Peds Flashcards
<div>Anatomic/Physiologic differences between Children/Adults in polytrauma</div>
c-spine: large head - use recessed spine board to protect<div>Airway/breathing: large tongue, short airway, anterior larynx, can have lung contusion without rib #</div><div>Circulation: BP reserve - can lose 30% blood volume before HoTN, increased risk of visceral injuries, organ failure ealy (during resus) use IO for access</div><div>Disability: hyperlaxity - SCIWORA risk, delayed neuro injury</div><div>Exposure: hypothermia risklarge body SA:volumre ratio</div><div><br></br></div><div>Trivia:</div><div>cause of death-head injury</div><div>fix fractures early to decrease Vent time/ICU stay</div><div>compartment syndrome - use analgesic requirement</div>
RFs for DDH? not a RC Q
“F’s<div>female</div><div>first born</div><div>frank breech</div><div>FHx up to 30%</div><div>fluid - oligohydramnios</div>”
Associations with DDH? not a RC Q
torticollis<div>foot: Metatarsus adductus (10%), CTEV (6%), calcaneovalgus</div><div>spine-scoliosis</div>
normal US angles for DDH? not a RC Q
“<div>Timing: 6 weeks to 4-6months</div>AAAA = alpha angle, acetabulum, above 60 deg (>60 deg is N)<div>BB = Beta, below 55 (<55 is N)</div><div><br></br></div><div><img></img><br></br></div>”
Defect in SCFE?
“Hypertrophic zone<div>Metaphyseal zone in renal osteodystrophy</div><div><br></br></div><div><img></img><br></br></div>”
Associations with PFFD? Not a RC Q
<ul> <li>Ulnar deficiency</li> <li>Coxa Vara</li> <li>Distal femoral focal defect</li> <li>ACL/PCL deficiency</li> <li>Fibular hemimelia (50-70%)</li> <li>Ball and Socket Ankle</li> <li>Lateral Ray Deficiency</li></ul>
Anteromed bowing - (1) assx anomalies, (2) Classification, (3) general tx?
“(1)<ul> <li>Upper extremity –> syndactyly, to extensive deficiency</li> <ul> <li>More common with bilateral involvement</li> </ul> <li>Hip: PFFD, coxa vara, congenital short femur (add to LLD), distal femoral hypoplasia (up to 93%)</li> <li>Knee: Genu valgum, ACL deficiency (95%), PCL def (60%) patella alta, hypoplastic patella</li> <li>Foot: Equinovalgus more common</li> <ul> <li>missing rays, tarsal coalition, ball in socket ankle, ankle instability</li> </ul></ul><div>(2)</div><div><div><img></img></div> <div></div> <img></img><br></br></div><div>(2) Tx depends on foot function and LLD</div><div>-indications for amputation: non-functional foot, predicted LLD>30%, 5cm discrepancy at birth, prolonged reconstructive course</div><div><img></img><br></br></div>”
Pirani Classification for CTEV?
“<ul> <li>Predictive of need for number of casts and need for TAL</li> <ul> <li>Pirani > 4 = 90% will need more than 3 casts</li> <li>Pirani > 5 = 85% will need TAL</li> </ul> </ul> <ul> <li>0:normal, 0.5 moderately abnormal, 1 severely abnormal</li> <li>Midfoot:</li> <ul> <li>(A) Curved lateral border</li> <li>(B) Medial crease</li> <li>(C) Talar head coverage</li> </ul> <li>Hindfoot</li> <ul> <li>Rigid equinus (D)</li> <li>Empty Heel (E)</li> <li>Posterior crease (F)</li> </ul> </ul> <div><img></img></div>”
Ponsetti technique?
”"”Serial above knee casting +/- TAL followed by abduction foot orthosis”“<div><br></br></div><div>Casts 5-6 weekly: correct supination, abduct foot around lateral talar pivot to 70 deg abduction and correct to hindfoot valgus, then DF to goal of 15 deg (TAL in 90%), then cast for 3/52</div><div><br></br></div><div>Move to foot abduction orthosis (Dennis Brown): 70 deg ER abd 10 DF 23 hr/d X3 month then 12-18hr/day up to 4 years</div><div><div><br></br></div></div>”
Soft tissue surgical Tx for clubfoot? not a RC Q
“Posteromedial release<div>-capsuleX4 - TT, subtalar, TN, CC</div><div>-musclesX4 - Achilles, PT, FHL, FDL (+Abd Hall, PF)</div><div><div> <div> <div><img></img></div> <div><img></img></div> </div></div></div>”
Causes of Cavovarus feet (not a RC)?
“<ul> <li>2/3 of pts with CV feet have neuro issue</li><li>unilateral - rule out tethered spinal cord or spinal cord tumor</li> </ul> <ul> <li>CNS:</li> <ul> <li>Cerebral palsy</li> <li>Freidrich’s Ataxia</li> </ul> <li>Spinal Abnormalities:</li> <ul> <li>Myelodysplasia</li> <li>Diastematomyelia</li> <li>Syringomyelia</li> <li>Poliomyelitis</li><ul><ul> </ul> </ul> <li>Spinal cord tumors, intrathecal lipoma, tethered cord syndrome, Guillain-Barre Syndrome</li> </ul> <li>Peripheral Nerves:</li> <ul> <li>Hereditary Sensorimotor Neuropathy (HSMN) - CMT</li><li><br></br></li><li>Other: polyneuritis, small muscular atrophy, atypical polyneuritis, neuromuscular choristoma</li> </ul></ul>”
Difference b/t oblique and vertical talus? not a RC Q
<div><div>Reduction of talocalcaneal angle and reduction of navicular on talus with forced PF view</div></div>
<ul> <li>Oblique talus </li> <ul> <li>Similar to true vertical talus but is passively correctable/reducible</li> <li>Plantarflexion lateral radiographs show talus aligns with 1st MT</li><li>Some need treatment</li> <ul> <li>< 10o dorsiflexion passively (tight Achilles)</li> <ul> <li>Will become symptomatic over time</li> </ul> </ul> </ul></ul>
Ortho and Non-ortho manifestations of DS?
