Pediatric Ortho Flashcards
Pediatric Orthopedic Conditions
Torticollis Scoliosis Nursemaid’s elbow Transient Synovitis Little league elbow Club Foot Rotational/Angular deformities of the legs Legg-Calves-Perthes Disease SCFE Developmental dysplasia of hip Osgood Schlatter’s Disease Sever’s disease Osteogenesis Imperfecta
Torticollis
contraction or contracture of the muscles of the neck that occurs and causes the head to be tilted to one side
Rotation of the chin to the opposite side of the contraction
>80% are congenital in nature the rest is trauma/disease
Congenital Torticollis
More common following breech deliveries
Can be associated w/ hip dysplasia and clubfoot
Unilateral contracture of SCM muscle
Fibrosis of SCM occurs w/ a resultant palpable “mass” in the SCM muscle
Mass resolves w/in a few weeks after birth, but it results in a shortened and contracted SCM
If untreated, facial asymmetry/skull deformity (plagiocephally) can occur as well as changes in the cervical vertebrae
Diagnosis for Congenital Torticollis
Clinical diagnosis based on physical examination and palpable “mass” of SCM muscle
X-ray of cervical spine recommended
Treatment for Congenital Torticollis
Conservative: stretching exercises several times/day to regain full ROM
May need Doc-band to help improve secondary plagiocephaly
Surgery: for patients who fail conservative treatment or those who are diagnosed late
Release of SCM muscle traction/casting and exercises
Plagiocephaly
Skull deformity that occurs secondary to external forces on the skull either in utero or during infancy
Scoliosis
Lateral curvature of the spine in the upright position
Usually accompanied by rotation as well as an increase in the normal kyphosis (thoracic) or lordosis (lumbar) of the spine
-occurs in 1-3% of population
Structural Classification of Scoliosis
Fixed, nonflexible, does not correct w/ side bending
Etiology:
Idiopathic (mechanism unknown, appears hereditary)- 80%
Congenital abnormalities
Neuromuscular (ex. Cerebral palsy, muscular dystrophy)
Dysmorphic syndromes (Neurofibromatosis, Marfan’s, osteogenesis imperfecta)
Non Structural Classification of Scoliosis
Flexible and corrects w/ side bending
Etiology:
Compensation d/t leg length discrepencies, local inflammation, muscle spasms
Idiopathic Scoliosis
4-5 times more common in girls
Serious curvatures are more frequent in fm
Progresses during rapid skeletal growth
Curve must be greater than 10 degrees
Right thoracic curvature is most common
Left thoracic curvature likely indicates a spinal disorder
Complications of Idiopathic Scoliosis
Cardiopulmonary dysfunction (most serious)
Progressive deformity
Pain with aging
Disability
Classification by age of idiopathic scoliosis
Infantile Occurs by age 3 M>Fm Usually resolves spontaneously Juvenile Occurs b/w ages 4-10 years Adolescent- MOST COMMON Occurs b/w age 10 until skeletal maturity Most significant and prevalent form Fm>M (girls age 10-12y and boys 14-16y)
Signs and Symptoms of Idiopathic Scoliosis
Usually asymptomatic
Pain is rare and if present is a red flag (look for secondary cause)
Diagnosis of Idiopathic Scoliosis
Confirmed with a standing (AP and lateral) X-ray of entire spine
Determine Cobb angle
Angle of spinal curvature
Identify the upper and lower end vertebrae of curve
Draw a line parallel to the end plate of each vertebrae
The angle at which they intersect is the Cobb angle
Risser Sign (skeletal maturity)
Sensitive indicator of skeletal maturity
Ossification progresses from lateral to medial (SI joint)
MRI for Idiopathic Scoliosis
Indicated if a secondary cause is suspected:
Significant pain
Abnormal neurological symptoms
Left thoracic curve (associated w/ spinal disorder)
Rapid progression
Progressive Facts for idiopathic scoliosis
Curves >20 degrees tend to progress in the young
Curves < 30 degrees at maturity have minimal progression as adults
Respiratory symptoms rarely develop in curves < 60 degrees
The greater the curve and the younger the patient, the more likely the curve will progress
Progression is more common in young children who are beginning their growth spurt
Curves in adolescent females are more likely to progress
