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Musculoskeletal Disorders and Conditions in Children Frank Caruso PA-C, MPS, EMT-P , Hearts & Private Parts 2019 Musculoskeletal Alterations • Overview: – Congenital • – Hereditary • Muscular dystrophy – Acquired • Legg-Calvé-Perthes – May be acute, chronic, or terminal – Common pediatric fractures Embryonic Development of

is the term for the formation of bone • There are two ways that bone can ossify during embryonic development: – Intramembranous ossification – Endochondral ossification Bone Formation • Intramembranous formation: – On or within the mesenchyme (stem cells) – Cranium, facial bones, and parts of the jaw bone (flatbones) arise from this fetal membrane called a mesenchyme • These bones grow by a process of intramembranous formation of bone (from skeletal tissue) • Endochondral formation: – embryonic cells (anlage): Defines the shape of the bone , usually found by 6 weeks gestation – : Contains cells that develop into – Periosteal collar: Osteoblasts that form a collar of bone, around a cartilage model – Secondary centers of ossification: result of the periosteal collar thickening and becoming wider toward the bone ends of the cartilage model. Intramembranous and Endochondral Bone formation • Intramembranous bones are always the flat bones • Endochondral bones include the long, short, and irregular bones • Most bones start off as cartilage and is later replaced by bone – endochondral ossification Intramembranous Ossification • Connective tissue forms in sheets at sites where flat bones will eventually be, highly invested with blood vessels which also contain osteoblasts • Osteoblasts begin laying down the bone, extracellular matrix, forming spongy bone • The osteoblasts get trapped within the hard matrix and then are called – this creates a sandwich where the connective tissue sheets are the “bread” and the spongy bone is the “meat” • This then forms the basis which the bone will finish developing. Endochondral Ossification

• Bone forms by replacing (the embryonic skeleton, early on is mainly made up of hyaline cartilage) • The cartilage is considered to simply be a “model” for the shape the bone should take on, and so it is often referred to as a “cartilaginous model” • This model is for most long, short and irregular bones Bone Growth

• Until adult stature achieved, bone growth occurs at the through endochondral ossification: – Cartilage cells at the epiphyseal side of the physeal plate multiply and enlarge – As rapidly new cartilage cells form, cartilage cells at the metaphyseal side of the plate are destroyed and replaced by bone • Distal physis in the contributes 80% of the overall growth in length in contrast to the proximal physis at the contributing only 20% of growth. • Epiphyseal closure: – Unites the and the – Occurs earlier in females than males because of earlier puberty in females

Growth in Diameter of Bone

• Occurs by deposition of new bone on an existing bone surface • Bone matrix is laid down by osteoblasts on the periosteal surface – at the same time bone resorption occurs on the endosteal surface – this allows for an increase in the diameter of the which contains marrow and spongy bone Cartilage : Ends of Long Bones

• Two regions of growing cartilage can be found at the end of long bones: – Articular cartilage over the free ends of bone – Physeal plate: layer of cartilage between the metaphyhsis and epiphysis: • Retains the ability to form and calcify new cartilage and deposit bone until the skeleton matures roughly one year after sexual maturity (11-15 females, 15-18 males)

Bone Formation

Bone Growth • Factors affecting bone growth – Growth hormone (secreted by pituitary) – Nutrition – General health – Many growth factors and regulators (fibroblast growth factor) Skeletal Development

• In the newborn, the entire spine is concave anteriorly (kyphosed) • In the first 3 months of life, the cervical spine begins to arch (lordotic) • Curve of lumbar spine develops with sitting • Compared to adult, a newborn has a large head, long spine, and short extremities Skeletal Development • (peaks by 2½ years) – Occurs in all newborns due to intrauterine stress – Bowleg • (peaks by 5-6 years) – Knock- • Persistence past peak times is pathologic 5 Adult 2 yrs like yrs Muscle Development • Between birth and maturity, muscle nuclei in the body increase 14 times in boys and 10 times in girls • The composition and size of muscles vary with age Congenital Defects • : most common congenital defect of the upper extremity: – Webbing of the fingers – Fusion of the soft tissues of the fingers – True syndactyly also includes fusion of the bones and nails • Vestigial tabs: – Extra digits