“<div> <div> <div> <div>MSK Manifestations</div> <ul> <li>General: </li> <ul> <li>Joint hypermobility/ligamentous laxity</li> <li>Shorter than average stature</li> <li>Polyarticular arthropathy NYD</li> <li>Delayed ambulation with walking at age 2 or 3, wide-based waddling gait</li> </ul> <li>Spine</li> <ul> <li>Odontoid hypoplasia</li> <li>Atlantoaxial instability</li> <li>Occipito-cervical instability</li> <li>Subaxial instability/cervical stenosis</li> <li>Scoliosis</li> </ul> <li>U/E: Clinodactyly (usually 5th digit)</li> <li>Pelvis</li> <ul> <li>Flared iliac wings</li> <li>Flat acetabulae</li> <li>Hip instability</li> <li>Hip dysplasia (acquired) with dislocation late in life</li> <li>High rates of SCFE</li> </ul> <li>Knee</li> <ul> <li>Genu valgum</li> <li>Subluxed/dislocated patellae</li> </ul> <li>Feet</li> <ul> <li>Flexible pes planovalgus</li> <li>Hallux valgus</li> </ul> </ul><div><div> <div> <div><img></img></div> </div></div></div> </div> </div></div>”
“<div>Friedreich Ataxia: (1) def’n, (2) triad, (3) ortho manifestations</div>”
“(1) spinocerebellar degen dz<div>(2) ataxia, absent patellar/achilles reflexes, upgoing toes</div><div>(3) scoliosis (AIS, SSEPs don’t work), rigid cavus foot (achilles tenotomy, TT, fusions)</div>”
Peri-op considerations for DMD? Not a RC Q
“<ul> <li>MALIGNANT HYPERTHERMIA common</li> <ul> <li>Avoid succinylcholine</li> <li>Can lead to lethal hyperkalemia even if frank MH doesn’t occur</li> </ul> <li>Cardiac evaluation (cardiomyopathy, late CHF, risk of intra-op cardiac arrythmias)</li> <li>Pulmonary function</li> <ul> <li>Decreased FVC starts around age 10 (Weakness/contractures of intracostal muscles)</li> </ul> <li>Increased intra-operative bleeding</li> <ul> <li>Lack of vasoconstriction from weak smooth muscle</li> <li>Consider TXA use</li> </ul> <li>Post-op wound complications and infections</li> <li>Stress dose steroids</li> <li>Curve progression</li> <li>Late pseudo-arthrosis</li></ul>”
MED vs LCDP hips?
<div>MED distinguished from LCPD by itssymmetric and bilateral presentation, early acetabular changes, and lack of metaphyseal cysts</div>
<div><br></br></div>
<div>MED always bilateral and symmetric</div>
<div>Only 13% of perthes are bilateral and 31% of these at same stage<br></br></div>
<div><br></br></div>
<div>MED will have other joint involvement - skeletal survey!</div>
Ortho manifestations of sickle cell? not a RC q
<div>-sickle cell crisis: hydroxyurea, hydration, analgesia</div>
-osteomyelitis<div>-AVN</div><div>-septic arthritis</div><div>-pathologic fracture</div>
RU Synostosis:<div>(1) position</div><div>(2) Investigations</div><div>(3) Tx and complications</div>
(1) presents at 2-5 years with fixed PRONATION (>60 deg is fxnally limiting)<div>(2) Xray, but MRI to r/o cartilaginous synostosis</div><div>(3) osteotomy through synostosis; injuries to PIN and high risk of CS if >85 deg correction</div>
EDS diagnostic criteria
<ul> <li>Major</li> <ul> <li>Beighton score >4</li> <li>Arthralgia for >3mo in 4 or more joints</li> </ul> <li>Minor</li> <ul> <li>Beighton score of 1, 2, or 3</li> <li>Arthralgia >3mo in 1,2,or 3 joints or back pain >3mo or spondylosis/spondylolysis/spondylolisthesis</li> <li>Dislocation or subluxation of more than one joint, or in one joint on more than one occasion</li> <li>Three or more soft tissue lesions (i.e. epicondylitis, tenosynovitis, bursitis)</li> <li>Marfanoid habitus</li> <li>Skin striae, hyperextensibility, thin skin, or abnormal scarring</li> <li>Occular signs (drooping eyelids, myopia, antimongoloid slant)</li> <li>Varicose veins, hernia, rectal or vaginal prolapse</li> <li>Mitral valve prolapse</li> </ul> <li>Positive if any of:</li> <ul> <li>2 major criteria</li> <li>1 major and 2 minor</li> <li>4 minor</li> <li>2 minor and unequivocally affected 1st degree relative</li> </ul></ul>
Alignment parameters for BBFA #s? Not A RCQ
<div> <div></div> <div>Angle</div> <div>Malrotation (°)</div> <div>Bayonet Apposition</div> <div>0-10 years</div> <div><15</div> <div><45</div> <div>Yes, if <1cm short</div> <div>≥10 years</div> <div><10</div> <div><30</div> <div>No</div> <div>Approaching skeletal maturity (<2y growth remaining)</div> <div>0</div> <div>0</div> <div>No</div> </div>
Etiologies of Physeal Arrest? not a RC Q
