Chapter 5 Pediatric Podiatry

5 Pediatric Podiatry
Russell Volpe, DPM
C o n t e n t s
5.1 Congenital Deformities . . . . . 420 5.2 Metatarsus Adductus . . . . . . 428 5.3 Serial Plaster Immobilization . 432 Of Congenital Foot Deformities 5.4 Podopediatric Exam . . . . . . . . 436 5.5 Collapsing Pes Plano Valgus . 440 5.6 Developmental Flatfoot . . . . . 444 5.7 Pediatric Orthoses. . . . . . . . . 445 5.8 Normal And Pathologic Gait In Children . . . . . . . . . . . 449 5.9 Rotational And Angular Disorders In Children. . . . . . . . . . . . . . . 456 5.10 The Pediatric Hip . . . . . . . . . 461 5.11 Pediatric Sports Medicine . . . 465 5.12 Knee. . . . . . . . . . . . . . . . . . . 468
5.13 5.14 5.15 5.16
ACL Injuries . . . . . . . . 471 Osteochondroses. . . . . 478 Toe Walking . . . . . . . . 481 Pediatric Neuromuscular Disorders . . . . . . . . . . 482 Pediatric Pharmacology. . 486 Skeletal Syndromes And Systemic Disorders In Pediatric Orthopedics . . . 490 Other Syndromes Involving Short Stature . . . . . . . 494 Malformations Of The Hand And Foot. . . . . . . . . . . 503
5.17 5.18
5.19
5.20
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5.1
Congenital Deformities
Definition Congenital deformity Usually unilateral can be bilateral 1-3/1000 live births Extreme dorsiflexion of ankle Decreased plantarflexion Referred to as up and out
Calcaneovalgus
Figure 1.
Etiology Abnormal intrauterine position Excessive internal limb rotation Rarely with congenital/neuromuscular/endocrine disease Associated findings Oligohydramnios Dislocated peroneal tendons Chromosomal abnormalities Thorough general, orthopedic, and neurologic physical recommended Uterine positions cause forefoot and calcaneus, to move on stable talus Open kinetic chain - talus in unit with leg, calcaneus, and foot move around it Pathologic Anatomy Navicular displaced laterally to talus Midfoot dorsiflexed and abducted on talus Distal calcaneus laterally displaced Prominent plantar-medial talar head Tight anterior and lateral musculature Pathologic anatomy Achilles tendon not contracted Talocalcaneal and plantar calcaneonavicular ligaments are relaxed Lack of rigidity (flexible congenital pes valgus) Clinical Features Excessive dorsiflexion Limited plantarflexion Forefoot touch anterior leg
420 The 2005 Podiatry Study Guide
Off w.b. calcaneus in valgus Forefoot varus Talar head prominent medially MTJ abducted and dorsiflexed Subtalar joint ROM normal or increased Flexible foot type Achilles tendon not taut even in maximum dorsiflexion Redundant skin folds anterior and lateral ankle Sinus tarsi depression on plantarflexion
Figure 2.
Radiographic findings Lateral View Plantarflexed talus- below cuboid if severe Forefoot dorsiflexed Talus overlaps anterior(distal) superior calcaneus Anterior break-cyma line Decreased calcaneal inclination Radiographic findings Dorso-plantar View Talar bisection falls medial to the 1st metatarsal Talo-calcaneal angle above 30-40 Altered cyma line Navicular not visible Radiographic differential diagnosis Stress lateral view taken with forefoot plantarflexed in radiograph talar-first metatarsal relationships will restore in calcaneovalgus; talar-first malalignment will persist in vertical talus. Classification Mild plantarflexion of ankle to 90(right angle) or beyond. Talar bisection central cuboid (lateral x-ray) Moderate - plantarflexion to less than 90. Talar bisection lower 1/3 cuboid Severe - plantarflexion to 80. Talar bisection below cuboid Treatment Rationale Prevent deleterious osseous adaptation Prevent abnormal joint relationships Support the superstructure function of foot altered by congenital pes valgus - ambulation may be delayed or awkward May produce muscle imbalance
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Result of Non-Treatment The untreated calcaneovalgus foot is predisposed to abnormal pronation after weightbearing and may lead to a symptomatic flatfoot in childhood and beyond Goal of Treatment in Infancy Reduce forefoot deformity on the rearfoot Reduce calcaneovalgus (dorsiflexion + eversion) Reduce muscular and ligamentous adaptation Prevent osseous adaptation Treatment - Mild Deformity in Infancy Manipulation - begin in neonate. Heel vertical, forefoot plantarflexed, and adducted (at midtarsal joint). Hold for 10 seconds 15 reps - diaper changes J-strap to hold Treatment - Moderate Deformity in Infancy Manipulation with strapping Tarsosupinator or straight last shoes D-B bar or Counter Rotation System - set straight or internal Serial plaster immobilization Treatment - Severe Deformity in Infancy Serial plaster immobilization Cast usually below-knee Maintenance with shoe, brace or splint Maintain for half as long as correction took Response is rapid Serial Casting For Calcaneovalgus Hold subtalar joint in neutral to slight varus Ankle in slight equinus Forefoot in neutral - reduce abducted/dorsiflexed MTJ Avoid using forefoot as lever arm to reduce up and out deformity at ankle and STJ
Figure 4.
Figure 5.
Figure 3.
Treatment - Mild Deformity Ambulatory High-top supportive shoes Heel wedges LA padding Pre-fabricated orthoses < 3yr Exercises / manipulation Custom orthoses > 3 yr. if concerns persist
Figure 6.
Treatment - Moderate Derfomity Ambulatory Shoes, wedges, LA pads, pre-fab orthoses if under age 3 Night-splint, tarso-supinator shoes Functional foot orthoses if > age 3, deep heel seat, medial flange recommended Treatment - Severe Deformity Ambulatory Night splints with tarso-supinator shoes High-top / supportive walking shoe Maximum-control pediatric foot orthoses - UCBL/DSIS Rehab intrinsic and extrinsic muscle groups Vertical Talus Convex Pes Valgus SYNONYMS Congenital rigid flatfoot Teratologic talo-navicular dislocation INCIDENCE First described by Henken in 1914 Relatively rare 50% bilateral Males over females Right leg predominance High percentage of associated anomalies (congenital, syndromal, neurologic) Components of Deformity Rigid rockerbottom (convex plantar aspect) Prominent talus medially and plantarly Navicular dislocates dorsally Equinovalgus deformity Forefoot abducted and dorsiflexed on rearfoot Rearfoot plantarflexed Tendoachilles tightness Heel perpendicular to slight valgus (not high valgus rearfoot as might be expected) Anterior and peroneal muscle tightness