Congenital Defects • Anomalies on the medial or radial aspect of the often associated with abnormalities of blood, heart, or kidneys • Lateral or ulnar-sided defects are less often associated with systemic anomalies and are far more rare Congenital Defects • Developmental dysplasia of the hip (Congenital dislocation of the hip): – Formerly: congenital dislocation of the hip – Abnormality of the proximal femur, acetabulum, or both – Risk factors: • Female, metatarsus adductus, torticollis, oligohydramnios, first pregnancy, and breech presentation – The hip can present as subluxated, dislocatable, or dislocated

Congenital Defects • Developmental dysplasia of the hip – Manifestations: • Asymmetry of gluteal or thigh folds • Limb length discrepancy • Limitation of hip abduction • Positive Ortolani sign • Positive Barlow test • Positive Trendelenburg gait • Pain

Developmental Dysplasia of the Hip Congenital Defects • Deformities of the foot: – Metatarsus adductus (forefoot adduction) • Mild, moderate, or severe (degree of deformity and flexibility) – Equinovarus deformity (clubfoot): • Positional equinovarus (in utero positioning) • Idiopathic congenital equinovarus

Congenital Defects • Treatment – Braces – Sequential casts – Surgery Osteogenesis Imperfecta • “Brittle bone disease” • Genetic defect in collagen production: – Bone and vessel collagen • Results in: – Osteoporosis – Bowed and deformed limbs – Short stature – Spine curvature – Bluish sclera • Can be evident before birth (in utero fractures)

Osteogenesis Imperfecta

• Severe – Child may be stillborn or die soon after birth; intrauterine fractures • Mild – May not be diagnosed until child begins to walk – May be mistaken for child abuse Osteogenesis Imperfecta Rickets

• Disorder causing mineralization failure, “soft” bones, and skeletal deformity • Causes: – Insufficient vitamin D – Insensitivity to vitamin D – Renal wasting of vitamin D – Inability to absorb calcium or vitamin D in the gut Rickets

Scoliosis • Rotational curvature of the spine: – Nonstructural: • Curvature is from a cause other than the spine – Structural: • Curvature associated with vertebral rotation • Skeletal abnormalities, neuromuscular disease, trauma, extraspinal contractures, bone infections of the vertebrae, metabolic bone disorders, disease, and tumors Evaluation

• Is there a curve? • Is it structural? • Is it idiopathic? • How large is the curve? • How mature is the patient? Scoliosis Scoliosis • Lateral curvature of the spine of > 10°: – Small curves are not scoliosis • Thoracic or lumbar spine (occasionally both): – Associated vertebral rotation with kyphosis or lordosis • May be congenital: – Vertebral anomalies • Commonly idiopathic • May be secondary to other disorder: • Cerebral palsy • Muscular dystrophy • Myelomeningocele Idiopathic Scoliosis

• Develops in early adolescence: – Male = female in curves < 10° – Female 7X more likely to have significant, progressive curve requiring treatment. – Progression typically girls at age 10-16 years – Not associated with pain • Pain suggests primary condition and requires further evaluation

Curve size Girls:Boys 6-10° 1:1 11-20° 1.4:1

>21° 5.4:1

*JBJS 60A:173,1978 Scoliosis • Physical exam: – Forward bending test: • Observe from behind • Elevation of cage, scapula or paravertebral muscle mass positive finding – Also assess: • Skin • Leg length • Feet alignment • Neuromuscular status – Beware! • Left side thoracic curves have high incidence of spinal cord abnormalities Scoliosis Is There A Curve? Is There A Curve?

Is The Curve Structural? Is The Curve Structural?

• Postural curves – Pain – Leg length inequality – Behavioral Is The Curve Structural?

• Congenital: – Vertebral anomalies • Neuromuscular: – Cerebral Palsy – Myelomeningocele – Muscular dystrophy – Polio • Miscellaneous: – Post surgical – Marfan syndrome – Trauma Congenital Scoliosis Beware!

• Unusual curves: – Left thoracic curves • Unusual symptoms: – Significant pain – Radiculopathy • Unusual findings: – Neurologic deficit – Skin changes – Hair patches (bottom of spine) – Asymmetry of lower extremities How Large is The Curve? How Large is The Curve?