<ul> <li>Trauma</li> <ul> <li>Salter Harris Type I and II fractures travel through hypertrophic zone so very little risk of arrest (1-7%)</li> <ul> <li>Risk factors</li> <ul> <li>Repeated, forceful manipulation/reduction</li> <li>Remanipulation >10d after injury</li> </ul> </ul> <li>Salter Harris Type III and IV fractures traverse reserve zone</li> <ul> <li>Increased risk of growth distrubance</li> <li>Malunion can bridge epiphysis to metaphysis</li> </ul> <li>Salter Harris Type V injuries have high energy and can affect all zones, high rate of arrest</li> <li>Usually injury not identified until arrest has occurred</li> </ul> <li>Vascular ischemia 20 to compartment syndrome</li> <ul> <li>Frostbite</li> <li>Both lead to cell death in reserve and proliferative zone</li> </ul> <li>Occlusion</li> <ul> <li>Can occur in hematological deraignment</li> <ul> <li>Sickle-cell disease</li> <li>Thalassemia</li> <li>Purpura fulminans</li> </ul> </ul> <li>Infection</li> <ul> <li>Usually more in the metaphysis and hypertrophic zone, as that is where blood flow slows in young bones</li> <ul> <li>Advanced infection can progress across physis to reserve zone and lead to growth arrest</li> </ul> <li>Subperiosteal abscess or septic arthritis can compress epiphyseal vessels -> secondary ischemic insult</li> </ul> <li>External beam radiation</li> <ul> <li>Direct death to chondrocytes in rapidly proliferating areas</li> <li>Also can have ischemic effects</li> </ul> <li>Tumors</li> <ul> <li>Can invade physis and destroy chondrocytes</li> <li>Can be damaged iatrogenicly during tumor resection</li> </ul> <li>Repetitive Stress</li> <ul> <li>Especially in gynmasts</li> <ul> <li>Can bear 10x body weight through their wrists</li> <li>Have increased incidence of positive ulnar variance compared to non-gymnasts</li> </ul> <li>Heuter-Volkman principle = compression across physis impairs growth, tension will increase growth</li> </ul></ul>
DDX for Vertebroplana
“<ul> <li>DDX for vertebroplana:</li> <ul> <li>F:fracture (trauma)</li> <li>E:eosinophilic granuloma</li> <li>T:tumor (e.g. metastases, myeloma, leukemia)</li> <li>I:infection</li> <li>S:steroids (<a>avascular necrosis</a>)</li> <li>H:hemangioma</li> </ul></ul>”
DDx for Kyphosis? Not a RC Q.
“<img></img>”
most common soft tissue mass in kids?
hemangioma<div><br></br></div><div><div>Hemangioma < 3 months of age, vascular malformation > 3months of age</div></div>
most common soft tissue and boney sarcoma in foot in peds? soft tissue tumor in general?
synovial<div>osteosarcoma</div><div>hemangioma</div><div><br></br></div>
Pavlik complications?
“<ul> <li>"”Pavlik Harness Disease””</li> <ul> <li>Damage to the femoral head despite failure of reduction</li> <li>Injury to acetabular cartilage</li> <li>Impaired bone growth</li> </ul> </ul> <ul> <li>Inferior dislocation resulting from the hyperflexion</li> <li>Femoral nerve compression from hyperflexion</li> <li>Brachial plexus palsy from shoulder straps</li> <li>Skin breakdown</li></ul>”
Principles of Open Reduction for DDH
“<ul> <li>Principles:</li> <ul> <li>Approach</li> <li>Identify acetabulum (cut psoas)</li> <li>Remove Obstacles</li> <li>Reduction</li> <li>Capsulorraphy</li> </ul><li><u>blocks</u></li><li>Extra-articular</li> <ul> <li>Iliopsoas tendon</li> <li>Contracted adductor longus</li> <li>Inferomedial hip capsule</li> </ul> <li>Intra-articular</li> <ul> <li>Pulvinar (fibro-fatty tissue that fills the acetabulum)</li> <li>Transverse acetabular ligament</li> <li>Inverted labrum (neolimbus)</li> <li>Hypertrophied ligamentum teres</li> </ul> <ul> <li></li> </ul> <div><img></img></div></ul>”
SCFE: classification and slippage grading?
“<ul> <li>Southwick Angle Classification - determines severity of slip</li> <ul> <li>Measurement of the difference on the Frog leg lateral of the epiphyseal-shaft angle</li> <li>Mild = <30°</li> <li>Moderate = 30-50°</li> <li>Severe = > 50°</li> <ul> <li><img></img></li> </ul><li>Orthobullets</li><li>Can also be done on AP If bilateral involvement, assume normal is 145 deg for AP and 10 deg for lateral<br></br></li> </ul></ul>”
SCFE Tx (buzzwords)
<ul> <li>gentle transfer to OR table</li><li>In-situ Single-screw fixation - 6.3mm screw into centre of the femoral head with >5 threads engaged, but >5mm from subchondral bone, staying perpendicular to physis</li> <ul> <li>Confirm screw not intra-articular with near-far method</li><li>ideally keep screw head lateral to intertroch line</li> </ul></ul>
Deformity in late SCFE and Osteotomy?
“<ul> <li>Deformity: apex anterior, ER, varus - present with impingement</li><li>Imhauser Osteotomy:</li> <ul> <li>Creates flexion, abduction, IR of distal fragment</li> <li>Fixation with blade plate</li> </ul> </ul> <div></div> <div><img></img></div>”
RFs for AVN following SCFE?
<ul> <li>Associated factors:</li> <ul> <li>Unstable SCFE</li> <li>Over reduction of unstable SCFE</li> <li>Attempted reduction of unstable SCFE</li> <li>Placement of pins in posterosuperior quadrant of epiphysis</li> <li>Cuneiform osteotomy</li> </ul> </ul>
<ul> <li>Risk factors for AVN: </li> <ul> <li>Sankar (JPO, 2010)</li> <ul> <li>Younger patients (11.7 vs 12.8 years)</li> <li>Shorter duration of prodromal symptoms (17.5 vs 65.9 days).</li> </ul> </ul> <li>(Tokomakova KP JBJS 2003, Palocaren T JPO 2010, Boyer DW JBJS 1981, Rattey T JBJS 1996)</li> <ul> <li>Severity of slip </li> <li>Complete or partial reduction </li> <li>Multiple pins</li> <li>Female sex</li> </ul></ul>
X-ray findings in SCFE?
