UK*TE 2022 Flashcards
(136 cards)
You see a three-year-old in clinic. Their legs appear as in the image below.
Bilateral varus deformity at the knee.
Which of the following is the most likely diagnosis?
A. Blount’s disease
B. Fibular hemimelia
C. Femoral anteversion
D. Physiological genu varum
E. Renal osteodystrophy
Answer: A. Blount’s disease
- Best divided into two distinct disease entities
o Infantile Blount’s: pathologic genu varum in children 2 to 5 years of age, male > female, more common, bilateral in 50%, centred at the tibia. Diagnosis is suspected clinically with presence of a genu varum/flexion/internal rotation deformity and confirmed radiographically with an increased metaphyseal-diaphyseal angle. RFs: early walking, large stature, obesity. Treatment ranges from bracing to surgery depending on patient age, severity of deformity, and presence of a physeal bar. Langenskiold classification. Bone involvement: proximal medial tibial physis producing genu varus, flexion, internal rotation AND MAY HAVE COMPENSATORY distal femoral VALGUS. Often self limited/bracing/surgery.
o Adolescent Blount’s: pathologic genu varum in children > 10 years of age, less common, less severe, more likely to be unilateral. RFs: Obesity. No radiographic classification. Bone involvement: Proximal tibia physis, AND may have distal femoral VARUS and distal tibia VALGUS. Progressive and never resolves spontaneously – therefore bracing unlikely to work and surgery only option.
- Pathophysiology: likely multifactorial but related to mechanical overload in genetically susceptible individuals including excessive medial pressure produces an osteochondrosis of the medial proximal tibial physis and epiphysis. Osteochondrosis can progress to a physeal bar
Physiologic genu varum:
- Normal in children <2 years
- Genu varum migrates to neutral at ~14 months
- Continues to a peak genu valgum at ~3 years of age
- Genu valgum then migrates back to normal physiologic valgus at ~7 years
Langenskiold Classification
o type I thru IV consist of increasing medial metaphyseal beaking and sloping
o type V and VI have an epiphyseal-metaphyseal bony bridge (congenital bar across physis)
o provides prognostic guidelines: Stage II and IV can exhibit spontaneous resolution.
Presentation:
- Genu varum/flexion/internal rotation deformity – usually bilateral
- Positive ‘cover up’ test.
- Leg length discrepancy
- Usually NO tenderness, restriction of motion, effusion
- Lateral thrust on walking
Radiographic findings suggestive of Blounts disease:
- varus focused at proximal tibia
- severe deformity
- asymmetric bowing
- medial and posterior sloping of proximal tibial epiphysis
- progressing deformity
- sharp angular deformity
- lateral thrust during gait
- metaphyseal beaking: different than physiologic bowing which shows a symmetric flaring of the tibia and femur
Measurements
- Metaphyseal-diaphyseal angle (Drennan): Angle between line connecting metaphyseal beaks and a line perpendicular to the longitudinal axis of the tibia
o >16 ° is considered abnormal and has a 95% chance of progression
o Drennan angles between 11-16° necessitate close observation for the progression of tibia vara
o <10 ° has a 95% chance of natural resolution of the bowing
- tibiofemoral angle: angle between the longitudinal axis of the femur and tibia
Causes of Pathologic Genu Varum:
* persistent physiological varus
* rickets
* osteogenesis imperfecta
* MED
* SED
* metaphyseal dysostosis (Schmidt, Jansen)
* focal fibrocartilaginous defect
* thrombocytopenia absent radius
* proximal tibia physeal injury (radiation, infection, trauma)
A child presents to the Emergency Department having sustained a femoral fracture.
Which scenario would prompt subsequent imaging in the form of a Skeletal Survey?
A. A 2 year old with a femoral fracture sustained playing with older sibling on a trampoline
B. A 6 year old with Cerebral Palsy with a femoral fracture sustained whilst having physiotherapy
C. A 14 year old with a femoral fracture sustained when knocked off their bicycle by a car
D. A 4 month old with a femoral fracture sustained crawling off the end of the bed
E. An 18 month old with a femoral fracture sustained slipping on the wet kitchen floor
Answer: D. A 4 month old with a femoral fracture sustained crawling off the end of the bed
- Pediatric Abuse is the second most common cause of death in children and 50% of fractures in children younger than 1 year of age are attributable to abuse.
- Diagnosis can be suspected with a pediatric injury that is inconsistent with the mechanism of injury, a delay in seeking care, long bone fractures in nonambulatory child, or presence of highly specific fractures.
- Treatment involves reporting abuse to the appropriate agency and hospital admission for multidisciplinary evaluation. Rarely, operative management of fractures may be required.
High specificity fractures
o long bone fractures in non-ambulatory child
o classic metaphyseal lesion
fracture at junction of metaphysis and physis (primary spongiosa)
torsional / traction-shearing strain when infant’s extremity is pulled or twisted violently
high specificity for child abuse
corner fractures: discrete avulsion of the metaphysis
bucket handle fractures: horizontal avulsion fracture with appearance of central and peripheral components gives the appearance of a bucket handle. Avulsed bone fragment may be seen en face
o transphyseal separation of the distal humerus
o rib fractures, especially posteromedial
o scapula fractures
o sternal fractures
o spinous process fractures
* moderate specificity fractures
o multiple fractures in various stages of healing
o vertebral body fractures and subluxations
o digital fractures
o complex skull fractures
* other injuries concerning for abuse - multiple bruises, burns
Skin lesions are most common presentation.
3.
A 12-year-old girl presents to the paediatric clinic with claw toes and a high medial longitudinal arch to both feet. She also has callouses underneath her 5th metatarsal heads.
When examining her feet, which movements around the foot and ankle are likely to be weak
A. Ankle Plantarflexion and Foot Inversion
B. Ankle Plantarflexion and Foot Eversion
C. Ankle Dorsiflextion and Foot Eversion
D. Ankle Dorsiflextion and 1st Ray Plantarflexion
E. Ankle Plantarflexion and 1st Ray Plantarflextion
Answer: C. Ankle Dorsiflextion and Foot Eversion
- Charcot-Marie-Tooth Disease, also known as peroneal muscular atrophy, is a common autosomal dominant hereditary motor sensory neuropathy, caused by abnormal peripheral myelin protein, that presents with muscles weakness and sensory changes which can lead to cavovarus feet, scoliosis, and claw foot deformities.
- Diagnosis is made with nerve conduction studies showing low nerve conduction velocities with prolonged distal latencies in the peroneal, ulnar, and median nerves.
- Treatment involves a multidisciplinary approach to address neuropathy, cavovarus and claw foot deformities, and scoliosis.
- Pathophysiology
o HMSN Type I
abnormal myelin sheath protein is the basis of this degenerative neuropathy.
results in a combination of motor and sensory disturbances.
o HSMN Type 2
intact myelin sheath with wallerian axonal degeneration that results in mild sensory and motor conduction velocities.
o pathoanatomy
peroneus brevis: peroneal involvement is typically first and most profound, results in muscle imbalance and varus deformity
tibialis anterior: weakness results in dropfoot
intrinsic muscles of hand and foot - check for wasting of 1st dorsal interosseous in hands - Genetics
o autosomal dominant duplication of chromosome 17 (most common): codes for peripheral myelin protein 22 (PMP 22) expressed in Schwann cells (most common) or X-linked connexin 32. But may also be autosomal recessive or X-linked. - Orthopedic manifestations: pes cavovarus, claw toes, hip dysplasia, Scoliosis, hand muscle atrophy and weakness
- Peroneus longus (more normal) overpowering weak tibialis anterior and weak intrinsics and contracted plantar fascia
- Varus caused by tibialis posterior (normal) overpowering weak peroneus brevis
Symptoms
* motor deficits: initial symptoms are distal weakness and atrophy of the distal muscles, instability during gait, clumsiness, frequent ankle sprains, difficulty climbing stairs
* lateral foot pain
* sensory deficits are variable
Physical exam
* Cavovarus foot: (similar to Freidreich’s ataxia) with hammer toes or clawing of toes, usually bilaterally and symmetric. Occurs due to unoposed pull of peroneus longus causing plantarflexion of the first ray and compensatory hindfoot varus. Initially flexible, but progresses to a rigid deformity
* motor weakness
o peroneal weakness: weakest muscles around foot and ankle
o anterior tibialis: weakens next, but typically stronger than the peroneals - can lead to drop foot in swing initially and later to a fixed equinus
o posterior tibialis: stays strong for a prolonged period of time
o weak intrinsics - including weak EDB and EHB
o clawtoes
* hyporeflexia or areflexia
* Coleman block test: test to determine if hindfoot varus deformity is secondary to plantar-flexed first ray vs an independent component.
o If deformity corrects with Coleman block, this suggests a forefoot driven varus deformity.
o If deformity does not correct with Coleman block, this suggests hindfoot driven varus deformity.
o a rigid hindfoot will not correct into neutral
* upper extremity: intrinsic wasting of hands, weak pinch and grasp
* spine: scoliosis may be evident on Adam’s forward bend test
- NCS: low nerve conduction velocities with prolonged distal latencies are noted in peroneal, ulnar, and median nerves. Can also see low amplitude nerve potentials due to axonal loss
- Genetic Testing: key component for diagnosis of CMT
o DNA analysis - PCR analysis used to detect peripheral myelin protein 22 (PMP22) gene mutations
o chromosomal analysis: duplication on chromosome 17 seen in autosomal dominant (most common) form
4.