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Figure 7.
Differential Diagnosis Oblique talus DDx on lateral plantarflexion (stress) x-ray Talipes calcaneovalgus Acquired flatfoot Spastic equinus flatfoot - cerebral palsy Iatrogenic rockerbottom (post TEV casting) Primary Diagnosis (Associated Syndromes) Arthrogryposis Myelodysplasia Epidermal Nevus Syndrome Sacral Agenesis Pathomechanics Growth disparity soft tissue/bone Dysplaisia of spring ligament leads to downward and medial rotation of the talar neck and head Absence of plantar intrinsics Aplasia of the anterior calcaneus Weakness of posterior tibial tendon associated with forward movement of the tendon along with the flexor digitorum longus tendon. The PT tendon now acts anteriorly as a dorsiflexor of the fore part of the foot Radiology AP/lateral/plantarflexion lateral (stress) views Increased talocalcaneal angle (>45 degrees) Calcaneus in equinus Navicular dislocation dorsally Plantarflexion lateral (stress) - No talar-first met congruity, i.e. the bisection of the talus will remain plantar to the 1st ray. In calcaneovalgus, the plantarflexion lateral will demonstrate the talar bisection approximately bisecting the first ray. Muscle Imbalances Posterior tibial and peroneals anteriorly displaced - ankle and forefoot dorsiflexor Medial column elongated Posterior tibial, peroneals, and long extensors shorten over time Goals of Treatment Restore Navicular/Talar/Calcaneal Relationship Plantigrade Foot
Painfree Function Minimize Arthritic Changes Non-Operative Treatment SERIAL PLASTER CASTING (USUALLY UNSUCCESSFUL) Stretch the soft-tissue preoperatively Stretch triceps surae Pressure on anterior calcaneus Plantarfex, adduct and invert forefoot Attempt closed reduction? Operative Correction Procedure to relocate midfoot plantarly and reduce the equinus of the rearfoot. Staged procedure Older children extra-articular subtalar arthrodesis Assessment Criteria (DeRosa, et al., Foot & Ankle, Vol. 5, No. 3) Assess these criteria to determine correction: Frontal plane heel position Residual equinus Lateral border alignment Medial talar prominence Subtalar joint mobility Range of plantar flexion Talipes Equino Varus Incidence 1-2 per 1000 live births 1/35 with a sibling who has TEV Ethnic diversity Polynesians 6.81/1000 2 -2.5/1 male/female 30 - 50% bilateral Etiology Arrest of fetal development at ninth fetal week Combination of genetic and environmental factors Primary germ plasm defect Two types one with positive family history the other without Morphological Features Dimple anterolateral Inversion, adduction of forefoot Varus of rearfoot Talocalcaneal equinus (little or no change on dorsiflexion lateral x-ray) External talar rotation (prominent laterally) Inverted and plantarflexed calcaneus Associated Internal tibial torsion Shorter/smaller calf Shorter/wider foot
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Tendoachilles notch Small, bean-shaped heel
Figure 8.
Figure 9.
ClassificationEtiology Based Congenital Idiopathic Intrinsic - type 1 rigid(genetic/teratologic) More likely to have calcaneal anomalies (smaller, inverted, or plantarflexed) Extrinsic -type 2 flexible Normal calcaneal anatomy Neurogenic Open or closed defects of the spina (spina bifida) Myogenic Osteogenic Collagenous/cartilagenous Aquired Neurogenic progressive neuromuscular disease, spinal cord tumors Vascular Volkmans ischemic contracture Traumatic abuse, serious injury Pathology Head and neck of talus medially and plantarly deviated on the body of the talus Superior surface of talus anteriorly displaced out of ankle mortise Calcaneus in equinovarus and internally rotated Contractures - Posterior Ankle capsule Subtalar capsule Calcaneofibular ligament Tendo achilles Contractures Medial Spring ligament Deltoid ligament Tibiales posterior Flexor digitorum Longus Flexor hallucis Longus Clinical Examination History and physical
Chief complaint Past medical history Prenatal Postnatal Growth and development Examination Musculoskeletal Neurophysiologic Special diagnostic
Radiographic Evaluation AP View Reduced talocalcaneal angle < 15 degrees to near parallel Superimposition of talar head on anterior surface of calcaneus Ossific center of navicular is medially displaced Lateral View Decreased calcaneal inclination angle Radiographic Angles Talocalcaneal index (on lateral) <40 degrees = talonavicular dislocation. This is the sum of the AP and lateral talocalcaneal angles. Simons rule of 15 (on AP). If talocalcaneal angle is less than 15 degrees and the talar-first metatarsal angle is greater than 15 degrees than the talo-navicular joint may be said to be dislocated. This is useful in an infant when the navicular is not yet ossified. Lateral T/C angle <35 on stress dorsiflexion Non-Operative Treatment Stretch soft-tissue Manipulate subluxed joints Maintain with casts Duration of Casting Weekly - neonates Bi-weekly - infants Maintain for half as long as to correct Manipulation Position Evert calcaneus Pressure over lateral talar head Abduct forefoot Reduce equinus at ankle/STJ take care to reduce equinus at the ankle joint (as opposed to the midtarsal joint). This prevents iatrogenic rockerbottom deformity from resulting.
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Figure 10.
Figure 11.
Treatment Outcomes Reduce equinovarus Reduce joint subluxations Create a plantigrade foot Functional ankle range of motion (minimum 5 ankle dorsiflexion) Maintenance Options Straight/abductory last shoes Night splints (as needed) Ankle foot orthoses UCBL/DSIS
Figure 12.
Figure 13.
5.2 Metatarsus Definition
Adductus
A transverse plane adduction deformity of the metatarsals at the tarsal-metatarsal articulation (Lisfrancs joint)
Incorrect Synonyms
Metatarsus varus (frontal plane) Forefoot adductus (midtarsal joint)
Incidence
1/1,000 live births No sex predilection If one child affected risk of second affected 1:10
Determining Metatarus Adductus

