Orthopaedics Flashcards
(138 cards)
1
Q
What is transient synovitis and what is it caused by?
A
Transient synovitis is sometimes referred to as irritable hip. It is caused by temporary (transient) irritation and inflammation in the synovial membrane of the joint (synovitis). It is often associated with a recent viral upper respiratory tract infection.
2
Q
What is the most common cause of hip pain in children aged 3 – 10 years?
A
Transient synovitis
3
Q
Transient synovitis vs septic arthritis presentation?
A
Both causes of hip pain
Transient synovitis usually associated with a recent viral URTI
Children with transient synovitis typically do not have a fever and are usually otherwise well. They should have normal paediatric observations and no signs of systemic illness. When other signs are present, consider alternative diagnoses.
Children with joint pain and a fever need urgent management for septic arthritis.
4
Q
Presentation of transient synovitis?
A
Symptoms of transient synovitis often occur within a few weeks of a viral illness.
They present with acute or more gradual onset of:
Limp
Refusal to weight bear
Groin or hip pain
Mild low grade temperature
Children with transient synovitis should be otherwise well. They should have normal paediatric observations and no signs of systemic illness. When other signs are present, consider alternative diagnoses.
5
Q
Management of transient synovitis?
A
General management of transient synovitis is symptomatic, with simple analgesia to help ease the discomfort.
The challenge is to establish the correct diagnosis and exclude other significant pathology, particularly septic arthritis.
NICE clinical knowledge summaries:
- Children aged 3 – 9 years with symptoms suggestive of transient synovitis may be managed in primary care if the limp is present for less than 48 hours and they are otherwise well, however they need clear safety net advice to attend A&E immediately if the symptoms worsen or they develop a fever.
- They should also be followed up at 48 hours and 1 week to ensure symptoms are improving and then fully resolve.
6
Q
According to NICE, children aged 3 – 9 years with symptoms suggestive of transient synovitis may be managed in primary care when?
A
If the limp is present for less than 48 HOURS
and they are otherwise well
However they need clear safety net advice to attend A&E immediately if the symptoms worsen or they develop a fever.
7
Q
How long does transient synovitis take to resolve?
A
Typically there is a significant improvement in symptoms after 24 – 48 hours.
Symptoms fully resolve within 1 – 2 weeks without any lasting problems.
8
Q
Prognosis of transient synovitis?
A
Typically symptoms fully resolve within 1-2 weeks without any lasting problems.
Transient synovitis may recur in around 20% of patients.
9
Q
What is SUFE?
A
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.
10
Q
Which demorgaphic typically present with slipped upper femoral epiphysis (SUFE/slipped capital femoral epiphysis (SCFE))?
A
More common in males
Presents between 8 – 15 years, with the
Average age of 12 in boys, presenting slightly earlier in females, with an average age of 11 years
More common in OBESE children
11
Q
What might you suspect in an adolescent, obese male undergoing a growth spurt presenting with a painful limp triggered by a minor trauma, with pain that is disproportionate to the severity of the trauma?
A
Slipped upper femoral epiphysis (SUFE/slipped capital femoral epiphysis (SCFE))?
12
Q
When examining a patient with slipped upper femoral epiphysis (SUFE)/slipped capital femoral epiphysis (SCFE), they will prefer to keep the hip in what position?
A
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.
13
Q
When examining a patient with slipped upper femoral epiphysis (SUFE)/slipped capital femoral epiphysis (SCFE), which movement will be particularly restricted?
A
RESTRICTED INTERNAL ROTATION
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.
14
Q
Presentation of slipped upper femoral epiphysis (SUFE)/slipped capital femoral epiphysis (SCFE)?
A
Hip, groin, thigh or knee pain (often preceeded by minor trauma - disproportionate to the pain)
Restricted range of hip movement
Painful limp
Restricted movement in the hip (particularly internal rotation, with the patient preferring to keep the hip externally rotated)
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.
15
Q
Investigating SUFE?
A
The initial investigation of choice in SUFE is X RAY
Other investigations that can be helpful in establishing the diagnosis are:
- Blood tests are normal, particularly inflammatory markers used to exclude other causes of joint pain
- Technetium bone scan
- CT scan
- MRI scan
16
Q
How is SUFE managed?
A
Surgery is required to return the femoral head to the correct position and fix it in place to prevent it slipping further.
17
Q
What is developmental dysplasia of the hip and why does it occur?
A
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.
18
Q
What problems does developmental dysplasia of the hip cause?
A
Instability in the hips + tendency/potential for subluxation or dislocation
Structural abnormalities have the potential to persist into adulthood leading to:
- Weakness
- Recurrent subluxation or dislocation
- Abnormal gait with early degenerative changes
19
Q
When might developmental dysplasia of the hip be detected?
