Pediatric MSK – FNP Prep

Newborn · Packaging Deformities

Congenital Packaging Deformities

Caused by intrauterine positioning — tight quarters, oligohydramnios, multiple gestation. Most resolve with stretching or time.

🎨 Analogy

Think of a baby in utero as a letter folded and stuffed into an envelope that's slightly too small. When there's not enough fluid or space, body parts get pressed into abnormal positions for weeks or months. At birth the "crease" is still there — but unlike a permanent fold, most of these packaging deformities unfold with time and gentle stretching, because the underlying bones and joints are completely normal.

Congenital Muscular Torticollis

Key Facts

Fibrosis/shortening of the sternocleidomastoid (SCM) muscle
Head tilts toward affected side, chin rotates away
May palpate firm SCM "mass" or "olive" in newborn
Associated: difficult delivery, forceps, breech presentation
Can cause plagiocephaly (asymmetric head shape) if untreated
Rule out: atlantoaxial instability, bony anomaly (Klippel-Feil), ocular torticollis

Management

Stretching exercises — first line; begin early (passive ROM, tilt head away from affected side)
Refer to PT if not improving by 1–2 months
Helmet therapy for significant plagiocephaly
Surgical SCM release if refractory (>12–18 months with no improvement)
Excellent prognosis if treated early

Congenital Talipes Equinovarus (Clubfoot)

Key Facts

Foot fixed in: equinus (plantar flexion) + varus (heel inward) + forefoot adduction + cavus
Mnemonic: CAVE — Cavus, Adductus, Varus, Equinus
1–2:1000 live births; male > female; bilateral 50%
Idiopathic (most common) vs. positional vs. teratologic (spina bifida, arthrogryposis)
Cannot be passively corrected (distinguishes from positional)

Management

Ponseti method — gold standard: serial casting × 6–8 weeks
Percutaneous Achilles tenotomy in 80–90% to correct equinus
Foot abduction brace (FAB) worn 23h/day × 3 months → nighttime until age 4–5
Surgery reserved for refractory/relapsed cases
Begin treatment within first weeks of life

Metatarsus Adductus

Key Facts

Forefoot turned inward (adducted) — most common foot deformity in infants
Heel and ankle are normal (distinguishes from clubfoot)
Flexible (passively correctable) vs. rigid
Associated with DDH — always examine hips!
Most cases resolve spontaneously by age 3–4

Management

Flexible: reassurance, gentle stretching — resolves spontaneously
Rigid: serial casting or corrective shoes
Surgery rare — only for persistent rigid deformity in older child
Always examine hips (associated DDH in 2–10%)

Newborn–Infant · Hip

Developmental Dysplasia of the Hip (DDH)

A spectrum from mild instability to frank dislocation — catch it early, treat it early.

🎨 Analogy

The hip is a ball-and-socket joint. In DDH, the socket (acetabulum) is too shallow — like a golf ball sitting on a barely-curved tee instead of nestled in a proper cup. The ball can wobble, sublux, or fully dislocate. The critical window is infancy: the socket is still cartilage and remodels beautifully around a correctly-positioned ball. Miss the window, and you're working with hardened bone — much harder to reshape, requiring surgery instead of a simple harness.

Risk Factors & Who

Female > Male (6:1) — ligamentous laxity from maternal estrogen
Firstborn, breech presentation, oligohydramnios
Family history (10× risk)
Left hip more common (against mother's spine in L occiput anterior)
Associated: torticollis, metatarsus adductus, clubfoot

Exam Findings by Age

Newborn:
- Barlow test — adduct + posterior force → hip dislocates
- Ortolani test — abduct + anterior force → "clunk" as hip reduces
Infant (after 3 months):
- Limited hip abduction (<60°)
- Asymmetric thigh/gluteal folds
- Galeazzi sign — unequal knee heights (shorter on affected side)
Toddler/walking child:
- Trendelenburg gait, leg-length discrepancy
- Lordosis, waddling gait (bilateral)

Diagnosis

<4–6 months: Hip ultrasound — first line (bones not yet ossified)
>4–6 months: X-ray pelvis — femoral head ossified, AP view
Universal US screening controversial — targeted screening for risk factors
X-ray findings: shallow acetabulum, lateral displacement of femoral head, ↑ acetabular index

Management by Age

<6 months — Pavlik Harness ⭐

Maintains hip in flexion/abduction. Success ~95% if started early. Worn 23h/day. Monitor with US.