Measure METATARSUS ADDUCTUS angle. Angle made by bisection of the lesser tarsus and the long axis of the 2nd metatarsal.
Radiographic Relationships
Bisect Lesser Tarsus Lateral aspect base of 4,5 mets Medial aspect base of 1st met Ant lateral aspect calcaneus Ant medial aspect calcaneus These four points create a box. Bisect this box. The metatarsus adductus angle is the angle made by this bisection and the long axis of the second metatarsal. Range of Normal Metatarus Adductus Angle Birth 15-35 degrees Beginning Walker 20 degrees Four to six Year Old 5-15 degrees Etiology Retention of fetal alignment Abnormal in-utero position producing muscle imbalance Abnormal amniotic compression with resultant contractures of medial soft tissues Untoward sleeping and sitting positions may accentuate deformity Clinical Features C-shaped appearance Convex lateral border Concave medial border Prominent styloid May be increased interval between hallux and 2nd digit (met primus adductus) Rearfoot neutral - normal varus
Figure 14.
Classification Flexible Rigid Dynamic (functional) Differentiate From Primus Adductus 95% excellent prognosis Proposed Etiology Demonstration of tight abductor hallucis
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Characteristic Radiographic Findings MA angle increased Severity of adductus decreases laterally Superimposition of mets at their bases decreasing laterally May be associated met primus adductus May be hypoplasia of cuboid Differential Diagnosis Metatarsus varus Met primus adducutus Talar neck adductus Forefoot adductus Metatarsus adductus and metatarsus varus = metatarsus adductovarus Talar Neck Adductus The angle formed between the head and neck and trochlear surface in the transverse plane 9-12th fetal week TNA = 33 degrees Adult TNA = 22 degrees Associated Fundings 75% of patients with metatarsus adductus have lack of external tibial torsion (or internal tibial torsion) Forefoot Adductus An adduction deviation of the forefoot on the rearfoot in the transverse plane occurring at the midtarsal joint Forefoot adductus Adult norm 10 Metatarsus adductus is not one-third of clubfoot deformity Adductus in TEV occurs at the midtarsal joint Talipes equino varus (TEV) Rearfoot equinus Marked varus Metatarsus adductus Rearfoot Normal Valgus on weight Normal dorsiflexion Skew or Z Foot Met adductus with marked calcaneal eversion and talo-navicular subluxation Implications Cosmesis Shoe-fitting Early deformity and dysfunction The hallmark deformity associated with metatarsus adductus is: Juvenile hallux abductovalgus Juvenile Digital Contractures Line of weight bearing normal foot L/M calcaneus, 5, 2, 1, hallux Line of weight bearing metatarsus adductus L/M calcaneus, 5,4,3-2, 3rd or 2nd digits Abnormal extensor alignment in met adductus results in digital contractures
Treatment Considerations The more flexible the deformity the more favorable the prognosis The earlier treatment is instituted the more favorable the prognosis Benefits of early correction include bony remodeling to more normal alignment CONSERVATIVE Manipulation Parental education Control of postural positions Shoe therapy Concomitant use of night splints Manipulation and serial plaster immobilization SURGICAL Soft-tissue Osseous Shoe Therapy Outflare last or straight last In shoe wedging (Tax) 1/8 inch felt Shaft of 1st metatarsal Cuboid
Figure 15.
Night Splints Purpose: To treat associated torsion and/or correct untoward sleeping positions Denis-Browne/Filauer bars Ganley splint Counter rotation splint (CRS)
Figure 16. Serial Maniopulations and Holding Plaster Immobilization
Figure 17.
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Manipulate foot for five minutes or one wk prior to visit Protect cutisz Stockinette Minimal padding Apply two to three inch plaster against deformity encompassing foot and ankle Supinate rearfoot and brace cuboid with palm Abduct mets with free hand by grasping forefoot and exerting pressure along shaft of first in abduction (not the hallux) Change cast q7 - 14 days Average Tx time 6 - 12 weeks To maintain correction utilize holding casts for one-half the time required to obtain correction
Figure 18.
Figure 19.
Criteria for the Cessation of Manipulative Plaster Immobilization Loss of C shape Lack of palpable styloid Decreased met adductus angle Possible Surgical Intervention Positive family history Persistent deformity Adequate trial of unsuccessful conservative therapy Summary The oftentimes innocuous appearing deformity of metatarsus adductus if left unrecognized, inadequately or inappropriately treated, will produce dysfunction and further deformity at an early age
5.3
Serial Plaster Immobilization of Congenital Foot Deformities

Based on age and severity of deformity
When to Cast
Age
Younger - greater joint mobility Older - increase risk of iatrogenic joint dysfunction Infants before the age of walking are the best candidates for casting
Severity
More severe deformities need casting
Purpose of the Cast

Apply external forces to redirect growth Stretch tight structures Avoid iatrogenic joint dysfunction
Manipulation
Stretch soft tissue contractures Precede cast application Five to 10 minutes to abnormal segment Practice hand positions - create sound habits
Figure 20.
Other Concepts
Maintenance Half as long as correction (cast or other device) Prevent recurrence Serial Radiographs Monitor progress Ensure correction is taking place at appropriate joint level
Preparation
Warm water in bucket Draping materials Skin preparant Stockinette/tube gauze Webril/elastic cast padding Two, three or four inch extra-fast-setting plaster rolls
Figure 21.
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Advice to Parents
Inform to reduce anxiety Child should be rested Bottle/pacifier Soak off casts before return
Cast Application
Prepare skin Apply minimal padding two to three layers Extra pad prominences Avoid wrinkling Wet plaster and leave saturated to allow set time Apply distal to proximal Six layers of plaster Reinforce plantar and posterior heel Fold end of layers to create tag for ease of removal Slipper cast then leg cast or single unit casting
Figure 22.
Figure 23.
Figure 24.
Figure 25.
Cast Modifications
Cast cutter removal not advised fearful to child Long leg to effect posterior muscles or align knee Synthetic or other new materials, - may be used to reinforce over plaster for walking cast. Not ideal for bottom layer as is less moldable Minimal or additional padding(to bony prominences)
Durations
Four to eight casts Weekly or bi-weekly
Removal
Soak at home just prior Add white vinegar to loosen bond
Metatarsus Adductus - Corrective Position Left Foot (Patient) - Right Hand (Clinician)
Stabilizes thenar eminence on cuboid Cup heel and rotate into slight varus Place cuboid plantar to navicular increasing MTJ stability Ankle joint at 90
Left Foot - Left Hand