• Diagnostic tests: – PA and lateral full- length radiographs with patient standing and knees straight – Measure Cobb angle: • Describe as if patient is being examined from behind Scoliosis Treatment

• If angle < 50° at skeletal maturity: – Progression usually ceases • If angle > 60° at skeletal maturity: – Progression into adulthood common and may compromise respiratory function: • Unusual if angle less than 90° and healthy • Back pain may occur in adulthood: – Not usually a major disability Scoliosis Treatment • Observation: – Frequency depends on curve and remaining growth • Bracing for progressive curves at 20-40°: – Goal is to stop progression – Not helpful for curves that are unlikely to progress or when little growth remains – Not helpful for large curves – May not work even with well made orthosis • Surgery: – Spinal fusion for curves of > 50° and for curves of 40 to 50 ° that are likely to progress Osteomyelitis

• Often associated with septic because infant’s bone has blood vessels that perforate the growth plate: • In children frequently begins as a blood abscess in the metaphysis of the bone • In adolescents and adults may involve the vertebrae – Back pain for several weeks may be only complaint – This age group is less often affected than younger populations Osteomyelitis • Much less common after the epiphyseal plates are closed, except in the vertebral body: – Infection may develop in any part of a bone, and abscesses spread slowly – Destruction of the cortex in a localized area may result in a pathologic fracture MOTH EATEN Osteomyelitis

• Infection spreads under the and along the bone shaft or into the – Sequestra: • Sections of dead bone from periosteal separation – Involucrum: • Periosteal new bone Osteomyelitis Juvenile (JRA) • Childhood form of rheumatoid arthritis • The basic pathophysiology of JRA is the same as the adult form • One difference is the mode of onset: – Arthritis in fewer than five – Arthritis in more than five joints – Systemic disease Juvenile Rheumatoid Arthritis (JRA) • Differences in JRA and adult RA: – Large joints are affected – Subluxation, ankylosis of the cervical spine – Joint pain is not as severe – Positive antinuclear antibody test – Chronic uveitis – Low detection of rheumatoid factor – Limited subcutaneous rheumatoid nodules • Common in heart, , eyes, and other organs

Osteochondrosis • Avascular diseases of the bone – Legg-Calvé-Perthes disease: • Interrupted blood supply to the femoral head • Self-limiting disease • Deformation due to ischemia is permanent – Osgood-Schlatter disease: • Tendinitis of the anterior patellar tendon and osteochondrosis of the tubercle of the tibia Legg-Calvé-Perthes Disease

Osgood-Schlatters • Osgood-Schlatter disease can cause a painful lump below the kneecap in children and adolescents experiencing growth spurts during puberty • Occurs most often in children who participate in sports that involve running, jumping and swift changes of direction — such as soccer, basketball, figure skating and ballet • More common in boys, the gender gap is narrowing as more girls become involved with sports • Affects as many as 1 in 5 adolescent athletes • Age ranges differ by sex because girls experience puberty earlier than do boys: • Boys ages 13 to 14 • Girls ages 11 to 12 • The condition usually resolves on its own, once the child's bones stop growing

Slipped Capital Femoral Epiphysis (SCFE) • One of the most important pediatric and adolescent hip disorders encountered in medical practice • Although SCFE is a rare condition, an accurate diagnosis combined with immediate treatment is critical • Despite the fact that the underlying defect may be multifactorial (eg, mechanical and constitutional factors), SCFE represents a unique type of instability of the proximal femoral growth plate • Clinically, the patient may report: —Hip pain —Medial thigh pain, and/or pain —Acute or insidious onset of a limp —Decreased range of motion of the hip Slipped Capital Femoral Epiphysis • Mean age at presentation: – 12 years for girls (range:10-14 years) – 13 years for boys (range: 11-16 years) – Onset before or after typical range is associated with endocrinopathy • Bilateral involvement seen in 40-50%: – Not always affected simultaneously • May be acute or chronic: – Early detection and treatment imperative Slipped Capital Femoral Epiphysis: Presentation

• Who? – 7 – 14 year olds – Growing FAST (or about to) – Obese or active more likely

• What complaint? – ANY hip/thigh/knee pain – Limp – Sits/runs/walks funny

Cerebral Palsy • Cerebral palsy is a disorder of movement, muscle tone or posture that is caused by an insult to the immature, developing brain, most often before birth • Signs (any or all): — Impaired movement associated with exaggerated reflexes, floppiness or rigidity of the limbs and trunk — Abnormal posture — Involuntary movements — Unsteadiness of walking — Difficulty with swallowing — Eye muscle imbalance — Reduced range of motion at various joints of their bodies due to muscle stiffness — Seizures — Blindness • The effect of cerebral palsy on functional abilities varies greatly: some people are able to walk while others are wheelchair bound; some people show normal to near normal intellectual function, but others may have intellectual disabilities