6–18 months — Closed reduction + spica cast

If Pavlik fails or late presentation. Under anesthesia.

>18 months — Open reduction ± osteotomy

Surgical. More complex. Acetabuloplasty if socket severely dysplastic.

⚠️ Board Sequence

Barlow = dislocates the hip. Ortolani = reduces it back. "Barlow Out, Ortolani In." Clunk = abnormal (vs. click = benign ligamentous).

Injuries · All Ages

Sprains · Strains · Fractures · Dislocations · Overuse

Sprains & Strains

Definitions & Grading

Sprain — ligament injury (bone-to-bone)
Strain — muscle or tendon injury (muscle-to-bone)
Grade I: microscopic tear, mild pain, no instability
Grade II: partial tear, moderate pain, mild instability
Grade III: complete tear, severe pain, frank instability → may need surgery
In children: physeal fractures more common than ligament tears — the growth plate is weaker than the ligament!

Management

RICE: Rest, Ice, Compression, Elevation
NSAIDs for pain/inflammation
Grade I–II: functional rehab, progressive weight-bearing
Grade III or physeal injury: ortho referral, possible immobilization/surgery
Always X-ray to rule out fracture in children — especially at growth plates

Fractures — Pediatric Pearls

Salter-Harris Classification ⭐

Growth plate (physeal) fractures — unique to children
Type I: through physis only — X-ray may be normal! Tenderness over growth plate = treat as fracture
Type II: through physis + metaphysis — most common (75%)
Type III: through physis + epiphysis — intraarticular
Type IV: through metaphysis + physis + epiphysis
Type V: crush injury of physis — worst prognosis, growth arrest
Mnemonic: SALTR — Straight, Above, Lower, Through, Ram (crush)

Pediatric Fracture Types

Greenstick: incomplete — cortex breaks one side, bends other. Like a green branch.
Torus (buckle): cortex buckles on compression side — very common, stable
Plastic deformation: bone bends without breaking — forearm bones
Toddler's fracture: spiral tibial fracture in toddlers from twisting — normal mechanism, but consider NAT if story doesn't fit
Clavicle fractures: most common fracture in children — usually mid-shaft, arm sling

⚠️ Non-Accidental Trauma (NAT)

Fractures highly concerning for abuse:
- Posterior rib fractures
- Classic metaphyseal lesions (corner/bucket-handle)
- Multiple fractures in different stages of healing
- Spiral fractures in non-ambulatory children
- Fractures inconsistent with history or developmental stage
Always get skeletal survey + ophthalmology (retinal hemorrhages)

Overuse Syndromes

Osgood-Schlatter Disease

Apophysitis of tibial tubercle — overuse traction injury at patellar tendon insertion
Active adolescents, males 12–15, females 8–12 (growth spurts)
Anterior knee pain ↑ with activity, ↓ with rest
Tender prominence at tibial tubercle
Tx: activity modification, stretching quads/hamstrings, NSAIDs, ice — self-limited

Sever's Disease

Apophysitis of calcaneal apophysis — Achilles tendon traction on heel growth plate
Active children 8–14, peak growth spurt
Heel pain with activity, bilateral common
Tender at posterior heel with medial-lateral squeeze
Tx: heel cups/lifts, stretching Achilles, activity modification, NSAIDs

Little League Elbow & Shoulder

Little League Elbow: medial epicondyle apophysitis from valgus overload — overhead/throwing athletes
Little League Shoulder: proximal humeral physeal stress fracture — shoulder pain with throwing
Both: rest from throwing, PT, gradual return
Pitch count limits recommended — prevention is key

Spinal · Adolescent

Adolescent Idiopathic Scoliosis (AIS)

Lateral curvature of the spine — screen every adolescent, manage based on curve magnitude.