A
During the newborn examinations
Later, when the child presents with:
- Hip asymmetry
- Reduced range of movement in the hip
- A limp
20
Q
Risk factors for developmental dysplasia of the hip?
A
First degree family history
Breech presentation from 36 weeks onwards
Breech presentation at birth if 28 weeks onwards
Multiple pregnancy
21
Q
When is DDH screened for?
A
At the neonatal examination at birth and 6-8 week old.
Public Health England provides newborn and infant physical examination (NIPE) guidance on picking up DDH.
22
Q
What is looked for when screening for DDH and what findings may suggest it is present?
A
When examining, look for symmetry in the hips, leg length, skin folds and hip movements.
Findings that may suggest DDH are:
- Different leg lengths
- Restricted hip abduction on one side
- Significant bilateral restriction in abduction
- Difference in the knee level when the hips are flexed
- Clunking of the hips on special tests
- Positive tests:
1.Ortolani test
2. Barlow test
23
Q
What special tests are used to look for DDH?
A
Ortolani test
Barlow test
24
Q
What is the Ortolani test performed to look for, and what does it involved?
A
Ortolani test is a special test looking for developmental dysplasia of the hip performed during the NIPE
Looking for ANTERIOR DISLOCATION of the hip
- Baby is on their back with the hips and knees flexed.
- Examiner places their palms on baby’s knees
- Examiner places their thumbs on the inner thigh
- Examiner places four fingers on the outer thigh
- Examiner used gentle pressure to abduct the hips and apply pressure behind the legs with the fingers to see if the hips will dislocate anteriorly
25
What is the Barlow test performed to look for, and what does it involve?
The Barlow test is a special test looking for developmental dysplasia of the hip, performed during the NIPE
Looking for POSTERIOR DISLOCATION of the hip
- Baby is on their back with hips adducted and flexed at 90 degrees, and knees bent at 90 degrees
- Examiner places gentle downward pressure on the knees through the femur to see if the femoral head with dislocate posteriorly
26
Clicking vs clunking - DDH
CLICKING - a common examination finding, 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 - more likely to indicate DDH, requires an ultrasound.
27
How is developmental dysplasia of the hip diagnosed?
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.
Xrays can also be helpful, particularly in older infants.
28
Below what age can a presentation of DDH be considered for management with a Pavlik harness?
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. T
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.
29
For how long is a Pavlik harness used?
Until the hips are more stable, usually after 6-8 weeks
30
When might surgical management be required for DDH?
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.
31
What is the role of the Pavlik harness in DDH?
The Pavlik harness is used when the child presents before 6 months of age
It is fitted and kept on permanently, adjusting for the growth of the baby.
It aims 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.
32
Management of developmental dysplasia of the hip?
PAVLIK HARNESS - if presenting before 6 months of age, fitted for around 6-8 weeks
SURGERY - if Pavlik harness fails or if child presents after 6 months of age, followed by immobilisation of the hip for a prolonged period with A HIP SPICA CAST
33
What is osteosarcoma and which sites are most commonly affected?
Osteosarcoma is a type of bone cancer.
The most common bone to be affected is the femur. Other common sites are the tibia and humerus.
34
What age range is usually affected by osteosarcoma?
Children and young adults 10 – 20 years.
35
How does osteosarcoma present?
The main presenting feature is persistent bone pain, particularly worse at night time. This may disturb or wake them from sleep.
Other symptoms that may be present include:
- bone swelling
- a palpable mass
- restricted joint movements
36
Osteosarcoma - investigations?
NICE guidelines recommend a very urgent direct access xray within 48 hours for children presenting with unexplained bone pain or swelling.
If the xray suggests a possible sarcoma they need very urgent specialist assessment within 48 hours.
Blood tests may show a raised alkaline phosphatase (ALP).
Further investigations is used to better define the lesion and stage the cancer:
CT scan
MRI scan
Bone scan
PET scan
Bone biopsy
37
X ray in osteosarcoma?
Xrays show a poorly defined lesion in the bone, with destruction of the normal bone and a “fluffy” appearance.
There will be a periosteal reaction (irritation of the lining of the bone) that is classically described as a “sun-burst” appearance.
There can an associated soft tissue mass.
38
Management of orthopaedics?
Management involves surgical resection of the lesion, often with a limb amputation.
Adjuvant chemotherapy is used alongside surgery to improve outcomes.
They will require support and input from the multidisciplinary team in addition to treatment of the tumour:
Paediatric oncologists and surgeons
Specialist nurses
Physiotherapy
Occupational therapy
Psychology
Dietician
Prosthetics and orthotics
Social services
The main complications are pathological bone fractures and metastasis.