“AP Pelvis<div><ul><li>Klein’s line - does not intersect with femoral head<ul><li>or is asymmetric between sides</li></ul></li><li>epiphysiolysis(growth plate widening or lucency)<ul><li>an early radiographic finding</li></ul></li><li>blurring of proximal femoral metaphysis (metaphyseal blanch sign of Steel)</li><ul><li>seen on AP due to overlapping of the metaphysis and posteriorly displaced epiphysis</li></ul></ul><div>Frog lateral</div></div><div><ul><li>identify subtle slip</li></ul></div>”
Stages of Perthes?
“Waldenstrom<div>-Fragmentation phase is where you aply: Herring, Catterall</div><div>-after remodelling: Stulberg classification<br></br><div><img></img><br></br></div></div>”
Stulberg Classifcation for Perthes?
“-Done after maturity/remodelling<div>-split into: spherical, non-spherical, incongruent hip joint</div><div><br></br></div><div><img></img><br></br></div>”
NHx of coronal knee alignment? DDx Genu Varum? How to differentiate Blounts from physiologic?
“<div><div>DDX Genu Varum</div> <ul> <li>Physiologic</li> <li>Blount’s</li> <li>Metabolic Bone Dz: Ricket’s</li> <li>Dysplasia: achondroplasia, pseudoachon</li> <li>Neoplastic</li></ul></div><div><br></br></div><img></img><div><br></br></div><div><ul> <li>Differentiating from physiological bowing</li> <ul> <li>Proximal tibial location of bowing</li> <li>Sharply angular deformity</li> <li>Asymmetric bowing of the two legs</li> <li>Progressive deformity on serial exams</li> <li>Lateral thrust during gait</li> <li>Very severe deformity</li> </ul></ul></div>”
“Tx algorithm for Blount’s disease?”
<ul> <li>General Algorithm</li> <ul> <li>MDA <9 - physiologic varus, no tx</li> <li>MDA 9-16 - observation</li> <li>MDA >16 - treat</li> <ul> <li>Brace</li> <ul> <li>Stage I and II in kids <3 years</li> </ul> <li>Operative</li> <ul> <li>Stage I and II in kids>3 years</li> <li>Stage >II</li> <li>Age>4</li> <li>Failure of bracing</li></ul></ul> </ul></ul>
<div><div> <div>Stage</div> <div>Treatment</div> <div>I and II</div> <div>Bracing before age 3</div> <div>Stage III</div> <div>Corrective osteotomy</div> <div>Stage IV</div> <div>Corrective osteotomy +/- physeal bar resection</div> <div>Stage V and VI</div> <div>Medial hemi-plateau elevation and proximal tibial realignment osteotomy, bar resection +/- lateral hemi-epiphysiodesis </div> </div></div>
Anterolateral bowing classification and treatment
“<div>1 - nondysplastic</div><div>2- failure of tubulation</div><div>3 - cystic pre-fracture</div><div>-types 1-3 clam shell brace/total contact orthosis or patellar tendon bone (PTB) cast</div><div>4 - pseudoarthrosis - operative</div><img></img><br></br><div>-Options: resection and graft, bone transport, VFG, amputation (syme)</div><ul><li>Fixation Principles: </li> <ul> <li>Resection of pseudoarthrosis</li> <ul> <li>Circumferential resection with periosteum</li> <li>Shorten for boney apposition</li> <li>Resect fibular pseudoarthrosis if present</li> </ul> <li>Correction of Angular Deformity</li> <li>Stabilize fibula</li> <li>Biologic bone bridging of defect</li> <li>Stable Fixation</li> </ul></ul>”
Tx for NF curves?
<ul> <li>Surgery when curve>20deg</li> <ul> <li>Front / back surgery if curve > 50o</li> </ul><li>Complications </li> <ul> <li>Both dystrophic and non dystrophic curves have higher rates of complication compared to AIS. </li> <li>Increased rate of pseudoarthrosis, particularly with dystrophic curves. </li> <li>Risk is 40% in a dystrophic curve with PSF only, and 10% with combined ASF and PSF.</li> </ul></ul>
CP: definition, causes/rfs?
“<div>Non-progressive, encephalopathy with permanent injury of the CNS secondary to a perinatal insult resulting in varying degrees of motor, cognitive and sensory dysfunction</div><div><br></br></div><div><img></img><br></br></div>”
Classification of CP?
“<div><img></img></div> <div>Physiologic</div> <ul> <li>Spastic (65-80%) –> involves the cortex; pyramidal</li> <ul> <li>Increased tone or rigidity with rapid stretch</li> <li>Pyramidal dysfunction</li> <li>Associated with periventricular leucomalacia (PVL) on MRI</li> <li>Most often benefit from surgery</li> </ul> <li>Dyskinetic - Athetoid/dystonic (10%) –> basal ganglia</li> <ul> <li>Involuntary movements, athetosis, dystonia</li> <li>Extrapyramidal dysfunction</li> <li>Poor candidates for Tendon transfers</li> <li>Associated with Rh issues, less common in modern medicine</li> </ul> <li>Ataxia (5%) –> cerebellum</li> <ul> <li>Cerebellar dysfunction</li> <li>Balance and coordination disturbance</li> <li>Usually part of another syndrome, rare for isolated CP</li> </ul> <li>Mixed (12%)</li> <ul> <li>Spastic children may not have athetoid or ataxic manifestations as they are masked by the spasticity</li> </ul> <li>Does not provide any useful information about functional abilities</li></ul><div><div>Anatomic (typically a descriptor for spastic CP):</div> <ul> <li>Hemiplegia</li> <ul> <li>Upper and lower extremities on same side, usually spastic</li> <li>Develop handedness early</li> <li>ALWAYS able to walk eventually</li> <li>Commonly have seizures (33%), 50% intellectual disability</li> </ul> <li>Diplegia:</li> <ul> <li>Lower extremity > upper extremity</li> <li>Most eventually walk</li> <li>May have normal IQ, often have strabismus</li> </ul> <li>Quadriplegia:</li> <ul> <li>Extensive involvement, low IQ, high mortality rate</li> <li>Usually unable to walk</li> </ul> <li>Whole Body:</li> <ul> <li>Quadriplegia + bulbar symptoms</li> </ul></ul></div>”
Tx overview for cp?