Key Facts

Lateral spinal curve ≥10° (Cobb angle) with vertebral rotation
Most common spinal deformity in children — 2–3% prevalence
Female > Male (progression risk); onset typically 10–12 years
"Idiopathic" — no known cause; genetic component
Right thoracic curve most common
Risk of progression: ↑ with remaining growth, larger initial curve, female sex

Screening & Diagnosis

Adam's forward bend test — child bends forward, observe from behind for rib hump (trunk rotation)
Scoliometer reading ≥7° → refer for X-ray
Standing PA X-ray — Cobb angle measurement
MRI if: atypical curve (left thoracic), rapid progression, neurologic symptoms, or <10 years old
Leg length discrepancy can cause functional scoliosis (not structural)

Management by Cobb Angle

<20° — Observation

Repeat X-ray every 4–6 months during growth. No treatment needed unless progressing.

20–40° + still growing — Bracing ⭐

TLSO brace (Boston brace or similar). Slows progression — does NOT correct curve. Worn 16–23h/day until skeletal maturity.

>45–50° — Surgical fusion

Posterior spinal fusion. Prevents cardiopulmonary compromise. Consider if >40° with significant remaining growth.

Red Flags (Not AIS)

Left thoracic curve → rule out intraspinal pathology (syrinx, Chiari)
Rapid progression (>5°/6 months)
Pain (AIS is usually painless)
Neurologic signs (weakness, bowel/bladder)
Age <10 → consider congenital or neuromuscular scoliosis

Lower Extremity · Normal Variants vs. Pathology

Genu Varum · Genu Valgum · In-Toeing · Idiopathic Toe-Walking

🎨 Analogy

A child's lower extremities follow a predictable developmental arc — like a pendulum swinging through normal positions before settling in the center. Newborns are bowed (physiologic genu varum), toddlers correct, then swing knock-kneed (genu valgum) around age 3–4, then straighten again by age 6–7. This is the developmental pendulum — not pathology, just timing. The question is always: is this child on the arc, or off it?

Condition	Age / Normal Peak	Features	When to Worry	Management
Genu Varum (bow-legs)	Normal until age 2	Legs bow outward; physiologic in infants/toddlers	Persistent after age 2, unilateral, asymmetric, short stature → Blount's disease, rickets	Reassurance if physiologic; Blount's → bracing or osteotomy
Genu Valgum (knock-knees)	Normal age 3–5; resolves by 7–8	Knees touch, feet apart; peak age 3–4	Severe (>10cm intermalleolar distance), asymmetric, persistence beyond age 8, obesity	Reassurance if physiologic; severe → ortho referral
In-Toeing	Varies by cause	Toes point inward with walking	Unilateral, painful, rigid, not improving	Cause-specific (see below)
Idiopathic Toe-Walking	Persistent after age 2–3	Walks on tiptoes, bilateral, flexible ankle	Unilateral, rigid, neurologic signs → rule out CP, autism, tethered cord, muscular dystrophy	Serial casting, Botox, AFOs; surgery if severe contracture

In-Toeing — Causes by Age

Metatarsus Adductus (Infant)

Forefoot adduction; heel normal
Most common cause of in-toeing in infants
Flexible: resolves spontaneously
Rigid: serial casting

Internal Tibial Torsion (Toddler)

Tibia rotated inward — most common cause in toddlers
Thigh-foot angle negative (< –10°)
Resolves spontaneously by age 4–5
No treatment needed; reassure parents

Femoral Anteversion (School-Age)

Increased internal rotation of femur — "W sitting" posture
Most common cause in school-age children
Wide range of internal hip rotation, limited external rotation
Resolves by adolescence in most cases
No treatment for physiologic; reassure

Pediatric Hip Disorders

SCFE · Legg-Calvé-Perthes Disease

SCFE — Quick Review

Obese adolescent, 10–16 years, male > female
Posterior-inferior slip of femoral epiphysis at physis
Obligate external rotation with hip flexion (Drehmann sign)
Knee pain = referred pain — always examine the hip!
X-ray: Klein's line fails to intersect epiphysis; "ice cream off cone"
Non-weight-bearing + urgent ortho; in situ pinning, never reduce
Unstable = surgical emergency (AVN risk up to 50%)
SCFE without obesity or <10 years → endocrine workup