A 12-month old child becomes acutely unwell with a painful knee following varicella infection.
What organism must you rule out?
A. Group A beta-haemolytic streptococcus
B. Group B beta-haemolytic streptococcus
C. Group C beta-haemolytic streptococcus
D. Group G beta-haemolytic streptococcus
E. Group D beta-haemolytic streptococcus
Answer: A. Group A beta-haemolytic streptococcus
Pediatric Septic Hip Arthritis is an intra-articular infection in children that peaks in the first few years of life.
While diagnosis may be suspected by a combination of history, physical exam, imaging, and laboratory studies, confirmation requires a hip aspiration.
Considered a surgical emergency and requires prompt recognition and urgent surgical I&D followed by IV antibiotics.
Hip joint involved in 35% of all cases of septic arthritis
Knee joint involved in 35% of all cases of septic arthritis
Risk factors: prematurity (relatively immunocompromised), cesarean section, patients treated in the NICU, invasive procedures such as umbilical catheterization, venous catheterization, heel puncture may lead to transient bacteremia
Joints with intra-articular metaphysis include: hip, shoulder, elbow, ankle (not KNEE)
Enzymatic destruction: release of proteolytic enzymes (matrix metalloproteinases) from inflammatory and synovial cells, cartilage, and bacteria which may cause articular surface damage within 8 hours
Increased joint pressure: may cause femoral head osteonecrosis if not relieved promptly
Group B streptococcus – most common in neonates with community acquired infection exposed during trans-vaginal delivery
Staph aureus – G+ve cocci in clusters, most common organism in >2years, most common nosocomial infection in neonates.
Neisseria gonorrhoeae – commonest organism in adolescents, g-ve diplococci, usually preceeding migratory polyarthralgia – multiple joint involvement, small red papules
Group A Beta-haemolytic strep – most common following varicella infection
HACEK organisms – Haemophilus (markedly decreased since vaccine), Actinobacillus, Cardiobacterium, Eikenella, and Kingella
Original Kocher Criteria (modified to include CRP)
WBC > 12,000 cells/µl of serum
inability to bear weight
fever > 101.3° F (38.5° C)
ESR > 40 mm/h
* Probability of septic arthritis may be as high as 99.6% when all four criteria above are present, if none of the above predictors are present, probability of having septic arthritis is <0.2%, 3% incidence of septic arthritis if 1/4 criteria present, 40% incidence if 2/4 criteria present, 93% incidence if 3/4 criteria present
5.
You review a 4-year-old with genu valgum of 14 degrees. Mum is concerned, what is your treatment plan?
A. Hemiepiphysiodesis
B. Bracing KAFO
C. Bracing and restricted weight bearing
D. Observation
E. Medial tibial epiphysiodesis
Answer: D. Observation
• Genu Valgum is a normal physiologic process in children which may also be pathologic if associated with skeletal dysplasia, physeal injury, tumors or rickets.
• Diagnosis is made clinically with presence of progressive genu valgum after the age of 7.
• Treatment is observation for genu valgum <15 degrees in a child <7 years of age. Surgical management is indicated for severe and progressive genu valum in a child > 7 years of age.
Distal femur is the more common location of pathological deformity.
Risk factors: prior infection or trauma, vit D deficiency/rickets, obesity, skeletal dysplasia, lysosomal disease.
- Genu varum <2 years
- Genu varum migrates to neutral at ~14 months
- Continues to a peak genu valgum at ~3 years of age (tibiofemoral angle 15-20 deg)
- Genu valgum then migrates back to normal physiologic valgus at ~7 years
o after age 7 valgus should not be worse than 12 degrees of genu valgum
o after age 7 the intermalleolar distance should be <8 cm
- lateral deviation of mechanical axis: decreased growth from lateral physis relative to medial physis
- patellar instability: increased Q-angle and shallow lateral femoral sulcus (lateral femoral condyle growth suppressed predisposing to lateral subluxation)
Associated conditions
- bilateral genu valgum: physiologic, renal osteodystrophy (renal rickets), skeletal dysplasia (Morquio syndrome, spondyloepiphyseal dysplasia, chondroctodermal dysplasia(Ellis-van Creveld))
- unilateral genu valgum: physeal injury from trauma, infection, or vascular insult, proximal metaphyseal tibia fracture (Cozen Phenomenon), benign tumors (fibrous dysplasia, osteochondromas, enchondromas), fibular hemimelia
• Normal lateral distal femoral angle (LDFA) = 85-90 degrees
• Normal medial proximal tibia angle (MPTA) = 85-90 degrees
• Hypoplastic lateral femoral condyle with shallow lateral femoral sulcus
• mechanical axis
o center of femoral head to center of ankle should pass through center of knee
o lateral deviation of mechanical axis in genu valgum, therefore lateral femoral condyle and lateral tibia plateau are subjected to increased loads
• mechanical loading on physis modulates growth
o Hueter–Volkmann law
compression inhibits growth
distraction stimulates growth
o greater proportion of change in growth rate from hypertrophic zone (75%) than proliferative (25%)
greater effect on growth seen from change in size of chondrocytes than number
Management:
- Non-operative is first line treatment – observation and medical management of risk/pathological factors. Bracing is rarely used (may provide temporary relief, but in-effective as long term solution).
o Indications: children <7 years old, tibiofemoral angle <15 deg
o Vast majority of physiological genu valgum will resolve spontaneously, medical management underlying etiology may slow progression.
- Operative:
o Indications: tibiofemoral angle >15 deg, intramalleolar distance 10cm after 10 years old, rapidly progressive deformity after 7 years.
o Medial hemi-epiphysiodesis (extra-periosteal placement to avoid physeal injury): usually temporary (8 plates), permanent hemi-epiphysiodesis (modified Phemister technique)
o Osteotomy: insufficient growth remaining to correct deformity with hemi-epiphysiodesis, skeletally mature patients, non-functional growth plates
Lateral distal femur opening wedge osteotomy: angular correction can be adjusted to desired correction, but requires grafting and is a less stable construct requiring prolonged immobilisation to allow graft to heal.
Medial distal femur closing wedge osteotomy: stable osteotomy, shorter period immobilisation, avoids distracting CPN, but more technically demanding to remove precise angular wedge.
HTO
- Deformity after a proximal metaphyseal tibia fracture (Cozen) should be observed as most remodel - maximum magnitude of deformity reached approximately 12-18 mo after injury, resolve spontaneously within 2-4 years.
6.
You review a 10-year-old boy with a varus deformity 2 years post fracture dislocation of the ankle.
There is a bony bridge involving 20% of the physis on CT scan.
How will you treat him?
A. Observation
B. Observation until skeletal maturity then realignment osteotomy
C. Bracing in AFO
D. Excision of physeal bar and interposition graft
E. Supramalleolar osteotomy
Answer: D. Excision of physeal bar and interposition graft
Physeal bridges commonly occur after Salter-Harris (SH) physeal fractures in early adolescence when the physis is thickest and the cartilage is weakest. Small (<25% of physeal area), central bridges have a better prognosis. There are 3 types of physeal bridges:
(1) Peripheral bridges cause angular deformity and may be amendable to excision.
(2) Elongated bridges involve involve the middle of the physis and are most commonly caused by SH III or IV fractures.
(3) Central bridges have a perimeter of healthy physis but act as a central tether and can tent/distort the articular surface.
When bar resection is performed, interposition options includes fat, cranioplast, bone wax, cartilage, muscle and silicone.
Growth arrest
• medial malleolus SH IV fractures have the highest rate of growth disturbance
• risk factors
o degree of initial displacement: 15% increased risk of physeal injury for every 1mm of displacement
o residual physeal displacement > 3mm - can represent periosteum entrapped in the fracture site, degree initial displacement greatest risk factor for premature physeal closure
o high-energy injury mechanism
o SH III and IV fractures
• types
o partial arrests can lead to angular deformity
distal fibular arrest results in ankle valgus deformity
medial distal tibia arrest results in varus deformity
o complete arrests can result in leg-length discrepancy
• treatment
o angular deformity
physeal bar resection
if < 20 degrees of angulation with < 50% physeal involvement and > 2 years of growth remaining
osteotomy: angular deformity >10-20degrees is an indication for osteotomy as the deformity will not correct spontaneously after bridge resection.
ipsilateral fibular epiphysiodesis
bar of >50% physeal involvement in a patient with at least 2 years of growth
fibular epiphysiodesis helps prevent varus deformity
o leg-length discrepancy
physeal bar resection
if < 50% physeal involvement and > 2 years of growth remaining
contralateral epiphysiodesis if near skeletal maturity with significant expected leg-length discrepancy
7.
You review a patient with osteochondritis dissecans whose MRI scan shows a detached lesion of 4 cm square area.
How would you treat them?
A. Microfracture
B. Fixation with buried variable pitch screw
C. Autograft OATS
D. Autologous chrondrocyte implantation
E. Non-operative management
Answer: C. Autograft OATS
• Osteochondritis Dissecans is a pathologic lesion affecting articular cartilage and subchondral bone with variable clinical patterns.
• Diagnosis may be made radiographically (notch view) but MRI usually required to determine size and stability of lesion, and to document the degree of cartilage injury.
• Treatment may be nonoperative with restricted weight bearing in children with open physis. Surgical treatment may be indicated in older patients (closed physis), lesions that are unstable and patients who have failed conservative management.
Knee is the most commonly affected, with the posterolateral aspect of medial femoral condyle in 70% of cases.