Nonoperative<ul><li><strong>physical therapy, bracing/orthotics, medications for spasticity</strong></li><ul><li>spasticity meds: botox, baclofen (intrathecal has less somnolence)</li></ul></ul><div>Operative<ul><li><strong>soft tissue procedures/releases</strong></li><ul><li>techniques</li><ul><li>tenotomiesfor continuously active muscles(e.g. hip adductor)</li><li>tendon lengtheningfor continuously active muscles(e.g. achilles tendon or hamstring)</li><li>tendon transfersfor muscles firing out of phase (e.g. rectus tendon or tibialis posterior)</li></ul></ul><li><strong>selective dorsal rhizotomy</strong></li><ul><li>indications<ul><li>ages 4 to 8, ambulatory spastic diplegia, and a stable gait patternthat is limited by lower extremity spasticity</li></ul></li><li>neurosurgical resection of dorsal rootlets that do not show a myographic or clinical response to stimulation</li><li>contraindications</li><ul><li>athetoid CP</li></ul></ul><li><strong>bony procedures/deformity correction</strong><ul><li>indications<ul><li>usually performed in later childhood / adolescence</li><li>static contractures, progressive joint breakdown, and certain patterned gait-deterioration can be treated with combinations of myotendonous unit lengthening, tendon transfers, and osteotomies</li></ul></li><li>SEMLS surgery (Single-Event, Multi-Level Surgery)</li></ul></li></ul></div>
Tendon transfer for brachial plexus palsy?
“<ul> <li>Hoffer Modification of L’Episcopo Procedure:</li> <ul> <li>Cosmetic axillary incision</li> <li>Release pectoralis major</li> <li>Transfer combined tendons of teres major and latissimus to posterior rotator cuff</li> <li>Average gain of 64o abduction and 45o external rotation at 2 year follow up</li> <li>Does not improve glenohumeral deformity</li> </ul></ul>”
RFs for brachial plexus palsy?
<ul> <li>Large for gestational age</li> <li>multiparous pregnancy</li> <li>prolonged labor</li> <li>difficult delivery</li> <li>fetal distress</li> <li>Shoulder dystocia</li> <li>breech position</li></ul>
preganglionic signs in bbpp?
<ul> <li>Pre-ganglionic (CNS)</li> <ul> <li>Horners syndrome (typically at C7)</li> <ul> <li>Miosis (pupil constriction); Anhidrosis (lack of sweat), Ptosis (drooping eyelid)</li> </ul> <li>Diaphragm paralysis (phrenic nerve) - RC EXAM</li> <li>Winged scapula (long thoracic nerve)</li> <li>Rhomboid absent (dorsal scapular nerve)</li> <li>Rotator cuff absent (suprascapular nerve)</li> <li>Latissimus dorsi absent (thoracodorsal nerve)</li> <li>More common in lower root (C8-T1)</li> </ul> <li>pre-ganglionic requires nerve transfer (neurotization)</li><li>oberlin works - ulnar nerve to biceps</li></ul>
Gait patterns in CP?
“<div>-jumped gait requires release at hip, knee and ankle</div><div>-crouch gait requires release at hip, knee, but ankle requires ground reaction AFO as it is in calcaneus from weak triceps surae<br></br></div><div>-apparent equinus has normal ankle DF/PF but likely has hip/knee flexion contracture (so address these)</div><img></img>”
OI treatment?
-medical: bisphosphonates (increase BMD, decrease fracture rate, improve vertebral shape - but no effect on scoliosis)<div>-scoliosis (70%): PSIF if curve >35 deg (use pedicle screws, 3 rod construct)</div><div>-basilar invagination: decompression and fusion</div><div>-fractures: never plate</div>
Osteogenesis imperfecta: ortho and non-ortho manifestations
“<ul><li>Orthopaedic manifestations<ul><li>bone fragilityand fractures<ul><li>fractures heal in normal fashion initially but thebone does not remodel</li><li>can lead to progressive bowing</li></ul></li><li>ligamentous laxity</li><li>short stature</li><li>scoliosis</li><li>codfish vertebrae (compression fx)</li><li>basilar invagination</li><li>olecranonapophyseal avulsion fx</li><li>coxa vara (10%)</li><li>congenital anterolateral radial head dislocations</li></ul></li><li><a></a><a></a><a></a><a></a><a></a>Non-Orthopaedic manifestations<ul><li>blue sclera</li><li>dysmorphic, triangle shaped facies</li><li>hearingloss<ul><li>50% of adults with OI</li><li>may be conductive, sensorial and mixed</li></ul></li><li>brownish opalescent teeth (dentinogenesisimperfecta)<ul><li>alteration in dentin</li><li>brown/blue teeth, soft, translucent, prone to cavities</li><li>affects primary teeth > secondary teeth</li></ul></li><li>wormianskull bones (puzzle piece intrasutural skull bones)</li><li>hypermetabolism<ul><li>increased risk of<b>malignant hyperthermia</b></li><li>hyperhidrosis, tachycardia, tachypnoea, heat intolerance</li></ul></li><li>thin skin prone to subcutaneous hemorrhage</li><li>cardiovascular<ul><li><b>mitral valve prolapse</b></li><li><b>aortic regurgitation</b></li></ul></li></ul></li></ul>”
OI CLASSIFICATION AND GENETICS
<ul> <li>90% have a mutation in COL 1A1 (chromosome 7q) and COL1A2 (17q)</li> <ul> <li>Abnormal collagen cross-linking via glycine substitution in pro-collagen molecule</li> <li>Prevents proper formation of collagen triple helix</li> </ul></ul>
<div><div> <div>Type 1</div><div><br></br></div> <div>AD</div> <div>Blue Sclera</div> <div>QUANTITATIVE. Mildest form. Present in preschool. Hearing deficit in 50%. </div> <div>Type 2</div><div><br></br></div> <div>AR</div> <div>Blue sclera</div> <div>Lethal in perinatal period</div> <div>Type 3</div><div><br></br></div> <div>AR</div> <div>Normal</div> <div>Fractures at birth. Most severe survivable form</div> <div>Type 4</div><div><br></br></div> <div>AD</div> <div>Normal</div> <div>Moderate severity. Bowing bones common. Normal hearing</div> </div></div>
CPx of Relapse in clubfoot and tx?