Muscular Dystrophies • Group of disorders that cause degeneration of skeletal muscle fibers • The muscular dystrophies cause progressive, symmetric weakness, and wasting of skeletal muscle groups Muscular Dystrophy • Group of genetic diseases in which muscle fibers are unusually susceptible to damage • Damaged muscles become progressively weaker and most patients will eventually need to use a wheelchair • There are many different kinds of muscular dystrophy: — Symptoms of the most common variety begin in childhood, primarily in boys — Other types of muscular dystrophy do not appear until adulthood • Signs: — Trouble breathing or swallowing — Limbs may also draw inward and become fixed in that position — contracture — Some varieties of the disease can also affect the heart and other organs • While there is no cure for muscular dystrophy, medications and therapy can slow the course of the disease Duchenne Muscular Dystrophy • Most common muscular dystrophy • X-linked recessive inheritance: – Deletion of segment of DNA or single gene defect on short arm of the X chromosome • Duchenne muscular dystrophy gene: – Encodes for the dystrophin protein – Dystrophin mediates the anchorage of the actin cytoskeleton of the skeletal muscle fiber to the basement membrane

Duchenne Muscular Dystrophy • Manifestations appear by 3 years of age: – Slow motor development – Progressive weakness – Muscle wasting – Sitting and standing are delayed – The child is clumsy, falls frequently, and has difficulty climbing stairs Muscular Dystrophy Fascioscapulohumeral Muscular Dystrophy • Facioscapulohumeral muscular dystrophy affects the upper body; it is not the same as Duchenne muscular dystrophy • A genetic disorder, it appears in both men and women and may develop in a child if either parent carries the gene for the disorder; in 10 to 30% of cases, the parents do not carry the genes • Facioscapulohumeral muscular dystrophy affects about 5 out of 100,000 people Bone and Muscle Tumors • Nonossifying fibroma • Simple bone cysts • Aneurysmal bone cysts • osteoma • Fibrous dysplasia • Osteosarcoma • Ewing sarcoma • Rhabdomyosarcoma Nonossifying Fibromas (NOF) • Most common benign bone tumor in children • They occur twice more often in males than in females • It is estimated that 30% to 40% of people under the age of 20 have NOFs, although few will have any symptoms • NOFs are often discovered by chance when a patient requires x-rays for another reason, such as a sports injury • NOFs do not become cancerous and they do not spread (metastasize) • In most cases, no treatment is necessary because these tumors typically go away on their own when a child is fully grown

Simple Bone Cysts (Unicameral) • A unicameral, or simple, bone cyst is a common, benign (noncancerous) bone tumor that primarily occurs in children and adolescents • Cavities within bone that are filled with fluid • They can develop in any bone, UBCs usually affect the long bones -- most often the upper arm bone () and the thighbone (femur) • Unicameral bone cysts are not painful, and are often discovered incidentally when an x-ray is obtained for another reason. • Because these cysts can weaken the surrounding bone, fractures through UBCs do occur • Treatment for a UBC is based on several factors, including the size and location of the cyst, and the risk for fracture; in some cases, surgery may be recommended

Aneursymal Bone Cyst (ABC) • An aneurysmal bone cyst is a benign blood-filled cyst in the bone that tends to expand or grow • It has a thin bony wall surrounding the growth, so it is sometimes called a bony tumor; although it is not cancerous, aneurysmal bone cysts grows aggressively, so they must be removed • ABCs can occur in the , extremities, and usually occurring in people age 20 or younger • About half of patients with aneurysmal bone cysts of the spine are children; most discover the cyst in their teen years • ABCs are the second-most common tumors in children, they are rare and account for only 1-6% of bony tumors • Aneurysmal bone cysts occur slightly more frequently in females than in males and there is a 20% recurrence rate with treatment (less often in the spine)

Osteoid Osteoma • An osteoid osteoma is a benign (non-cancerous) bone tumor • It has a center of growing cells, called a nidus, surrounded by a hard shell of thickened bone • They do not spread throughout the rest of the body • Tend to be small—less than 1.5 cm in size and they may occur in any bone in the body —Most common in long bones, such as the thigh bone (femur) and leg bone (tibia), but are also found in the hands, fingers, and spine • May occur at any age, and are most common in patients between the ages of 4 and 25 years old • Males are affected approximately three times more commonly than females