39
What blood marker may be raised in osteosarcoma?
ALP
40
What investigations may be done to stage osteosarcoma?
CT scan
MRI scan
Bone scan
PET scan
Bone biopsy
41
What is talipes and when does it present?
Talipes is a fixed abnormal ankle position that presents at birth.
It is also known as clubfoot. It can occur spontaneously or be associated with other syndromes.
It is usually identified at birth or during the newborn examination.
42
What talipes equinovarus?
Talipes equinovarus describes the ankle in plantar flexion and supination.
43
What is seen here?
Talipes equinovarus
44
What is talipes calcaneovalgus?
Talipes calcaneovalgus describes the ankle in dorsiflexion and pronation.
45
How is talipes managed?
Talipes is treated with the “Ponseti method” with good results.
Surgery may be required if the Ponseti method fails or cannot be used.
46
What is the ''Ponseti method'' of treating talipes?
The Ponseti method is a way of treating talipes without surgery.
It is usually very successful.
Treatment is started almost immediately after birth. It is performed by a properly trained therapist.
The foot is manipulated towards a normal position and a cast is applied to hold it in position.
This is repeated over and over until the foot is in the correct position.
At some point an achilles tenotomy to release tension in the achilles tendon is performed, often in clinic.
After treatment with the cast is finished a brace is used to hold the feet in the correct position when not walking until the child is around 4 years old. This brace is sometimes referred to as “boots and bars”.
47
What is positional talipes and how does it differ from talipes?
Positional talipes is a common condition where the resting position of the ankle is in plantar flexion and supination, however it is not fixed in this position and there is no structural boney issue in the ankle.
The muscles are slightly tight around the ankle but the bones are unaffected.
The foot can still be moved into the normal position.
This requires referral to a physiotherapist for some simple exercises to help the foot return to a normal position.
Positional talipes will resolve with time.
48
What is seen here?
Talipes calcaneovalgus
49
What happens in Perthe's disease and which part of the bone is affected?
Perthes disease involves disruption of blood flow to the femoral head, causing avascular necrosis of the bone. This affects the epiphysis of the femur, which is the bone distal to the growth plate (physis)
Over time there is revascularisation or neovascularisation and healing of the femoral head.
There is remodelling of the bone as it heals.
50
Which ages and sex are mostly affected by Perthes disease?
It occurs in children aged 4 – 12 years, mostly between 5 – 8 years, and is more common in boys.
51
Why does avascular necrosis of the femoral head occur in Perthes disease?
It is described as idiopathic, meaning there is no clear cause or trigger for the avascular necrosis.
One theory suggests that repeated mechanical stress to the epiphysis may interrupt the blood supply.
52
What is the main complication of Perthes disease?
The main complication is a soft and deformed femoral head, leading to early hip osteoarthritis.
This leads to an artificial total hip replacement in around 5% of patients.
53
How does Perthes disease?
Perthes disease present with a slow onset of:
Pain in the hip or groin
Limp
Restricted hip movements
There may be referred pain to the knee
There will be no history of trauma.
54
In Perthes disease there will not be a history of trauma - what might you consider as a DDx instead?
If the pain is triggered by minor trauma, think about slipped upper femoral epiphysis, particularly in older children.
55
Investigating ?Perthes disease?
The initial investigation of choice in Perthes disease is an xray, however this can be normal.
Other investigations that can be helpful in establishing the diagnosis are:
Blood tests are typically normal, particularly inflammatory markers that are used to exclude other causes
Technetium bone scan
MRI scan
56
Management of Perthes disease?
The severity of Perthes disease varies between patients.
Initial management in younger and less severe disease is conservative. The aim of management to maintain a healthy position and alignment in the joint and reduce the risk of damage or deformity to the femoral head. This is with:
Bed rest
Traction
Crutches
Analgesia
Physiotherapy is used to retain the range of movement in the muscles and joints without putting excess stress on the bone.
Regular xrays are used to assess healing.
Surgery may be used in severe cases, older children or those that are not healing. The aim is to improve the alignment and function of the femoral head and hip.
57
What is rickets?
Rickets is a condition affecting children where there is defective bone mineralisation causing “soft” and deformed bones. In adults the same process leads to a condition called osteomalacia. Osteo– means bone and –malacia means soft.
58
What is the adult equivalent of Rickets?
Osteomalacia
Rickets is a condition affecting children where there is defective bone mineralisation causing “soft” and deformed bones. In adults the same process leads to a condition called osteomalacia.