“<ul> <li>Treatment</li> <ul> <li><2 years: trial recasting</li> <li>>2 years: trial recasting with higher chance of need TA transfer</li> <ul> <li>Even in adolescents with severe deformity, serial casting can reduce the extent of surgery so it’s reasonable to try</li> </ul> </ul> <li>Forms of relapse</li> <ul> <li>Equinus relapse</li> <ul> <li>Correct by applying serial long-leg casts with the foot abducted and knee flexed. </li> <li>Continue weekly casting until the foot can be brought to about 10 ̊ of dorsiflexion </li> <li>If this is not achieved in 4–5 casts in children under 4 years of age repeat the percutaneous heel-cord tenotomy and resume the nighttime bracing program </li> </ul> <li>Varus relapse</li> <ul> <li>Varus heel relapses are more common than equinus relapses </li> <li>Should be treated by re-casting in the child between age 12 and 24 months, followed by resuming of a strict bracing program. </li> </ul> <li>Dynamic supination</li> <ul> <li>Usually between ages 3 and 4 years</li> <li>Supination deformity will benefit from an anterior tibialis tendon transfer if the deformity is dynamic and not fixed</li> <ul> <li>Need to have 10 degrees of DF</li> </ul> <li>Delay the procedure until after 30 months of age when the lateral cuneiform becomes ossified </li> <li>Bracing is not required after the transfer </li> <ul> <li>The tendon transfer PREVENTS recurrence due to muscle imbalance and does not TREAT recurrence.</li> </ul> </ul> </ul></ul>”
PM release goals?
<ul> <li>Operation goals</li> <ul> <li>Lateral border of foot is straight.</li> <li>Heel is in slight valgus with the foot at 90 degrees to the tibia. </li> <li>Prior to repair of the tendons, the ankle range of motion should be 20+ degrees of dorsiflexion and 30+ degrees of plantarflexion. </li> <li>After repair of the tendons, the ankle dorsiflexion should be to neutral or 0 degrees. </li> <li>The talar head is reduced under the forefoot, with the navicular palpated to be slightly proud medially. </li> <li>The TN joint should be flush dorsally and plantarly. </li> <li>The first metatarsal should be in line with the talus on the lateral radiograph and should be in 0 to 30 degrees valgus relative to the talar axis on the anteroposterior (AP) radiograph. </li> <li>The talocalcaneal angle should be >25 degrees on the lateral and AP radiographs.</li> </ul></ul>
Residual Clubfoot Tx
“<img></img>”
Important Exam findings in cavovarus foot eval?
NEURO EXAM<div>(hx of neuro features, or bowel/bladder, etc)</div><div><br></br></div><div>consider mr brain and spine if positive</div>
X-rays angles for cavovarus foot?
“<div><img></img></div> <div>Meary’s Angle:</div> <ul> <li>Long axis of the talus and the long axis of the first metatarsal</li> <li>Usually 0-5o</li> <ul> <li>Increased in cavovarus feet</li> </ul> </ul> <div>Calcaneal Pitch:</div> <ul> <li>Angle between undersurface of calcaneus and floor</li> <li>Normally about 30o</li> <ul> <li>Decreased pitch indicates forefoot equinus</li> <li>Increased pitch indicates calcaneocavus</li> <ul> <li>Marked dorsiflexion of the calcaneus with normal medial forefoot</li> </ul> </ul> </ul> <div>Hibb’s Angle:</div> <ul> <li>Calcaneus and axis of first MT</li> <ul> <li>Normally <45o</li> <li>Increased in cavus foot</li> </ul></ul>”
Cavovarus reconstruction?
-soft tissue: PT to dorsum foot, PL to PB, TAL, PF release<div>-boney: medial cuneiform dorsiflexion osteotomy, cuboid lateral closing wedge</div><div>-forefoot: jones procedure - EHL transfer to MT1 neck with IP fusion</div>
CVT etiology
<ul> <li>Idiopathic (50% - Kiefer says less than 20%)</li> <ul> <li>20% of idiopathic have family history (AD)</li> </ul> <li>similar to CTEV: arthrogryposis, myelomeningocele</li> <li>CNS (NTD) Defect:</li> <ul> <li>Myelomeningocele (10% of myelo patients)</li> <li>Diastematomyelia</li> <li>Sacral Agenesis</li> </ul> <li>Neuromuscular Disorders - 36%</li> <ul> <li>Arthrogryposis</li> <li>Neurofibromatosis</li> <li>Spinal muscular atrophy</li> </ul> <li>Genetic Disorder</li> <ul> <li>Trisomy 13, 15, 18</li> <li>NF, Prune-Belly Syndrome, Rasmussen Syndrome</li> <li>HOXD10 single gene mutation</li> </ul> <li>Rare Syndromes --> De Barsy, Costello, Rasmussen</li></ul>
DDx vertical talus
<ul> <li>Oblique talus</li> <li>Calcaneovalgus foot --> calcaneus is also dorsiflexed (break is in the ankle, not midfoot)</li> <ul> <li>Usually passively correctable</li> <li>Usually normal by age 6-8 months</li> </ul> <li>Posteromedial bowing of tibia</li> <ul> <li>Apex of deformity is in distal tibia</li> <li>Can result in limb length discrepancy</li> </ul> <li>tarsal coalition, pes planus valgus</li></ul>
Talocalcaneal coalition:<div>(1) associated foot pathology</div><div>(2) x-ray that can help</div><div>(3) treatment</div>
(1) associated with flat feet (rigid)<div>(2) harris axis</div><div>(3) medial approach between FDL and nvb for resection and interposition, then assess foot position - if in valgus - do MDCO.</div>
DDx rigid flatfoot?