Fibrous Dysplasia

• Fibrous dysplasia is a chronic condition of the skeleton where a portion of a bone develops abnormally • The condition begins before birth • It is caused by a gene mutation that affects the cells that produce bone • The abnormal bone forms before birth, its presence is often not discovered until childhood, adolescence, or even adulthood

Osteosarcoma

• Osteosarcoma is a type of bone cancer that begins in the cells that form bones • Most often found in the long bones in and legs, though it can occur in any bone • Osteosarcoma tends to occur in children and young adults, but it can also occur in older adults • Treatment involves surgery, chemotherapy and radiation therapy

Ewing Sarcoma

• Ewing sarcoma is a cancerous tumor that grows in bones or soft tissue near bones and usually affects adolescents • Named after Dr. James Ewing, the American pathologist who identified the cancer in the 1920s • It can develop anywhere in the body, but most commonly affects the arms, legs, ribs, spinal column, and pelvis Ewings Sarcoma

• Treatment for Ewing sarcoma involves a combination of chemotherapy, surgery, and/or radiation. With early diagnosis and proper treatment, many kids who develop it have a good chance of recovery

Rhadomyosarcoma • A type of sarcoma • Cancer of soft tissue (such as muscle), connective tissue, (such as tendon or cartilage) or bone • Usually begins in muscles that are attached to bones associated with movement • The most common type of soft tissue sarcoma in children • It can begin in many places in the body Rhadomyosarcoma • There are three main types of rhabdomyosarcoma: – Embryonal: This type occurs most often in the head and neck area or in the genital or urinary organs; it is the most common type – Alveolar: This type occurs most often in the arms or legs, chest, abdomen, genital organs, or anal area; it usually occurs during the teen years – Anaplastic: This type rarely occurs in children

Common Pediatric Fractures Pediatric vs Adult Fracture Healing

• DIFFERENCES BETWEEN PEDIATRIC AND ADULT FRACTURE HEALING • One of the primary differences between pediatric and adult bone is that the periosteum in children is very thick • The periosteum around the fracture site walls off the hematoma and is stripped from the bone as bleeding occurs—a primary factor in the amount of new bone formed around a fracture Pediatric vs Adult Fracture

• The area of bone necrosis on either side of the fracture surface must be replaced by viable bone through the process of bone resorption and deposition • This process leads to an initial radiographic appearance of sclerosis at the fracture site because new bone is being formed on the existing necrotic bone • The area around the necrotic bone elicits an inflammatory response • Because pediatric bone is more vascular than adult bone, the inflammatory (hyperemic) response is more rapid and significant; temperatures as high as 40 °C may be noted after fracture INJURY PATTERN IN GROWING BONES

• Bones tend to BOW rather than BREAK • Compressive force= TORUS fracture – Aka. Buckle fracture • Force to side of bone may cause break in only one cortex= GREENSTICK fracture – The other cortex only BENDS • In very young children, neither cortex may break= PLASTIC DEFORMATION INJURY PATTERN IN GROWING BONES

• Bones tend to BOW rather than BREAK • Compressive force= TORUS fracture – Aka. Buckle fracture • Force to side of bone may cause break in only one cortex= GREENSTICK fracture – The other cortex only BENDS • In very young children, neither cortex may break= PLASTIC DEFORMATION INJURY PATTERN IN GROWING BONES

• Bones tend to BOW rather than BREAK • Compressive force= TORUS fracture – Aka. Buckle fracture • Force to side of bone may cause break in only one cortex= GREENSTICK fracture – The other cortex only BENDS • In very young children, neither cortex may break= PLASTIC DEFORMATION INJURY PATTERN IN GROWING BONES

• Bones tend to BOW rather than BREAK • Compressive force= TORUS fracture – Aka. Buckle fracture • Force to side of bone may cause break in only one cortex= GREENSTICK fracture – The other cortex only BENDS • In very young children, neither cortex may break= PLASTIC DEFORMATION INJURY PATTERNS IN GROWING BONES

• Point at which metaphysis connects to physis is an anatomic point of weakness • Ligaments and tendons are stronger than bone when young – Bone is more likely to be injured with force – Periosteum is biologically active in children and often stays intact with injury • This stabilizes fracture and promotes healing INJURY PATTERNS IN GROWING BONES

