartment. It is not able to stretch or expand.

Acute compartment syndrome is an orthopaedic emergency requiring surgery (fasciotomy) to relieve the pressure within the compartment and restore blood flow. Without prompt treatment, tissue necrosis (death) and permanent damage can occur.

Compartment syndrome can be classified as acute or chronic. Most of this section relates to acute compartment syndrome.

Acute compartment syndrome is usually associated with an acute injury, where bleeding or tissue swelling (oedema) associated with the injury increases the pressure within the compartment.

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37
Q

Presentation of compartment syndrome

A

Acute compartment syndrome most often affects one of the fascial compartments in the legs, but it can also affect the forearm, feet, thigh and buttocks.

It usually presents after an acute injury, particularly:

Bone fractures
Crush injuries

Acute compartment syndrome presents with the 5 P’s:

P – Pain “disproportionate” to the underlying injury, worsened by passive stretching of the muscles
P – Paresthesia
P – Pale
P – Pressure (high)
P – Paralysis (a late and worrying feature)

Note that pulseless is not a feature, differentiating it from acute limb ischaemia. The pulses may remain intact depending on which compartment is affected.

TOM TIP: Disproportionate pain is a key characteristic of compartment syndrome. The pain is so severe that pain medications are not effective. If you see a patient with disproportionate pain after an injury in your exams, the diagnosis is probably compartment syndrome.

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38
Q

Managing acute compartment syndrome

A

Acute compartment syndrome is primarily a clinical diagnosis based on clinical signs and symptoms.

Needle manometry can be used to measure the compartment pressure. A device (manometer) measures the resistance to injecting saline through a needle into the compartment.

Initial management involves:

Escalating to the orthopaedic registrar or consultant
Removing any external dressings or bandages
Elevating the leg to heart level
Maintaining good blood pressure (avoiding hypotension)

Emergency fasciotomy is the definitive management. Ideally, this should be as soon as possible after injury (e.g., within 6 hours). If it is delayed, irreversible damage may occur, and fasciotomy may not be beneficial.

Fasciotomy involves a surgical operation to cut through the fascia, down the entire length of the compartment, and release the pressure. The compartment is explored to identify and debride any necrotic muscle tissue. The wound is left open and covered with a dressing.

Patients require repeated trips to theatre (every few days) to explore the compartment for necrotic tissue, which needs to be debrided. As the swelling improves, the wound can be gradually closed, which can take several weeks. A skin graft may be required if the wound cannot be closed around the compartment.

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39
Q

Chronic compartment syndrome

A

Chronic compartment syndrome (also called chronic exertional compartment syndrome) is usually associated with exertion. During exertion, the pressure within the compartment rises, blood flow to the compartment is restricted, and symptoms start. During rest, the pressure falls, and symptoms begin to resolve. It is not an emergency.

Symptoms are usually isolated to a specific location at the affected compartment. Symptoms include pain, numbness or paresthesia (pins and needles). They are made worse by increasing activity and resolve quickly with rest.

Needle manometry can be used to measure the pressure in the compartment before, during and after exertion to confirm the diagnosis. It may be treated with a fasciotomy.

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40
Q

Osteomyelitis

A

Osteomyelitis refers to inflammation in a bone and bone marrow, usually caused by bacterial infection.

Haematogenous osteomyelitis refers to when a pathogen is carried through the blood and seeded in the bone. This is the most common mode of infection. Alternatively, osteomyelitis can occur due to direct contamination of the bone, for example, at a fracture site or during an orthopaedic operation.

Staphylococcus aureus causes most cases of osteomyelitis.

Osteomyelitis can be acute or chronic. Patients may develop recurring or chronic infections after treatment for acute osteomyelitis.

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41
Q

Risk factors for osteomyelitis

A

The key risk factors for developing osteomyelitis are:

Open fractures
Orthopaedic operations, particularly with prosthetic joints
Diabetes, particularly with diabetic foot ulcers
Peripheral arterial disease
IV drug use
Immunosuppression

Infection in a prosthetic joint is a big problem. This occurs in around 1% of joint replacements, and extensive measures are taken to prevent it, such as perioperative prophylactic antibiotics. It is more likely to occur in revision surgery rather than during the initial joint replacement.

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42
Q

Presentation of osteomyelitis

A

The typical presentation of osteomyelitis is with:

Fever
Pain and tenderness
Erythema
Swelling

The presentation of osteomyelitis can be quite non-specific, with generalised symptoms of infection such as fever, lethargy, nausea and muscle aches.

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43
Q

Investigating osteomyelitis

A

X-rays often do not show any changes, particularly in early disease. They cannot be used to exclude osteomyelitis. The potential signs of osteomyelitis on an x-ray are:

Periosteal reaction (changes to the surface of the bone)
Localised osteopenia (thinning of the bone)
Destruction of areas of the bone

MRI scans are the best imaging investigation for establishing a diagnosis.

Blood tests will show raised inflammatory markers (e.g., WBC, CRP and ESR).

Blood cultures may be positive for the causative organism.

Bone cultures can be performed to establish the causative organism and the antibiotic sensitivities.

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44
Q

Managing osteomyelitis

A

Management involves a combination of:

Surgical debridement of the infected bone and tissues
Antibiotic therapy

Prolonged courses of antibiotics are required to treat osteomyelitis. The BNF page on osteomyelitis recommends for acute osteomyelitis:

6 weeks of flucloxacillin, possibly with rifampicin or fusidic acid added for the first 2 weeks

Alternatives to flucloxacillin are:

Clindamycin in penicillin allergy
Vancomycin or teicoplanin when treating MRSA

Chronic osteomyelitis usually requires 3 months or more of antibiotics.

Osteomyelitis associated with prosthetic joints (e.g., a hip replacement) may require complete revision surgery to replace the prosthesis.

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45
Q

Sarcoma

A

Sarcomas are cancers originating in the muscles, bones or other types of connective tissue. There are many subtypes of sarcoma, which vary in their histology, location and degree of malignancy.

Types of bone sarcoma include:

Osteosarcoma – the most common form of bone cancer
Chondrosarcoma – cancer originating from the cartilage
Ewing sarcoma – a form of bone and soft tissue cancer most often affecting children and young adults

Types of soft tissue sarcoma include:

Rhabdomyosarcoma – originating from skeletal muscle
Leiomyosarcoma – originating from smooth muscle cancer
Liposarcoma – originating from adipose (fat) tissue
Synovial sarcoma – originating from soft tissues around the joints
Angiosarcoma – originating from the blood and lymph vessels
Kaposi’s sarcoma – cancer caused by human herpesvirus 8, most often seen in patients with end-stage HIV, causing typical red/purple raised skin lesions but also affecting other parts of the body

The prognosis depends greatly on the type, location, size and stage of the sarcoma. It can range from a greater than 90% 5-year survival for well-differentiated and resectable liposarcoma, to less than 10% for angiosarcoma affecting the liver.

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46
Q

Presentation of sarcoma

A

The presenting symptoms of sarcoma will vary dependent on the location and size of the lesion. The key features that should raise suspicions are:

A soft tissue lump, particularly if growing, painful or large
Bone swelling
Persistent bone pain

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47
Q

Investigating sarcoma

A

X-ray is the initial investigation for bony lumps or persistent pain.

Ultrasound is the initial investigation for soft tissue lumps.

CT or MRI scans may be used to visualise the lesion in more detail and look for metastatic spread (particularly a CT thorax, as sarcoma most often spreads to the lungs).

Biopsy is required to look at the histology of the cancer.

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48
Q

Staging sarcoma

A

Staging is either with the TNM staging system or a number system that grades the cancer from stage 1 (earliest) to stage 4 (most advanced).

The most common location for sarcoma to metastasise to is the lungs.

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49
Q

Managing sarcoma

A

Management will be guided by the sarcoma multidisciplinary team (MDT). There are specialist sarcoma centres in various locations in the UK that specialise in managing sarcoma. This concentrates the expertise about these relatively rare and often challenging cancers to ensure patients get the best care.

Sarcoma treatment will depend on the type, location, size and stage of the sarcoma. This may involve:

Surgery (surgical resection is the preferred treatment)
Radiotherapy
Chemotherapy
Palliative care

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50
Q

Back pain and sciatica

A

Low back pain is very common and has many causes. Lumbago is another term for low back pain. Non-specific or mechanical lower back pain refers to the majority of patients who do not have a specific disease causing their lower back pain.

Sciatica refers to the symptoms associated with irritation of the sciatic nerve.

Acute low back pain should improve within 1-2 weeks. Recovery can take longer (4-6 weeks) for sciatica.

Chronic lower back pain can have a massive impact on the patient’s quality of life and be difficult to manage.

There are several challenges with managing patients with lower back pain:

Identifying serious underlying pathology
Speeding up recovery
Reducing the risk of chronic lower back pain
Managing symptoms in chronic lower back pain

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51
Q

Causes of mechanical back pain

A

Muscle or ligament sprain
Facet joint dysfunction
Sacroiliac joint dysfunction
Herniated disc
Spondylolisthesis (anterior displacement of a vertebra out of line with the one below)
Scoliosis (curved spine)
Degenerative changes (arthritis) affecting the discs and facet joints

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52
Q

Causes of neck pain

A

Muscle or ligament strain (e.g., poor posture or repetitive activities)
Torticollis (waking up with a unilaterally stiff and painful neck due to muscle spasm)
Whiplash (typically after a road traffic accident)
Cervical spondylosis (degenerative changes to the vertebrae)

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53
Q

Red-Flag Causes of Back Pain

A

It is essential to look out for features that may indicate underlying:

Spinal fracture (e.g., major trauma)
Cauda equina (e.g., saddle anaesthesia, urinary retention, incontinence or bilateral neurological signs)
Spinal stenosis (e.g., intermittent neurogenic claudication)
Ankylosing spondylitis (e.g., age under 40, gradual onset, morning stiffness or night-time pain)
Spinal infection (e.g., fever or a history of IV drug use)

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54
Q

Other causes of back pain

A

Keep in mind that back pain may not always be related to the spine. There is a long list of abdominal or thoracic conditions that can cause back pain, including:

Pneumonia
Ruptured aortic aneurysms
Kidney stones
Pyelonephritis
Pancreatitis
Prostatitis
Pelvic inflammatory disease
Endometriosis

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55
Q

Sciatica

A

The spinal nerves L4 – S3 come together to form the sciatic nerve. The sciatic nerve exits the posterior part of the pelvis through the greater sciatic foramen, in the buttock area on either side. It travels down the back of the leg. At the knee, it divides into the tibial nerve and the common peroneal nerve.