<ul> <li>Tarsal Coalition</li> <li>Inflammatory Arthritis</li> <li>Accessory Navicular</li> <li>Post-traumatic</li> <li>Neoplastic lesions</li></ul>
X-ray features of coalition?
<ul> <li>Talar beaking</li> <li>Broadening of lateral process of anterior facet of calc (ant-eater sign)</li> <li>Narrowing/irregularity of the subtalar joint (esp on Harris heel view)</li> <li>Concave undersurface of the talus</li> <li>C-sign</li></ul>
Factors to consider when doing reduction in isthmic spondy?
“<ul> <li>Local Deformity</li> <ul> <li>Lumbosacral kyphosis has worse HRQoL</li> </ul> <li>Global Sagittal Balance:</li> <ul> <li>C7 plumb line should be posterior to hip joints</li> <li>Relates to PI in that people with low (?) PI are able to compensate more with their pelvis</li> </ul><li>Consider reduction if:</li> <ul> <li>High local lumbosacral kyphosis</li> <li>Global imbalance of spine</li> </ul><li><img></img><br></br></li></ul><div><br></br></div><div>-L5 nerve root at risk (in L5-S1 spondy)<br></br></div>”
Delbet Classification
“<img></img><div>Type I: Transphyseal (with or without dislocation of the capital femoral epiphysis - A/B)</div><div>- A: 38% (40) risk of AVN</div><div>- B: 100%</div><div><br></br></div><div>Type II: Transcervical</div><div>- 28% (30) risk AVN</div><div><br></br></div><div>Type III: Cervicotrochanteric</div><div>- 18% (20) risk AVN</div><div><br></br></div><div>Type IV: Intertrochanteric</div><div>- 5% risk AVN</div>”
LLD General Tx
- <2-2.5cm: shoe lift<div>- 2.5-5cm: C/L shortening</div><div>- >5cm: distraction osteogenesis</div><div><br></br></div><div>Closed femoral shortening >5cm may lead to quadriceps insufficiency</div><div>Note: Phemister = physeal ablation by removing a segment of the bone and inserting it in a flipped position</div>
Most common interposed anatomic structure in a flexion type SC#?
Ulnar nerve
Condition with rhizomelic dwarfism and FGF-3 mutation - which spine finding is not seen?<div>A: foramen magnum stenosis</div><div>B: Thoracolumbar gibbus deformity, kyphosis</div><div>C: Short pedicles, narrowed interpedicular distance</div><div>D: Sacral agenesis</div>
Achondroplasia<div>Answer is D<br></br><div><br></br></div></div>
When compared with intravenous (IV) antibiotics via a peripherally inserted central catheter, postdischarge treatment of pediatric acute osteomyelitis with oral antibiotics is associated with a:<div>A: lower rate of treatment failure</div><div>B: high rate of treatment failure</div><div>C: lower rate of rehospitalization or return visit to ED</div><div>D: high rate of rehospitalization or return visit to ED</div>
C<div><br></br></div><div>In the management of pediatric acute osteomyelitis, early transition to oral antibiotic therapy has been demonstrated to have a similar risk of treatment failure as prolonged IV therapy via a peripherally inserted central catheter (PICC).Transition to oral antibiotic therapy can avoid the substantial risks of a PICC complication, which can result in a higher rate of rehospitalization or return visit to the emergency department.<br></br></div>
“Risk factors for little leaguer’s elbow”
- > 80 pitches per game<div>- >8 months of competitive pitching/year</div><div>- Fastball speed >85mph</div><div>- Continued pitching despite arm fatigue/pain</div><div>- Participating in showcases</div>
How does risk of recurrent or C/L ACL injury compare in pediatric vs. adult patients undergoing ACL-R
Significantly higher risk of secondary ACL injury (ipsilateral and C/L) in peds
Femur fractures, when suitable for spica: pros/cons of single vs. double leg immobilization
Single leg: may have decreased complications and decreased time to healing. Increased cost for double. Parents may need more time off work for double. Single leg fits better in car seats.