Wilson’s Test: pain with internally rotating the tibia during extension of the knee between 90 and 30 deg, then relieving the pain with tibial external rotation
MRI: characterises size of lesion, status subchondral bone and cartilage, signal intensity surrounding lesion, presence loose bodies.
Osteochondral grafting: indicated in lesions >3cm
Osteochondritis dissecans (OCD) is a disorder of subchondral bone, which secondarily affects the overlying articular cartilage. Separation of a fragment of articular cartilage, complete with a layer of its subchondral bone, occurs in end-stage disease.1 The layer of bone can be very thin, or even absent. Patients may be asymptomatic or present with pain and mechanical symptoms. The knee is most commonly affected. It classically affects skeletally immature patients who are keen on sport. In this group, the condition is usually described as juvenile OCD, but also occurs in adults for whom the prognosis is worse.2
Although OCD was first named by Konig in 18873 its cause, management and prognosis are still not fully understood. It has been our observation, and also that of others, that the proposed management strategies for patients are highly variable.4
With appropriate treatment, it is possible to heal lesions, particularly in juveniles.5 However, lesions that do not heal can lead to premature joint degeneration.4,5 Therefore, early identification and treatment of OCD is essential in order to maximise healing potential.
OCD is one of several types of osteochondral defect. These can be divided into focal and degenerative lesions. Focal defects are well delineated and include OCD, traumatic chondral and osteochondral fractures and osteonecrosis, whereas degenerative defects are typically poorly demarcated.6 Differentiation between the types of defect is based on a combination of history, clinical and radiological findings, and is essential as it will affect the management, and possibly the outcome.
Presenting symptoms for OCD will vary according to the pathological stage of the lesion and its site. In juvenile OCD, if the lesion is still attached and is stable, the symptoms (if there are any) are of vague poorly localised pain, which is often longstanding, and exacerbated by activity, and can intermittently cause an antalgic gait.11 Quadriceps atrophy may be present if there has been a long history.1 Unfortunately, late diagnosis is common due to the vague nature of the symptoms and lack of awareness of the diagnosis among sports coaches, parents and medical staff.
In more advanced cases, where lesions are unstable or displaced, mechanical symptoms such as locking and catching occur, and may be associated with swelling.
Diagnostic imaging is valuable. Plain radiographs including a flexed anteroposterior ‘tunnel view’ will allow most mature lesions to be identified.4,8 MRI is used to identify all OCD lesions and to determine their stability.12
Within the knee, OCD lesions are most commonly seen on the lateral aspect of the medial femoral condyle. In a large multicentre study involving over 500 knees, Hefti et al5demonstrated that 77% of lesions affect the medial femoral condyle, of which 51% are on the lateral aspect, 19% central and 7% medial. In comparison, only 17% were in the lateral femoral condyle, 7% in the patella and only 0.2% arose from the tibial plateau. Lesions of the trochlea have been reported as being the most rare, occurring in 1% of patients.13 In young elite athletes, it is possible that trochlear lesions are more common than this, and patellar lesions less prevalent. However, this is based on our anecdotal experience, and there is no evidence in the literature to support this.
Classification Systems:
XR – Berndt & Hardy: Stage 1-4
MRI – Dipaola et al: Type I - IV
Arthroscopy – Guhl: Type I - IV
The most important aspect of any classification of OCD is to establish whether the lesion is stable or unstable as this will influence how the lesion is treated.
Prognosis
A review by the Research on OsteoChondritis of the Knee (ROCK) study group reported rates of healing for OCD lesions being between 50% and 98%.4
Patient age is a significant factor, which affects the prognosis. Adult onset symptoms are associated with worse outcomes than those found in skeletally immature patients.5 Furthermore, in skeletally immature patients, a younger age is also associated with a more favourable outcome.16
The prognosis also varies with the size and site of the lesion, and the stability of the OCD fragment.5 Medial femoral condylar lesions, narrow lesions and cysts, when present, of < 1.3 mm when visualised on MRI are good prognostic factors16whereas patellar lesions have a poor prognosis.7 This may be due to these lesions having a higher rate of instability compared with condylar lesions.13
If, at diagnosis, the situation is favourable in terms of patient age, location and size of the lesion, these patients will do significantly better with conservative treatment than with precipitant surgery. However, if there are signs of separation of the lesion operative treatment will produce better results.5
Treatment
There are two main aims of treatment of OCD. One is to promote the healing of subchondral bone and the overlying articular cartilage, and the other is to ensure joint congruity in order to protect the opposing joint surface and mitigate circumstances which may bring about the development of osteoarthritis.
Stable lesions
Stable lesions should usually be treated non-operatively, in view of the potential for healing, particularly in juvenile OCD.5 However, some cause persisting pain and although radiographically ‘stable’, benefit from the operative treatment described later in this paper.
Non-operative treatment
The rationale for treatment is to reduce the loading from the affected articular cartilage to facilitate spontaneous healing of the defect, thus preserving the patient’s native hyaline cartilage. In the literature, several authors make recommendations for the conservative treatment of OCD including Kocher et al1and Wall et al,17 who suggest an initial period of six weeks immobilisation in a cast with protected weight-bearing. However, their progression of treatment after this period varies. Kocher et al1 advocate removal of immobilisation and increased weight-bearing over the next six weeks, at which point if the patient is free of pain, a gradual return to sport starting at three to four months. However, Wall et al17 would continue with the initial immobilisation for a further six weeks unless radiographs demonstrated re-ossification of the lesion. Other non-operative treatments have included modification of activities, bracing and physiotherapy, but there is no evidence available regarding specific protocols. Although the evidence for specific treatments is inconclusive, there is agreement that conservative treatment should continue for at least three months.4
In any event, if symptoms are not improving, surgery is indicated and the MRI helps to guide this. If pain has resolved and the MRI is improved, weight-bearing exercises are begun and a graded increase in activity is started to enable return to sports after a further four weeks. If the MRI is not resolving but pain is better, running or sport is still not allowed for another 12 weeks, after which the MRI is repeated. If there is still no improvement, then operative treatment is undertaken. However, if the MRI is improved then activity is increased as already described.
Symptomatic OCD after failed conservative treatment
Although there is a consensus that surgery should be offered when patients have not responded to conservative treatment, there is no clear evidence to show which surgical procedure should be used, or at what time.18 A guiding principle is that the best articular cartilage is the patient’s own, and so the treatment strategy is to preserve the articular surface.
Symptomatic radiographically stable lesions
The MRI will show bone oedema adjacent to the lesion but no separation of the lesion. Although there is a consensus that surgical treatment is indicated in these cases there is no clear evidence which technique is most effective. However, arthroscopic drilling of these lesions is a common treatment which has been shown to be successful, particularly in juveniles.1,8 Both retrograde and transarticular drilling techniques have been described1 and can lead to healing. We recommend arthroscopically-assisted drilling of the lesion directly through the articular surface using a 1.2 mm diameter Kirschner-wire. The drilling should be orthogonal to the joint surface and so supplementary portals may be needed, including if necessary, drilling via the patellar tendon. If there is any doubt about stability, bio-absorbable pin fixation is used) in addition to drilling of the lesion. Typically, two to four of these implants are required and the lengths are chosen to avoid violating the growth plate. Though drilling through healthy articular cartilage may be criticised, it is effective and the joint surface damage is minimal. Nevertheless, some surgeons undertake retrograde drilling with fluoroscopic guidance or the use of drill guides. This is technically more difficult and it is harder to achieve accurate placement and depth,8 increasing the risk of surgical morbidity. It is often hard to locate these lesions visually and probing can be essential to reveal a softer area corresponding with the position of the lesion shown on MRI.
Unstable lesions
Unstable lesions are treated surgically, except for those that are asymptomatic (often in adults) identified by chance on imaging and that have clearly remained in situ for a long time. These require follow-up with serial imaging.
To safeguard joint congruity, the aim is to prevent dislodgment of undisplaced OCD fragments or to replace and maintain displaced fragments within their defect area. Every effort should be made to salvage displaced fragments, as the native hyaline cartilage of the fragment is thought to be superior to the hybrid hyaline-like cartilage provided by techniques, such as microfracture and autologous chondrocyte implantation (ACI).19 Even a loose body, which detached months beforehand, will have living articular cartilage at its surface, which has been nourished via the synovial fluid and therefore continued to grow. Whether a lesion has detached from its host completely, or the lesion is still attached peripherally to healthy articular cartilage, the displaced fragment will have grown to be too big for its host crater. Although traditionally separated lesions were removed, there is still potential for healing, even when surgical treatment is delayed. Even apparently unfavourable lesions can be salvaged, leading us to believe that the outcomes are more positive than previously thought, but the operative technique needs to be scrupulous. Simply pushing these lesions back and ‘fixing in situ’ will not work as the adherent fibrous tissue must be removed first20 to ensure a close fit and stimulate healing.
Multiple techniques for OCD fixation have been described9,18,20-23 and include metallic and bio-absorbable implants and biological fixation using osteochondral plugs. Although there is a consensus that symptomatic patients should be offered surgery, there is no reliable evidence or consensus as to which specific surgical technique should be used.
An arthroscopy is first carried out to retrieve any loose bodies and to assess whether arthroscopic surgery is possible. Although the procedure is commonly carried out arthroscopically,8 we recommend open surgery in most cases as greater access allows the steps below to be carried out more easily and thoroughly. Although there is increased surgical morbidity, the chance for better preparation of the displacement and fixation often offers greater healing potential. The base of the lesion is curetted clear of fibrous tissue and the shiny, corticated surface is prepared with a burr to increase bleeding and promote healing. It is also drilled to create ‘vascular channels’ in order to maximise the chance of revascularisation.