Osteo– means bone and –malacia means soft.
59
A deficiency in what leads to rickets? Where can they come from/be produced from?
Rickets is caused by a deficiency in vitamin D or calcium.
Vitamin D is either produced by the body in response to sunlight or obtained through foods such as eggs, oily fish or fortified cereals or nutritional supplements.
Calcium is found in dairy products and some green vegetables.
60
What causes Rickets?
Usually deficiency in vitamin D or calcium
There is a rare form of rickets caused by genetic defects that result in low phosphate in the blood.
- This is called hereditary hypophosphataemic rickets.
- The most common form is x-linked dominant, however it also has other modes of inheritance.
61
What is the pathophysiology of rickets?
Vitamin D is essential in calcium and phosphate absorption from the intestines and kidneys.
Vitamin D is also responsible for regulating bone turnover and promoting bone reabsorption to boost the serum calcium level.
Inadequate vitamin D leads to a lack of calcium and phosphate in the blood.
Since calcium and phosphate are required for the construction of bone, low levels result in defective bone mineralisation.
Low calcium causes a secondary hyperparathyroidism as the parathyroid gland tries to raise the calcium level by secreting parathyroid hormone.
Parathyroid hormone stimulates increased reabsorption of calcium from the bones.
This causes further problems with bone mineralisation.
62
Why does vitamin D deficiency occur?
Vitamin D is a hormone (not technically a vitamin) created from cholesterol by the skin in response to UV radiation.
Patients with darker skin require a longer period of sun exposure to generate the same quantity of vitamin D.
A standard diet contains inadequate levels of vitamin D to compensate for a lack of sun exposure.
Reduced sun exposure without vitamin D supplementation leads to vitamin D deficiency.
Patients with malabsorption disorders (such as inflammatory bowel disease) are more likely to have vitamin D deficiency.
The kidneys are essential in metabolising vitamin D to its active form, therefore vitamin D deficiency is common in chronic kidney disease.
63
What is the role of vitamin D
Vitamin D is essential in calcium and phosphate absorption from the intestines and kidneys.
Vitamin D is also responsible for regulating bone turnover and promoting bone reabsorption to boost the serum calcium level.
64
Presentation of Rickets
Lethargy
Bone pain
Swollen wrists
Bone deformity
Poor growth
Dental problems
Muscle weakness
Pathological or abnormal fractures
65
What bony deformity is seen in Rickets?
Bowing of the legs, where the legs curve outwards
Knock knees, where the legs curve inwards
Rachitic rosary, where the ends of the ribs expand at the costochondral junctions, causing lumps along the chest
Craniotabes, which is a soft skull, with delayed closure of the sutures and frontal bossing
Delayed teeth with under-development of the enamel
66
What bony deformity is seen here?
Bowing of the legs, where the legs curve outwards
seen in Rickets
67
What bony deformity is seen here?
Knock knees, where the legs curve inwards
seen in Rickets
68
What bony deformity is seen here?
Rachitic rosary, where the ends of the ribs expand at the costochondral junctions, causing lumps along the chest
seen in Rickets
69
What bony deformity is seen here?
Craniotabes, which is a soft skull, with delayed closure of the sutures and frontal bossing
seen in rickets
70
Risk factors of Rickets
darker skin
low exposure to sunlight
living in colder climates
spending the majority of time indoors.
71
Investigating Rickets?
Serum 25-hydroxyvitamin D is the laboratory investigation for vitamin D.
A result of less than 25 nmol/L establishes a diagnosis vitamin D deficiency, which can lead to rickets.
Xray is required to diagnose rickets. X-rays may also show osteopenia (more radiolucent bones).
Other investigation results include:
Serum calcium may be low
Serum phosphate may be low
Serum alkaline phosphatase may be high
Parathyroid hormone may be high
NICE clinical knowledge summaries suggest additional investigations to look for other pathology:
Full blood count and ferritin, for iron deficiency anaemia
Inflammatory markers such as ESR and CRP, for inflammatory conditions
Kidney function tests, for kidney disease
Liver function tests, for liver pathology
Thyroid function tests, for hypothyroidism
Malabsorption screen such as anti-TTG antibodies, for coeliac disease
Autoimmune and rheumatoid tests, for inflammatory autoimmune conditions
72
Management of Rickets?
Children with vitamin D deficiency can be treated with vitamin D (ergocalciferol). The doses for treatment of vitamin D deficiency depend on the age
Children with features of rickets should be referred to a paediatrician.
Vitamin D and calcium supplementation is used to treat rickets.
73
Prevention of rickets?
Prevention is the best management for rickets.