Treatment for idiopathic scoliosis
Early detection is key to prevent progression
Referral to a specialist is mandatory for all patients
Depends on the age of the patient and the angle of the curve
Non-surgical treatment methods will not fully correct the curve (it may improve the curve in some cases), but will prevent progression of the curve and maintain flexibility
Surgical treatment will correct the curve, but it also reduces flexibility
Immature and Older children idiopathic scoliosis treatment
Immature patients:
Observation every 6-12 months till the curve reaches 20 degrees
Curves >20-25 degrees will require treatment
Older child (growth has slowed)
Observation if a small curve is present b/c it is less likely to progress
Non surgical treatment for idiopathic scoliosis
Spinal Bracing
Indicated in curves <20 degrees if they are progressing
Indicated in curves between 20-40 degrees, particularly in a skeletally immature patient
Ex. Milwaukee Brace and Thoracolumbosacral orthotic (TLSO)
23 hours/day for 2 years or longer
Exercises while in the brace to improve appearance and decrease the curve
Surgical Treatment for idiopathic scoliosis
Indicated for curves >45 degrees
2 components:
Deformity correction with intraoperative instrumentation
Spinal fusion
Success rates are high
Results in decreased spine motion which can be quite limiting
Nursemaids/ pulled elbow
Head of the radius subluxes distally through the annular ligament
Etiology of Nursemaids/ pulled elbow
Children age 1-3 are most affected, rare after age 6
Etiology
Toddler being pulled or swung by an extended arm (longitudinal traction w/ elbow extended and forearm pronated)
Trauma
Clinical Signs and Symptoms of Nursemaid elbow
May hear a snap when the radial head subluxes
Immediate elbow pain that increase w/ movement
Arm is held with the elbow flexed and the forearm pronated
Tenderness to radial head
Diagnosis and imaging for nursemaid elbow
Clinical diagnosis based on history and PE
Imaging
Typically not indicated unless the history suggests trauma or an unusual mechanism
Usually appear normal
Presumably d/t spontaneous reduction before or during the X-ray with radiographic positioning
Treatment for Nursemaids elbow
Reduction
Start w/ the elbow extended and the forearm pronated
Supinate the forearm and flex the elbow simultaneously while applying manual pressure over the radial head
A palpable click can be palpated when reduction occurs
Pain resolves immediately and the toddler will start using the arm
Immobilization is not recommended following the injury except for recurrent subluxations
Little League Elbow
A traction injury to the medial epicondylar physis related to repetitive throwing
Pathophysiology
Repetitive valgus stress results in shearing, inflammation, traction and abnormal bone development
Symptoms of Little League Elbow
Acute or gradual Acute suggests avulsion injury Pain to medial epicondyle Swelling Stiffness Decrease in performance Weakness
Signs of Little League Elbow
Tenderness to medial epicondyle
Pain worsened by valgus stress
May have decreased range of motion (ROM)
Wrist flexion and forearm pronation may bring on pain
Diagnosis of Little League Elbow
Imaging is not required but an X-raymay show widening of the apophysis
Treatment of Little League Elbow
Complete rest from throwing activities
Stretching and strengthening (PT) is helpful
Prevention is key (proper throwing mechanics, proper conditioning, limiting # of pitches and 3-4 days of rest b/w games pitched)
Dysplasia
abnormal growth or development
Dislocated Hip
Femoral head is not in contact with the acetabulum
Subluxation of hip
Femoral head is w/in the acetabulum but can partially come out of the socket w/ a provocative maneuver
Development of dysplasia of the hip
Term used to describe a spectrum of hip disorders in young children
Congenital hip dysplasia is the most common
Others include conditions associated with neuromuscular abnormalities
98% of the cases are reversible
2% are severe and irreversible
Epidemiology for dysplasia of the hip
Incidence: 1-2 cases per 1,000 live births in the US
Frequently bilateral