Corrective force in transverse plane First web space at medial 1st metatarsal head IPJs of thumb and fingers fully extended Apply pressure parallel to heel to keep forefoot to rearfoot perpendicular
Internal Tibial Position - Corrective Position

Diagnosed with excessive rotation in internal direction One hand stabilizes distal thigh Other hand rotates leg in appropriate direction Knee flexed at 30 Apply short-leg cast Correct foot deformities
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Apply thigh cast - leave knee uncovered Flex knee to 30 Rotate leg to correction Join cast with three or four inch roll
Talipes Calcaneovalgus-Corrective Position

Right Foot (Patient) - Right Hand (Clinician) Cup heel and invert and plantarflex Right Hand - Left Hand Thumb at plantar distal calcaneus Dorsal pressure to talus Plantarflex and adduct at MTJ
Talipes Equinovarus - Left Hand (Clinician)

Left Foot (Patient) - Left Hand (Clinician) Over navicular-plantarflex, abduct and evert to pronate medial column Left Foot - Right Hand Evert and externally rotate heel Pull proximal posterior heel plantigrade to reduce equinus Long-leg cast - block g/s equinus Talipes Equinus (Toe Walking) Congenitally short g/s complex - soft tissue contracture Lengthen to avoid compensation Long-leg cast in pre-walker Can short-leg in walking child as gait has knee extension Talipes Equinus-Corrective Position Short-leg cast Invert heel to place cuboid below navicular to prevent CC joint pronation with dorsiflexion Dorsiflex foot to resistance Thigh cast Join cast with three or four-inch roll Keep knee gently extended
5.4
Podopediatric
Thumb to forearm - two points Fifth digit extension - two points Elbow hyperextends - two points Knee hyperextends - two points Toe touch ability - two points Maximum - ten points (higher score more laxity)
Ligamentous Laxity
Spinal Exam
Curvatures - scoliosis Rotations Palpable defects - tumors, other masses Hairy patches and dimples myelomeningocoele, dysraphism, etc.
Neurologic Exam
Reflexes deep tendon and superficial (pathologic) Spontaneous movements General tone Overall integrity
Hip Exam
Femoral shortening flexion (all is test) and extension Skin fold irregularities Loss of abduction in flexion Ortolani clunk in neonate (reduce DDH) Provoke located hip with Barlow maneuver
Exam Positioning of a Child

Sitting up Lying back only when needed defenseless position scary for child Use parents lap Legs facing examiner
General Observation
Limb shortening Limb angulation Limb rotation Limb - trunk proportions
Facial Exam
Parietal bossing Blue sclarae High-arched palate Low-set ears Ear irregularities Tooth anomalies Facial symmetry These may suggest genetic syndromes with orthopedic or lower extremity implications.
Hand Exam
Square Long tapering fingers Nail anomalies Thumb in palm Single palmar crease These may suggest genetic syndromes with orthopedic or lower extremity implications.
Gait Exam
See Gait section for details Short-legged Antalgic Trendelenburg Neurogenic Rotational Angular
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Joint Exam
Look - skin, shape, position Feel - skin, soft-tissue , bones Move - active, passive, power X-ray
Torsional Assessment
Total foot rotation Femoral rotations Tibial rotations Ryders test Malleolar position Angular assessment
Figure 26.
Figure 27.
Figure 28.
Genu Valgum
Measure intermalleolar distance, record patient height, as a given distance is more significant in a shorter person. Knees will be touching in genu valgum
Figure 29.
Angular Assessment
Genu varum - measure intercondylar distance Ankles will be touching in genu varum
Tips for Assessment

Consider pseudo-bowing (displaced gastroc secondary to internal torsion) In-toe Check patellar position Inward - femoral segment Outward - tibial/foot segment Gentle bow - physiologic Sharp, angular bow - true tibia vara (Blounts)
Figure 30.
Foot Exam
Mobile Deformities POSITIONAL In utero Attitudinal SECONDARY Compensatory Neuromuscular Ligamentous laxity
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Rigid Deformities PRIMARY Talipes equino varus Vertical talus SECONDARY Neuromuscular Tarsal coalition JRA
General Exam Tips

Watch child remove clothing - check use of hands and limbs Observe trip to examination room from waiting area - early gait exam Examine painful area last Sit for exam - go to foot and leg level Toe and heel walk with limp to eliminate fake limps stress gait
Torsional Screening
Perform total foot rotation Perform thigh rotation If total foot was abnormal and thigh rotation normal suggests tibial torsion Perform total foot rotation Perform thigh rotation If total foot is abnormal and thigh rotation is abnormal, deformity likely in proximal segment
Prognosis
Consider natural history Metatarsus adductus - treat Torsions - rapid growth - best chance for spontaneous correction and treatment under 18 months 18 months - four years active growth - amenable to treatment After five - static growth treatment less successful
Lower Extremity Exam

A R M Method Attitude-at-rest - include hopscotch technique Relationship of parts Measurement - quantify relationships JIM GANLEY, DPM JAPMA, FEB. 1981
Conclusion
Child is unique Focus exam Master tips Natural history to guide treatment
5.5
Collapsing Pes Plano Valgus

Is flatfoot a pathological condition that effects foot function? If so, how do we determine which ones to treat and how aggressively to treat them?
Concerns
Flatfoot As Pathology In The Literature

Oxygen consumption decreased with arch support - Otman, et.al. A cause of spontaneous osteonecrosis of the navicular in otherwise healthy adults - Haller, et.al. Susceptibility to stress fractures correlates to pes planus - Sullivan, et.al. There is a relationship between pes valgus and hallux abducto valgus - Inman, Hohman, Kalen, Brecher.
End-Stage Flatfoot
A painful tarsal enthesopathy which is the result of severe long-term pronation of the foot about the subtalar and other joints
Signifigance
Those authors who dismiss the flatfoot as trivial, normal, or as something that is outgrown over time invariably neglect to connect this condition with the many disabling conditions it creates Mahan, K.T., Comp Text - Foot Surgery ed. McGlamry
Classification
Congenital Calc. Valgus Vertical talus Peroneal spasm Developmental Accessory navicular Tarsal coalition Z-foot Equinus Acquired Trauma Infection Arthritis PT dysfunction Neuromuscular Biomechanical
Classification
Rigid Flatfoot Convex pes plano valgus Tarsal coalition Trauma Neuropathy Flexible Flatfoot Forefoot varus Flexible forefoot valgus Rearfoot equinus Calcaneovalgus Torsions Muscle abnormalities Neurotropic - early Medial weight shift
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Clinical Features
Everted heel Abduction of the forefoot on the rearfoot Collapse of the medial column Flexibility of the foot with reducibility of deformity Pronated throughout gait, notably after heel lift Posterior equinus as a primary force or secondary adaptation
Figure 31.
Figure 32.
Why Treat The Pes Planovalgus Foot?