Breastfed babies are at higher risk of vitamin D deficiency compared with formula fed babies, as formula feed is fortified with vitamin D.
Breastfeeding women and all children should take a vitamin D supplement.
NICE clinical knowledge summaries recommend supplements containing 400 IU (10 micrograms) per day for children and young people.
74
What is osteomyelitis and acute vs chronic osteomyelitis?
Osteomyelitis is an infection in the bone and bone marrow.
This typically occurs in the metaphysis of the long bones.
The most common bacteria is staphylococcus aureus.
Chronic osteomyelitis is a deep seated, slow growing infection with slowly developing symptoms.
Acute osteomyelitis presents more quickly with an acutely unwell child.
75
Where does osteomyelitis typically occur?
Metaphysis of the long bones
76
What organism is most commonly implicated in osteomyelitis?
Staphylococcus Aureus
77
Which children are more commonly affected by osteomyelitis?
Boys under 10
78
There is often a predisposing risk factor to osteomyelitis, such as?
Open bone fracture
Orthopaedic surgery
Immunocompromised
Sickle cell anaemia
HIV
Tuberculosis
79
Presentation of osteomyelitis?
Osteomyelitis can present acutely with an unwell child, or more chronically with subtle features. Signs and symptoms are:
Refusing to use the limb or weight bear
Pain
Swelling
Tenderness
They may be afebrile, or may have a low grade fever. Children with acute osteomyelitis may have a high fever, particularly if it has spread to the joint causing septic arthritis.
80
Investigating osteomyelitis?
Xrays are often the initial investigation, but can be normal in osteomyelitis.
MRI is the best imaging investigation for establishing a diagnosis.
A bone scan is an alternative.
Blood tests will show raised inflammatory markers (CRP and ESR) and white blood cells in response to the infection.
Blood culture is important in establishing the causative organism. A bone marrow aspiration or bone biopsy with histology and culture may be necessary.
81
What is the best imaging investigation for establishing a diagnosis of osteomyelitis?
MRI
Xrays are often the initial investigation, but can be normal in osteomyelitis.
A bone scan is an alternative.
82
How is osteomyelitis managed?
Treatment requires extensive and prolonged antibiotic therapy. They may require surgery for drainage and debridement of the infected bone.
83
What is Achondroplasia?
Achondroplasia is the most common cause of disproportionate short stature (dwarfism). It is a type of skeletal dysplasia.
84
What genetics are implicated in achondroplasia?
The achondroplasia gene, fibroblast growth factor receptor 3 (FGFR3), is on chromosome 4.
Achondroplasia results from either a sporadic mutation or inheritance of an abnormal copy of this gene.
The condition is inherited in an autosomal dominant pattern.
Homozygous gene mutations, meaning two abnormal gene copies with one from each parent, is fatal in the neonatal period.
Therefore, patients with achondroplasia have one normal gene and one abnormal gene.
Mutations in the FGFR3 gene causes abnormal function of the epiphyseal plates (growth plates).
This restricts the bone growth in length, leading to short bones and short stature.
85
Features of Achondroplasia?
Patients with achondroplasia have disproportionate short stature.
The average height is around 4 feet.
The limbs are most affected by reduce bone length.
The femur and humerus (proximal limbs) are affected more than the bones of the forearm and lower leg.
The spine length is less affected and patients have a normal trunk length. Intelligence and life expectancy are not affected by the condition.
Other features of the condition:
Short digits
Bow legs (genu varum)
Disproportionate skull
Foramen magnum stenosis
Different areas of the skull grow by different methods, some of which are affected more than others.
This leads to a disproportionate skull.
The skull base grows and fuses via endochondral ossification, which is affected by achondroplasia and leads to a flattened mid-face and nasal bridge and foramen magnum stenosis.
The cranial vault grows and fuses via membranous ossification, which is unaffected by achondroplasia and leads to a normal sized vault and frontal bossing (prominent forehead).
86
Associations with Achondroplasia?
Recurrent otitis media, due to cranial abnormalities
Kyphoscoliosis
Spinal stenosis
Obstructive sleep apnoea
Obesity
Foramen magnum stenosis can lead to cervical cord compression and hydrocephalus
87
Management of achondroplasia?
There is no cure for the underlying genetic condition.
Management will involve the multidisciplinary team to support the patient with development and maximise functioning:
Paediatricians
Specialist nurses
Physiotherapists
Occupational therapists
Dieticians
Orthopaedic surgeons
ENT surgeons
Geneticists
Leg lengthening surgery can add height, but requires extensive surgery and recovery.
It involves cutting the bone (osteotomy) and separating the two parts, creating a gap between them (distraction).
Over a long period of time bone will form between the two parts, creating a longer bone.
