Orthopaedics: Osgood-Schlatter disease; osteochondritis dissecans; SUFE Flashcards
Describe the pathophysiology of Osgood-Schlatters disease [5]
The patella tendon inserts into the tibial tuberosity.
The tibial tuberosity is at the epiphyseal plate.
Stress from running, jumping and other movements at the same time as growth in the epiphyseal plate result in inflammation on the tibial epiphyseal plate.
There are multiple small avulsion fractures, 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 bump is tender due to the inflammation, but has the bone heals and the inflammation settles it becomes hard and non-tender.
Describe the presentation of Osgood Schlatter disease [4[
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 and relieved by rest
* Osgood-Schlatter disease is most commonly unilateral (70% of cases) but can also be bilateral (30%) though the severity in each knee can vary.
What is chondromalacia and how do you differentiate this from OSD? [2]
Chondromalacia patella
Similarities:
- knee pain presenting in sporty teenagers, managed conservatively
Differences:
- typically presents with pain on anterior or inner side of the knee
Chondromalacia patellae is a condition where there is damaged cartilage behind the patella (kneecap). It is like a softening or wear and tear of the cartilage.
How do you distinguish between OSD and Osteochondritis dissecans? [1]
Osteochondritis dissecans
Similarities:
- activity-related knee pain with localised bony tenderness
Differences:
- presents with mechanical features as knee intermittently locks and gives way. Effusion and joint crepitus present on examination
Per NICE Clinical Knowledge Summary recommendations, Osgood-Schlatter disease should be initially managed conservatively. This includes: [4]
Reassurance
* Advise patient that pain will eventually settle as growth spurt slows and there is no adverse progressive pathology
Simple analgesia
* Paracetamol +/- NSAIDs
* Ice packs
* Compression using athletic tape or knee pads
Physiotherapy and modified exercise regimes
* Stretching recommended to prevent muscle contraction and improve joint stability
Activity modification
* Limiting the amount movement that involves strong quadriceps contraction (e.g. running or jumping)
* In most cases, patients should be encouraged to remain active but to alter the physical exercises they do
Describe what is meant by osteochondritis dissecans [1]
Osteochondritis dissecans (OCD) is a pathological process affecting the subchondral bone (most often in the knee joint) with secondary effects on the joint cartilage, including pain, oedema, free bodies and mechanical dysfunctions.
Describe the clinical features osteochondritis dissecans [3]
Patients typically present with a subacute onset of:
* Knee pain and swelling, typically after exercise
* Knee catching, locking and/or giving way - more constant and severe symptoms are associated with the presence of loose bodies
* Feeling a painful ‘clunk’ when flexing or extending the knee - indicating the involvement of the lateral femoral condyle
What are the clinical signs of osteochondritis dissecans [5]
Joint effusion
Full range of movement in the joint without signs of ligamentous instability
External tibial rotation when walking - if medial femoral involvement
Tenderness on palpation of the articular cartilage of the medial femoral condyle, when the knee is flexed
Wilson’s sign for detecting medial condyle lesion - with the knee at 90° flexion and tibia internally rotated, the gradual extension of the joint leads to pain at about 30°, external rotation of the tibia at this point relieves the pain
Describe the investigations used for osteochondritis dissecans [4]
X-ray (anteroposterior, lateral and tunnel views)
- may show the subchondral crescent sign or loose bodies
MRI
- used to evaluate cartilage, visualise loose bodies, stage and assess the stability of the lesion
CT
- may be used in preoperative planning and in cases where MRI is not available or contraindicated
Scintigraphy
- may be used to guide treatment as it may show increased uptake in the fragments - a sign of osteoblastic activity
Describe the pathophysiology of SUFE [1]
Slipped upper femoral epiphysis (SUFE) is also known as slipped capital femoral epiphysis (SCFE). It is where the head of the femur is displaced (“slips”) along the growth plate.
- It is characterised by a posterior and medial slippage of the proximal femoral epiphysis on the metaphysis (femoral neck) within the hypertrophic zone of the physeal plate.
Which endocrine abnormalities are associated with SUFE? [3]
hypothyroidism, growth hormone supplementation and renal osteodystrophy
Slipped capital femoral epiphysis (SCFE) can be classified based on several parameters, including duration of symptoms, stability of the slip, and degree of displacement.
What (and describe) the different classifications? [3]
Duration:
* Acute: Symptoms have been present for less than three weeks.
* Chronic: Symptoms have been present for more than three weeks.
Stability:
* Stable SCFE: The patient is able to walk with or without crutches.
* Unstable SCFE: The patient cannot bear weight on the affected hip, even with crutches. This type is associated with a higher risk of avascular necrosis and chondrolysis.
Degree of Displacement:
* Mild (< 33%): Only slight displacement of the femoral head is seen radiographically.
* Moderate (33-50%): A moderate amount of displacement is noted on imaging.
* Severe (>50%):The femoral head is significantly displaced from the neck.
The [] angle can also be used to quantify the degree of slippage in SCFE. It compares the angle between a line parallel to the physis and a line perpendicular to the shaft of the femur in both normal and affected hips. A greater angle indicates increased severity.
The Southwick angle can also be used to quantify the degree of slippage in SCFE. It compares the angle between a line parallel to the physis and a line perpendicular to the shaft of the femur in both normal and affected hips. A greater angle indicates increased severity.
What age group does SUFE most commonly occur in? [1]
It is more common in boys and typically presents aged 8 – 15 years, with the average age of 12 in boys. It presents slightly earlier in females, with an average age of 11 years. It is more common in obese children.
Describe the presentation of SUFE
The typical exam presentation is an adolescent, obese male undergoing a growth spurt. There may be a history of minor trauma that triggers the onset of symptoms. Suspect SUFE if the pain is disproportionate to the severity of the trauma.