The sciatic nerve supplies sensation to the lateral lower leg and the foot. It supplies motor function to the posterior thigh, lower leg and foot.

Sciatica causes unilateral pain from the buttock radiating down the back of the thigh to below the knee or feet. It might be described as an “electric” or “shooting” pain. Other symptoms are paraesthesia (pins and needles), numbness and motor weakness. Reflexes may be affected depending on the affected nerve root.

The main causes of sciatica are lumbosacral nerve root compression by:

Herniated disc
Spondylolisthesis (anterior displacement of a vertebra out of line with the one below)
Spinal stenosis

Bilateral sciatica is a red flag for cauda equina syndrome.

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56
Q

Assessing back pain

A

Key symptoms in the history are:

Major trauma (spinal fracture)
Stiffness in the morning or with rest (ankylosing spondylitis)
Age under 40 (ankylosing spondylitis)
Gradual onset of progressive pain (ankylosing spondylitis or cancer)
Night pain (ankylosing spondylitis or cancer)
Age over 50 (cancer)
Weight loss (cancer)
Bilateral neurological motor or sensory symptoms (cauda equina)
Saddle anaesthesia (cauda equina)
Urinary retention or incontinence (cauda equina)
Faecal incontinence (cauda equina)
History of cancer with potential metastasis (cauda equina or spinal metastases)
Fever (spinal infection)
IV drug use (spinal infection)

Key findings on examination are:

Localised tenderness to the spine (spinal fracture or cancer)
Bilateral neurological motor or sensory signs (cauda equina)
Bladder distention implying urinary retention (cauda equina)
Reduced anal tone on PR examination (cauda equina)

The sciatic stretch test can be used to help diagnose sciatica. The patient lies on their back with their leg straight. The examiner lifts one leg from the ankle with the knee extended until the limit of hip flexion is reached (usually around 80-90 degrees). Then the examiner dorsiflexes the patient’s ankle. Sciatica-type pain in the buttock/posterior thigh indicates sciatic nerve root irritation. Symptoms improve with flexing the knee.

TOM TIP: It is worth remembering the main cancers that metastasise to the bones. A history of these in an exam patient presenting with back pain should make you think of possible cauda equina or spinal metastases. You can remember them with the PoRTaBLe mnemonic:

Po – Prostate
R – Renal
Ta – Thyroid
B – Breast
Le – Lung

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57
Q

Investigating back pain

A

Generally, patients with mechanical/non-specific lower back pain can be diagnosed clinically and do not require further investigations.

X-rays or CT scans can be used to diagnose spinal fractures.

An emergency MRI scan is required in patients with suspected cauda equina (within hours of the presentation).

Investigations for suspected ankylosing spondylitis are:

Inflammatory markers (CRP and ESR)
X-ray of the spinal and sacrum (may show a fused “bamboo spine” in later-stage disease)
MRI of the spine (may show bone marrow oedema early in the disease)

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58
Q

STarT Back Screening Tool

A

The STarT Back tool was developed by Keele University to stratify the risk of a patient presenting with acute back pain developing chronic back pain. This helps guide the intensity of the initial interventions (e.g., referral for group exercises, physiotherapy and cognitive behavioural therapy).

It involves 9 questions that assess the patient’s function and psychological response to the back pain. It gives a:

Total score (out of 9)
Subscore on the 4 psychosocial questions (out of 4)

The interpretation gives a risk of developing chronic back pain:

Low Risk
Medium Risk
High Risk

Total Score
3 or less
More than 3
More than 3

Subscore
3 or less
3 or less
More than 3

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59
Q

Managing acute lower back pain

A

First, exclude serious underlying causes. If concerned about symptoms or signs of an underlying condition, arrange further investigations and refer appropriately. For example:

Same-day referral to the on-call orthopaedic team for an urgent MRI scan if cauda equina is suspected
Inflammatory markers and an urgent rheumatology review if ankylosing spondylitis is suspected
Full in-line spinal immobilisation, admission to a trauma unit and x-rays/CT scans for spinal injury after major trauma

Patients with neurological symptoms or signs on examination, particularly if progressive or severe, may require referral to orthopaedics or neurosurgery (potentially urgently).

The StarT Back tool can be used to stratify the risk of developing chronic back pain.

The NICE clinical knowledge summaries (updated 2020) give the options for managing non-specific low back pain based on the outcome of risk stratification, as briefly summarised below (always check the latest guidelines when treating patients).

Patients at low risk of chronic back pain can generally be managed with:

Self-management
Education
Reassurance
Analgesia
Staying active and continuing to mobilise as tolerated

Additional options for patients at medium or high risk of developing chronic back pain include:

Physiotherapy
Group exercise
Cognitive behavioural therapy

The NICE clinical knowledge summaries advise for analgesia:

NSAIDs (e.g., ibuprofen or naproxen) first-line
Codeine as an alternative
Benzodiazepines (e.g., diazepam) for muscle spasm (short-term only – up to 5 days)

They specifically state not to use opioids, antidepressants, amitriptyline, gabapentin or pregabalin for low back pain.

Patients need safety-net advice to report red flag symptoms, such as saddle anaesthesia or incontinence.

Radiofrequency denervation may be an option in patients with chronic low back pain originating in the facet joints. Radiofrequency is used to target and damage the medial branch nerves that supply sensation to the facet joints associated with the back pain. This is done under a local anaesthetic.

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60
Q

Managing sciatica

A

The initial management of sciatica is mostly the same as acute low back pain.

The NICE clinical knowledge summaries (updated 2020) state not to use medications such as gabapentin, pregabalin, diazepam or oral corticosteroids for sciatica. They state not to use opioids for chronic sciatica.

They suggest considering a neuropathic medication if symptoms are persisting or worsening at follow up, but not gabapentin or pregabalin, leaving at the main choices of:

Amitriptyline
Duloxetine

Specialist management options for chronic sciatica include:

Epidural corticosteroid injections
Local anaesthetic injections
Radiofrequency denervation
Spinal decompression

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61
Q

Pathophysiology of cauda equina syndrome

A

Cauda equina syndrome is a surgical emergency where the nerve roots of the cauda equina at the bottom of the spine are compressed. It requires emergency decompression surgery to prevent permanent neurological dysfunction. However, even with immediate decompression, patients may still not regain full function.

Pathophysiology

The cauda equina (translated as “horse’s tail”) is a collection of nerve roots that travel through the spinal canal after the spinal cord terminates around L2/L3. The spinal cord tapers down at the end in a section called the conus medullaris. The nerve roots exit either side of the spinal column at their vertebral level (L3, L4, L5, S1, S2, S3, S4, S5 and Co).

The nerves of the cauda equina supply:

Sensation to the lower limbs, perineum, bladder and rectum
Motor innervation to the lower limbs and the anal and urethral sphincters
Parasympathetic innervation of the bladder and rectum

In cauda equina syndrome, the nerves of the cauda equina are compressed. There are several possible causes of compression, including:

Herniated disc (the most common cause)
Tumours, particularly metastasis
Spondylolisthesis (anterior displacement of a vertebra out of line with the one below)
Abscess (infection)
Trauma

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62
Q

Red flags of cauda equina syndrome

A

Saddle anaesthesia (loss of sensation in the perineum – around the genitals and anus)
Loss of sensation in the bladder and rectum (not knowing when they are full)
Urinary retention or incontinence
Faecal incontinence
Bilateral sciatica
Bilateral or severe motor weakness in the legs
Reduced anal tone on PR examination

TOM TIP: A common way people ask about saddle anaesthesia when taking a history is to ask, “does it feel normal when you wipe after opening your bowels?”

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63
Q

Managing cauda equina syndrome

A

Cauda equina is a neurosurgical emergency. It requires:

Immediate hospital admission
Emergency MRI scan to confirm or exclude cauda equina syndrome
Neurosurgical input to consider lumbar decompression surgery

Surgery should be performed as soon as possible to increase the chances of regaining function. Even with early surgery, patients can be left with bladder, bowel or sexual dysfunction. Leg weakness and sensory impairment can also persist.

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64
Q

Metastatic spinal cord compression

A

When a metastatic lesion compresses the spinal cord (before the end of the spinal cord and the start of the cauda equina), this is called metastatic spinal cord compression (MSCC). This is different to cauda equina, which specifically refers to compression of the cauda equina.

MSCC presents similarly to cauda equina, with back pain and motor and sensory signs and symptoms. A key feature is back pain that is worse on coughing or straining.

MSCC is an oncological emergency and requires rapid imaging and management. There are specialist MSCC coordinators who should be involved early to coordinate the imaging and treatment of patients with MSCC.

Treatments will depend on individual factors. They may include:

High dose dexamethasone (to reduce swelling in the tumour and relieve compression)
Analgesia
Surgery
Radiotherapy
Chemotherapy

TOM TIP: Cauda equina presents with lower motor neuron signs (reduced tone and reduced reflexes). The nerves being compressed are lower motor neurons that have already exited the spinal cord. When the spinal cord is being compressed higher up by metastatic spinal cord compression, upper motor neuron signs (increased tone, brisk reflexes and upping plantar responses) will be seen.

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65
Q

Spinal stenosis

A

Spinal stenosis refers to the narrowing of part of the spinal canal, resulting in compression of the spinal cord or nerve roots. This usually affects the cervical or lumbar spine. This section focuses on lumbar spinal stenosis, which is the most common type.

Spinal stenosis is more likely to occur in patients older than 60 years, relating to degenerative changes in the spine.