The fragment is then trimmed using a scalpel in order to fit it into the host area. Rather than widening the crater, we recommend trimming the fragment in the belief it is easier for a smaller fragment to revascularise. With a wet gauze swab to hold the fragment more safely, its bony surface can be ‘freshened’ with bone nibblers or a burr used with great care.
Once the fragment has been resized, a decision regarding the type of fixation should be made. There are multiple implants available, all with advantages and disadvantages, and therefore the choice of fixation should be based on the size and type of fragment to be fixed.
Standard metal small fragment cancellous lag screws provide good compression,9whereas the threads of some other metal screws are too fine to grip properly. Metal screws have the disadvantage of making MRI interpretation difficult and also that their heads need countersinking with resultant articular cartilage damage. They should also be removed after one to two years as they have a tendency to back out even with good healing of the lesion, and can damage the articular cartilage of the opposing joint surface.4 If the fragment has a reasonable layer of bone, as is commonly the case, our fixation of choice is a small metallic cancellous lag screw as we feel this offers the best compression.
Bioabsorbable screws are at risk of breaking during tightening in hard, corticated bone even with pre-tapping and it is possible that they fail to provide adequate compression, for a sufficient duration, for healing to occur.23 However, if the fragment is almost entirely articular cartilage, absorbable devices such as barbed nails are more appropriate. In fragments that are too fragile for any fixation device, peripheral suturing can suffice. With this technique there is a risk of sutures ‘cutting out’. This risk may be reduced by lubricating 6/0 vicryl with sterile petroleum jelly taken from dressings.
An alternative fixation is a mosaicplasty of osteochondral plugs placed through the mobile fragment. However, again there is only limited evidence for this method.24
The presence of an underlying subchondral cyst can affect healing and therefore should be addressed. The walls of the cyst should be curetted and drilled to increase vascularisation and to form a favourable cavity into which to impact bone graft. This can be harvested locally from the tibial metaphysis or, if large amounts are needed, the iliac crest. Cysts of up to 2 mm to 3 mm do not require grafting. Bone grafting may also be required in large defects, even without cysts, in order to support the fragment and restore joint congruency.4,8
In adverse lesions, osteotomy or patellar re-alignment procedures may be considered as discussed below.
Unsalvageable lesions
Fixation of OCD lesion is not always possible due to excessive fragmentation or the small size of the fragment, in which case the fragment should be excised. Although the presence of an unfilled defect will lead to osteoarthritis, the results of removal of the fragment can be surprisingly good and sustained, particularly in smaller lesions. Therefore, if the diameter of a lesion in this situation is 2 cm or less, this should be the first choice of treatment.
Should symptoms persist, or the lesion is larger, chondral resurfacing techniques should be considered. Microfracture drilling has been recommended for chondral lesions between 2 cm2 and 4cm2 in size.21 However, the subchondral bone needs to be intact. In contrast to traumatic chondral lesions this is rarely the case in OCD and it should be remembered that treatment with microfracture alone does not restore joint congruency.
Autologous chondrocyte implantation (ACI) or matrix- induced autologous chondrocyte implantation (MACI) has the same issue of not restoring congruity, although the bony defect can be dealt with using bone grafting. Peterson et al25demonstrated favourable outcomes following ACI in 58 patients with OCD of the knee at a mean follow-up of 5.6 years. However, in some studies of ACI and MACI, the type of chondral defect is not clearly specified.26,27 In OCD, due to the pathological subchondral bone, it is possible that the effectiveness of ACI could be impaired compared with its use for chondral defects following trauma.
Osteochondral grafting, whether using autologous grafts from ‘non-weight-bearing’ surfaces of the joint, or allograft, can address the underlying bony defect. Although osteochondral autologous transplantation (OATs) is thought to have better long-term results than microfracture for the treatment of juvenile OCD, particularly in lesions over 2 cm,21 it can have problems with donor-site morbidity. Osteochondral allografts remove the problem of donor site morbidity and have been successful,28 however, there are technical challenges and the long-term results in OCD patients are unclear.1
In addition to the size and location of the lesion, other factors that affect their healing potential should also be taken into account.
Osteotomy should be considered to address adverse limb alignment, thereby offloading the lesion. Applying the same logic, patellofemoral re-alignment procedures may need to be considered. In a small number of older patients, focal metallic implants (e.g., Hemicap, Arthrosurface, Franklin, Massachusetts) may be appropriate.
8.
You review a child in A&E with a proximal femoral fracture. At what age does the greater trochanter ossification centre appear?
A. 3 years
B. 4 years
C. 5 years
D. 6 years
E. 7 years
Answer: B. 4 years
Greater trochanter appears by 4 years, closes at 16-17 years
Lesser trochanter appears by 14 years, closes at 16-17years
Femoral head appears by 1 year, closes by 16-17 years (F), 17-18years (M)
Proximal femur anatomy
• femoral head: center of femoral head should be at the level of the tip of the greater trochanter
o femoral neck: anteverted 15 degrees (in relation to femoral condyles), neck shaft angle of 125 degrees
Blood supply to femoral head:
• Birth to 4 years of age: medial and lateral circumflex and ligamentum teres
• 4 years of age to adult: posterosuperior and posteroinferior retinacular vessels from medial femoral circumflex. Therefore piriformis start nails damage posterosuperior retinacular vessels and can cause AVN of femoral head
• adult age: medial femoral circumflex, therefore avoid transection the quadratus during posterior approach and damaging the MFC artery
• Ligamentum teres: arterial branch of the posterior division of the obturator artery to the femoral head - not significant in adults
• Abdominal aorta
o external iliac artery
common femoral artery: at risk during screw placement in anterosuperior quadrant during THA
profunda femoris
lateral femoral circumflex: ascending branch at risk during the direct anterior approach
medial femoral circumflex: major blood supply to femoral head, at risk during psoas tenotomy
femoral artery perforators: supply vastus lateralis
o internal iliac artery
obturator (posterior branch): supplies transverse acetabular ligament - at risk with screw placement and acetabular retractors in the anteroinferior quadrant
superior gluteal
inferior gluteal: supplies short external rotators and gluteus maximus. Runs along the piriformis after it exits the greater sciatic notch
internal pudendal
re-enters pelvis via lesser sciatic notch
• Corona Mortis
o vascular connection between
inferior epigastric branch of the external iliac vessels
obturator vessels
9.
You perform a rotational profile on a patient in clinic. What is the normal femoral anteversion at birth?
A. 0-10 degrees
B. 10-20 degrees
C. 30-40 degrees
D. 40-50 degrees
E. 50-60 degrees
Answer: C. 30-40 degrees
Is based on degree of anteversion of femoral neck in relation to the femoral condyles
o at birth, normal femoral anteversion is 30-40°
o typically decreases to normal adult range of 15° by skeletal maturity
o minimal changes in femoral anteversion occur after age 8
• Femoral Anteversion is a common congenital condition caused by intrauterine positioning which lead to increased anteversion of the femoral neck relative to the femur with compensatory internal rotation of the femur.
• Diagnosis is made clinically with the presence of intoeing combined with an increase in internal rotation of the hip of greater than 70° with an accompanying decrease in external rotation of the hip of less than 20°.
• Treatment is observation with parental reassurance as most cases resolve by age 10. Rarely, surgical management is indicated in the presence of less than 10° of hip external rotation in children greater than 10 years of age.
• Femoral anteversion is characterized by
o increased anteversion of the femoral neck relative to the femur
o compensatory internal rotation of the femur
o lower extremity intoeing
• There are three main causes of intoeing including
o femoral anteversion (this topic)
o metatarsus adductus (infants)
o internal tibial torsion (toddlers)
• Pathophysiology
o a packaging disorders caused by intra-uterine positioning
o most spontaneously resolve by age 10
• Associated conditions
o can be seen in association with other packaging disorders
DDH
metatarsus adductus
congenital muscular torticollis
10.
On post-natal checks it was discovered that a newborn had partial absence of the posterior ring of C1. Conservative management was employed but he is now 5 years old and is affected by head tilt, suboccipital pain and decreased range of movement about the c‐spine.
What would you offer him?
A. Excision of tumour
B. Immobilisation and NSAIDs
C. Distal and proximal release
D. Posterior fusion
E. Observation
Answer: D. Posterior fusion
Congenital anomalies of the posterior arch of the atlas (C1) are relatively common anomalies. They may range from partial defects presenting as clefts to complete absence of the posterior arch (aplasia).
These anomalies are classified according to Currarino. It should not be confused with Currarino triad (an inherited congenital disorder of the sacrum and anus or rectum).
Currarino Classification: combination of morphology and clinical presentation
* morphological types
o type A: failure of posterior midline fusion of the two hemiarches
o type B: unilateral defect
o type C: bilateral defects
o type D: absence of the posterior arch, with persistent posterior tubercle
o type E: absence of the entire posterior arch, including the tubercle
* clinical subgroups
o 1: incidental imaging finding, asymptomatic
o 2: neck pain or stiffness after trauma to the head or neck
o 3: chronic symptoms referable to the neck
o 4: various chronic neurological problems
o 5: acute neurological symptoms following minor cervical trauma
Type A and subgroup 1 are by far the commonest (approximating 80% of cases) and are encountered in 4% of the general population 7. In contrast, all other morphological types (B to E) are encountered in only 0.69% of the population
This anomaly is a developmental failure of chondrogenesis (lack of chondrification). In the embryological period C1 is usually formed from three primary ossification centres:
* an anterior centre developing into the anterior tubercle
* two lateral centres giving rise to the lateral masses and posterior arch
In ~2% of the population, an additional ossification centre develops in the posterior midline, subsequently forming into a posterior tubercle.