Pain Reduction of activity Reduced social interaction Fatigue Overuse Cramping Discomfort Joint Degeneration Slow, consider the effects over time Associated Deformities Hallux valgus Metatarsalgia Digital pathology
Planal Dominance
Allows the treatment to address the pathology on the basis of clinical and radiographic findings. Understanding the primary plane of both deformity and compensation introduces a greater measure of predictability and precision in the selection of treatment.
Planal Dominance As A Management Concept

Determine clinically and radiographically Increased vertical subtalar axis increases transverse motion Increased horizontal subtalar axis increases frontal plane motion
Planal Dominance On X-ray

Transverse Plane Deformity Inc. T-C angle - AP view Inc. Cuboid abductus angle -AP view Dec. Forefoot adductus angle -AP Dec. T-N congruency Frontal Plane Wide lesser tarsus - AP view Dec. first met declination - lateral Dec. height of sustentaculum Inc. superimposition of lesser tarsus on lateral view SAGITTAL PLANE Inc. Talar declination - lateral Navicular - cuneiform breach Inc. T-C angle - lateral Dec. calcaneal inclination - lateral
Clinical Evaluation
General structural Muscle inventory Biomechanical Radiographic Hubscher maneuver Dynamic evaluation Other clinical exams and tests
Management
PEARLS FOR THOUGHT Even in the absence of symptoms the child with a collapsing pes plano valgus will adapt their activities, lifestyles, personality and vocation ... The astute clinician will probe further...and unveil an entire lifestyle and personality adapted to the function of the deformed feet. MAHAN, K.T. COMP TEXT - FOOT SURGERY
Pre-Walkers
Serial casting Rx shoes Splints - Ganley, CRS ... Many of the changes labeled as compensatory, such as rearfoot pronation associated with forefoot varus, are truly primary because they may be observed before the child ever takes a step...
Toddler
Orthoses Pre-fab Custom Night splints Rx shoes Evaluate equinus influence
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Figure 33.
Childhood And Adolescence

Custom orthoses Stretching, strengthening programs Night splints Evaluate equinus influence
Figure 34.
Adolescence To Adults
Custom orthoses Role changes to motion control and minimization of further deformity Surgery - failed conservative Tx
Surgical Indications
At least one of the following: Pain - in spite of control Progression - in spite of control Instability - abnormal joint stress Deformity - impossible to control
5.6
Development of Flat Foot

Since most childrens feet are flat, dont hurt, and are not deformed they are assumed to be normal Childrens feet are flat due to an increased plantar fat pad Dont worry theyll grow out of it!
Common Myths
Facts
80% of the population will suffer from foot problems at one time or another in their lives The vast majority of these problems begin in childhood and are musculoskeletal in nature Often symptomatology and/or deformity is not apparent till the third or fourth decade
Differential - Pes Valgus

Calcaneovalgus Convex pes valgus Os Tibiales externum Neurologic disorders Syndrome component Iatrogenic Mechanical Developmental Mechanical Equinus- forefoot, met, gastroc-soleus, hamstring, ileopsoas Genu valgum Transverse plane deficiencies Forefoot varus Mortons syndrome Limb length discrepancy
5.7
Pediatric Orthoses
Objective - Motion Control Pes plano valgus Ligamentous laxity Objective - Accomodation Talipes equino varus Convex pes plano valgus Peroneal spasm Juvenile arthritides Inflammatory conditions
Criteria For Selection
Shell Selection
Motion Control Thermoacrylics Thermoplastics Lamination of softer materials Accomodation Thermoplastics Toprelle Leather EVA Cork PPT Plastizote
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Specialty Devices
Dynamic Stabilizing Innersole System (DSIS) 5 degree varus offset heel seat High medial and lateral flange Longitudinal split Individual control of medial and lateral column
Figure 35.
University of California Biomechanics Laboratory (UCBL) Deep heel seat High medial and lateral flanges Brace-level control
Figure 36.
Blake Inverted Orthosis (BIO) Pour and balance positive 15-45 inversion 20 mm heel seat Increase supination moment to STJ Severe pes valgus Medial axis deviation Ligamentous laxity Gait Plate Rigid to alter lever arm Extend past 4/5 MPJs Shoe with flexible ball Must have available hip motion (at least 30 external) More severe case gait plate less effective Enhance with valgus FF post
Figure 37
Posting
Rearfoot Stabilizes the device Resist rapid pronation at heel strike Forefoot Avoid under age six May be necessary in unstable foot/supinatus Consider with rigid valgus
Figure 38.
Shoe Selection
Properties Of The Shoe Rigid counter Firm sole in sagittal plane Firm shank Flexible ball High top in severe pes valgus
Impression Casting
Plaster - single splint in small child Hold STJ neutral from behind helps to resist childs movement Avoid biofoam, which makes a weak, wide cast in a moving child Dorsiflex hallux plantarflex first metatarsal Dorsiflex digits increases arch height
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Figure 39.
Cast Modifications
Calcaneal pitch Plaster removed from positive to lock calcaneocuboid joint one-fourth to one-half inch Moderate to severe pes valgus Need range of motion to tolerate Do not add plaster except to smooth Increases control of device Narrow the positive Reduce a wide negative Alter the positive to reduce a metatarsus adductus
Figure 40.
Figure 41.
Alternatives
Pre-Fabricated Best under three Choose carefully Flanges, depth, etc. Better than nothing
Figure 42.
Supramalleolar Orthoses Control the ankle Follow failed orthosis Superstructural deformity Neuromuscular disease Better tolerated than AFO
Figure 43.
5.8
NORMAL AND PATHOLOGIC GAIT IN CHILDREN