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66
Q

Types of spinal stenosis

A

Central stenosis – narrowing of the central spinal canal
Lateral stenosis – narrowing of the nerve root canals
Foramina stenosis – narrowing of the intervertebral foramina

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67
Q

Causes of spinal stenosis

A

Several conditions can cause the spinal canal to narrow, including:

Congenital spinal stenosis
Degenerative changes, including facet joint changes, disc disease and bone spurs
Herniated discs
Thickening of the ligamenta flava or posterior longitudinal ligament
Spinal fractures
Spondylolisthesis (anterior displacement of a vertebra out of line with the one below)
Tumours

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68
Q

Presentation of spinal stenosis

A

Symptoms of spinal stenosis tend to have a gradual onset (as opposed to cauda equina syndrome or sudden disc herniation with cord compression).

The severity of symptoms will depend on the degree of narrowing and spinal cord. Symptoms may be subtle with mild compression. Severe compression can present with features of cauda equina syndrome (saddle anaesthesia, sexual dysfunction and incontinence of the bladder and bowel), requiring emergency management.

Intermittent neurogenic claudication is a key presenting feature of lumbar spinal stenosis with central stenosis. It is sometimes referred to as pseudoclaudication. Typical symptoms are:

Lower back pain
Buttock and leg pain
Leg weakness

The symptoms are absent at rest and when seated but occur with standing and walking. Bending forward (flexing the spine) expands the spinal canal and improves symptoms. Standing straight (extending the spine) narrows the canal and worsens the symptoms.

Lateral stenosis and foramina stenosis in the lumbar spine tends to cause symptoms of sciatica.

The term radiculopathy refers to compression of the nerve roots as they exit the spinal cord and spinal column, leading to motor and sensory symptoms.

TOM TIP: The important thing for your exams is to spot the typical symptoms of intermittent neurogenic claudication. At first glance, they are similar to peripheral arterial disease. The exam question might specify that the peripheral pulses or the ankle-brachial pressure index (ABPI) are normal, in which case the diagnosis is more likely to be spinal stenosis. Additionally, patients with spinal stenosis are more likely to struggle with back pain, whereas back pain is not a feature of peripheral arterial disease.

69
Q

Investigating spinal stenosis

A

MRI is the primary imaging investigation for diagnosing spinal stenosis.

Investigations to exclude peripheral arterial disease (e.g., ankle-brachial pressure index and CT angiogram) may be appropriate where symptoms of intermittent claudication are present.

70
Q

Managing spinal stenosis

A

Management will be guided by a spinal specialist based on individual factors. Options include:

Exercise and weight loss (if appropriate)
Analgesia
Physiotherapy
Decompression surgery where conservative treatment fails (with variable results)

Laminectomy refers to the removal of part or all of the lamina from the affected vertebra. The laminae are the bony parts that form the posterior part of the vertebral foramen (forming the spinal canal) and attaches to the spinous process.

The benefits of epidural injections with local anaesthetic and corticosteroids are unclear, and they are not generally used.

71
Q

Meralgia paraesthetica

A

Meralgia paraesthetica refers to localised sensory symptoms of the outer thigh caused by compression of the lateral femoral cutaneous nerve. It is a mononeuropathy, meaning it only affects a single nerve.

72
Q

Anatomy of lateral femoral cutaneous nerve

A

The lateral femoral cutaneous nerve originates from varying combinations of L1, L2 and L3 nerve roots. It comes from behind the psoas muscle, around the surface of the iliacus muscle and under the inguinal ligament onto the thigh, just medial and inferior to the anterior superior iliac spine (ASIS).

It supplies sensory innervation to the upper-outer thigh. Pressure, deformity or trauma to the nerve can occur at several places.

The lateral femoral cutaneous nerve only carries sensory signals. Therefore, there are no motor symptoms with meralgia paraesthetica.

73
Q

Presentation of meralgia paraesthetica

A

Patients present with abnormal sensations (dysaesthesia) and loss of sensation (anaesthesia) in the lateral femoral cutaneous nerve distribution. The skin of the upper-outer thigh is affected. Patients may describe symptoms of:

Burning
Numbness
Pins and needles
Cold sensation
There may also be localised hair loss.

Symptoms are aggravated by walking or standing for a long duration and improve when sitting down.

Symptoms are often worse with extension of the hip on the affected side. This can be used to reproduce symptoms on examination.

74
Q

Diagnosing meralgia paraesthetica

A

The diagnosis is mainly clinical, based on history and examination findings. Other investigations may be used to rule out other causes (e.g., nerve root compression in the spine or pelvic tumours compressing the nerve).

75
Q

Managing meralgia paraesthetica

A

Symptoms vary from mild and self-limiting to severe and persistent.

Management can be conservative, medical or surgical.

Conservative management involves:

Rest
Looser clothing (tight clothes such as belts may add pressure to the nerve)
Weight loss (if appropriate)
Physiotherapy

Medical management is based around analgesia if pain is a feature, such as:

Paracetamol
NSAIDs
Neuropathic analgesia (e.g., amitriptyline, gabapentin, pregabalin or duloxetine)
Local injections of steroids or local anaesthetics

Surgical management may involve:

Decompression – removing pressure on the nerve
Transection – cutting the nerve
Resection – removing the nerve

76
Q

Trochanteric bursitis

A

Trochanteric bursitis refers to inflammation of a bursa over the greater trochanter on the outer hip.

It produces pain localised at the outer hip, referred to as greater trochanteric pain syndrome.

Bursae are sacs created by synovial membrane filled with a small amount of synovial fluid. They are found at bony prominences (e.g., at the greater trochanter, knee, shoulder and elbow). They act to reduce friction between the bones and soft tissues during movement.

Bursitis refers to inflammation of a bursa. This causes thickening of the synovial membrane and increased fluid production, causing swelling.

This inflammation can have several causes:

Friction from repetitive movements
Trauma
Inflammatory conditions (e.g., rheumatoid arthritis)
Infection – referred to as septic bursitis

77
Q

Presentation of trochanteric bursitis

A

The typical presentation is a middle-aged patient with gradual-onset lateral hip pain (over the greater trochanter) that may radiate down the outer thigh. The pain is described as aching or burning. It is worse with activity, standing after sitting for a prolonged period and trying to sit cross-legged. It may disrupt sleep and be difficult to find a comfortable lying position.

On examination, there is tenderness over the greater trochanter. There is not usually any swelling (unlikely bursitis in other areas).

The NICE clinical knowledge summaries (updated 2016) suggest special tests to establish the diagnosis:

Trendelenburg test
Resisted abduction of the hip
Resisted internal rotation of the hip
Resisted external rotation of the hip

The Trendelenburg test involves asking the patient to stand one-legged on the affected leg. Normally, the other side of the pelvis should remain level or tilt upwards slightly. A positive Trendelenburg test is when the other side of the pelvis drops down, suggesting weakness in the affected hip.

To perform the resisted movements, ask the patient to resist while you move their hip. For example, with the patient lying supine, abduct their leg at the hip while they try to resist the movement. This causes the soft tissues associated with the bursa to tighten, causing pain. Pain on resisted movement supports a diagnosis of bursitis.

78
Q

Managing trochanteric bursitis

A

The diagnosis is based on the history and examination findings.

Management options are:

Rest
Ice
Analgesia (e.g., ibuprofen or naproxen)
Physiotherapy
Steroid injections

Rarely, trochanteric bursitis can be caused by infection. This may present with warmth, erythema, swelling and pain over the bursa. The patient may have a fever. Treatment involves antibiotics.

It can take 6-9 months to recover fully, sometimes longer.

79
Q

Knee anatomy

A

The knee is a hinge joint. Between the femur and the tibia are the menisci. There is a medial and lateral meniscus. The rounded bones at the end of the femur (condyles) do not match the slightly convex areas (also called condyles) at the top of the tibia. Therefore, the menisci help the femur and tibia fit together and move smoothly across each other. They act as a shock absorber, distribute weight throughout the joint and help stabilise the joint.

Also in the knee is a joint between the anterior femur and the patella (patellofemoral joint). The patella sits in a groove on the femur called the trochlea (or patellofemoral groove). The quadriceps tendon attaches to the patella, which is attached to the tibia by the patellar ligament. Contraction of the quadriceps muscles causes knee extension by pulling through the patella.

There are four ligaments in the knee:

Anterior cruciate ligament
Posterior cruciate ligament
Lateral collateral ligament
Medial collateral ligament

80
Q

Presentation of meniscal tears

A

Meniscal tears often occur during twisting movements in the knee. In young patients, this often happens when playing sports.

With increasing age, the meniscus becomes more prone to injury. Tears can occur with minor twisting movements in older patients (e.g., standing from seated with an awkward twist in the knee).

The initial injury can be accompanied by a “pop” sound or sensation.

Symptoms include:

Pain
Swelling
Stiffness
Restricted range of motion
Locking of the knee
Instability or the knee “giving way”

Pain may be referred to the hip or lower back.

Examination findings are:

Localised tenderness on the joint line
Swelling
Restricted range of motion

Traditionally, the two key special tests for meniscal tears are McMurray’s test and Apley grind test. These are generally not used or recommended in clinical practice as they can cause pain and may worsen the meniscal injury.

81
Q

McMurray’s Test

A

McMurray’s test involves the patient lying supine. The examiner takes the leg and flexes the knee.

While internally rotating the tibia (by turning the foot inwards) and applying varus pressure to the knee (applying outward pressure to the inside of the knee), carefully extend the knee. Pain or restriction indicates lateral meniscal damage.

Repeating the flexed to extended movement with external rotation of the tibia and valgus (inward) pressure on the knee tests for medial meniscal damage.

82
Q

Apley Grind Test

A

The Apley grind test involves the patient lying prone and flexing the knee to 90 degrees with the thigh flat on the couch. Downward pressure is applied through the leg into the knee, and the tibia is internally and externally rotated at the same time. Pain indicates a positive result, suggesting meniscal damage. The pain is localised to the area of damage (e.g., medial or lateral meniscus).

83
Q

Ottawa Knee Rules

A

Bone fractures are worth considering as a differential diagnosis in patients presenting with acute knee injuries. The Ottawa knee rules can be used to determine whether a patient requires an x-ray of the knee after an acute knee injury to look for a fracture.