Females > Males
Left hip > Right hip
RF for dysplasia of the hip
First born child Female born in breech position musculoskeletal abnormalities (metatarsus adductus, clubfoot and torticollis) Certain syndromes (Trisomy 21) FH of DDH
congenital dysplasia of the hip
Hip is fully formed by 11th weeks of gestation
Proper growth of the acetabulum requires a round femoral head
In congenital dysplasia, the hip forms normally but dislocates around the time of birth
Once the normal articulation is disrupted, the acetabulum and femoral head grow abnormally and this will progress if not treated early
Acetabulum shallower, saucerlike
Femoral head flattened and anteverted
Joint capsule loose/lax
prognosis for dysplasia of the hip
If untreated, leads to deformity, disability and painful arthritis in adults
Early diagnosis and early intervention is KEY
Signs/symptoms for dysplasia of the hip
Very subtle and can be easily missed
In infants, you can’t see any abnormality, you can only feel it
In children 3-12 months (not walking)
Restricted hip abduction is the hallmark sign
Shortening of thigh compared to contralateral side
Abnormal skin folds
Unilateral Signs/symptoms of dysplasia of the hip in an older child
Unilateral
Painless limp and a lurch to the affected side
Leg length discrepency
Positive Trendelenburg sign (weakness of gluteus medius)
Bilateral Signs/symptoms of dysplasia of the hip in an older child
Loss of hip abduction
Waddling gait
Flexion contracture of the hips with secondary hyperlordosis of lumbar spine
Infant hip exam with 2 special tests
Examine one hip at a time
Examine supine on exam table
Examine the patient when they are calm and comfortable
2 tests should be performed:
Barlow Maneuver- hip is purposefully dislocated and then reduced by doing the Ortolani Maneuver
Ortolani Maneuver- Gentle reduction of the dislocated hip
Barlow Maneuver
Loosen the diaper but do not remove completely
Stabilize the pelvis by grasping the pubic symphysis and sacrum firmly w/ one hand
Place your examining hand on the baby’s bare thigh w/ your thumb along the medial thigh, your fingers along the lateral thigh and your first web space or index finger over the anterior knee
Flex the hip to 90 degrees and slight adduction, create an axial load along the femur using the first web space or index finger
Trying to push the femoral head posteriorly out of the acetabulum over the posterior rim
You would be able to feel the dislocation w/ the tip of your index finger/ring finger
Ortolani Maneuver
Hands are in the same position as in the Barlow Maneuver
Widely abduct the hip
Palpate the greater trochanter as you abduct the hip and reduce the hip into the socket
A palpable clunk of the femoral head as it reduces back into the acetabulum is a positive Ortolani sign
Imaging for Dysplasia of the hip
Not reliable in children < 6 weeks of age
6 weeks to 4 months: Ultrasound is the imaging test of choice
>6 months: X-ray is the imaging test of choice
Treatment for Dysplasia of the hip
Short window of opportunity for conservative treatment; therefore early diagnosis is key
The sooner the hip can be reduced and maintained, the better the outcome
Birth to 6 weeks is the most opportune time
Birth to 6 months:
Pavlik harness- gold standard
Maintains hip flexion of 100 degrees and prevents adduction
Safe and effective in 80-90% of cases
Worn several weeks until the hip is stable
Treatment Surgery for Dysplasia of the hip
Failure to obtain or maintain a stable reduction
Dislocated hips that are missed
Closed or open reduction and casting +/- osteotomy
Delays in treatment make reduction more difficult and complicated
Legg Calve Perthes Disease (LCPD)
Disruption of blood supply to the femoral head resulting in avascular necrosis of the proximal femoral head
Avascular necrosis- necrosis of bone followed by replacement of new bone
Epidemiology of LCPD
Highest incidence b/w the ages of 4-10
M>Fm (4:1)
Bilateral in 15% of cases
Early/Initial Stage for LCPD
Synovitis of hip joint w/ effusion and early ischemic changes in the ossific nucleus of the femoral head
X-ray shows joint swelling and possible lateral displacement of the femoral head d/t swelling