During ossification different anomalies can develop, comprising:
* median cleft(s) of the posterior arch
* varying degrees of posterior arch dysplasia
o either with or without the presence of posterior tubercle (see above)
Fusion of ossicles usually occurs during age 3 to 5 years. Incomplete posterior fusion may even be normal in children up to 10 years old.
Associations:
* Arnold-Chiari malformation
* gonadal dysgenesis
* Klippel-Feil syndrome
* Down syndrome
* Turner syndrome
Treatment and prognosis
Anomalies of the posterior arch of C1 are usually considered benign 4, but may give rise to severe neurological compromise. Especially groups C and D (i.e. isolated posterior ossicle) may be considered a risk factor for neurological morbidity rather than a developmental variant of normal 7.
In cases of doubt (e.g. post-traumatic symptoms not clearly related to the anomaly, type C or D without symptoms) imaging studies may include 7:
* cervical lateral plain radiography, optimally as flexion and extension study
* cervical CT with multiplanar reconstruction and/or 3D
* cervical MRI, possibly with the neck in extension
o including medullary and soft-tissue sequences to depict spinal cord changes and mapping of ligamentous structures
For asymptomatic cases, no treatment or follow-up is needed, as considered a benign anatomical variant. Some authors including Currarino suggest advising patients with type C and D to avoid contact sports. Prevention of cumulative damage to the cord by surgery at an early stage may also be prudent in these types with a posterior tubercle. In cases with symptomatic compression, surgery with excision of the posterior arch is considered curative 7.
Differential diagnosis
When patients with arch anomalies present with trauma, the radiographs may be confusing and misleading. Hence thorough knowledge of these abnormalities is essential to avoid misinterpretation as an osteolytic lesion, fracture or dislocation, e.g. atlantoaxial subluxation.
11.
An 11-year-old girl presents with a left thoracic rib hump. Neurological examination reveals absent abdominal reflexes. X‐rays show a 30-degree curve.
What is the next appropriate step?
A. Observation
B. Bracing
C. MRI
D. Anterior spinal fusion
E. Posterior spinal fusion
Answer: C. MRI
MRI should extend from posterior fossa to conus – purpose is to rule out intraspinal anomalies.
Other indications for MRI:
- Atypical curve pattern (left thoracic, short angular curve, apical kyphosis)
- Rapid progression
- Excessive kyphosis
- Structural abnormalities
- Neurological symptoms or pain
- Midline skin defects (hairy patches, dimples, naevi – signs of spinal dysraphism), café au lait spots,
- Foot deformities (suggest neural axis abnormalities)
- Asymmetric abdominal reflexes (syringomyelia). A syrinx is associated with abnormal abdominal reflexes and a curve without significant rotation.
Adolescent Idiopathic Scoliosis is a coronal plane spinal deformity which most commonly presents in adolescent girls from ages 10 to 18 (10:1 female to male ratio for curves >30deg).
Cobb angle >10deg = scoliosis
Spinal Balance: coronal balance is determined by alignment of C7 plumb line to central sacral vertical line. Sagittal balance is based on C7 plumb from centre of C7 to the posterior-superior corner of S1.
Stable zone = between lines drawn vertically from lumbosacral facet joints.
Stable vertebrae = most proximal vertebrae that is most closely bisected by central sacral vertical line.
Apical vertebrae = vertebra deviated farthest from the centre of the vertebral column.
Diagnosis is made with full-length standing PA and lateral spine radiographs.
Right thoracic curve is commonest, left thoracic curves are rate and indicate MRI to rule out cysts or syrinx.
Treatment can be observation, bracing, or surgical management depending on the skeletal maturity of the patient, magnitude of deformity, and curve progression.
Curve progression risk factors:
- Curve magnitude: >25 deg before skeletal maturity will continue to progress, after skeletal maturity thoracic curves >50deg will progress at 1-2deg/year and lumbar curves >40deg will progress 1-2deg/year.
- Remaining skeletal growth: Peak growth velocity is the best predictor of curve progression, <12 years at presentation, Tanner stage <3, Risser 0-1 (Risser 0 covers the first 2/3rd of the pubertal growth spurt and correlates with the greatest velocity of skeletal growth). Open triradiate cartilage. If curve is >30deg before peak height velocity, there is a strong likelihood of the need for surgery.
- Curve type: thoracic curves more likely to progress than lumbar, and double curves more likely to progress than single curves.
12.
You review an x-ray of a 1-year-old girl with DDH.
What is the name of the horizontal line drawn through the tri-radiate cartilages on a pelvic radiograph?
A. Shenton
B. Perkin
C. Acetabular index
D. Hilgenreiner
E. Klein
Answer: D. Hilgenreiner
Hilgenreiner’s line: horizontal line through the right and left triradiate cartilage – femoral head ossification should be inferior to this line.
Perkin’s line: line perpendicular to Hilgenreiner’s line through a point at the lateral margin of the acetabulum – femoral head ossification should be medial to this line.
Shenton’s line: arc along the inferior border of the femoral neck and the superior margin of the obturator foramen – arc line should be continuous.
Delayed ossification of the femoral head is seen in cases of dislocation.
Acetabular teardrop not typically present prior to hip reduction for chronic dislocations since birth – development of teardrop after reduction is thought to be a good prognostic sign for hip function.
Acetabular Index: angle formed by Hilgenreiner’s line and a line from a point on the lateral triradiate cartilage to a point on lateral margin of acetabulum – should be <25deg in patients older than 6 months.
Centre-edge angle of Wiburg: angle formed by Perkin’s line and a line from the centre of the femoral head to the lateral edge of the acetabulum, <20deg is considered abnormal, only reliable in patients >5years.
Developmental Dysplasia of the Hip is a disorder of abnormal development resulting in dysplasia, subluxation, and possible dislocation of the hip secondary to capsular laxity and mechanical instability.
Diagnosis can be confirmed with ultrasonography in the first 4 months and then with radiographs after femoral head ossification occurs (~ 4-6 months).
Treatment varies from Pavlik bracing to surgical reduction and osteotomies depending on the age of the patient, underlying etiology, and the severity of dysplasia.
Risk factors: firstborn, female, breech, packing disorders, family history, macrosomia, limited hip abduction, talipes, swaddling
Dysplasia: shallow or underdeveloped acetabulum
Subluxation: displacement of the joint with some contact remaining between the articular surfaces
Dislocation: complete displacement of the joint with no contact between the original articular surfaces
Teratologic hip: dislocated in utero and irreducible on neonatal exam, presents with a pseudoacetabulum - associated with neuromuscular conditions and genetic disorders. Commonly seen with arthrogryposis, myelomeningocele, Larsen’s syndrome, Ehlers-Danlos
Late (adolescent) dysplasia: mechanically stable and reduced but dysplastic
Typical deficiency is anterior or anterolateral acetabulum, BUT in spastic cerebral palsy acetabular deficiency is posterosuperior – needs to be considered when planning pelvic osteotomies!
Dysplasia leads to subluxation and gradual dislocation, repetitive subluxation of the femoral head leads to the formation of a ridge of thickened articular cartilage called the limbus.
Chronic dislocation leads to the development of secondary barriers to reduction: pulvinar thickens, ligamentum teres thickens and elongates, TAL hypertrophies, hip capsule and iliopsoas form hourglass configuration. Anatomic changes include increased femoral anteversion, flattening of the femoral head, increased acetabular anteversion, increased obliquitiy and decreased concavity of the acetabular roof, thickening of the medial acetabular wall.
Associated with other packing deformities: congenital muscular torticollis (20%), metatarsus adductus (10%), congenital knee dislocation.
Barlow: dislocates a dislocatable hip by adduction and depression of a flexed femur – ‘click of exit”
Ortolani: reduces a dislocated hip by elevation and abduction of the flexed femur – ‘click of entry’
Galeazzi (Allis): apparent limb length discrepancy due to unilateral dislocated hip with hip flexed at 90 degrees and feet on the table – femur appears shortened on dislocated side.
Klisic test: for bilateral dislocations: line from long finger placed over the greater trochanter and the index finger over the ASIS should point to the umbilicus – if the hip is dislocated, the line will point halfway between the umbilicus and pubis.
13.
A 13-year-old girl presents with progressive development of cavus feet.
What would be the most appropriate first line investigation when she is first seen by you in clinic?
A. Nerve conduction velocity studies
B. Biopsy of the quadriceps femoris muscle.
C. Biopsy of the sural nerve.
D. DNA testing.
E. Chromosomal analysis
Answer: A. Nerve conduction velocity studies
- Charcot-Marie-Tooth Disease, also known as peroneal muscular atrophy, is a common autosomal dominant hereditary motor sensory neuropathy, caused by abnormal peripheral myelin protein, that presents with muscles weakness and sensory changes which can lead to cavovarus feet, scoliosis, and claw foot deformities.
- Diagnosis is made with nerve conduction studies showing low nerve conduction velocities with prolonged distal latencies in the peroneal, ulnar, and median nerves.