This is controversial and has the potential to lead to significant problems, including chronic pain and reduced function.
88
Achondroplasia prognosis?
Patients have a normal life expectancy if they are not affected by complications.
Patients have a tendency to become relatively overweight due to small stature.
There are psychosocial implications to the disproportionate short stature.
89
What is Osgood-Schlatter disease?
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.
90
Which age and sex does Osgood-Schlatter disease usually affect?
It typically occurs in patients aged 10 – 15 years, and is more common in males.
91
Osgood Schlatter disease - pathophysiology
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.
92
What symptoms does Osgood-Schlatters disease present with?
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
Management of Osgood-Schlatter's Disease
Initial management focuses on reducing the pain and inflammation.
Reduction in physical activity
Ice
NSAIDS (ibuprofen) for symptomatic relief
Once symptoms settle, stretching and physiotherapy can be used to strengthen the joint and improve function.
94
Prognosis/complications - Osgood-Schlatter's disease
Symptoms will fully resolve over time. The patient is usually left with a hard boney lump on their knee.
A rare complication is a full avulsion fracture, where the tibial tuberosity is separated from the rest of the tibia.
This usually requires surgical intervention.
95
What is osteogenesis imperfecta?
Osteogenesis imperfecta is a genetic condition that results in brittle bones that are prone to fractures. It is also knowns as brittle bone syndrome.
It is caused by a range of genetic mutations that affect the formation of collagen.
Collagen is a protein that is essential is maintaining the structure and function of bone, as well as skin, tendons and other connective tissues.
There are 8 types of osteogenesis imperfecta depending on the underlying genetic mutation, and they vary in their severity.
96
Osteogenesis imperfecta presents how and with what associated features?
Osteogenesis imperfecta presents with recurrent and inappropriate fractures. There are several associated features:
Hypermobility
Blue / grey sclera (the “whites” of the eyes)
Triangular face
Short stature
Deafness from early adulthood
Dental problems, particularly with formation of teeth
Bone deformities, such as bowed legs and scoliosis
Joint and bone pain
97
Blue sclera is associated with what MSK condition?
Osteogenesis imperfecta
98
What causes osteogenesis imperfecta?
It is caused by a range of genetic mutations that affect the formation of collagen.
Collagen is a protein that is essential is maintaining the structure and function of bone, as well as skin, tendons and other connective tissues.
99
How is osteogenesis imperfecta diagnosed?
Osteogenesis imperfecta is a clinical diagnosis. Xrays can be helpful in diagnosing fractures and bone deformities. Genetic testing is possible but not always done routinely.
100
Management of osteogenesis imperfecta?
The underlying genetic condition cannot be cured.
Medical treatments include:
Bisphosphates to increase bone density
Vitamin D supplementation to prevent deficiency
Management is done by the multidisciplinary team, with:
- Physiotherapy and occupational therapy to maximise strength and function
- Paediatricians for medial treatment and follow up
- Orthopaedic surgeons to manage fractures
- Specialist nurses for advice and support
- Social workers for social and financial support
101
What is septic arthritis and when does it usually occur?
Septic arthritis refers to infection inside a joint.
This can occur at any age, but is most common in children under 4 years.
Infection in a joint is an emergency, as the infection can quickly begin to destroy the joint and cause serious systemic illness. Septic arthritis has a mortality around 10%. Therefore, early recognition and management is essential.
Septic arthritis is a common and important complication of joint replacement. It occurs in around 1% of straight forward hip or knee replacements. This percentage is higher in revision surgery.
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Under what age is septic arthritis more common?
Under 4 years
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How does septic arthritis present?
Septic arthritis usually only affects a single joint. This is often a knee or hip.
It presents with a rapid onset of:
Hot, red, swollen and painful joint
Refusing to weight bear
Stiffness and reduced range of motion
Systemic symptoms such as fever, lethargy and sepsis
Septic arthritis can be subtle in young children, so always consider it as a differential when a child is presenting with joint problem
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Common bacteria causing septic arthritis
Staphylococcus aureus - most common causative organism.
Other bacteria:
Neisseria gonorrhoea (gonococcus) in sexually active teenagers
Group A streptococcus (Streptococcus pyogenes)
Haemophilus influenza
Escherichia coli (E. coli)
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Differential diagnosis for septic arthrits?
Transient sinovitis
Perthes disease
Slipped upper femoral epiphysis
Juvenile idiopathic arthritis
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Management of septic arthritis?
Patients with suspected septic arthritis require admission to hospital and involvement of the orthopaedic team.
The joint should be aspirated prior to giving antibiotics where possible.