Femoral head appears denser
Mean duration- 6 months
Regenerative/Fragmentation Stage LCPD
Necrotic area begins to be replaced by new bone
X-ray shows fragmentation and compression of the femoral head w/ widening of the femoral neck
Duration- 1 to 2 years
Reossification Stage LCPD
Femoral head starts healing (shape may be normal or irregular and flat (coxa plana))
Complications for LCPD
Osteoarthritis if untreated
Permanent femoral head deformity (affects motion and gait)
Symptoms for LCPD
Onset is gradual Mild hip pain Referred knee/thigh pain Limp Limited ROM Pain is relieved by rest and aggravated by weightbearing
Signs of LCPD
Decreased abduction and IR
Tenderness over the anterior hip joint
+/- Leg length discrepency
+/- Thigh and calf muscle atrophy
Imaging used for LCPD
X-ray: Gold standard
AP and lateral frog view of both hips
MRI: Can assess the extent of the necrosis
Treatment Goals for LCPD
Ultimate Goal: to prevent deformity of the femoral head while healing which decreases risk of DJD
Initial Goal: relieve pain and maintain ROM
Rest
Treatment based on age for LCPD
6 years/older child:
Abduction brace to keep the femoral head w/in the acetabulum (helps mold the femoral head and prevent deformity)
Worn continuously for up to 2 years
Surgery in select cases
Prognosis depends on what for LCPD
Age of onset
Degree of involvement
Adequacy of treatment
Slipped Capital Femoral Epiphysis (SCFE)
Displacement of the proximal femoral epiphysis due to disruption of the grown plate
Results in upward and anterior displacement of the femoral neck
Bilateral in 25% of cases (up to 1-2 years after the initial episode)
Can occur acutely in the setting of trauma (Salter I fracture)
Primarily gradual onset
Epidemiology of SCFE
Uncommon
Most common in boys 10-17 years old (during rapid growth spurt)
Occurs earlier in females d/t advanced skeletal maturity
More common in African Americans
Occurs more commonly in 2 body types:
Overweight/obese adolescents
Tall and thin
Etiology of SCFE
Trauma (acute slippage)
Suspected to be hormonal (gradual slippage)
Has been associated with hypothyroidism
Complications for SCFE
Traumatic cases have a worse prognosis Avascular necrosis severe arthritis Gradual cases Does not commonly cause avascular necrosis Slight leg shortening Mild external rotation deformity Osteoarthritis if delayed treatment
Symptoms of SCFE
Hip/groin pain Referred medial knee pain Limp Usually gradual onset of symptoms over weeks/months Sudden if d/t trauma
Signs of SCFE
Antalgic gait
Tenderness over hip
External rotation deformity (toing out)
Limited ROM (IR, abduction, flexion)
Imaging for SCFE
X-ray imaging (AP and lateral views- both hips)
Preslippage:
Widening of the epiphyseal plate and joint swelling
Slippage:
Displacement of the femoral head
Best seen on lateral view
Klein’s line (X-ray finding)
Think of it as an ice cream scoop slipping off a cone
Treatment for SCFE
Refer to orthopedic surgeon immediately
Non-weightbearing with crutches
Surgery:
May have traction prior to surgery to reduce the slip
Internal fixation of the head of the femur to the neck of the femur (pinning)
Non-weightbearing for several months till the epiphyseal place closes
Prognosis and Prophylaxis for SCFE
Good particularly in a gradual slip Poor if d/t an acute, traumatic slip Prophylaxis Pinning of contralateral hip (controversial) Not recommended
Transient Synovitis of Hip
Self-limited, nonspecific synovial inflammation of the hip joint resulting in a joint effusion
Most common cause of hip pain in children Fm
Cause is unknown (viral infection suspected-URI/GI in prior 4 weeks)
Diagnosis of exclusion
Symptoms of Transient Synovitis of Hip
Acute onset
Hip/groin pain
Referred knee pain
Limp or refusal to WB
Signs of Transient Synovitis of Hip
Temp of 37.3-38.2C may be present
Hip held in slight flexion, abduction and ER
Decreased ROM
Diagnosis of Transient Synovitis of Hip
Rule out other hip pathology such as septic hip, SCFE, LCPD, developmental conditions, trauma, osteomyelitis
Observation alone if child is well-appearing, afebrile, mobile, symptoms <48hrs and a reliable caretaker