Legg-Calvé-Perthes Disease (LCPD)

Idiopathic avascular necrosis of the femoral head — unknown etiology
Age: 4–8 years; Male > Female (4:1)
Gradual onset limp, hip/groin pain, ↓ internal rotation and abduction
Bilateral in 10–12% (sequential, not simultaneous)
X-ray: flattened, fragmented, sclerotic femoral head
MRI: most sensitive early (shows AVN before X-ray changes)
Bone scan: "cold spot" early

LCPD — Management

Goal: containment — keep femoral head inside acetabulum while it heals and remodels
<6 years: observation, activity restriction, NSAIDs — good prognosis
>8 years or severe: surgical containment (femoral/pelvic osteotomy)
Bracing (Petrie cast/abduction brace) — moderate evidence
Prognosis: younger age at onset = better remodeling potential
Complications: coxa magna, early OA, femoral head deformity

Hip Disorders — Rapid Differential

Condition	Age	Onset	Key Feature	X-ray	Treatment
DDH	Newborn–infant	At birth	Ortolani/Barlow+, limited abduction	Shallow acetabulum	Pavlik harness → surgery
Transient Synovitis	3–8 years	Sudden	Limp, low fever, well-appearing, self-limited	Normal (US: effusion)	NSAIDs, rest
LCPD	4–8 years	Gradual	Limp, idiopathic AVN, remodeling phase	Flattened, fragmented head	Containment ± surgery
SCFE	10–16 years	Gradual/acute	Obese, obligate ER, knee pain	Klein's line fails	In situ pinning
Septic Arthritis	Any	Sudden	Toxic, high fever, won't move hip	Joint space widening	Emergent drainage + IV abx

Infectious / Inflammatory

Osteomyelitis · Septic Arthritis · Transient Synovitis

Osteomyelitis

🎨 Analogy

Bone is like a fortified city with a wall (cortex) and an interior (medullary canal). In children, the fortification is still under construction — the rich metaphyseal blood supply and relatively sluggish sinusoidal flow near the growth plate create a perfect ambush point for bacteria. Hematogenous seeding delivers the invaders, they set up camp in the metaphysis, and inflammation spreads. The pressure inside the bone builds like a sealed pipe — and if not drained, bursts through the cortex into soft tissue (subperiosteal abscess).

Osteomyelitis — Key Facts

Most common: hematogenous spread in children
Most common site: metaphysis of long bones (distal femur, proximal tibia, proximal humerus)
Most common organism: S. aureus (all ages)
Neonates: GBS, S. aureus, gram-negatives
Sickle cell patients: Salmonella (+ S. aureus)
Puncture wound through shoe: Pseudomonas

Presentation & Diagnosis

Fever, localized bone pain, point tenderness, soft tissue swelling, refusal to use limb
Labs: ↑ WBC, ↑ ESR, ↑ CRP (ESR + CRP together most sensitive)
Blood cultures — positive in ~50%
MRI — gold standard imaging (most sensitive/specific)
X-ray: normal early (<7–10 days); periosteal elevation + lytic lesion later
Bone scan: sensitive early; "hot spot"
Bone aspiration/biopsy — definitive culture

Management

IV antibiotics → oral step-down when clinically improving + ↓ CRP
Empiric: anti-staphylococcal coverage (nafcillin, oxacillin, or vancomycin if MRSA risk)
Total duration: 4–6 weeks
Surgical drainage if: subperiosteal abscess, no response to 48–72h IV abx, adjacent septic joint
MRSA risk: community-acquired, no prior abx, severe infection → vancomycin

Septic Arthritis

Key Facts & Presentation

Surgical emergency — cartilage destruction begins within hours
Most common organism: S. aureus
Neonate: GBS; sexually active teen: N. gonorrhoeae
Most common joint: hip (especially in young children)
Presentation: fever, toxic appearance, severe joint pain, refusal to move joint, joint held in position of comfort
Hip held in: flexion, abduction, external rotation (FABER position)