• Point at which metaphysis connects to physis is an anatomic point of weakness • Ligaments and tendons are stronger than bone when young – Bone is more likely to be injured than soft tissue – Periosteum is biologically active in children and often stays intact with injury • This stabilizes fracture and promotes healing PHYSEAL INJURIES

• Many childhood fractures involve the physis – 20% of all skeletal injuries in children – Can disrupt growth of bone – Injury near but not at the physis can stimulate bone to grow more

SALTER HARRIS

• Classification system to delineate risk of growth disturbance: – Higher grade fractures are more likely to cause growth disturbance – Growth disturbance can happen with ANY physeal injury SALTER HARRIS CLASSIFICATION • I – Fracture passes transversely through physis separating epiphysis from metaphysis • II • III • IV • V SALTER HARRIS CLASSIFICATION

• I • II – Transversely through physis but exits through metaphysis – Triangular fragment • III • IV • V SALTER HARRIS CLASSIFICATION

• I • II • III – Crosses physis and exits through epiphysis at joint space • IV • V SALTER HARRIS CLASSIFICATION

• I • II • III • IV – Fracture extends upwards from the joint line, through the physis and out the metaphysis • V SALTER HARRIS CLASSIFICATION

• I • II • III • IV • V – Crush injury to growth plate IT’S GOOD TO BE YOUNG

• Children tend to heal fractures faster than adults: – Advantage: shorter immobilization times – Disadvantage: misaligned fragments become “solid” sooner • Anticipate remodeling if child has > 2 years of growing left: – Mild angulation deformities often correct themselves – Rotational deformities require reduction (do not remodel) IT’S GOOD TO BE YOUNG

• Fractures in children may stimulate longitudinal bone growth: – Some degree of bone overlap is acceptable and may even be helpful • Children do not tend to get as stiff as adults after immobilization: • After casting, callus is formed but still may be fibrous: – Avoid contact activities for 2-4 weeks once out of cast COMMON FRACTURES

• Distal radius • • Tibia DISTAL RADIUS

• Peak injury time correlates with peak growth time – Bone is more porous • Check sensation: median and ulnar nerve • Nerve injury more likely to occur with significant angulation of fragment or with significant swelling • Examine elbow (supracondylar) and wrist (scaphoid) DISTAL RADIUS

• Torus fractures – Usually nondisplaced- strong periosteum – Subtle, may be best seen on lateral • Greenstick fractures – Compression of dorsal cortex, apex volar angulation • Complete (transverse) fractures TORUS FRACTURES

• No reduction needed • If > 48 hours old, may cast at first visit: – Otherwise splint and cast at 5-7 days • Short arm cast for 4 weeks • Repeat x-rays unnecessary unless no clinical improvement after 4 weeks • Splint an additional 2 weeks GREENSTICK FRACTURES

• If non-displaced: – Short arm cast • If displaced >15 degrees, reduce and immobilize in long arm • 4 weeks cast, 2 weeks splint DISTAL RADIUS PHYSIS FRACTURE

• Non-displaced Salter I can appear normal on plain films • Presence of pronator fat pad along volar distal radius on lateral film = occult fracture • If tender over physis, treat as fracture • SALTER HARRIS II DISTAL RADIUS FRACTURES

• Displaced fractures= reduce asap • Non-displaced fractures= short arm cast for 3- 6 weeks – The older the child, the longer immobilization • If x-rays are normal initially but tenderness is over growth plate, immobilize for 2 weeks – Bring child back to re-examine and re-xray – If no callus, fracture is unlikely ELBOW

• 10% of all fractures in children • Diagnosis and management complex – Early recognition and referral • Most are supracondylar fractures – Sequence of ossification: • Come Read My Tale Of Love • Capitellum, Radial head, Medial epicondyle, Trochlea, Olecranon, Lateral epicondyle • Age 1, 3, 5, 7, 9, 11 ELBOW FRACTURE EXAMINATION • Check neurovascular status – Flex and extend fingers and wrist – Oppose thumb and little finger – Palpate brachial and radial pulses – Capillary refill in fingers • Immobilize elbow before radiographs to avoid further injury from sharp fragments – Flexion 20-30 degrees = least nerve tension Know basic landmarks on lateral view to give clues to distinguish fracture from normal

AnteriorRadiocapitellarDisruption humeral = line line—— middlepointsdisplaced directly1/3 capitellum fracture to capitellum