A 5-year-old girl with increasing lower extremity bowing and short stature is diagnosed to have X-linked hypophosphatemic rickets. The underlying pathology is due to:<div><br></br></div><div>A: Fibroblast growth factor 23 protein increase</div><div>B: ALP deficiency</div><div>C: 1 alpha-hydroxylase deficiency</div><div>D: Carbonic anhydrase deficiency</div>
<div><div><div><div><div> <div>X-linked hypophosphatemic rickets is the most common form of inheritable rickets and is inherited in an X-linked dominant fashion. It is caused by mutations in the phosphate–regulating endopeptidase homolog X-linked gene (PHEX), which are expressed in osteocytes. Mutation of this gene results in an increase in fibroblast growth factor -23, which then leads to reduction of the proteins involved in renal phosphate reabsorption and 1,25-OH vitamin D production. This leads to phosphaturia and ultimately in decreased mineralization of the long bones and teeth.<div></div>Alkaline phosphatase deficiency causes hypophosphatasia and is a recessive condition.1 α-hydroxylase deficiency patients cannot convert 25-hydroxyvitamin D3 to its active form 1,25 dihydroxyvitamin D3, and therefore develop clinical rickets. Carbonic anhydrase deficiency prevents the osteoclasts from acidifying the extracellular space at their ruffled border, which then leads to osteoclast dysfunction and diminished reabsorption of the bone and osteopetrosis.</div> </div> </div> </div> </div> </div>
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4 Anatomic sites with highest risk of concomitant pediatric septic arthritis and osteomyelitis:
Proximal humerus<div>Proximal radius</div><div>Proximal femur</div><div>Distal fibula</div><div><br></br></div><div>- 4 intra-articular metaphyses</div>
CA-MRSA vs. MSSA
<div>CA-MRSA is one of the most common organisms causing severe musculoskeletal infections in children. In contrast to its methicillin-sensitive counterpart, CA-MRSA is associated with a much more severe disease burden, including the need for more operative procedures before it is cleared.<div></div>CA-MRSA is more likely to be diagnosed when the C-reactive protein level is >5 mg/dL. Currently, clindamycin and vancomycin are the first-line antibiotics used for treatment of CA-MRSA; linezolid is reserved for severe resistant cases or allergies, as it is not indicated otherwise for use in children. CA-MRSA is much more likely to cause associated deep venous thrombosis and pulmonary thromboembolism than hospital-acquired-MRSA, due to a much higher propensity for the former to carry the <b>Panton-Valentin leukocidin gene</b>.<br></br></div>
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Most common deformity after ACL reconstruction in a skeletally immature patient
Valgus, due to injury to the distal lateral femoral physis
An 11-year-old boy goes to the emergency department after a twisting injury to his left knee during a soccer game. Radiographs reveal a McKeever type 3 tibial eminence fracture. The most common associated finding with this injury is:<div><br></br></div><div>A. Meniscal tear</div><div>B. Meniscal entrapment</div><div>C. Displaced chondral fracture</div><div>D. PCL injury</div>
“B.Concomitant injuries are increasingly recognized with displaced type III tibial eminence fractures. Although meniscal tears, chondral injuries, and posterior cruciate ligament injuries are associated findings, <b>the most common finding is meniscal entrapment</b><div><b><br></br></b></div><div><img></img><br></br></div>”
Larsen Syndrome<div>- Mutation (and inheritance)</div><div>- Facial features</div><div>- MSK findings</div>
<div>(Filamin, Face (flat), Floppy (generalized laxity, hypotonia - multiple joint dislocations), Feet (clubfoot)</div>
- Filamin B, autosomal dominant<div>- Hypertelorism, depressed nasal bridge</div><div>- Joint dislocations (look for B/L knee, radial head dislocations), scoliosis, clubfeet, cervical kyphosis (may present with myelopathy)</div>
Jaffe Campanacci Syndrome
“<img></img><div>- Presence of multiple non-ossifying fibromas in long bones</div><div>- Mandibular giant cell lesions</div><div>- Cafe-au-lait macules without neurofibromas</div><div>- Mental retardation</div><div>- Heart, eyes, gonads involved</div><div>- Most have pathogenic germline mutation in NF1 (may actually have NF1) - neurofibromin gene</div>”
<div>What halo placement configuration is most appropriate in a skeletally immature patient?</div>
<div>A. Four pins at 2-4 inch-pounds of torque</div>
<div>B. Four pins at 6-8 inch-pounds of torque</div>
<div>C. Eight pins at 2-4 inch-pounds of torque</div>
<div>D. Eight pins at 6-8 inch-pounds of torque</div>
C. Eight pins at 2-4 inch-pounds of torque<div>Halo pin placement into a pediatric skull is performed in cases of pediatric cervical spine injury or after occipital and/or cervical spine surgery. <b>The ideal configuration of pins in a skeletally immature patient is eight pins at 2 to 4 inch-pounds of torque, which is often “finger-tight” in very young children. Because children have thinner skulls than adults, a higher number of pins with less torque are required to prevent penetration into a child’s skull.</b> Children younger than 10 years should also have a CT scan to evaluate skull thickness and prevent placing pins into a thin area of bone. Halo placement in adults usually requires four pins placed at 6 to 8 inch-pounds of torque.<br></br></div>
A 19-year-old pregnant woman presents with a bilateral cleft hand deformity. What is the most common mode of genetic inheritance?<div>A. Autosomal recessive</div><div>B. Autosomal dominant</div><div>C. X-linked recessive</div><div>D. Mitochondrial</div>
<div>B. AD</div>
Cleft (or split) hand and foot deformity is a rare congenital condition that is seen most often in insular or genetically isolated communities (eg, the Amish population). Although cosmetically this condition can be undesirable many patients have very good function, especially if they can achieve prehensile grasp. The most common mode of hereditary transmission is autosomal dominance with penetrance of approximately 70%. Although sporadic reports of autosomal recessive and X-linked cases occur, they are very few and far between.
What are the pearls/pitfalls/potential complications with surgical management of tibial spine avulsion fractures?
Pearls<div>- Continually palpate calf compartments</div><div>- Address concomitant pathology before managing the avulsion fracture</div><div>- Disengage any interposed soft tissue</div><div><br></br></div><div>Pitfalls</div><div>- Remove only the necessary portions of the intermeniscal ligament</div><div>- Leave at least 1-2cm between tunnels</div><div>- Maintain tension of all sutures while each one is tied</div><div><br></br></div><div>Potential complications</div><div>- Loss of motion/arthrofibrosis</div><div>- Residual displacement or laxity</div><div>- Nonunion or malunion</div><div>- Growth disturbance</div>