- Treatment involves a multidisciplinary approach to address neuropathy, cavovarus and claw foot deformities, and scoliosis.
- Pathophysiology
o HMSN Type I
abnormal myelin sheath protein is the basis of this degenerative neuropathy.
results in a combination of motor and sensory disturbances.
o HSMN Type 2
intact myelin sheath with wallerian axonal degeneration that results in mild sensory and motor conduction velocities.
o pathoanatomy
peroneus brevis: peroneal involvement is typically first and most profound, results in muscle imbalance and varus deformity
tibialis anterior: weakness results in dropfoot
intrinsic muscles of hand and foot - check for wasting of 1st dorsal interosseous in hands - Genetics
o autosomal dominant duplication of chromosome 17 (most common): codes for peripheral myelin protein 22 (PMP 22) expressed in Schwann cells (most common) or X-linked connexin 32. But may also be autosomal recessive or X-linked. - Orthopedic manifestations: pes cavovarus, claw toes, hip dysplasia, Scoliosis, hand muscle atrophy and weakness
- Peroneus longus (more normal) overpowering weak tibialis anterior and weak intrinsics and contracted plantar fascia
- Varus caused by tibialis posterior (normal) overpowering weak peroneus brevis
Symptoms
* motor deficits: initial symptoms are distal weakness and atrophy of the distal muscles, instability during gait, clumsiness, frequent ankle sprains, difficulty climbing stairs
* lateral foot pain
* sensory deficits are variable
Physical exam
* Cavovarus foot: (similar to Freidreich’s ataxia) with hammer toes or clawing of toes, usually bilaterally and symmetric. Occurs due to unoposed pull of peroneus longus causing plantarflexion of the first ray and compensatory hindfoot varus. Initially flexible, but progresses to a rigid deformity
* motor weakness
o peroneal weakness: weakest muscles around foot and ankle
o anterior tibialis: weakens next, but typically stronger than the peroneals - can lead to drop foot in swing initially and later to a fixed equinus
o posterior tibialis: stays strong for a prolonged period of time
o weak intrinsics - including weak EDB and EHB
o clawtoes
* hyporeflexia or areflexia
* Coleman block test: test to determine if hindfoot varus deformity is secondary to plantar-flexed first ray vs an independent component.
o If deformity corrects with Coleman block, this suggests a forefoot driven varus deformity.
o If deformity does not correct with Coleman block, this suggests hindfoot driven varus deformity.
o a rigid hindfoot will not correct into neutral
* upper extremity: intrinsic wasting of hands, weak pinch and grasp
* spine: scoliosis may be evident on Adam’s forward bend test
- NCS: low nerve conduction velocities with prolonged distal latencies are noted in peroneal, ulnar, and median nerves. Can also see low amplitude nerve potentials due to axonal loss
- Genetic Testing: key component for diagnosis of CMT
o DNA analysis - PCR analysis used to detect peripheral myelin protein 22 (PMP22) gene mutations
o chromosomal analysis: duplication on chromosome 17 seen in autosomal dominant (most common) form
14.
You are in the Ponseti clinic treating a 3-week old boy. The stages in correction of the clubfoot deformity proceed in the following order:
A. Elevation of the first ray to correct cavus, abduction, then dorsi-flexion with a Tendo-achilles tenotomy
B. Pronation, dorsiflexion, abduction, Tendo-achilles tenotomy
C. Correction of varus, then supination then dorsiflexion with a Tendoachilles tenotomy
D. Elevation of the first ray to correct cavus, then dorsiflexion with a TA tenotomy followed by a final abduction cast
E. Elevation of the first ray to correct cavus, then dorsiflexion with a TA tenotomy
Answer: A. Elevation of the first ray to correct cavus, abduction, then dorsi-flexion with a Tendo-achilles tenotomy
CAVE
Clubfoot, also known as congenital talipes equinovarus, is a common idiopathic deformity of the foot that presents in neonates.
Diagnosis is made clinically with a resting equinovarus deformity of the foot.
Half of cases are bilateral and in 80%, clubfoot is an isolated deformity.
Genetic component is strongly suggested - recent link to PITX1.
Associated with arthrogryposis.
Pathophysiology
Muscle contractures contribute to the characteristic deformity that includes (CAVE):
- Cavus (tight intrinsics, FHL, FDL)
- Adductus of forefoot (tight tibialis posterior)
- Varus (tight tendoachilles, tibialis posterior, tibialis anterior)
- Equinus (tight tendoachilles)
Bony deformity consists of medial spin of the midfoot and forefoot relative to the hindfoot
- talar neck is medially and plantarly deviated
- calcaneus is in varus and rotated medially around talus
- navicular and cuboid are displaced medially
15.
You are asked to review a 7-year-old boy in A&E with early Perthes disease. Which of the following features would you expect to see on Pelvic X-Rays?
A. Bilateral symmetrical changes
B. Early acetabular changes
C. Irregular delayed proximal femoral ossification centres
D. Smaller sclerotic epiphysis with medial joint space widening
E. Femoral head deformity with widening and flattening
Answer: D. Smaller sclerotic epiphysis with medial joint space widening
XR findings:
Earliest findings: joint space widening (due to less ossification of head), irregularity of femoral head ossification, crescent sign (subchondral fracture).
Other investigations include MRI for earlier diagnosis, and an arthrogram to assess coverage and containment of the femoral head to help guide potential management.
Histology: femoral epiphysis and physis show areas disorganized cartilage, with areas of hypercellularity and fibrillation.
Legg-Calve-Perthes Disease is an idiopathic avascular necrosis of the proximal femoral epiphysis in children.
Diagnosis can be suspected with hip radiographs. MRI may be required for diagnosis of occult or early disease.
12% of cases are bilateral – usually asynchronous asymmetrical involvement – if symmetrical then is suggestive of multiple epiphyseal dysplasia.
Treatment is typically observation in children less than 8 years of age, with analgesia, activity modification and physio to maintain/improve ROM, and consideration for proximal femoral or acetabular osteotomy if required for containment.
Proximal Femoral Varus Osteotomy: for extrusion in early stages – aims to reposition femoral head into the acetabulum for containment purposes.
Valgus osteotomy considered if hinge abduction – lateral extrusion of the capital femoral epiphysis producing a painful hinge affect on the lateral acetabulum during abduction.
Shelf/Chiari osteotomies when femoral head is no longer containable.
Osteonecrosis occurs secondary to disruption of blood supply to femoral head, followed by revascularization with subsequent resorption and later collapse. Remodelling by creeping substitution after collapse. Repeated subclinical trauma and mechanical overload lead to bone collapse and repair. Damage results from epiphyseal bone resorption, collapse and the effect of subsequent repair during the course of disease.
Associated with coagulopathy, maternal/passive smoking, ADHD.
Lateral Pillar Classification – prognostic – patient needs to have entered the fragmentation stage radiographically.
Group A: lateral pillar maintains full height, no density changes identified – consistently good outcome.
Group B: Maintains >50% height, poor outcome if bone age >6years
Group B/C: Lateral pillar is narrowed (2-3mm) or poorly ossified with approximately 50% height.
Group C: Less than 50% of lateral pillar height is maintained – poor outcomes in all patients.
Waldenstrom Classification (Stages)
Initial – infacrtion produces a smaller, sclerotic epiphysis with medial joint space widening (XR may be occult for 3-6 months)
Fragmentation – begins with presence of subchondral lucent line (crescent sign). Femoral head appears to fragment/dissolve as a result of revascularisation process with bone resorption producing collapse with subsequent patchy density and lucencies. Lasts 6months – 2years. Symptoms most prevalent in this stage.
Reossification: ossific nucleus undergoes re-ossification, with new bone appearing as necrotic bone is resorbed. May last up to 18 months.
Remodelling: femoral head remodels until skeletal maturity – begins once ossific nucleus is completely reossified – trabecular pattern returns.
Caterall at risk signs with poor outcome: Gage sign (V-shaped lucency in lateral portion of the epiphysis and/or adjacent metaphysis), calcification lateral to the epiphysis, metaphyseal cyst, lateral subluxation of the femoral head, horizontal proximal femoral physis.
Stulberg Classification – for rating residual femoral head deformity and joint congruence.
Coxa magna = widened femoral head
Coxa plana = flattened femoral head
Presents with insidious onset intermittent hip, knee, groin or thigh pain, hip stiffness – loss of IR and abduction, altered gait (antalgic/Trendelenberg – decreased abductor tension), LLD is late
Good prognostic indicators: younger bone age (<6years @ presentation), spherity of femoral head and congruency at skeletal maturity (Stulberg classification), lateral pillar classification.
Poor prognosis: females, decreased hip abduction, heavy patient, longer duration from onset to complete healing, stiffness with progressive loss of ROM, Catterall at risk signs.
16.
You are in theatre performing a pelvic osteotomy on a 7-year-old. Which of the following is a salvage osteotomy?
A. Dega
B. Salter Innominate
C. Shelf
D. Pemberton
E. Triple
Answer C. Shelf
periacetabular osteotomy (PAO) for symptomatic dysplasia in an adolescent or adult with a concentrically reduced hip and congruous joint space with a preserved range of motion. Triradiate cartilage must be closed.
Intraoperative dynamic testing of hip motion is needed to determine the need for femoral osteotomy (minimum of 90° flexion and 15° internal rotation to prevent FAI)
Multiple osteomies in pubis, ilium and ischium near the acetabulum, technically most challenging.