The Ottawa knee rules state that a patient requires a knee x-ray if any of the following are present:

Age 55 or above
Patella tenderness (with no tenderness elsewhere)
Fibular head tenderness
Cannot flex the knee to 90 degrees
Cannot weight bear (cannot take 4 steps – limping steps still count)

84
Q

Investigating meniscal tears

A

MRI scan is usually the first-line imaging investigation for establishing the diagnosis.

Arthroscopy can be used to visualise the meniscus within the joint and is the gold-standard investigation for diagnosing a meniscal tear. Arthroscopy can also be used to repair or remove damaged sections of the meniscus.

85
Q

Managing meniscal tears

A

The NICE clinical knowledge summaries on knee pain (updated 2017) recommend urgent referral in patients with an acute onset of knee pain associated with symptoms suggestive of an acute meniscal tear. Local pathways vary, and this may involve sending the patient to A&E or the fracture clinic. Key symptoms include:

A “pop”
Rapid onset swelling
Instability or giving way
Locking

Conservative management of most acute soft tissue injuries, including meniscal tears, is with the RICE mnemonic:

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

NSAIDs are usually used first-line for analgesia in MSK injuries.

Physiotherapy can be used for rehabilitation after the initial pain and swelling have settled.

Surgery may be required. This involves arthroscopy (keyhole surgery) of the knee joint. The main options are:

Repair of the meniscus if possible
Resection of the affected portion of the meniscus (this often results in osteoarthritis)

86
Q

Anterior cruciate ligament injury

A

Injury to either the anterior cruciate ligament (ACL) or posterior cruciate ligament (PCL) can cause instability in the knee. Damage to the ACL is common, particularly amongst athletes. PCL injuries are less common.

Basic Anatomy

At the top of the tibia, there are the medial and lateral condyles, which are slightly convex surfaces that correspond to the condyles of the femur. Between the condyles, there is an intercondylar area. The cruciate ligaments are named after where they attach to the tibia:

The ACL attaches at the anterior intercondylar area on the tibia
The PCL attaches at the posterior intercondylar area on the tibia

There are rounded areas of bone at the end of the femur, which are also called condyles. At the back of the distal end of the femur is an intercondylar notch, which is a groove between the two condyles. Both cruciate ligaments originate from the intercondylar notch, the ACL on the lateral aspect and the PCL on the medial aspect.

The ACL stops the tibia from sliding forward in relation to the femur. The PCL stops the tibia sliding backwards in relation to the femur.

87
Q

Presentation of ACL injury

A

The ACL is typically damaged during a twisting injury to the knee. The injury causes:

Pain
Swelling
“Pop” sound or sensation

Patients with ACL injuries will have instability of the knee joint. The tibia can move anteriorly below the femur. The knee can buckle, and patients often feel a lack of confidence that the knee is stable. Over time, muscle weakness develops, and there is an increased risk of other knee injuries (e.g., meniscal tears).

The anterior drawer test can be used to assess for anterior cruciate ligament damage. The patient is supine with the hip flexed to 45 degrees and the knee flexed to 90 degrees, with the foot flat on the couch. The examiner sits on the patient’s toes to stabilise the foot. The examiner holds the leg just below the knee and pulls the proximal tibia anteriorly, sliding it forward from the femur at the knee. In a normal knee, there will be slightly anterior movement of the proximal tibia but a definite end-point to movement, as the ACL holds the joint securely. With ACL damage, the tibia can move an excessive distance anteriorly, and the examiner will not be able to feel a clear end-point to the movement.

The Lachman test is similar to the anterior drawer test, but the knee is tested while flexed at around 20-30 degrees.

Examination can be difficult to interpret shortly after the injury due to pain and swelling. Examination after the acute pain and swelling has settled is more likely to be accurate.

88
Q

Investigating ACL injury

A

MRI scan is usually the first-line imaging investigation for establishing the diagnosis.

Arthroscopy can be used to visualise the cruciate ligament and is the gold-standard investigation for diagnosing a cruciate ligament tear.

89
Q

Managing ACL injury

A

The NICE clinical knowledge summaries on knee pain (updated 2017) recommend urgent referral in patients with an acute onset of knee pain associated with symptoms suggestive of an acute anterior cruciate ligament tear. Local pathways vary, and this may involve sending the patient to A&E or the fracture clinic. Symptom suggestive of an acute anterior cruciate ligament tear include:

A “pop”
Rapid onset swelling
Instability or giving way

Conservative management involves RICE:

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

NSAIDs are usually used first-line for analgesia in MSK injuries.

Crutches and knee braces may be required to help protect the knee while mobilising.

Physiotherapy can be used before and after surgery for rehabilitation.

Arthroscopic surgery to reconstruct the ligament is often required, particularly in active and young patients. The type and timing of surgery will be based on individual factors, such as the extent of the ACL injury and the patient’s activities (e.g., are they a young competitive athlete or a sedentary older patient). A new ligament is formed using a graft of tendon from another location. Options for graft tendons used to reconstruct the ACL include:

Hamstring tendon
Quadriceps tendon
Bone-patellar tendon-bone (taking part of the patella tendon as well as the bone it inserts into)

90
Q

Osgood-Schlatter disease

A

Osgood-Schlatter disease is caused by inflammation at the tibial tuberosity where the patella ligament inserts. It is a common cause of anterior knee pain in adolescents.

It typically occurs in patients aged 10 – 15 years and is more common in males. Osgood-Schlatter disease is usually unilateral, but it can be bilateral.

91
Q

Pathophysiology of Osgood-Schlatter disease

A

The patella tendon inserts into the tibial tuberosity. In patients with Osgood-Schlatter disease, multiple minor avulsion fractures occur where the patella ligament pulls away tiny pieces of the bone. This leads to growth of the tibial tuberosity, causing a visible lump below the knee. Initially, this lump is tender due to inflammation. As the bone heals and inflammation settles, the lump becomes hard and non-tender.

A hard, non-tender lump is then permanently present at the tibial tuberosity.

92
Q

Presentation of Osgood-Schlatter disease

A

Osgood-Schlatter disease presents with a gradual onset of symptoms:

Visible or palpable hard and tender lump at the tibial tuberosity
Pain in the anterior aspect of the knee
The pain is exacerbated by physical activity, kneeling and on extension of the knee

93
Q

Managing Osgood-Schlatter disease

A

Initial management focuses on reducing pain and inflammation.

Reduction in physical activity
Ice
NSAIDS (e.g., ibuprofen) for symptomatic relief

Once symptoms settle, stretching and physiotherapy can be used to strengthen the joint and improve function.

94
Q

Prognosis of Osgood-Schlatter disease

A

Symptoms will fully resolve over time. The patient is usually left with a hard bony lump on their knee.

A rare complication is a complete avulsion fracture, where the tibial tuberosity is separated from the rest of the tibia. This requires surgical intervention.

95
Q

Baker’s cysts and popliteal fossa

A

Baker’s cysts are also called popliteal cysts. A Baker’s cyst is a fluid-filled sac in the popliteal fossa, causing a lump.

The popliteal fossa is the diamond-shaped hollow area formed by the:

Semimembranosus and semitendinosus tendons (superior and medial)
Biceps femoris tendon (superior and lateral)
Medial head of the gastrocnemius (inferior and medial)
Lateral head of the gastrocnemius (inferior and lateral)

Pathophysiology

In adults, Baker’s cysts are usually secondary to degenerative changes in the knee joint. They can be associated with:

Meniscal tears (an important underlying cause)
Osteoarthritis
Knee injuries
Inflammatory arthritis (e.g., rheumatoid arthritis)

Synovial fluid is squeezed out of the knee joint and collects in the popliteal fossa. A connection between the synovial fluid in the joint and the Baker’s cyst can remain, allowing the cyst to continue enlarging as more fluid collects there.

Baker’s cysts are contained within the soft tissues. They do not have their own epithelial lining.

96
Q

Presentation of Baker’s Cyst

A

Patients may present with symptoms localised to the popliteal fossa:

Pain or discomfort
Fullness
Pressure
A palpable lump or swelling
Restricted range of motion in the knee (with larger cysts)

On examination, the lump will be most apparent when the patient stands with their knees fully extended. The lump will get smaller or disappear when the knee is flexed to 45 degrees (Foucher’s sign).

Oedema may occur if the cyst compresses the venous drainage of the leg.

97
Q

Ruptured Baker’s Cyst

A

Baker’s cysts can rupture if the pressure is large enough.

Ruptured Baker’s cyst causes inflammation in the surrounding tissues and calf muscle, presenting with:

Pain
Swelling
Erythema

A critical differential diagnosis of a ruptured Baker’s cyst is a deep vein thrombosis (DVT).

A ruptured Baker’s cyst can rarely cause compartment syndrome.

98
Q

The key differential diagnoses of a lump in the popliteal fossa are

A

Baker’s cyst
Deep vein thrombosis
Abscess
Popliteal artery aneurysm
Ganglion cyst
Lipoma
Varicose veins
Tumour

99
Q

Investigations for Baker’s Cyst

A

Ultrasound is usually the first-line investigation to confirm the diagnosis. It is also used to rule out a DVT.

MRI can evaluate the cyst further if required, for example, before surgery. They can also demonstrate underlying knee pathology, such as meniscal tears.

100
Q

Managing Baker’s Cyst

A

No treatment is required for asymptomatic Baker’s cysts.

Non-surgical management for symptomatic Baker’s cysts include:

Modified activity to avoid exacerbating symptoms
Analgesia (e.g., NSAIDs)
Physiotherapy
Ultrasound-guided aspiration
Steroid injections

Surgical management typically involves arthroscopic procedures to treat underlying knee pathology contributing to the cyst, such as degenerative changes or meniscal tears. Resection of the cyst is difficult, and the cyst is likely to recur, particularly when another knee pathology is present.

101
Q

Achilles Tendinopathy

A

The Achilles tendon connects the calf muscles (gastrocnemius and soleus) to the heel (the calcaneus bone). Flexion of the calf muscles pulls on the Achilles and causes plantar flexion of the ankle.

Achilles tendinopathy involves damage, swelling, inflammation and reduced function in the Achilles tendon.