Flat-foot strike Knee/ankle flexion Reciprocal arm swing absent Wide base Abrupt and choppy Low velocity (increase with cadence) Short step length (lack neural control to increase) Externally rotated limb with circumduction
Onset Of Ambulation
Figure 44.
Two Year Old Gait

Greater ankle DF at contact/lose foot drop Heel strike in large % Knee flexion after heel-strike Knee extension before toe-off Swing phase ankle DF 75% have arm swing Single support 35%
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Three Year Old Gait

Adult hip and knee motions High stance ankle DF Increasing single support Greater velocity Slower cadence Awaiting control of ankle PF to increase step length
Maturation Of Gait
Presence of heel strike Reciprocal arm swing Narrow base in double support Mature initial knee flexion wave Absence of swing phase equinus
Final Determinants Of Gait

Increasing single support 38% by age seven Increasing velocity Age one - 60 cm/s Age seven - 120 cm/s Decreasing cadence - greatest ages 1-3 Increasing step length with ankle PF control Ankle spread to pelvic width decreases
Age Parameters For Motor Maturity

Six months - roll-over Six months - sitting Nine months - crawling 9-15 months - walking (average 12 months) Two factors needed to walk: Maturation of myelin Overcome inherent difficulties of learning a complex task
Gait Assessment
Complete motor evaluation Muscle strength and tone Range of joint motion DTRs - upper and lower Presence of involuntary movements Evaluation for joint pain Spinal exam Lordosis/kyphosis Scoliosis Derm markers? Hemangiomas Lipomas
Caf au lait spots Bony abnormalities Muscle mass
Examination Of Gait
Standing Posture Wide base? Bring knees and toes together -cerebella ataxia Close eyes - sensory ataxia. Normal = 30 secs Check Gait Barefoot In shoes In shoes with device
Observation of Gait
Arm swing Pelvic position Leg swing Hip and knee in sagittal plane Step symmetry Foot weight-bearing patterns Listen while you look
Techniques To Bring Out Pathlogy

Run Heel walk Heel lift Away on toes/return on heels Is ground clearance equal? Arm weakness may emerge
Stressing Gait
Tandem walking Tests cerebellar function Can perform by age 4-5 years Proficient by age 6-7 Aptitude may vary If absence suspect mid-line cerebella disease Tumor? Confirm ask to execute quick turns - if base widens (+)
Stressing Gait
Suspected proximal or gluteal weakness Stair climbing Rise from floor Gowers sign
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Non-Neurologic Abnormal Gait

Antalgic Gait Affected leg favored Limp results Caused by pain or inflammation Muscle strength and tone normal DTRs may be reduced from guarding Numerous causes Thorough work-up indicated to find cause Short Leg Gait Sagittal plane head movement manifests as up and down head movements Step up in stance to long side Step down in swing to short side Minimal sideward head or trunk movement Pain and antalgia usually absent Common compensations include: Toe walking, flexion of the long limb, vaulting and circumduction of the long limb Limp Consider age and nature of limp 2 year old: DDH short - leg or abductory twist not antalgic Septic hip - antalgic Toxic synovitis - antalgic Juvenile RA - antalgic Diskitis - antalgic School-aged child Decreased incidence of DDH and septic hip Calve-Legg Perthes incidence increases antalgic Trauma Pre-teen and Teen Septic hip Calve-Legg Perthes Slipped Capital Femoral Epiphysis Conversion Reacton Gait Hysterical gait - most common ages 10-16 Variable, normal walking interspersed May be simple or complex Strength, tone, reflexes and sensation normal May lurch but will rarely fall Complex tasks will confirm Circle walk Walk backwards Assume ballet positions
Neurologic Abnormal Gait

Hemplegia-Detection Noted in swing Extended knee Hip hike Semicircular swing Lateral foot drop Reduced reciprocal arm swing Weak heel walking reduced height of the foot Evaluate other limb for compensatory effects Hemplegia-Causes Cerebral palsy Corticospinal lesion above the medulla contralateral to affected limb CVA Porencephalic cyst Intracerebral mass Spastic - Detection Increased tone with out-of-phase muscle activity Scissoring due to increased adductor tone Toe-walking Partial crouch - hip and knee flexion Equinovarus or valgus Increased DTRs Ankle clonus Spastic - Causes Bilateral corticospinal tract lesions Hypoxic ischemic injury Diffuse inflammatory disease - encephalitis Demyelinating disease - early MS Cerebellar Ataxia - Detection Divergence from the line of progression Erratic with lurching Wide base esp. in turns Stress gait may reveal instability Reduced single support Increased double support Acute onset Toxic ingestion or post-viral Increased tone Slurred speech Altered mentation
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Cerebellar Ataxia - Causes Static Cerebella hypoxic/ischemic Progressive Posterior fossa cyst/tumor Spinocerebellar deterioration - Friedrichs ataxia Acute onset Toxic ingestion or post-viral Increased tone Slurred speech Altered mentation Sensory Ataxia - Detection Disruption of proprioceptive input to cerebellum Cannot sense feet touching ground Raise leg unusually high Eyes fixed to ground Sensory Ataxia - Causes Posterior column disease Friedrichs ataxia Demyelinating disease Polyneuritis Meningeal myelitis Subacute combined systemic degeneration Neurologic Abnormal Gait Steppage - Detection DF weakness of foot Swing phase foot drop Increased hip and knee flexion May resemble sensory ataxia if bilateral Test heel walking Prancing horse Steppage - Causes Anterior Horn Cell disease Peripheral nerve disorders Charcot Marie Tooth disease Guillain-Barre Progressive muscle atrophy Distal myopathy Polio Paralytic CVA
Extrapyramidal - Detection Difficulty initiating gait Base normal Steps short and shuffling Arms close to body Elbow and wrist flexion Forward tilt Catch up to COG Decreased automatic movements Muscle rigidity Extrapyramidal - Causes Basal ganglia disease Hypoxic/ischemic injury Juvenile Parkinsons Inherited metabolic disease Wilsons disease Hallervorder-Spatz Post-streptococcal disease Sydenhams chorea Toxic ingestion Phenytoin Carbemazapine Apraxic - Detection Glue-foot Difficulty initiating gait Lacks acceleration and shuffle of extra-pyramidal gait Difficulty initiating complex acts Dementia + primitive reflexes Apraxic - Causes severe frontal lobe disease hydrocephalus bifrontal tumor Waddling - Detection Labored/wide-base Side-to-side pelvic rotation Weak abductors and extensors Increased lumbar lordosis Equinovarus Gowers sign Trendelenburg gait
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Waddling - Causes Myopathies Duchennes muscular dystrophy Poliomyositis Anterior Horn Cell disease Spinal muscle atrophy Developmental dislocated hip
5.9
Rotational and Angular Disorders in Children