F/U in 48 hours: if improving or symptoms resolve w/in 1 week, diagnosis is confirmed
Clinical Intervention for Transient Synovitis of Hip
child is ill appearing, immobile, febrile, or the pain is rapidly progressing, then w/u required:
Clinical Intervention
Labs (CBC, ESR, CRP, aspiration of joint fluid w/ cx)
Imaging
X-ray to r/o Fracture, SCFE, LCPD, osteomyelitis
U/S to detect effusion and for guidance during arthrocentesis
Does not differentiate transient synovitis from septic arthritis
Treatment and Follow up for Transient Synovitis of the Hip
Treatment Conservative treatment Rest NSAIDS (ibuprofen) Non-weightbearing till symptoms improve
Follow Up
Within 48 hours and 1 week to confirm symptom improvement
Repeat X-ray at 6 weeks to assess for LCPD or sooner if persistent limp/pain
Angular/Rotational Deformities of Legs
Genu Varum Blount’s Disease Genu Valgum In-Toeing: MOST COMMON Internal Tibial Torsion Metatarsus Adductus Femoral Anteversion Out-Toeing Femoral Retroversion (external femoral torsion) External Tibial Torsion Flat Feet
Genu Varum
Bowleg”
Normal till age 3
Usually secondary to tibial rotation
Refer if persists past age 2, worsens rather than improves, occurs in only 1 leg
Blount’s Disease
Pathologic, developmental bowing secondary to disrupted growth of the upper medial tibial epiphysis
Etiology unknown
More common in obese early walkers and African Americans and positive FH
May be unilateral or bilateral
2 forms:
Infantile- begins before age 3
Adolescent- begins after age 8
Progressively worsens unlike physiological bowing
Tx: Bracing if started early (<3yr) and Surgery
Genu Valgum
“Knock-knee”
Occurs from age 3-8 years of age
May be caused by skeletal dysplasia and rickets
Refer if persists past age 8, worsens rather than improves, occurs in only 1 leg, or if associated with short stature
Usually resolves, though bracing and/or osteotomy may be necessary
Toeing in
Most common rotational deformity
Etiology:
Metatarsus adductus/varus of foot in infants
Internal tibial torsion in toddler
Increased femoral torsion in child >10 yrs old
Most are benign and self-limited
Tx: reassurance and education of parents
Toeing In: Internal Tibial Torsion
Toeing in”
Rotation of the lower leg b/w the knee and ankle
Normal at birth (20 degrees) but returns to neutral by 16 months
Can be increased by laxity of knee ligaments
Present if toeing in and patella faces straight forward (deformity is distal to knee)
Self-limiting and resolves by itself w/ increased growth
Stretching and corrective shoes show no benefit
Toeing In: Metatarsus Varus
Lateral border of foot is convex and medial border is concave
Vertical crease in medial aspect of arch if rigid
10-15% of cases have associated hip dysplasia
Treatment depends on if the deformity is fixed
If flexible- stretching exercises and wearing a straight/reverse shoe is helpful
If fixed (unable to passively correct)- corrective casts if caught early, otherwise surgery
Toeing In: Femoral Anteversion
“Toeing in” beyond age 2-3 years old
More internal rotation of the hip than external rotation
Present if toeing in and the patella faces medially (deformity proximal to knee)
Improves with growth
External rotation exercises are encouraged (bike riding, skating)
Out Toeing and Treatment
Often associated w/ genu valgum
May be aggravated by sleeping in prone position and using wide diapers
Treatment
Observation and reassurance
Avoid wide diapers and wide canvas slings
stretching
Osgood-Schlatter’s Disease
Disturbance of the patella tendon attachment to the tibial tubercle apophysis
Early adolescent males are most commonly affected
20% occur bilaterally
Common cause of knee pain in adolescents
Most common in athletic adolescents (running sports, jumping sports, etc)
Osgood-Schlatter’s Disease Etiology
Unknown, suspect partial avulsion
Contributing factors:
Repetitive micro-avulsion (overuse) of tibial tubercle
Traction-type injury on apophysis where patella tendon attaches (tendon growth can’t keep up with bone growth)
Osgood-Schlatter’s Disease Background
Proximal tibial epiphysis fuses to the shaft of the femur by age 20.