There are two types of Achilles tendinopathy:

Insertion tendinopathy (within 2cm of the insertion point on the calcaneus)
Mid-portion tendinopathy (2-6 cm above the insertion point)

102
Q

Risk factors for achilles tendinopathy

A

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

103
Q

Presentation of achilles tendinopathy

A

The typical presentation is with a gradual onset of:

Pain or aching in the Achilles tendon or heel, with activity
Stiffness
Tenderness
Swelling
Nodularity on palpation of the tendon

104
Q

Managing achilles tendinopathy

A

Achilles tendinopathy is a clinical diagnosis and does not usually require any investigations to diagnose. It is essential to exclude Achilles tendon rupture, for example, using Simmonds’ calf squeeze test. Ultrasound is used to diagnose Achilles tendon rupture.

Management options are:

Rest and altered activities
Ice
Analgesia
Physiotherapy
Orthotics (e.g., insoles)
Extracorporeal shock-wave therapy (ESWT)
Surgery, to remove nodules and adhesions or alter the tendon, may be used where other treatments fail

Steroid injections into the Achilles tendon are avoided due to the risk of tendon rupture.

105
Q

Achilles tendon rupture

A

Achilles tendon rupture is a sudden onset injury resulting in rupture of the Achilles tendon and a loss of the connection between the calf muscles (gastrocnemius and soleus) to the heel (the calcaneus bone).

106
Q

Risk factors for achilles tendon rupture

A

Sports that stress the Achilles (e.g., basketball, tennis and track athletics)
Increasing age
Existing Achilles tendinopathy
Family history
Fluoroquinolone antibiotics (e.g., ciprofloxacin and levofloxacin)
Systemic steroids

TOM TIP: It is worth remembering the association between fluoroquinolone antibiotics and Achilles tendinopathy and rupture. Rupture can occur spontaneously within 48 hours of starting treatment. This knowledge is commonly tested in exams. It is also important to warn patients to look out for any signs of Achilles tendinitis and stop treatment if they occur.

107
Q

Presentation of achilles tendon rupture

A

The typical presentation is:

Sudden onset of pain in the Achilles or calf
A snapping sound and sensation
Feeling as though something has hit them in the back of the leg

There are often no prior warning signs or Achilles symptoms.

Signs on examination are:

When relaxed in a dangled position, the affected ankle will rest in a more dorsiflexed position
Tenderness to the area
A palpable gap in the Achilles tendon (although swelling might hide this)
Weakness of plantar flexion of the ankle (dorsiflexion is unaffected)
Unable to stand on tiptoes on the affected leg alone
Positive Simmonds’ calf squeeze test

Simmonds’ calf squeeze test is the special test for Achilles tendon rupture. The patient is positioned prone or kneeling with the feet hanging freely off the end of the bench or couch. When squeezing the calf muscle in a leg with an intact Achilles, there will be plantar flexion of the ankle. Squeezing the calf pulls on the Achilles. When the Achilles is ruptured, the connection between the calf and the ankle is lost. Squeezing the calf will not cause plantar flexion of the ankle in a leg with a ruptured Achilles. A lack of plantar flexion is a positive result.

108
Q

Diagnosing achilles tendon rupture

A

Ultrasound is the investigation of choice for confirming the diagnosis.

109
Q

Managing achilles tendon rupture

A

Patients with suspected Achilles rupture should be reviewed by orthopaedics on the same day.

Immediate management involves:

Rest and immobilisation
Ice
Elevation
Analgesia

Venous thromboembolism prophylaxis needs to be considered while the ankle is immobilised.

There is a debate between non-surgical and surgical management. Healing rates are similar between the two. Non-surgical management avoids the risks associated with surgery (e.g., anaesthetic risks, poor wound healing and infection) but has a higher risk of re-rupture.

Non-surgical management involves applying a specialist boot to immobilise the ankle. The first boot involves full plantar flexion of the ankle. Over time, the boots are altered to gradually move the ankle from full plantar flexion to a neutral position. This process takes 6-12 weeks while the Achilles tendon heals. A long rehabilitation process is required to get back to full pre-injury function.

Surgical management involves surgically reattaching the Achilles. After surgery, a similar process is followed to non-surgical management, with boots that immobilise the ankle initially in a plantar-flexed position, gradually adjusted to a neutral position. This is followed by a long rehabilitation process to get back to full pre-injury function.

110
Q

Plantar Fasciitis

A

Plantar fasciitis is inflammation of the plantar fascia.

The plantar fascia is thick connective tissue. It attaches to the calcaneus at the heel, travels along the sole of the foot and branches out to connect to the flexor tendons of the toes.

Presentation is with a gradual onset of pain on the plantar aspect of the heel. This is worse with pressure, particularly when walking or standing for prolonged periods. There is tenderness to palpation of this area.

111
Q

Managing plantar fasciitis

A

Management involves:

Rest
Ice
Analgesia (e.g., NSAIDs)
Physiotherapy
Steroid injections (can be very painful and rarely cause rupture of the plantar fascia or fat pad atrophy)

Rarely, specialist management may be required, with:

Extracorporeal shockwave therapy
Surgery

112
Q

Fat pad atrophy

A

Fat pad atrophy affects the fat pad over the heel of the foot (under the calcaneus). The fat pad protects the heel from impact.

Atrophy (wasting away) of the fat pad can occur with age or inflammation from repetitive impacts, such as jumping activities, running, walking, and obesity. Local steroid injections (used to treat plantar fasciitis) can cause fat pad atrophy.

Symptoms are similar to plantar fasciitis, with pain and tenderness over the plantar aspect of the heel. Symptoms are worse with activities, particularly when barefoot on hard surfaces.

The thickness of the fat pad can be measured with an ultrasound scan.

Management involves comfortable shoes, custom insoles, adapting activities (e.g., avoiding high heels) and weight loss if appropriate.

113
Q

Morton’s Neuroma

A

Morton’s neuroma refers to the dysfunction of a nerve in the intermetatarsal space (between the toes) towards the top of the foot. The abnormal nerve is usually located between the third and fourth metatarsal. It is caused by irritation of the nerve relating to the biomechanics of the foot. High-heels or narrow shoes may exacerbate it.

Typical symptoms are:

Pain at the front of the foot at the location of the lesion
The sensation of a lump in the shoe
Burning, numbness or “pins and needles” felt in the distal toes

There are several ways to test for Morton’s neuroma:

Deep pressure applied to the affected intermetatarsal space on the dorsal foot causes pain
Metatarsal squeeze test – squeezing the forefoot with one hand to create a concave shape to the plantar aspect while using the other hand to press the affected area on the plantar side of the foot causes pain
Mulder’s sign – a painful click is felt when using two hands on either side of the foot to manipulate the metatarsal heads to rub the neuroma

Ultrasound or MRI can be used to confirm the diagnosis.

Management options include:

Adapting activities (e.g., avoiding high heels)
Analgesia (NSAIDs if suitable)
Insoles
Weight loss if appropriate
Steroid injections
Radiofrequency ablation
Surgery (e.g., excision of the neuroma)

114
Q

Bunions (Hallux Valgus)

A

The medical name for bunions is hallux valgus (hallux refers to the big toe, and valgus refers to the angle of the deformity).

A bunion is a bony lump created by a deformity at the metatarsophalangeal joint (MTP) at the base of the big toe. The first metatarsal becomes angled medially, the big toe (hallux) become angled laterally (towards the other toes), and the MTP joint becomes inflamed and enlarged. Over time, additional stress on the joint can result in osteoarthritis.

Bunions develop slowly. The cause is not clear. They can be painful, particularly when walking and wearing tight shoes.

Weight-bearing x-rays can be used to assess the extent of the deformity.

Conservative management is with wide, comfortable shoes and analgesia. Patients can use bunion pads to protect the bunion from friction inside their shoes.

Surgery is the definitive treatment. There are various options depending on individual factors. The aim is to realign the bones and correct the deformity.

115
Q

Gout

A

Gout is a common cause of pain and swelling in the metatarsophalangeal joint (MTP) at the base of the big toe. It can also affect the ankle, wrists, base of the thumb or knee.

Gout is a type of crystal arthropathy associated with chronically high blood uric acid levels. Urate crystals collect in the joint, causing it to become acutely hot, swollen and painful.

Diagnosis is usually made clinically. It is essential to exclude septic arthritis as a differential diagnosis. This may require joint fluid aspiration.

Aspirated fluid will show:

No bacterial growth
Needle shaped crystals
Negatively birefringent of polarised light
Monosodium urate crystals

116
Q

Frozen shoulder

A

Frozen shoulder is also called adhesive capsulitis. It is a relatively common cause of shoulder pain and stiffness. The loss of range of motion and function in the shoulder joint can significantly impair activities.

It most commonly affects people in middle age. Diabetes is a key risk factor.

Adhesive capsulitis can be:

Primary – occurring spontaneously without any trigger
Secondary – occurring in response to trauma, surgery or immobilisation

Pathophysiology

The glenohumeral joint is the ball and socket joint in the shoulder. The glenohumeral joint is surrounded by connective tissue that forms the joint capsule.

In adhesive capsulitis, inflammation and fibrosis in the joint capsule lead to adhesions (scar tissue). The adhesions bind the capsule and cause it to tighten around the joint, restrict movement in the joint.

117
Q

Presentation of frozen shoulder

A

There is a typical course of symptoms, with three phases:

Painful phase – shoulder pain is often the first symptom and may be worse at night
Stiff phase – shoulder stiffness develops and affects both active and passive movement (external rotation is the most affected) – the pain settles during this phase
Thawing phase – there is a gradual improvement in stiffness and a return to normal

The entire illness lasts 1 – 3 years before resolving (e.g., 6 months in each phase). However, a large number of patients (up to 50%) have persistent symptoms.

118
Q

Differentials in a patient presenting with shoulder pain

A

The main differentials in a patient presenting with shoulder pain not preceded by trauma or an acute injury are:

Supraspinatus tendinopathy
Acromioclavicular joint arthritis
Glenohumeral joint arthritis

Rare but important differentials to keep in mind are:

Septic arthritis
Inflammatory arthritis
Malignancy (e.g., osteosarcoma or bony metastasis)

Shoulder pain preceded by trauma or an acute injury may be due to:

Shoulder dislocation
Fractures (e.g., proximal humerus, clavicle or rarely the scapula)
Rotator cuff tear

119
Q

Supraspinatus tendinopathy

A

Supraspinatus tendinopathy involves inflammation and irritation of the supraspinatus tendon, particularly due to impingement at the point where it passes between the humeral head and the acromion. The empty can test (AKA Jobe test) can be used to assess for supraspinatus tendinopathy. This involves the patient abducting the shoulder to 90 degrees and fully internally rotating the arm as though they are emptying a can of water. The examiner pushes down on the arm while the patient resists. The test is positive if there is pain or the arm gives way.