Presenting symptoms can be vague. These can be:
* Hip, groin, thigh or knee pain
* Restricted range of movement in the hip
* Painful limp
* 11/12 year old
* When examining the patient, they will prefer to keep the hip in external rotation. They will have limited movement of the hip, particularly restricted internal rotation.
Describe the limited range of motion seen in hip movements of a child w SUFE [3]
There may be restriction in hip movements, especially internal rotation, abduction and flexion. Forced passive internal rotation often exacerbates the pain.
Describe the x-ray findings of SUFE [1]
The AP view can demonstrate the characteristic posterior displacement or ‘slip’ of the femoral epiphysis, while the lateral view can confirm it
- Changes in the Shenton’s line, metaphyseal blanch sign of Steel, or widening of the physis may also be visible.
Describe the management of SUFE
The management of slipped capital femoral epiphysis (SCFE) is primarily surgical, aiming to stabilise the epiphysis and prevent further slippage. The specific management steps are as follows:
In Situ Pinning:
- This is the most common treatment for stable SCFE. A single screw or pin is inserted percutaneously into the femoral head to secure it in place. In unstable SCFE, multiple screws may be used.
Open Reduction and Internal Fixation (ORIF):
- In severe cases or when closed methods fail, open reduction followed by internal fixation can be performed. This involves surgically exposing the hip joint, realigning the displaced femoral head under direct vision and then securing it with screws.
Osteotomy:
- If there is significant deformity or chronic SCFE, an osteotomy may be required. This procedure involves cutting and realigning the bone to correct its position and orientation.
Describe what is meant by developmental dysplasia of the hip [1]
Developmental dysplasia of the hip (DDH) is a condition where there is a structural abnormality in the hips caused by abnormal development of the fetal bones during pregnancy.
- This leads to instability in the hips and a tendency or potential for subluxation or dislocation.
- These structural abnormalities have the potential to persist into adulthood leading to weakness, recurrent subluxation or dislocation, an abnormal gait and early degenerative changes.
What are the risk factors for DDH? [4]
- First degree family history
- Breech presentation from 36 weeks onwards
- Breech presentation at birth if 28 weeks onwards
- Multiple pregnancy
When does screening for DDH occur? [2]
Describe the screening used for DDH [2]
DDH is screened for on the neonatal examination at birth (NIPE) and 6-8 week old.
Ortolani test
- is done with the baby on their back with the hips and knees flexed.
- Palms are placed on the baby’s knees with thumbs on the inner thigh and four fingers on the outer thigh.
- Gentle pressure is used to abduct the hips and apply pressure behind the legs with the fingers to see if the hips will dislocate anteriorly.
Barlow test
- is done with the baby on their back with the hips adducted and flexed at 90 degrees and knees bent at 90 degrees.
- Gentle downward pressure is placed on knees through femur to see if the femoral head will dislocate posteriorly.
NB: Clicking is a common examination finding and is usually due to soft tissue moving over bone. When this is the cause an ultrasound will be normal. Isolated clicking without any other features does not usually require an ultrasound unless there are other concerns. Clunking is more likely to indicate DDH and requires an ultrasound.
Where children are suspected of having DDH, [] of the hips is the investigation of choice and can establish the diagnosis. All children with risk factors or examination findings suggestive of DDH should have an ultrasound.
Where children are suspected of having DDH, ultrasound of the hips is the investigation of choice and can establish the diagnosis. All children with risk factors or examination findings suggestive of DDH should have an ultrasound.
Treatment typically involves a Pavlik harness if the baby presents at less than 6 months of age
- The Pavlik harness is fitted and kept on permanently, adjusting for the growth of the baby.
- The aim is to hold the femoral head in the correct position to allow the hip socket (acetabulum) to develop a normal shape.
- This harness keeps the baby’s hips flexed and abducted.
- The child is regularly reviewed and the harness is removed when their hips are more stable, usually after 6 – 8 weeks.
Surgery
- is required when the harness fails or the diagnosis is made after 6 months of age.
- After surgery is performed, an hip spica cast is used to immobilises the hip for a prolonged period.
- Open reduction: For children older than two years, or when closed reduction is unsuccessful, surgical intervention in the form of an open reduction may be required. Additional procedures, such as femoral or pelvic osteotomies, may be needed to achieve optimal hip stability and congruity.
Describe which ages determine different treatment methods for DDH [3]
Pavlik harness:
- Under 6 months
Closed reduction and spica casting:
- In infants aged six months to two years
- or when Pavlik harness treatment fails
Open reduction:
- For children older than two years, or when closed reduction is unsuccessful
Describe early [3] and late [3] complications of DDH
Early Complications:
Osteonecrosis:
- This is one of the most severe early complications. It involves death of bone tissues due to limited blood flow, leading to femoral head deformity and growth disturbance.
Residual dysplasia:
- Despite adequate treatment, some patients may still exhibit residual dysplasia. This refers to persistent abnormality in the shape or position of the hip joint, predisposing it to premature degenerative changes.
Subluxation or dislocation:
- If not adequately treated or managed, DDH can result in subluxation (partial dislocation) or complete dislocation of the hip joint.
Late Complications:
Osteoarthritis:
- Untreated or poorly managed DDH often leads to early onset osteoarthritis. This degenerative disease results from wear and tear on the hip joint over time, causing pain, stiffness and reduced mobility.
Gait abnormalities:
- These are common in individuals with untreated DDH. Abnormalities such as limping or waddling gait can affect mobility and quality of life.
Hip impingement:
- Also known as Femoroacetabular Impingement (FAI), this condition occurs when there’s an abnormal contact between the femoral head and acetabulum. It can cause pain and limit movement in the hip joint.