B/w the ages of 7-14 year, an extension of the epiphysis is visible on X-ray and forms the anterior tibial tuberosity
Anterior tibial tuberosity is where the patella tendon attaches
Osgood-Schlatter’s Disease Pathophys
Localized traction tendonitis as a result of constant traction of the patella tendon at it’s insertion avulsion of small amounts of cartilage and bone
Recurrent irritation of the growth plate by the patella tendon from repetitive injury chronic inflammation
Osgood-Schlatter’s Disease Complications
Osteoarthritis (OA)
Painful ossicle in the distal patella tendon
Painful kneeling
Displaced avulsion fracture of tibial tubercle
Permanent bump (“Knobby knees”) at tibial tubercle
Osgood-Schlatter’s Disease Signs/ Symptoms
Anterior knee pain (point over tibial tubercle)
Swelling over tibial tubercle
Pain worsened by kneeling, squatting and going up/down stairs
Point tenderness over tibial tubercle
Often with a noticable lump
Often bilateral
Osgood-Schlatter’s Disease Diagnosis
Clinical based on hx and examination
X-rays not indicated unless acute onset of pain or following trauma to r/o an avulsion fracture
May be normal or may show fragmentation at tibial tubercle
Osgood-Schlatter’s Disease Treatment
Conservative
Activity restriction, ice, NSAIDS, protective padding, quad/hamstring stretching and strengthening and time
May take several months to resolve
Condition heals once the epiphysis closes
Prognosis for Osgood Schlatter’s Disease
Excellent
Bony prominence will persist into adulthood
May get minor pain when kneeling
Severs Disease
AKA Calcaneal apophysitis
Similar in nature to Osgood-Schlatter’s Disease
Definition:
Low grade inflammation at the insertion of the Achilles tendon to the calcaneal apophysis
More common in boys aged 8-14 years old
Often bilateral
Common in high impact activities/sports
Sever’s Disease Etiology
Overuse
Improper footwear
Tightness in calf muscle and achilles tendon
Signs/ Symptoms of Sever’s Disease
Local pain, tenderness and swelling to the heal over the apophysis
Pain is aggravated by activity
Imaging and Diagnosis for Sever’s Disease
Imaging:
X-ray not always indicated but will reveal sclerosis of the apophysis
Diagnosis:
Clinical based on history and examination
Treatment and Prognosis for Sever’s Disease
Treatment:
NSAIDS, ice, activity restriction, heel cord stretching, calf strengthening
Heel cup (insert) may help
Brief immobilization with a walking boot or cast for rare, resistant cases followed by PT
Prognosis:
Excellent
Self limiting
Club Foot
AKA: Talipes Equinovarus Occurs in 1:1000 live births More frequent in males 3 categories: Idiopathic May be hereditary Neurogenic Associated with syndromes (arthrogryposis and Larsen syndrome)
3 Features used for Clinical Diagnosis for Club Foot
3 features must be present: Plantar flexion of the foot at the ankle joint (equinus) Inversion deformity of the heel (varus) Medial deviation of the forefoot (varus) Other common features: Unable to dorsiflex ankle >90 degrees Foot resists realignment Calf muscle may be shortened and underdeveloped
Treatment for Club foot depending on age
Newborn to 3 months- serial casting
3-6 months- serial casting and possible surgery
6-9 months- surgical release of soft tissue
>18 months- Bone surgery
>4 years- tendon transfers if recurrent
Treatment for Club Foot
Treatment:
The earlier the treatment, the faster the correction
Need to have patience!!
Stretch the contracted tissues followed by casting to hold the correction
Long term treatment:
Night braces may be necessary for several years
Osteogenesis Imperfecta (OI)
Rare genetic connective tissue disorder characterized by multiple and recurrent fractures
Multiple types (I-VII) with varying degrees of illness
Type I is most common
Some types result in fetal death (Type II)
Affected patients are frequently suspected of having suffered child abuse
Common PE findings for OI
Moderately affected children have numerous fractures and are dwarted due to bony deformities and growth retardation Common PE findings: Blue sclera Thin skin Hyperextensibility of ligaments Otosclerosis w/ hearing loss Hypoplastic and deformed teeth Wormian bones (accessory skull bones that are completely surrounded by cranial sutures)
Prognosis of OI
Depends on the type
Type I: Patients attain normal height with minimal functional limitations
Type II: fatal in perinatal period
Remainder of types results in decreased height, they can be fully mobile to completely wheelchair bound depending on the type
Diagnosis and Treatment of OI
Diagnosis:
Genetic testing and X-ray findings
Treatment:
Bisphosphonates to decrease incidence of fractures
Surgery to correct deformities of long bones
Preventive measures: intramedullary rod placement to prevent deformity from fracture malunion