Kocher Criteria (Hip)

Used to differentiate septic arthritis from transient synovitis
4 criteria:
- Fever >38.5°C
- Non-weight-bearing
- ESR >40 mm/hr
- WBC >12,000
0 criteria: <0.2% probability septic
1 criterion: ~3%
2 criteria: ~40%
3 criteria: ~93%
4 criteria: ~99.6% → go to OR
CRP >2 mg/dL added to enhance specificity

Diagnosis & Management

Joint aspiration — definitive: WBC >50,000–80,000 cells/mm³, ↑ neutrophils, ↓ glucose, + culture
Ultrasound: effusion present (also seen in transient synovitis)
MRI: distinguishes septic arthritis from adjacent osteomyelitis
Emergent surgical drainage + irrigation
IV antibiotics: anti-staphylococcal ± vancomycin
Complications: AVN (especially hip), growth disturbance, joint destruction, chronic osteomyelitis

Transient Synovitis

Key Facts

Most common cause of acute hip pain in children 3–8 years
Benign, self-limited inflammatory synovitis — often post-viral
Unilateral hip pain, limp, mildly reduced ROM
Afebrile or low-grade fever — child looks well
Labs: WBC and ESR normal or mildly elevated
Ultrasound: hip effusion (indistinguishable from early septic arthritis by imaging alone)

Transient Synovitis vs. Septic Arthritis

Use Kocher criteria — if low probability, can observe
Transient synovitis: afebrile, well-appearing, able to bear weight, normal WBC/ESR
Septic arthritis: toxic, high fever, refuses to move, ↑↑ labs
If uncertain → joint aspiration
Transient synovitis management: NSAIDs, rest, follow-up in 24–48h
Resolves in 1–4 weeks; small risk of LCPD later (<2%)

Neuromuscular · Ch 35

Cerebral Palsy · Muscular Dystrophy

Cerebral Palsy (CP)

What Is CP

Group of permanent, non-progressive disorders of movement/posture from early brain injury
Most common cause of physical disability in children
Etiology: periventricular leukomalacia (premature), hypoxic-ischemic injury, stroke, infection, kernicterus
Associated: intellectual disability, epilepsy, visual/hearing impairment, feeding difficulties

Types of CP

Spastic (most common — 70–80%): upper motor neuron; increased tone, hyperreflexia, scissor gait
Dyskinetic/athetoid: basal ganglia injury; involuntary writhing movements; associated with kernicterus
Ataxic: cerebellar; poor balance, wide-based gait
Mixed: most common combination = spastic + dyskinetic
Distribution: hemiplegia, diplegia (legs > arms, premature infants), quadriplegia (most severe)

Diagnosis & Early Signs

Clinical diagnosis — no single test
Early red flags: persistent primitive reflexes (Moro, ATNR beyond 6 months), hand preference before 18 months, hypotonia or hypertonia
MRI brain — identifies lesion in 80–90%
Hearing and vision screen, EEG if seizures, developmental evaluation

Management

Multidisciplinary: PT, OT, speech, orthotics, social work
Spasticity: baclofen (oral/intrathecal), botulinum toxin injections, selective dorsal rhizotomy
Seizure management if epilepsy present
Feeding support: GT if aspiration risk
Ortho management: hip surveillance (dislocation risk in quadriplegia), scoliosis monitoring
Non-progressive — but complications evolve with age

Muscular Dystrophy — Duchenne (DMD)

Duchenne Muscular Dystrophy

X-linked recessive — mutation in dystrophin gene (Xp21)
Males affected; females are carriers
Onset: 2–5 years
Progressive proximal muscle weakness — legs before arms
Gowers' sign — uses hands to "walk up" thighs to stand from floor ⭐
Pseudohypertrophy of calves (fat + fibrous tissue replacing muscle)
Delayed motor milestones, frequent falls, waddling gait