Advantages:
provides hyaline cartilage coverage
preserved integrity of the posterior column, which allows patients to weight bear as tolerated postoperatively (posterior column and pelvic ring remain intact).
large multidirectional corrections
preserves external rotators
delays need for arthroplasty
outcomes
reliably improves radiographic parameters and symptomatology
92% survivorship at 15 years in avoiding THA
Chiari = salvage osteotomy for unreduced hip - recommended for patients with inadequate femoral head coverage and incongruous joint (concentric reduction cannot be obtained) - Osteotomy starts above the acetabulum to the sciatic notch and ileum is shifted lateral beyond the edge of the acetabulum.
Depends on fibrocartilage
metaplasia for successful results.
Medializes the acetabulum via iliac osteotomy
Shelf: salvage in patients >8 years, add bone to the lateral weight bearing aspect of the acetabulum by placing extra-articular buttress of bone over the subluxed femoral head.
Depends on fibrocartilage metaplasia for successful results.
Salter - redirectional: younger patient with open triradiate cartilage - single transverse cut above the acetabulum through the ilium to sciatic notch. Acetabulum then hinges through pubis symphysis - improves anterolateral coverage (may length leg up to 1cm)
Triple (Steele) is Salter with additional cuts through superior and inferior rami - redirectional for anterolateral coverage)
Dega - volume reducing. favoured in neuromuscular dislocation and patients with posterior acetabular deficiency - for severe cases.
Osteotomy from acetabular roof to triradiate cartilage (incomplete cuts through peri-capsular of the innominate bone).
Acetabulum hinges through the triradiate cartilage. Does not enter the sciatic notch and is therefore stable and does not require internal fixation.
Improves anterior, central or posterior coverage.
Pemberton = volume reducing, moderate to severe. Triradiate cartilage must be open. stable as osteotomy does not enter sciatic notch.
17.
You are performing an arthrogram on a child. On an arthrogram, which one of the following is NOT seen in DDH?
A. A ‘rosethorn’ appearance on the antero‐superior aspect of the joint.
B. Inverted labrum
C. Pooling of the contrast
D. Gage’s sign
E. Hourglass constriction
Answer: D. Gage’s sign
Gage’s sign is seen in Perthes Disease – not DDH: Caterall at risk signs with poor outcome: Gage sign (V-shaped lucency in lateral portion of the epiphysis and/or adjacent metaphysis)
Dysplasia leads to subluxation and gradual dislocation, repetitive subluxation of the femoral head leads to the formation of a ridge of thickened articular cartilage called the limbus.
Chronic dislocation leads to the development of secondary barriers to reduction: pulvinar thickens, ligamentum teres thickens and elongates, TAL hypertrophies, hip capsule and iliopsoas form hourglass configuration. Anatomic changes include increased femoral anteversion, flattening of the femoral head, increased acetabular anteversion, increased obliquitiy and decreased concavity of the acetabular roof, thickening of the medial acetabular wall.
Developmental Dysplasia of the Hip is a disorder of abnormal development resulting in dysplasia, subluxation, and possible dislocation of the hip secondary to capsular laxity and mechanical instability.
Diagnosis can be confirmed with ultrasonography in the first 4 months and then with radiographs after femoral head ossification occurs (~ 4-6 months).
Treatment varies from Pavlik bracing to surgical reduction and osteotomies depending on the age of the patient, underlying etiology, and the severity of dysplasia.
Risk factors: firstborn, female, breech, packing disorders, family history, macrosomia, limited hip abduction, talipes, swaddling
Dysplasia: shallow or underdeveloped acetabulum
Subluxation: displacement of the joint with some contact remaining between the articular surfaces
Dislocation: complete displacement of the joint with no contact between the original articular surfaces
Teratologic hip: dislocated in utero and irreducible on neonatal exam, presents with a pseudoacetabulum - associated with neuromuscular conditions and genetic disorders. Commonly seen with arthrogryposis, myelomeningocele, Larsen’s syndrome, Ehlers-Danlos
Late (adolescent) dysplasia: mechanically stable and reduced but dysplastic
Typical deficiency is anterior or anterolateral acetabulum, BUT in spastic cerebral palsy acetabular deficiency is posterosuperior – needs to be considered when planning pelvic osteotomies!
Associated with other packing deformities: congenital muscular torticollis (20%), metatarsus adductus (10%), congenital knee dislocation.
Barlow: dislocates a dislocatable hip by adduction and depression of a flexed femur – ‘click of exit”
Ortolani: reduces a dislocated hip by elevation and abduction of the flexed femur – ‘click of entry’
Galeazzi (Allis): apparent limb length discrepancy due to unilateral dislocated hip with hip flexed at 90 degrees and feet on the table – femur appears shortened on dislocated side.
Klisic test: for bilateral dislocations: line from long finger placed over the greater trochanter and the index finger over the ASIS should point to the umbilicus – if the hip is dislocated, the line will point halfway between the umbilicus and pubis.
18.
A 5‐year‐old boy presents with a limp and pain over the medial aspect of the foot. He is diagnosed with Kohler’s disease.
Orthotics have failed to improve his symptoms. What is the next appropriate management of this condition?
A. Core decompression
B. Triple arthrodesis
C. Subtalar fusion
D. IV antibiotics with irrigation and debridement
E. Symptomatic treatment with analgesia/short period of rest in cast/orthotica
Answer: E. Symptomatic treatment with analgesia/short period of rest in cast/orthotica
- Kohler’s Disease is a rare idiopathic condition caused by avascular necrosis of the navicular bone that occurs in young children and presents with pain on the dorsal and medial surface of the foot. More common in boys, aged 4-7 years, can be bilateral in up to 25% of cases. Presents with mid-foot pain and a limp, may be asymptomatic. May have swelling, warmth & redness with point tenderness over navicular.
- Diagnosis is made with radiographs of the foot showing sclerosis, fragmentation, and flattening of tarsal navicular bone – most re-organise after disease has run it’s course, but even when continue to be deformed almost all are asymptomatic.
- Treatment is usually nonoperative with NSAIDs and a short period of cast immobilization as the condition typically resolves over time. XRs typically improve 6-48 months after onset, with no reports of long-term disability.
Surgery is not indicated – typically self limiting, intermittent symptoms may remain for 1-3 years after diagnosis.
Blood supply to the central third of the navicular is a watershed zone – accounting for the susceptibility to avascular necrosis and stress fractures. The navicular is the last bone to ossify (therefore increased vulnerability to mechanical compression and injury).
19.
A 20-year-old man attends clinic following an MRI which has confirmed a diagnosis of Kienbock’s disease.
Which of the following is NOT thought to contribute to Kienbock’s disease?
A. Ulnar negative variance
B. Lunate geometry
C. Ulnar positive variance
D. Vascular anatomy of lunate
E. Decreased radial inclination
Answer: C. Ulnar positive variance
Kienbock’s Disease is the avascular necrosis of the lunate which can lead to progressive wrist pain and abnormal carpal motion. Most commonly affecting males 20-40years old.
Diagnosis can be made with wrist radiographs in advanced cases but may require MRI for detection of early disease.
Treatment is NSAIDs and observation in minimally symptomatic patients. A variety of operative procedures are available depending on severity of disease and patient’s symptoms.
Risk factors:
- Ulnar negative variance (leads to increased radial-lunate contact area)
- Decreased radial inclination
- Repetitive trauma
- Lunate geometry
- Vascular supply to lunate – patterns of arterial blood supply (3 patterns: Y-pattern, X-pattern, I-pattern (highest risk AVN)) have differential incidence of AVN – disruption of venous outflow leading to increased intraosseous pressure. Blood supply to capitate is also poor and may lead to AVN.
Presents with dorsal wrist pain usually activity related, may be swelling, decreased flexion/extension arc, decreased grip strength.
MRI is best for diagnosis of early disease and rules out ulnar impaction.
CT is most useful once lunate collapse has already occurred – for showing extent of necrosis, trabecular destruction and lunate geometry.
Lichtman Classification:
Stage I: changes on MRI only – immobilisation & NSAIDs
Stage II: Sclerosis of lunate – consider joint levelling procedure (in ulnar negative patients), radial wedge osteotomy or STT fusion (in ulnar neutral patients), distal radius core decompression, revascularisation procedures.
Stage IIIA: Lunate collapse, no scaphoid rotation – same treatment as Stage II
Stage IIIB: lunate collapse, fixed scaphoid rotation – proximal row carpectomy, STT fusion or SC fusion
Stage IV: degenerated adjacent intercarpal joints – wrist fusion, PRC, limited intercarpal fusion.
20.
A 25-year-old man has presented with a radial head fracture that you have decided is for surgical fixation. When planning for surgery you decide to use the Kaplan interval for your approach.
Which is the intermuscular interval that you will use?
A. Brachioradialis and ECRL
B. Anconeus and ECU
C. ECU and EDC
D. ECRB and EDC
E. ECRB and ECRL
Answer: D. ECRB and EDC
Kocher: ECU (PIN) and anconeus (radial N) - palpate the radial head and lateral epicondyle - 5cm oblique posterolateral incision in line. Need to repair LUCL.
Kaplan: EDC (PIN) and ECRB (radial N) more anterior therefore more caution re: PIN
Anteromedial Hotchkiss approach:
- Mark out medial epicondyle, ulnar nerve and olecranon ridge
- 10cm curving incision from medial epicondyle
- Internervous plane: FCU (ulnar nerve) and FCR(medial nerve)/PL
- Identify medial supracondylar ridge of humerus, peel of brachialias, extend interval down to capsule and coronoid.