120
Q

Acromioclavicular (AC) joint arthritis

A

Acromioclavicular (AC) joint arthritis can be demonstrated on examination by:

Tenderness to palpation of the AC joint
Pain is worse at the extremes of the shoulder abduction, from around 170 degrees onwards when the arm is overhead
Positive scarf test – pain caused by wrapping the arm across the chest and opposite shoulder

121
Q

Diagnosing frozen shoulder

A

Adhesive capsulitis is a clinical diagnosis based on the history and examination and excluding other causes of shoulder pain and stiffness. Imaging investigations are not usually required.

X-rays are usually normal. However, they are helpful for diagnosing osteoarthritis as a differential.

Ultrasound, CT or MRI scans can show a thickened joint capsule.

122
Q

Basic anatomy of rotator cuff

A

The rotator cuff is made of four muscles, each with a specific action at the shoulder (mnemonic is SITS):

S – Supraspinatus – abducts the arm
I – Infraspinatus – externally rotates the arm
T – Teres minor – externally rotates the arm
S – Subscapularis – internally rotates the arm

123
Q

Presentation of rotator cuff tears

A

Rotator cuff tears may present either with an acute onset of symptoms after an acute injury, or with a gradual onset of symptoms. Patients typically present with:

Shoulder pain
Weakness and pain with specific movements relating to the site of the tear (e.g., abduction with a supraspinatus tear)

Patients may find it difficult to get comfortable at night due to pain in the shoulder, disrupting sleep.

124
Q

Investigating rotator cuff tears

A

X-rays will not show soft tissue injuries such as rotator cuff tears. They may be helpful for excluding bony pathology, such as osteoarthritis.

Ultrasound or MRI scans can diagnose a rotator cuff tear.

125
Q

Managing rotator cuff tears

A

Patients with degenerative rotator cuff tears may be managed conservatively, particularly where they are at increased risk of complications from surgery. Active or young patients and those with acute or full-thickness tears are more likely to be managed with surgery. Surgery may be used where physiotherapy fails.

Non-surgical options are:

Rest and adapted activities
Analgesia (e.g., NSAIDs)
Physiotherapy

There are many options for surgical management, depending on individual factors. The main option is arthroscopic rotator cuff repair, where the tendon is reattached to the bone during an arthroscopy (keyhole surgery).

126
Q

Shoulder dislocation

A

Shoulder dislocation is where the ball of the shoulder (head of the humerus) comes entirely out of the socket (glenoid cavity of the scapula).

Subluxation refers to a partial dislocation of the shoulder. The ball does not come fully out of the socket and naturally pops back into place shortly afterwards.

More than 90% of shoulder dislocations are anterior dislocations. This is where the head of the humerus moves anteriorly (forward) in relation to the glenoid cavity. This can occur when the arm is forced backwards (posteriorly) whilst abducted and extended at the shoulder. Picture someone reaching up and out to try and catch a heavy rock travelling towards them.

Posterior dislocations are associated with electric shocks and seizures.

TOM TIP: Exam questions might challenge you to distinguish between anterior and posterior dislocations. The answer is almost certainly an anterior dislocation unless the patient has had a seizure or an electric shock.

127
Q

Associated damage of shoulder dislocation

A

The glenoid labrum surrounds the glenoid cavity. The labrum is a rim of cartilage that creates a deeper socket for the head of the humerus to fit into. When the shoulder dislocates, the labrum can tear along one edge.

Bankart lesions are tears to the anterior portion of the labrum. These occur with repeated anterior subluxations or dislocations of the shoulder.

Hill-Sachs lesions are compression fractures of the posterolateral part of the head of the humerus. As the shoulder dislocates anteriorly, the posterolateral part of the humeral head impacts with the anterior rim of the glenoid cavity. Part of the humeral head is damaged, making the shoulder less stable and at risk of further dislocations.

Axillary nerve damage is a key complication. The axillary nerve comes from the C5 and C6 nerve roots. Damage causes a loss of sensation in the “regimental badge” area over the lateral deltoid. It also leads to motor weakness in the deltoid and teres minor muscles.

Fractures can occur alongside shoulder dislocations, affecting the:

Humeral head
Greater tuberosity of the humerus
Acromion of the scapula
Clavicle

Rotator cuff tears may occur with shoulder dislocations, particularly in older patients.

TOM TIP: Axillary nerve damage is a common association with anterior dislocations to remember for your exams. This knowledge may be tested in MCQs, where you are asked to identify the nerve, location of sensory loss or muscle affected by weakness.

128
Q

Presentation of shoulder dislocation

A

Patients with a shoulder dislocation usually present after the acute injury. They will almost certainly be aware that the shoulder is dislocated. Shortly after the shoulder is dislocated, the muscles will go into spasm and tighten around the joint.

They will hold their arm against the side of their body. The deltoid will appear flattened, and the head of the humerus will cause a bulge and be palpable at the front of the shoulder.

It is important to assess patients with a shoulder dislocation for:

Fractures
Vascular damage (e.g., absent pulses, prolonged capillary refill time and pallor)
Nerve damage (e.g., loss of sensation in the “regimental patch” area)

129
Q

Apprehension test

A

The apprehension test is a special test to assess for shoulder instability, specifically in the anterior direction. It is likely to be positive after previous anterior dislocation or subluxation of the shoulder. This may be performed after recovery from any acute injuries.

The patient lies supine. The shoulder is abducted to 90 degrees, and the elbow is flexed to 90 degrees. The shoulder is then slowly externally rotated in this position while watching the patient. As the arm approaches 90 degrees of external rotation, patients with shoulder instability will become anxious and apprehensive, worried that the shoulder will dislocate. There is no pain associated with the movement, only apprehension.

130
Q

Investigating shoulder dislocation

A

X-rays may be used in an acute presentation to confirm a dislocation and exclude fractures. They are not always required before reduction, depending on the clinical findings and risk of a fracture (see local policies and ask seniors). X-rays are performed after reduction to confirm the shoulder is reduced and assess for fractures.

Magnetic resonance arthrography is an MRI scan of the shoulder with a contrast injected into the shoulder joint. This can be used to assess the shoulder for damage (e.g., Bankart and Hill-Sachs lesions) and planning for surgery.

Arthroscopy involves inserting a camera into the shoulder joint to visualise the structures.

131
Q

Acute management of shoulder dislocation

A

Ideally, the shoulder should be relocated as soon as safely possible. Muscle spasm occurs over time, making it harder to relocate the shoulder and increasing the risk of neurovascular injury during relocation.

Acute management of a shoulder dislocation involves:

Analgesia, muscle relaxants and sedation as appropriate
Gas and air (e.g., Entonox) may be used, which contains a mixture of 50% nitrous oxide and 50% oxygen
A broad arm sling can be applied to support the arm
Closed reduction of the shoulder (after excluding fractures)
Dislocations associated with a fracture may require surgery
Post-reduction x-rays
Immobilisation for a period after relocation of the shoulder

There are various options for closed reduction of shoulder dislocations. See local guidelines and get experienced senior input when managing shoulder dislocations and for guidance on relocation techniques.

132
Q

Ongoing management of shoulder dislocation

A

There is a high risk of recurrent dislocations, particularly in younger patients.

Physiotherapy is recommended to improve the function of the shoulder and reduce the risk of further dislocations.

Shoulder stabilisation surgery may be required to improve stability and prevent further dislocations. This may be an arthroscopic or an open procedure. Underlying structural problems are corrected, such as:

Repairing Bankart lesions
Tightening the shoulder capsule
Bone graft using bone from the coracoid process to correct a bony injury to the glenoid rim (Latarjet procedure)
Correcting Hill-Sachs lesions (Remplissage procedure)

There is a prolonged period of recovery and rehabilitation after shoulder stabilisation surgery (3 months or more).

Recurrent instability and dislocations can occur in up to 20% of patients after surgery.

133
Q

Olecranon bursitis

A

Olecranon bursitis refers to inflammation and swelling of the bursa over the elbow. The olecranon is the bony lump at the elbow, which is part of the ulna bone.

Bursae are sacs created by synovial membrane filled with a small amount of synovial fluid. They are found at bony prominences (e.g., at the greater trochanter, knee, shoulder and elbow). They act to reduce the friction between the bones and soft tissues during movement.

Bursitis is inflammation of a bursa. This causes thickening of the synovial membrane and increased fluid production, causing swelling. This inflammation can be caused by a number of things:

Friction from repetitive movements or leaning on the elbow
Trauma
Inflammatory conditions (e.g., rheumatoid arthritis or gout)
Infection – referred to as septic bursitis

Olecranon bursitis is sometimes called “student’s elbow”, as students may lean on their elbow for prolonged periods while studying, resulting in friction and mild trauma leading to bursitis. It can also occur with people with occupations that require leaning on the elbow, such as plumbers or drivers.

134
Q

Presentation of olecranon bursitis

A

The typical presentation is a young/middle-aged man with an elbow that is:

Swollen
Warm
Tender
Fluctuant (fluid-filled)

It is important to identify where bursitis is caused by infection. Features of infection are:

Hot to touch
More tender
Erythema spreading to the surrounding skin
Fever
Features of sepsis (e.g., tachycardia, hypotension and confusion)

An important differential diagnosis is septic arthritis. Consider septic arthritis if there is:

Swelling in the joint (rather than the bursa)
Painful and reduced range of motion in the elbow

135
Q

Aspiration of olecranon bursitis

A

The NICE clinical knowledge summaries (updated January 2021) recommend aspiration of fluid from the bursa when an infection is suspected. They advise that the appearance can give an indication of the underlying cause:

Pus indicates infection
Straw-coloured fluid indicates infection is less likely
Blood-stained fluid may indicate trauma, infection or inflammatory causes
Milky fluid indicates gout or pseudogout

Aspiration should ideally be performed before starting antibiotics. The fluid is sent to the lab for microscopy and culture. During microscopy, they will examine for crystals (gout and pseudogout) and gram-staining for bacteria.