Send the sample for gram staining, crystal microscopy, culture and antibiotic sensitivities.
The joint fluid may be purulent (full of pus).
The gram stain will come back quite quickly and may give a clue about the organism.
The full culture will take longer.
Empirical IV antibiotics should be given until the microbial sensitivities are known.
Antibiotics are usually continued for 3 to 6 weeks in total when septic arthritis is confirmed.
The choice of antibiotic depends on the local guidelines.
Patients may require surgical drainage and washout of the joint to clear the infection in severe cases.
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Joint pain is a common paediatric presentation, particularly an acute limp.
Hip pain will present differently depending on the developmental age of the child. They may present how?
Limp
Refusal to use the affected leg
Refusal to weight bear
Inability to walk
Pain
Swollen or tender joint
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Joint pain 0-4 years
Septic arthritis
Developmental dysplasia of the hip (DDH)
Transient sinovitis
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Joint pain 5-10 years
Septic arthritis
Transient sinovitis
Perthes disease
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Joint pain 10-16 years?
Septic arthritis
Slipped upper femoral epiphysis (SUFE)
Juvenile idiopathic arthritis
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Red flags for hip pain?
Child under 3 years
Fever
Waking at night with pain
Weight loss
Anorexia
Night sweats
Fatigue
Persistent pain
Stiffness in the morning
Swollen or red joint
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Criteria for urgent referral for assessment in a limping child, according to NICE clinical knowledge summaries?
Child under 3 years
Child older than 9 with a restricted or painful hip
Not able to weight bear
Evidence of neurovascular compromise
Severe pain or agitation
Red flags for serious pathology
Suspicion of abuse
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Joint pain - investigations?
Blood tests including inflammatory markers (CRP and ESR) for JIA and septic arthritis
Xrays are used to diagnose fractures, SUFE and other boney pathology
Ultrasound can establish an effusion (fluid) in the joint
Joint aspiration is used to diagnose or exclude septic arthritis
MRI is used to diagnose osteomyelitis
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Which part of the bone is strongest in children?
Growth plate (epiphyseal plates)
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What are epiphyseal plates?
Growth plates (epiphyseal plates) are found in the bones of children but not adults.
They are the area at the ends of long bones that allow the bones to grow in length.
They are made of hyaline cartilage and sit between the epiphysis and the metaphysis.
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What are epiphyseal plates made of and where do they sit?
They are made of hyaline cartilage and sit between the epiphysis and the metaphysis.
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What do epiphyseal plates become in adults?
Once the epiphysis and the metaphysis fuse during the teenage years, the growth plates become the epiphyseal lines.
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Bones in adults vs children
Children have growth plates, whereas adults do not.
Children have more cancellous bone, which is the spongy, highly vascular bone in the centre of long bones.
Adults have more cortical bone, which is the compact, hard bone around the outside.
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Why are children more prone to green stick fractures?
Children have growth plates, whereas adults do not.
Children have more cancellous bone, which is the spongy, highly vascular bone in the centre of long bones.
This makes children’s bones are more flexible but less strong.
This makes children prone to “greenstick” fractures, where one side of the bone breaks whilst the other stays intact.
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Why do bones heal better in children?
Bones in children have very good blood supply and are able to heal much more quickly with less long term deformity compared with adults.
When bones fracture in children, they are more likely to break cleanly in two compared with adults.
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Adult vs children fractures
The younger the child, the better and faster the healing of fractures. When bones fracture in children, they are more likely to break cleanly in two compared with adults.
Children are more likely to have greenstick fractures, where only one side of the bone breaks whilst the other side of the bone stays intact.
Children are more likely to have a buckle fracture (or torus fracture), due to less strength against compression.
Bone remodelling is the process where bone tissue is taken from areas of low tension and deposited in areas of high tension. This allows bone to change to the optimum shape for function. Bones in children have a high capacity for remodelling, which means that even if they are set at an incorrect angle, they will remodel over time to return to the correct shape.
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What is bone remodelling?
Bone remodelling is the process where bone tissue is taken from areas of low tension and deposited in areas of high tension.
This allows bone to change to the optimum shape for function.
Bones in children have a high capacity for remodelling, which means that even if they are set at an incorrect angle, they will remodel over time to return to the correct shape.
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Types of fracture
Buckle (torus)
Transverse
Oblique
Spiral
Segmental
Salter-Harris (growth plate fracture)
Comminuted
Greenstick
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Fractures through the growth plate can cause issues with growth in that bone. Growth plate fractures are graded using what classification?
The Salter-Harris classification. The higher the Salter-Harris grade, the more likely the fracture is to disturb growth.
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Salter-Harris classification of growth plate structures?