...rotational deformities of the lower limbs of infants are a frequent cause for orthopedic evaluation. The most common deformities are medial tibial torsion and metatarsus adductus... These conditions often present in older children as treatment options decline The greatest number of management options exist for the infant and toddler
Rotational Deformities - Overview
Significance
Why does it matter? Abnormal gait Cosmetic Compensatory pes plano valgus Increased arthritic changes due to malalignment of joints
Etiology
Intrauterine constraints Birth weight Sleeping positions Genetic
Intrauterine Constraints
... etiology of these deformities is related to extrinsic factors in the later weeks of gestation... ... metatarsus adductus is rare in preterm infants with gestational age <30 weeks ...medial tibial torsion is rare in preterm infants with gestational age <30 weeks...
Differential Diagnosis
FOOT - Adductus TIBIA - Internal Tibial Torsion KNEE - Pseudotorsion FEMUR - Femoral antetorsion HIP - Internal Femoral Position
Figure 46.
Mixed Deformity
...it is not uncommon for these conditions to occur together, 75% of metatarsus adductus has internal tibial torsion, etc... ...rotational deformity at multiple levels can be additive leading to more severe in-toe...
Assessment
FOOT Blecks Test X-ray -base of 5th Photograph TIBIA - Malleolar position KNEE - Transverse plane rotation FEMUR - Ryders test HIP - Hip rotation -flexed/extended
Exam - Malleolar Position

Place patella in frontal plane Take care not to move knee during exam Find apex of malleoli Transection of malleoli is angle Parallel is 0 Lateral malleolus posterior is external
Figure 47.
Exam - Hip Range Of Motion

Externally and internally rotate hip Hold leg above knee Use other hand on ankle only to assist Rotate only to resistance - do not over-rotate Use dot on patella to determine rotation
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Exam - Ryders Test

Palpate greater trochanter laterally Rotate hip to place trochanter on frontal plane Find transcondylar axis of distal femur Measure transcondylar axis Parallel is 0
Figure 48.
Gait Assessment
Where is the knee? Where is the foot? Are they both pointing in? Is the knee in with the foot straight or out? Is the knee straight or out with the foot straight or in?
Explaining The Diagnosis

Failure to derotate or unwind Developmental lag Assist with development
Management Theory
... it seems prudent to use cast treatment in deformities classified as moderate to severe ... spontaneous correction of MA may occur by abduction at the MTJ and perpetuate an illusion of successful observational management... ... the evidence supports...that compensations in the distal segments of the closed kinetic chain often account for perceived improvements in the angle of gait... ... although 90% of children with femoral anteversion are said to have spontaneous resolution...in only 10% of cases did the gait become normal through anatomic normalization of the anteversion...in the remaining cases straightening of the angle of gait occurred by compensations in the distal structures... Goals Of Management Correct Malrotation Treatment of underlying deformity Improve Function Modify the angle of gait
Treatment Of Underlying Deformity

Best used in infants and toddlers: Casts Denis-Browne Splint or Counter Rotation System (CRS) Ganley Splint
Wheaton brace - leg extender
Figure 49.
Figure 50
Figure 51.
Management Theory - Bars And Casts

... even extremely mild forces on growing bone can inhibit or modify epiphyseal growth... ... there was a significant increase in the Static Foot Angle after even splinting... ...such changes associated with night splinting would be considered clinical improvement...
Improve Function/Prevent Compensations

Gait plate/orthoses Rigid shell Sneaker/flexible ball 20+ external hip rotation 0 rearfoot post Valgus forefoot post
Figure 52.
Shoe Wedging These are often necessary when the child is older Improve Function/Prevent Compensations Foot orthoses to reduce compensatory pes valgus resulting from persistent transverse plane influences Control of pes valgus may accentuate in-toe Modify the Angle of Gait Pelvic band Ashley brace Severe in-toe Worn best under clothing Elastic tension produces external rotation
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Figure 53.
Figure 54.
Angular Assessment Gait - observe for level Genu varum - intercondylar distance Genu valgum - intermalleolar distance Measure leg length to monitor significance of change Normal Values < two years = genu varum Two to four years = straight Four to seven years = genu valgum Seven to twelve years = straight 13-18 years = genu valgum Adult = straight Geriatric = genu varum Varum Differential Physiologic genu varum Physiologic tibial varum True tibial varum - Blounts disease Metabolic bowing -Rickets Pseudobowing - underlying ITT
Figure 55.
Valgum
Differential Physiologic genu valgum Lateral growth plate disruption Secondary to collapsing pes plano valgus Systemic ligamentous laxity
Figure 56.
Treatment - Varum Tincture of time for physiologic KAFO for true vara Bars for pseudobowing Treatment - Valgum Tincture of time for physiologic KAFO for true valgum Foot orthoses Stabilization for ligamentous laxity Conclusions ... these apparent improvements in gait are gained at the expense of undesirable compensatory changes of the knee, tibia and foot. They are potentially damaging to the distal structures over time...
5.10
The Pediatric Hip
Developmental Dislocated Hip