136
Q

Managing olecranon bursitis

A

Management options for olecranon bursitis include:

Rest
Ice
Compression
Analgesia (e.g., paracetamol or NSAIDs)
Protecting the elbow from pressure or trauma
Aspiration of fluid may be used to relieve pressure
Steroid injections may be used in problematic cases where infection has been excluded

When infection is suspected or cannot be excluded, management involves:

Aspiration of the fluid for microscopy and culture
Antibiotics

The NICE CKS recommend flucloxacillin first-line, with clarithromycin as an alternative.

Patients that are systemically unwell (e.g., immunocompromised or have sepsis) need admission to hospital for further management, including:

Bloods (including lactate)
Blood cultures
IV antibiotics
IV fluids

137
Q

Causes of repetitive strain injury

A

Repetitive strain injury is an umbrella term that refers to soft tissue irritation, microtrauma and strain resulting from repetitive activities. It can affect the muscles, tendons and nerves. Lateral epicondylitis (tennis elbow) is a specific example of a repetitive strain injury.

Causes

Almost any repetitive movement can result in repetitive strain injury if done long enough. It often results from occupational activities, where the same movement is performed for many hours at a time, day after day. Some common examples of activities are:

Working on an assembly line in a factory, doing the same movements over and over
Using a computer mouse or keyboard (affecting the wrist and forearm)
Having a poor posture for an extended period whilst reading or using a computer (affecting the neck and shoulders)
Texting or scrolling on a smartphone (affecting the base of the thumb)

Certain characteristics of an activity increase the risk of repetitive strain injury, such as:

Small repetitive activities (e.g., scrolling on a smartphone)
Vibration (e.g., using power tools)
Awkward positions (e.g., painting a ceiling)

138
Q

Presentation of repetitive strain injury

A

Usually, there will be a history of repetitive activities, often related to work.

Symptoms will be located in an area related to the activity. They can include:

Pain, exacerbated by using the associated joints, muscles and tendons
Aching
Weakness
Cramping
Numbness

On examination, the area may be tender to palpation. There may be mild swelling in the area. It may be possible to recreate the pain by having the patient perform specific movements that add resistance to the affected soft tissues.

139
Q

Diagnosing repetitive strain injury

A

The diagnosis is usually made clinically, based on the history and examination findings, without investigations.

Investigations may be necessary to rule out other differential diagnoses (e.g., arthritis, inflammatory conditions or nerve compression), such as:

X-rays (e.g., to look for osteoarthritis)
Ultrasound (e.g., to look for synovitis in rheumatoid arthritis or rotator cuff tears)
Blood tests (e.g., inflammatory markers and rheumatoid factor for rheumatoid arthritis)

140
Q

Managing repetitive strain injury

A

The RICE mnemonic can be applied to most soft tissue injuries. This stands for:

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

Rest and adapting activities are essential. If the repetitive movement continues, the condition will get worse. This often involves the patient discussing their duties with the occupational health department at their place of work to amend their work tasks.

Other potentially helpful options include:

Analgesia (e.g., NSAIDs)
Physiotherapy
Steroid injections (in specific scenarios)

141
Q

Epicondylitis

A

Epicondylitis refers to inflammation at the point where the tendons of the forearm insert into the epicondyles at the elbow. It is a specific type of repetitive strain injury.

There is a medial epicondyle and a lateral epicondyle on the distal end of the humerus, either side of the elbow joint.

The tendons of the muscles that insert into the:

Medial epicondyle act to flex the wrist
Lateral epicondyle act to extend the wrist

Epicondylitis is the result of repetitive use and injury to the tendons at the point of insertion. Symptoms gradually worsen over weeks to months. It most commonly affects patients in middle age.

142
Q

Lateral epicondylitis

A

Lateral epicondylitis is often called tennis elbow.

Lateral epicondylitis causes pain and tenderness at the lateral epicondyle (outer elbow). The pain often radiates down the forearm. It can lead to weakness in grip strength.

Mill’s test involves stretching the extensor muscles of the forearm while palpating the lateral epicondyle. The elbow is extended, the forearm pronated, and the wrist is flexed. The examiner holds the patient’s elbow with pressure on the lateral epicondyle. If this causes pain, the test is positive, indicating lateral epicondylitis.

Cozen’s test starts with the elbow extended, forearm pronated, wrist deviated in the direction of the radius and hand in a fist. The examiner holds the patient’s elbow with pressure on the lateral epicondyle. The examiner applies resistance to the back of the hand while the patient extends the wrist. If this causes pain, the test is positive, indicating lateral epicondylitis.

143
Q

Medial Epicondylitis

A

Medial epicondylitis is often called golfer’s elbow.

Medial epicondylitis causes pain and tenderness at the medial epicondyle (inner elbow). The pain often radiates down the forearm. It can lead to weakness in grip strength.

A golfer’s elbow test involves stretching the flexor muscles of the forearm while palpating the medial epicondyle. The elbow is extended, the forearm supinated, and the wrist and fingers are extended. The examiner holds the patient’s elbow with pressure on the medial epicondyle. If this causes pain, the test is positive, indicating medial epicondylitis.

144
Q

Managing epicondylitis

A

Epicondylitis is a clinical diagnosis based on the signs and symptoms.

In most patients, epicondylitis is self-limiting and resolves with time. However, symptoms can take several years to resolve.

Management options for epicondylitis include:

Rest
Adapting activities
Analgesia (e.g., NSAIDs)
Physiotherapy
Orthotics, such as elbow braces or straps
Steroid injections
Platelet-rich plasma (PRP) injections
Extracorporeal shockwave therapy

Rarely, surgery may be required to debride, release or repair damaged tendons.

145
Q

De Quervain’s tenosynovitis

A

De Quervain’s tenosynovitis is a condition where there is swelling and inflammation of the tendon sheaths in the wrist. It primarily affects two tendons:

Abductor pollicis longus (APL) tendon
Extensor pollicis brevis (EPB) tendon

It is a type of repetitive strain injury and results in pain on the radial side of the wrist.

One notable cause of bilateral De Quervain’s tenosynovitis is in new parents repetitively lifting newborn babies in a way that stresses the tendons of the thumb. For this reason, it is sometimes referred to as “mummy thumb”.

146
Q

Pathophysiology of De Quervain’s tenosynovitis

A

The abductor pollicis longus acts to abduct the thumb and abduct the wrist. The tendon inserts into the base of the first metacarpal bone (at the base of the thumb).

The extensor pollicis brevis also acts to abduct the thumb and abduct the wrist. The tendon inserts into the base of the proximal phalanx of the thumb.

Tendon sheaths can surround tendons. A tendon sheath is formed by connective tissue (synovial membrane) that covers the tendons and is filled with synovial fluid. They help lubricate and protect the movement of the tendons within them.

The extensor retinaculum is a fibrous band that wraps across the back (dorsal side) of the wrist. The APL and EPB pass underneath the extensor retinaculum. Repetitive movement of the APL and EPB under the extensor retinaculum result in inflammation and swelling of the tendon sheaths.

147
Q

Presentation of De Quervain’s tenosynovitis

A

Patients present with symptoms at the radial aspect of the wrist near the base of the thumb. Typical symptoms include:

Pain, often radiating to the forearm
Aching
Burning
Weakness
Numbness
Tenderness

There is a special test for De Quervain’s tenosynovitis called Finkelstein’s test. There is some confusion about what this is, depending on where you look. Most sources describe the first manoeuvre below as Finkelstein’s test, but it may be Eichhoff’s test.

Finkelstein’s test (or maybe Eichhoff’s test) involves the patient making a fist with their thumb inside their fingers. Then, the wrist is adducted (ulnar deviation), causing strain on the APL and EPB tendons. If this movement causes pain at the radial aspect of the wrist, the test is positive, indicating De Quervain’s tenosynovitis.

The original Finkelstein’s test involves the patient resting their forearm on a surface in a neutral position with the wrist hanging off and unsupported. The examiner holds the patient’s thumb and passively flexes the thumb into the palm, causing the wrist to adduct (ulnar deviation), putting strain on the APL and EPB tendons. If this causes pain at the radial aspect of the wrist, the test is positive, indicating De Quervain’s tenosynovitis.

148
Q

Managing De Quervain’s tenosynovitis

A

Management can involve:

Rest and adapting activities
Using splints to restrict movements
Analgesia (e.g., NSAIDs)
Physiotherapy
Steroid injections

Rarely, surgery may be required to release (cut) the extensor retinaculum, releasing the pressure and creating more space for the tendons.

149
Q

Trigger finger

A

Trigger finger is a condition causing pain and difficulty moving a finger. It is also known as stenosing tenosynovitis.

Pathophysiology

The flexor tendons of the fingers pass through several tunnels (sheaths) along the length of the fingers. In trigger finger, there is thickening of the tendon or tightening of the sheath. This prevents the tendon from smoothly moving through the sheath when the finger is flexed and extended, causing pain, stiffness, or catching symptoms.

The most commonly affected part of the sheath is the first annular pulley (A1) at the metacarpophalangeal (MCP) joint.

There may be a nodule on the tendon. When the finger is flexed, the nodule is outside the A1 pulley. As the finger is extended from a flexed position, the tendon nodule can get stuck at the entrance to the A1 pulley. This causes the finger to lock or get stuck in the bent position. It may release suddenly with a painful pop or click.

150
Q

Risk factors for trigger finger

A

Patients more likely to be affected by trigger finger are:

In their 40s or 50s
Women (more often than men)
People with diabetes (more with type 1, but also type 2)

151
Q

Presentation of trigger finger

A

The typical presentation is with a troublesome finger, that:

Is painful and tender (usually around the MCP joint on the palm-side of the hand)
Does not move smoothly
Makes a popping or clicking sound
Gets stuck in a flexed position

Symptoms are typically worse in the morning and improve during the day.