Use the SALTR mnemonic to remember the types:
Type 1: Straight across
Type 2: Above
Type 3: BeLow
Type 4: Through
Type 5: CRush
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Principles of fracture management
The first principle is to achieve mechanical alignment of the fracture by:
Closed reduction via manipulation of the joint
Open reduction via surgery
The second principle is provide relative stability for a period of time, to allow healing. 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
K wires
Intramedullary wires
Intramedullary nails
Screws
Plate and screws
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Safeguarding in children with fractures?
Always keep safeguarding in mind when children present with fractures. Does the story make sense? Has this happened before? When there is doubt, discuss the case with a senior and consider a safeguarding referral.
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Pain management in paediatric fractures?
Pain management in children is slightly different than adults. The World Health Organisation have a pain ladder for children that has only two steps:
Step 1: Paracetamol or ibuprofen
Step 2: Morphine
If a child requires morphine they generally need admission for a serious illness.
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Which common analgesics are not used in children and why not?
Codeine and tramadol are not used in children as there is unpredictability in their metabolism, so the effects vary too greatly to make them safe and effective options.
Aspirin is contraindicated in children under 16 due to the risk of Reye’s syndrome (except in certain circumstances such as Kawasaki disease).
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Recognised radiological feature of rickets
Rickets can present as widening of the wrist joints due to an excess of non-mineralized osteoid at the growth plate
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A number of fractures have been recognised as highly specific to non-accidental than
accidental injury - including?
* Metaphyseal fractures (so-called bucket handle fracture or corner fracture)
* present in up to 39-50% of abused infants <18 months.
* said to be virtually pathognomonic of NAI.
* Rib fractures
* especially posterior ribs.
* may have no overlying bruising.
* although vigorous CPR can occasionally cause anterior rib fractures, posterior rib
fractures do not occur.
* Skull fractures: suspicious features include:
* non-parietal skull fracture (a parietal fracture is more suggestive of accidental injury)
* involves multiple bones
* crosses sutures; sutural d
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Fractures moderately suspicious for NAI?
* bilateral fractures with fractures of differing ages.
* digital fractures in non-ambulant children.
* vertebral fractures or vertebral subluxation.
* spiral humeral fractures.
* separation of epiphysis.
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Fractures with low specificity for NAI
* middle clavicular fractures.
* linear simple fractures of parietal bone (tibia or fibula).
* single fractures in diaphysis (spiral humeral fracture is an exception)
* greenstick fractures.
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Which investigations are considered first-line in a child who presents with a
fracture due to suspected NAI?
A bone profile that includes calcium, phosphate and alkaline phosphatase is important to
exclude any underlying metabolic bone disease as a cause for fractures such as Paget’s
disease, hyperparathyroidism etc. Osteogenesis imperfecta (commonly called brittle bone
disease) can also lead to frequent low impact fractures. Clinical features are blur sclera and
skeletal survey findings are osteoporosis and Wormian bones (extra bones within skull
sutures).
A full blood count would help identify children with malabsorption disorders resulting in
reduced bone strength.
A skeletal survey is a series of radiographs taken to systemically examine the skeleton. It is a
very important part of investigating NAI as it can reveal multiple fractures which vary in stage
of healing, a feature highly suggestive of NAI.
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Generally, first line investigations for
bruising in children suspected of physical abuse are what?
* Clotting screen
* Full blood count and film
* Factor VIIIc (haemophilia A)
* Von-Willebrand factor
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CHILD, CARER and FAMILY risk factors for NAI
1. Child
a. failure to meet parental expectations and aspirations, e.g. disabled, ‘wrong’ gender,
‘difficult’ child.
b. born after forced, coercive, or commercial sex.
2. Parent/carer
a. mental health problems
b. parental indifference, intolerance, or over-anxiousness
c. alcohol, drug abuse.
3. Family
a. step-parents
b. domestic violence.
c. multiple/closely spaced births.
d. social isolation or lack of social support.
e. young parental age.
f. poverty, poor housing
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Typical sites of NAI?
. Head/neck: Ears – especially pinch marks involving both sides of ear.
Black eyes, especially if bilateral.
Soft tissues of cheeks.
Intra-oral injuries.
b. Torso: The [triangle of safety’: ears, side of face and neck, top of shoulders.
Back and side of trunk except over the bony spine.
Chest and abdomen.
Any groin or genital injury.
c. Limbs: Forearms – when raised to protect self.
. Inner aspects of arms or thigh.
Soles of feet.
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Typical sites of accidetnal injury?
Head injuries tend to involve parietal bones, occiput, forehead.
Nose, chin
Palm of hand
Knee, shins.