Radial head fracture - Mason (modified by Hotchkiss and Broberg-Morley) 1-4: 1- non/minimally displaced, no mechanical block to rotation, II - displaced > 2mm or angulation, possible mechanical block to forearm rotation, III - comminuted and displaced, mechanical block to rotation, IV - radial head fracture with associated elbow dislocation. (Usually a posterolateral dislocation)
O’Driscoll’s Classification:
Elbow Stabilisers:
Primary: MCL, LCL, ulnohumeral joint
Secondary: flexor and extensor muscles, radial head, capsule
O’Driscoll terrible triad: radial head, coronoid, fractures, elbow dislocation
21.
A 30-year-old lady is seen in a follow up clinic complaining that she is only able to fully flex one finger following an operation to repair a structure in her hand following a glass laceration.
Which structure has been repaired?
A. Flexor digitorum profundus
B. Flexor digitorum superficialis
C. Flexor pollicis longus
D. Extensor pollicis longus
E. Extensor digitorum communis
Answer: A. Flexor digitorum profundus
22.
A Martin-Gruber anastomosis is:
A. Median nerve to ulnar nerve in the forearm
B. Ring finger to middle finger common digital nerve in the hand
C. Between recurrent branch median and deep motor branch ulnar in the hand
D. Ulnar nerve branches into medial nerve in the forearm
E. Ulnar nerve to musculocutaneous nerve in the arm
Answer: A. Median nerve to ulnar nerve in the forearm
Marti-Gruber anastomosis: communicating nerve crossing over from the median to ulnar nerve in the forearm; (motor connections but not sensory connections). Can cause confusion both clinically and on EMG. Incidence around 15%
it occurs in two patterns:
- from median nerve in proximal forearm to ulnar nerve in middle to distal third of forearm, & from AIN to ulnar nerve, innervating the intrinsic muscles in the hand.
Occurs more commonly on the right side and can be Autosomal dominant.
A lesion of the median nerve above the communicating branch will affect the median nerve muscles.
A lesion of the ulnar nerve below the anastomosis will not affect the median nerve muscles, it will spare the thenar motor intrinsics.
Isolated ulnar nerve lesion at the elbow unusual pattern of intrinsic muscle paralysis.
Damage to the ulnar nerve at the wrist more severe deficit of intrinsics and hand function than expected.
Marinacci anastomosis: ulnar to median in forearm (reverse of Martin-Gruber)
Riche-Cannieu anastomosis: ulnar to median anastomosis in the hand – connection between the deep branch of ulnar nerve and recurrent branch of the median nerve. It carries motor fibres and the anastomosis usually occurs in the region of the thenar and adductor pollicis muscles.
Berrettini anastomosis: communication between the digital nerves (sensory!) arising from the ulnar and median nerves in the hand. Most common nerve anastomosis pattern.
23.
In which order are the following articulations disrupted in a lesser arc perilunate injury, as established by Mayfield?
A. Scapholunate - Lunotriquetral -Capitolunate - Radiocarpal
B. Radiocarpal - Scapholunate - Lunotriquetral -Capitolunate
C. Scapholunate - Capitolunate - Lunotriquetral - Radiocarpal
D. Capitolunate - Lunotriquetral - Scapholunate - Radiocarpal
E. Capitolunate - Lunotriquetral - Radiocarpal - Scapholunate
Answer: C. Scapholunate - Capitolunate - Lunotriquetral - Radiocarpal
- Sequence of events:
o scapholunate ligament disrupted –>
o disruption of capitolunate articulation –>
o disruption of lunotriquetral articulation –>
o failure of dorsal radiocarpal ligament –>
o lunate rotates and dislocates, usually into carpal tunnel
Peri-lunate Injuries:
- Piece of pie sign, spilled tea cup sign, Gilulla’s lines
- Dislocation of lunate from carpus – is a rare, high energy injury that involves ligamentous +/- boney components, and can -> complex carpal instability, degenerative change, decreased range of movement, grip strength.
- Devastating injury but innocuous on XR, can be easily missed therefore important to always get an AP and a lateral.
- 25% are missed at presentation – delayed reconstruction can -> poor outcomes
- Gilula’s lines:
o Proximal edge of distal carpal bones
o Distal edge proximal carpal bones
Proximal edge proximal carpal bones
o
Mayfield classification:
- Originally purely soft tissue
- A predictable pattern of injury occurs:
o Hyperextended wrist is taken in ulnar deviation
o Capitate becomes the centre of rotation -> injury to soft tissue on the radial side of the wrist occurs first
o As the forces progresses through the carpus -> intercarpal supination which is centred through the triquetrum -> injury to the soft tissue on the ulnar side of the wrist:
1. Scapholunate ligament injury
2. Scapholunate ligament injury + midcarpal ligament injury
3. Scapholunate ligament injury + midcarpal ligament injury + lunotriquetral ligament injury - “Classic” Perilunate
4. Injury to radiolunate ligaments – associated with median nerve compression
Johnson Classification:
Lesser Arc injuries: purely ligamentous
Greater Arc: ligamentous disruptions with associated fractures of the radius, ulnar, or carpal bones – bone involvement = ‘trans’ injury
Ligaments:
- Intrinsic: Origin and insertion within the same row e..g scapholunate, lunotriquetral
- Extrinsic:
o Palmar ligaments: 2 parallel chevrons, between which is an area of relative weakness (space of Poirier – this is the area through which the lunate dislocates in a Mayfield 4) – radioscaphocapitate (distal), long and short radiolunate (proximal), Ulnalunate ligament
o Dorsal ligaments: (Berger’s approach)
Proximal limb: dorsoradiocarpal ligament
Distal limb: dorsal intercarpal ligament
Carpal Instability – 4 main types
1. Adaptive carpal instability (post distal radius fracture non-union)
2. Carpal instability dissociative – between bones in the same row, most commonly proximal row (scapholunate/lunotriquetral)
3. Carpal instability NON-dissociative – instability between the proximal and distal rows – i.e. the rows themselves remain well aligned.
4. Complex carpal instability = combination of 2&3 (Mayfield 2,3 & 4)
Scapholunate syndrome = trans-scaphoid, transcapitate therefore proximal pole of the capitate can rotate up to 180 degrees, leading to significant mid carpal degeneration
Assessment:
Emergent Management: Assess for any median nerve symptoms! Reduce the carpus – use your thumb to support the lunate whilst hyperextending, then flexing. 20-30mins of fingertraps can aide ligamentotaxis.
CT scan – then refer to local hand team.
If you take to theatre to reduce then you MUST also decompress the median nerve – won’t know if you have caused median nerve compression on reduction while patient anaesthetised!
If closed reduction is unsuccessful:
- Mayfield 4 -> palmar approach
- Mayfield 3 -> palmar +/- dorsal approach
Principles of definitive management:
1. Reduce the lunate
2. Hold reduced
3. Reconstruct injured structures
4. Protect repairs until healed
Palmar approach – release transverse carpal ligament to decompress median nerve and reduce the lunate
Dorsal Approach: landmarks = Lister’s tubercle, EPL
- Longitudinal midline dorsal incision (used interval between 3rd and 4th extensor compartments – flex the common extensors away)
Berger/Mayo flap:
- K-wire: 1x into distal pole of scaphoid and 1x into lunate (converging) – site the wires parallel to the concavity of the lunate (in normal reduced anatomy this wire should then be at 90degrees so acts to aide fracture reduction. Then bend wires towards eachother and this will reduce the scapho-lunate joint.
- Then use a scapholunate wire to protect the SLL, triquetrolunate wire to protect lunotriquetral ligament, then scaphocapitate and triquetrohamate to stabilise mid-carpal row.
Then move on to soft tissue reconstruction e.g. suture anchors/Miteks etc
Greater arc injuries: fix bone 1st, work proximal to distal i.e. radius then scaphoid, then reconstruct ligaments.
Outcomes: 75% range of movement, 75% grip strength (according to retrospective 10 year follow up – Forli et al)
24.
Which of these structures is NOT part of the triangular fibrocartilage complex?
A. Meniscus homolog
B. ECU subsheath
C. Radioscaphocapitate ligament
D. Ulnotriquetral ligament
E. Radioulnar ligament
Answer: C. Radioscaphocapitate ligament
TFCC is made up of:
- Dorsal and volar radioulnar ligaments: deep ligaments, known as ligamentum subcruetum, which insert into the ulnar fovea, and superficial fibres that insert in the ulnar styloid. They originate at the sigmoid notch of the radius and converge at the base of the ulna styloid.
- Central articular disc
- Meniscus homolog
- Ulna collateral ligament
- ECU subsheath
- Origin of ulnolunate and ulnotriquetral ligaments
The periphery is well vascularised, whereas the central portion is avascular.
TFCC injury is a common cause of ulnar-sided wrist pain, diagnosis is pain worse on ulnar deviation and a positive ‘fovea’ sign, MRI can confirm the diagnosis, although arthroscopy remains the most accurate method of diagnosis.
Type 1 traumatic injury: most common mechanism is a fall on extended wrist with forearm pronation or a traction injury to the ulnar wrist.
Type 2 degenerative injury: associated with positive ulnar variance and ulnocarpal impaction.
Treatment is generally conservative (NSAIDS and immobilisation). Surgical debridement, TFCC repair or ulnar shortening procedures may be indicated depending on severity of symptoms and underlying cause.