152
Q

Diagnosing trigger finger

A

Trigger finger is a clinical diagnosis based on the history and examination findings.

153
Q

Managing trigger finger

A

Management options include:

Rest and analgesia (a small number resolve spontaneously)
Splinting
Steroid injections
Surgery to release the A1 pulley

154
Q

Dupuytren’s contracture

A

Dupuytren’s contracture is a condition where the fascia of the hand becomes thickened and tight, leading to finger contractures.

A contracture is a shortening of the soft tissues that leads to restricted movement in a joint. In Dupuytren’s contracture, the finger is tightened into a flexed position and cannot fully extend.

Pathophysiology

The palmar fascia of the hand forms a triangle of strong connective tissue on the palm.

In Dupuytren’s contracture, the fascia of the hands becomes thicker and tighter and develops nodules. Cords of dense connective tissue can extend into the fingers, pulling the fingers into flexion and restricting their ability to extend (contracture).

It is unclear why the fascia becomes thicker and tighter. However, it is thought to be an inflammatory process in response to microtrauma.

155
Q

Risk factors for Dupuytren’s Contracture

A

Age
Family history (autosomal dominant pattern)
Male
Manual labour, particularly with vibrating tools
Diabetes (more with type 1, but also type 2)
Epilepsy
Smoking and alcohol

156
Q

Presentation of Dupuytren’s Contracture

A

The first sign of Dupuytren’s contracture is the development of hard nodules on the palm. There may be skin thickening and pitting. Slowly, the fascia becomes thicker, and the finger is pulled into flexion. It becomes impossible to extend the affected finger fully.

A thick, nodular cord can be palpated from the palm into the affected finger.

The ring finger is most often affected. The index finger is least likely to be affected.

Dupuytren’s contracture can significantly affect the function of the hand. However, patients do not usually experience pain with the condition.

The table-top test is a straightforward test for Dupuytren’s contracture. The patient tries to position their hands flat on a table. If the hand cannot rest completely flat, the test is positive, indicating Dupuytren’s contracture.

157
Q

Managing Dupuytren’s Contracture

A

The options for Dupuytren’s contracture are essentially to do nothing (conservative management) or to treat it surgically. There are three options for surgical management.

Needle fasciotomy (also known as needle aponeurotomy) involves inserting a needle through the skin to divide and loosen the cord that is causing the contracture.

Limited fasciectomy involves removing the abnormal fascia and cord to release the contracture.

Dermofasciectomy involves removing the abnormal fascia and cord, as well as the associated skin. A skin graft is used to replace the removed skin.

158
Q

Carpal Tunnel Syndrome

A

Carpal tunnel syndrome is caused by compression of the medial nerve as it travels through the carpal tunnel in the wrist, causing pain and numbness in the median nerve distribution on the hand.

Basic Anatomy and Pathophysiology

The flexor retinaculum is a fibrous band that wraps across the front (palmar side) of the wrist. It is also known as the transverse carpal ligament. Between the carpal bones and the flexor retinaculum is a passageway from the forearm and the hand called the carpal tunnel. The median nerve and the flexor tendons of the forearm travel through the carpal tunnel.

Compression of the contents of the carpal tunnel (causing carpal tunnel syndrome) is the result of either:

Swelling of the contents (e.g., swelling of the tendon sheaths due to repetitive strain)
Narrowing of the tunnel

The palmar digital cutaneous branch of the median nerve (which passes through the carpal tunnel) is responsible for sensory innervation of the palmar aspects and full fingertips of the:

Thumb
Index and middle finger
The lateral half of ring finger

Note that the palmar cutaneous branch of the median nerve provides sensation to the palm. However, this branch originates before the carpal tunnel and does not travel through the carpal tunnel. Therefore, it is not affected by carpal tunnel syndrome.

The median nerve also supplies the motor function to the three thenar muscles. These muscles make up the muscular bulge at the base of the thumb that is responsible for thumb movements:

Abductor pollicis brevis (thumb abduction)
Opponens pollicis (thumb opposition – reaching across the palm to touch the tips of the fingers)
Flexor pollicis brevis (thumb flexion)

The other muscle that controls thumb movement is the adductor pollicis (thumb adduction). However, this is innervated by the ulnar nerve. Whether this is classed as one of the thenar muscles depends on where you look.

159
Q

Risk factors for carpal tunnel syndrome

A

In most cases, carpal tunnel syndrome is idiopathic, meaning no clear cause is found.

There are a number of key risk factors:

Repetitive strain
Obesity
Perimenopause
Rheumatoid arthritis
Diabetes
Acromegaly
Hypothyroidism

TOM TIP: When I was preparing for the PACES exam, the link between bilateral carpal tunnel syndrome and acromegaly came up several times. Cases would present a patient with symptoms of bilateral carpal tunnel syndrome. The challenge was not only to diagnose carpal tunnel syndrome but also to identify the features of the underlying cause. Whenever you see a patient in an OSCE station that has a diagnosis, ask yourself whether that diagnosis might have an underlying cause and look for features of that cause. For example, if you see a patient with bilateral carpal tunnel syndrome, look for features that might suggest underlying rheumatoid arthritis, diabetes, acromegaly or hypothyroidism. This will take you from average exams scores to the very top scores.

160
Q

Presentation of carpal tunnel syndrome

A

Carpal tunnel syndrome usually has a gradual onset of symptoms. Initially, the symptoms are intermittent. Often, they are worse at night time.

Carpal tunnel syndrome causes sensory symptoms in the distribution of the palmar digital cutaneous branch of the median nerve, affecting the palmar aspects and full fingertips of the:

Thumb
Index and middle finger
The lateral half of ring finger

Sensory symptoms include:

Numbness
Paraesthesia (pins and needles or tingling)
Burning sensation
Pain

Patients often find the sensory symptoms worse at night. The symptoms may cause them to wake up from sleep. They may describe shaking their hand to try and relieve symptoms.

Motor symptoms of carpal tunnel syndrome affect the thenar muscles, with:

Weakness of thumb movements
Weakness of grip strength
Difficulty with fine movements involving the thumb
Wasting of the thenar muscles (muscle atrophy)

161
Q

Special tests for carpal tunnel syndrome

A

There are two special tests for carpal tunnel syndrome:

Phalen’s test
Tinel’s test

Phalen’s test involves fully flexing the wrist and holding it in this position. Often this is done by asking the patient to put the backs of their hands together in front of them with the wrists bent inwards at 90 degrees. The test is positive when this position triggers the sensory symptoms of carpal tunnel, with numbness and paraesthesia in the median nerve distribution.

Tinel’s test involves tapping the wrist at the location where the median nerve travels through the carpal tunnel. This is in the middle, at the point where the wrist meets the hand. The test is positive when this position triggers the sensory symptoms of carpal tunnel, with numbness and paraesthesia in the median nerve distribution.

TOM TIP: I think of tapping a tin can (Tinel’s) to remember the difference between Phalen’s and Tinel’s test.

162
Q

Carpal tunnel questionaire

A

The Kamath and Stothard carpal tunnel questionnaire (CTQ) gives a score based on the symptoms. It can be used to predict the likelihood of a diagnosis of carpal tunnel syndrome. A high score on the questionnaire may replace the need for nerve conduction studies to confirm the diagnosis.

It scores based on questions such as:

Do symptoms wake you at night?
Do you have trick movements (e.g., shaking the hand) to improve symptoms?
Is your little finger affected? (Answering yes scores negatively, making carpal tunnel syndrome less likely)

163
Q

Nerve conduction studies for carpal tunnel syndrome

A

Nerve conduction studies are the primary investigation for establishing the diagnosis.

A small electrical current is applied by an electrode (nerve stimulator) to the median nerve on one side of the carpal tunnel. Recording electrodes over the median nerve on the other side of the carpal tunnel record the electrical current that reaches them. This demonstrates how well signals are passing through the carpal tunnel along the median nerve.

164
Q

Managing carpal tunnel syndrome

A

Management options for carpal tunnel syndrome are:

Rest and altered activities
Wrist splints that maintain a neutral position of the wrist can be worn at night (for a minimum of 4 weeks)
Steroid injections
Surgery

Carpal tunnel syndrome surgery is usually performed as a day case procedure under local anaesthetic. It can be performed by open (with a vertical incision at the wrist) or endoscopic (keyhole) surgery. The flexor retinaculum (AKA transverse carpal ligament) is cut to release the pressure on the median nerve.

165
Q

Ganglion cysts

A

Ganglion cysts are sacs of synovial fluid that originate from the tendon sheaths or joints. They commonly occur in the wrist and fingers but can occur anywhere there is a joint or tendon sheath.

Ganglion cysts are thought to occur when the synovial membrane of the tendon sheath or joint herniates, forming a pouch. Synovial fluid flows from the tendon sheath or joint into the pouch, forming a cyst (a fluid-filled sac).

166
Q

Presentation of ganglion cysts

A

Ganglion cysts can appear rapidly (over days) or gradually. Patients present with a visible and palpable lump. It is not usually painful. Rarely, they may compress nerves, leading to sensory or motor symptoms.

On examination, ganglion cysts:

Range in size from 0.5 to 5cm or more (most are 2cm or less)
Firm and non-tender on palpation
Well-circumscribed
Transilluminates (shining a torch into the cyst causes the whole lump to light up)

167
Q

Diagnosing ganglion cysts

A

Ganglion cysts are mostly diagnosed clinically, based on the history and examination findings.

X-rays will show normal bones and joints (unless there are co-existing conditions).

Ultrasound can help confirm the diagnosis and exclude other causes of lumps.

168
Q

Managing ganglion cysts

A

Ganglion cysts may be managed conservatively, without any intervention. 40-50% of cysts will resolve spontaneously, but this can take several years.

Active management options for ganglion cysts are:

Needle aspiration (draining the cyst by aspirating the fluid with a needle)
Surgical excision (open or endoscopic removing the cyst, usually under local anaesthetic)

Needle aspiration has a high rate of recurrence (50% or more).

Surgical excision involves removing the entire cyst and the affected part of the joint capsule or tendon sheath. Therefore, the recurrence rate is low. However, there is a risk of complications, such as infection and scarring.

169
Q
A