Diagnosis

CK (creatine kinase) — massively elevated (10–100× normal) ⭐
Genetic testing: dystrophin gene deletion/duplication
Muscle biopsy: absent dystrophin staining (if genetic testing inconclusive)
EMG: myopathic pattern
Echo + ECG: cardiomyopathy monitoring
Becker MD: milder, later onset, partial dystrophin

Management & Prognosis

Corticosteroids (prednisone/deflazacort) — slow progression, preserve function
Exon-skipping therapy (eteplirsen) — some mutations
PT, OT, orthotics, spinal bracing (scoliosis)
Cardiac: ACE inhibitors when cardiomyopathy develops
Pulmonary: nocturnal BiPAP as respiratory muscles weaken
Loss of ambulation: typically 9–12 years
Life expectancy: late 20s–30s with modern respiratory + cardiac support

Board Pearls — DMD

Boy with developmental delay, frequent falls, waddling gait → check CK first
Gowers' sign = proximal weakness, not cerebellar
Pseudohypertrophy of calves = classic; muscle replaced by fat/fibrosis
Becker MD = same gene, partial function, milder course
Female carrier: may have ↑ CK and mild weakness
Confirm with genetic testing before muscle biopsy

Board Quick Quiz · Flip to Reveal

MSK Flash Cards

tap any card to flip ↓

Newborn with head tilted to left, chin rotated right. Firm mass palpated in left neck. Diagnosis and first-line treatment?

Congenital muscular torticollis (SCM fibrosis). First-line: passive stretching exercises + PT referral. Surgery only if refractory after 12–18 months.

What does CAVE stand for in clubfoot?

Cavus · Adductus · Varus · Equinus. Gold standard treatment: Ponseti serial casting + tenotomy + foot abduction brace.

Barlow test vs. Ortolani test — what does each do?

Barlow = adduct + posterior push → dislocates hip. Ortolani = abduct + anterior lift → reduces it (clunk). "Barlow Out, Ortolani In."

6-month-old with DDH not yet treated. What is first-line management?

Pavlik harness — maintains hip in flexion/abduction. 95% success if started early. Monitor with ultrasound. Worn 23h/day.

Salter-Harris Type II fracture — what bones are involved?

Physis + Metaphysis. Most common type (75%). Generally good prognosis. Growth plate + the bone above it.

What fractures are most suspicious for non-accidental trauma (child abuse)?

Posterior rib fractures, classic metaphyseal lesions (corner/bucket-handle), multiple fractures at different healing stages, spiral fractures in non-ambulatory infants.

When does a child with scoliosis need bracing vs. surgery?

Bracing: 20–40° Cobb angle + still growing. Surgery (spinal fusion): >45–50°. Observation only: <20°. Brace slows progression, doesn't correct curve.

4 Kocher criteria for septic arthritis of the hip — name them.

Fever >38.5°C · Non-weight-bearing · ESR >40 mm/hr · WBC >12,000. 4/4 = ~99.6% probability septic → emergent OR.

Most common organism in pediatric osteomyelitis and septic arthritis?

S. aureus — all ages. Exception: Salmonella in sickle cell disease; Pseudomonas in puncture wound through shoe; GBS in neonates.

5-year-old with sudden limp, mild hip pain, low-grade fever, well-appearing, normal WBC. Ultrasound shows effusion. Diagnosis?

Transient synovitis — most common cause of acute hip pain in 3–8 year olds. Use Kocher criteria to rule out septic arthritis. Treat with NSAIDs + rest.

Boy age 3 with frequent falls, waddling gait, and calf enlargement. What test do you order first?

CK (creatine kinase) — massively elevated in Duchenne MD. Then confirm with genetic testing. Gowers' sign and pseudohypertrophy of calves are classic.

What is the difference between LCPD and SCFE in terms of age and mechanism?

LCPD: age 4–8, idiopathic AVN of femoral head, gradual limp, flattened head on X-ray. SCFE: age 10–16, obese, physis slips, Klein's line fails, obligate ER. Both cause limp — age is the key differentiator.

Pediatric MSK Disorders

SCFE — Full Guide Available