 Fat pad sign may be only clue if non-displaced • Fat Pad sign (aka. Sail Sign) – Anterior fat pad sign can be normal – Posterior always abnormal SUPRACONDYLAR FRACTURES • Weakest part of the elbow joint where humerus flattens and flares – Most common fracture is extension type – Olecranon driven into humerus with hyperextension • Marked pain and swelling of elbow • Potential for vascular compromise – Check pulse!!! Reduce fracture if pulse compromised – Check nerve function in hand SUPRACONDYLAR FRACTURE CLASSIFICATION • Type I- non-displaced or minimally displaced • Type II- displaced distal fragment with intact posterior cortex • Type III- displaced with no contact between fragments Radiocapitellar Line Anterior Humeral Line

SUPRACONDYLAR FRACTURES MANAGEMENT • Most are displaced and need surgery • Type I can be managed with long arm cast, forearm neutral, elbow 90o for 4 wks • Bivalve cast if acute • Follow-up xrays 3-7 days later to document alignment • Xrays at 4 weeks to document callus • Once callus noted at 4 weeks, discontinue cast and start active ROM LATERAL CONDYLAR FRACTURES • Most common x-ray findings: – Fracture line begins in distal humeral metaphysis and extends to just medial to capitellar physis into the joint – Neurovascular injury rarely

 MEDIAL  LATERAL LATERAL CONDYLAR FRACTURES

• Second most common elbow fracture • Most common physeal elbow injury • Exam: focal swelling at lateral distal humerus CLAVICLE

• Most occur in the middle third of the bone – 80% • 15% distal third, 5% proximal third • Fall on , direct trauma • Clinical: pain with any shoulder movement, holds arm to chest • Point tender over fracture, subQ crepitus • Often obvious deformity CLAVICULAR FRACTURE

• AP view often sufficient to diagnose if midshaft • Consider 45o cephalic tilt view if needed CLAVICULAR FRACTURE

• In displaced fracture: sternocleidomastoid pulls upward to displace medial clavicle, lateral fragment pulled downward by weight of arm

CLAVICULAR FRACTURE MANAGEMENT • Sling versus figure-of-eight bandage • Fracture fully healed when pt has painless ROM at shoulder and non tender to palpation at fracture • Generally back to full activity by 4 weeks • Protect from contact sports x 6 weeks • Warn of the healed ‘bulge’ TIBIA

• Tibia and fibula fractures often occur together – If you see a tibial fracture, hunt for a fibular one – Fibular fracture could be plastic deformity • Mechanism: falls and twisting injury of the foot – Low force, intact periosteum and support from fibula prevent displacement commonly TIBIAL FRACTURE

• When to refer: – Displaced fracture – Tib/fib fractures – Fractures with > 15o varus angulation TIBIAL FRACTURE MANAGEMENT • Posterior lower leg splint if acute • Non-displaced fractures: long leg cast for 6-8 weeks • Repeat radiographs weekly to check position • Refer if angulates more than 15o TODDLER’S FRACTURES

• Children younger than 2 years old learning to walk • No specific injury notable most of the time • Child refuses to bear weight on leg – Examine hip, thigh and knee to r/o other causes of limping TODDLER’S FRACTURES

• If you suspect it, get AP and lateral views of entire tib/fib area • Typical: nondisplaced spiral fracture of tibia with no fibular fracture • Initial x-ray often normal, diagnosis on f/u films with lucent line or periosteal reaction CONCLUSIONS

• Nearly 20% of children with injury have a fracture • Always take post-reduction x-rays • Physeal injuries are common and may have no radiographic findings – Treat as fracture!! • Don’t forget to tell Mom and Dad about possible growth problems Nonaccidental Trauma • “Corner” metaphyseal fractures – Long bone fractures caused by a twisting force – Transverse tibial fractures are the most common – Associated with child abuse, but osteogenesis imperfecta must be ruled out Nonaccidental Trauma FRACTURES OF ABUSE

• Majority of fractures in child < 1 year are from abuse – High percentage of fractures <3yo = abuse • Greater risk of abuse: first-born, premature infants, stepchildren, children with learning or physical disabilities • Most common sites: femur, humerus, tibia • Also: radius, skull, spine, ribs, ulna, fibula Child Abuse Concerns

• Unexplained fractures in different stages of healing as shown on radiology • Femoral fracture in child < 1 year • Scapular fracture in child without a clear history of violent trauma • Epiphyseal and metaphyseal fractures of the long bones • Corner or “chip” fractures of the metaphyses