Contributing Factors Family history Breech delivery C-section Abnormal position Congenital foot deformities Torticollis First born female Clinical Exam Limited abduction Thigh/perineal fold asymmetry Ortolani clunk (relocate dislocated hip) Barlow maneuver (provoke dislocatable hip) Galeazzi sign Leg length discrepancy Gait changes
Ortolani Test Distract joint Abduct hip Pop femoral head into acetabulum
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Figure 57.
Barlow Maneuver Adduct flexed limb Provoke down and out Ortolani to reduce
Figure 58.
Diagnostic Testing Clinical not radiological X-rays variable < four to six months Bony nucleus forms then May be located on x-ray then dislocate X-rays not useful till after treatment window Useful to determine hip position in treatment Diagnostic Ultrasound Dynamic real-time Non- invasive Operator dependent Perform barlows during exam Follow-up in brace X-ray Angles Hilgenreiners line horizontal line across the upper edge of the ishiopubic bone in the area of the triradiate cartilage. Normally, the metaphysis is well below this line and the epiphysis should only just reach to this line Perkins vertical line a perpendicular to Hilgenreiners line dropped through the anterior inferior ileac spine. The femoral epiphysis should be on the medial side of Perkins line Shentons line along the upper margin of the obdurator foramen and continues outward and downwards along the under surface of the femoral neck and the medial aspect of the shaft of the femur. This should be unbroken in a normal hip
Acetabular index A line is drawn as a tangent to the acetabular roof. The angle this line makes to Hilgenreiners line is the Acetabular Index. Normal is about 20 and in dislocated hips it is said to increase to 30 to 40.
Figure 59.
Treatment - Infancy
Ortolani positive Concentric reduction in abduction and flexion Triple diapers Pavlik harness Freijka pillow Craig splint Von Rosen splint
Goals Of Treatment
Maintain flexed/abducted Hip flexed > 90 Posterior strap prevents adduction - too tight avn Harnesses seldom effective after six mos. Document reduction - x-ray/sono Watch femoral nerve palsy
Treatment - Older Child

Closed reduction - general anesthesia Skin traction Adductor tenotomy Spica cast Failed or > two yrs - open reduce
Calve-Legg Perthes
Necrosis of the bony nucleus May affect the physis May lead to remodeling of regenerated bone Loss of blood to physis May need multiple episodes to get clinical picture
Incidence And Presentation

Age of onset 3 to 10 Boys: girls 5:1 Insidious onset limp Pain-activity related - groin, thigh, or knee Limited hip ROM especially abduction and internal rotation
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Differential
Toxic synovitis Infection Juvenile rheumatoid arthritis Rheumatic fever Tuberculosis Tumors Sickle cell/Gaucher - AVN
Radiology
First seen with absorption and replacement of ossific nucleus - several months Revascularization with bony resorption leads to micro fractures Replaced by soft plastic bone - deformity may result
Phases
Initial Fragmentation Reossification or reparative Healed
Classification (Catterall)
Group 1 - small, central necrosis Group 2 - up to one half of head, lateral buttress intact Group 3 - greater that one half, lateral buttress lost Group 4 - whole head involved lateral buttress collapsed
Prognosis
Best - Catterall one and two, younger child Worst - Catterall three and four, older child
Management Goals
Containment - abduction setting Jell-O in a bowl Eliminate hip irritability Restore and maintain ROM Prevent femoral head extrusion/subluxation Goal is as spherical a head as possible after disease
Management Methods
Complete bed rest Intermittent traction Ambulatory orthotics Toronto brace Scottish Rite brace If bracing a problem - osteotomy
Slipped Capital Femoral Epiphysis

Definition Displacement of the femoral head to the femoral neck Etiology Hormonal Mechanical Vascular Incidence Most common hip disorder in adolescence Incidence 2:100,000 Obese, skeletally immature More common in boys Propensity to left hip Bilateral in 40-80% Types Acute Acute on chronic Chronic Management Goals Stabilize to prevent further slip Stimulate early closure Prevent AVN and chondrolysis Management Methods Recumbency cast immobilization In situ fixation Osteotomy
5.11
Pediatric Sports Medicine
Injury Rates
Boys Girls Football Wrestling Track and Field Basketball Soccer Softball Gymnastics Track and Field Volleyball 81% 75% 33% 31% 30% 44% 40% 35% 10%
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Intrinsic Factors
Strength Flexibility and bulk Associated disease states Potential for growth
Extrinsic Factors
Environment Equipment Training program
The Child As Athlete

Potential to heal and remodel quickly Open growth plates unique injuries Rapid growth rate
Injury Types
High-Energy Macrotrauma (Acute) Fractures Dislocations Sprains Ligament tears Repetitive Microtrauma (Overuse) Stress fractures Apophysitis Factors Rigorous training Biomechanical imbalances
Injuries - Hip And Pelvic

Acute fractures - rare from sports Avulsion Fractures Hamstring from ischial tuberosity * Most common - leads to sig. functional disability Ileopsoas from lesser trochanter Rectus femoris from ASIS sartorius from ASIS Abdominals from ileac crest Incidence Ages 13-17 Rapid growth Inflexible Secondary center has appeared - not yet fused Males > females High-Risk Sports Kicking Sprinting Jumping
Symptoms Acute onset Local pain and swelling Guarding with decreased muscle use Stages Non-displaced apophyseal injury (Apophysiolysis) Acute avulsion Chronic non-union
Management Non-operative Rest Partial WB Position extremity to reduce muscle strain If pain persists surgical excision Rehabilitation 5 STEP REHAB Patient can return to pre-injury level within 4 monthsMetzmaker and Pappas Protected gait Protected gait and guided exercise Progressive resistance training Gradual return to athletics Gradual return to competition
Ileac Apophysitis
Traction apophysitis - anterior and posterior Distance runners Gradual onset of local tenderness Pain on resisted hip abduction Oblique abdominals Treatment - three to four weeks rest - resume training
Anterior Tensor fascia lata Gluteus medius Posterior Latisimus dorsi Gluteus maximus
Hip Dislocation
Rare Mild to moderate trauma in athletics Average age seven to ten Most are posterior - shortened/flexed/adducted Football injury Fracture of posterior acetabulum Anterior - abducted/flexed/external rotated
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Complications AVN Neuro exam - sciatic injury Treatment Closed or open reduction Protected weight-bearing four to six weeks Muscle Contusion 38% of pediatric athletic injuries Quadriceps - football/tackle Opponents knee to quads Pain, swelling, restricted passive knee flexion Treatment Phase I - RICE Phase II - active knee ROM with full extension >90 flexion Phase III -resistance training Return to athletics with full strength and ROM Considerations May develop myositis ossificans Severity Re-injury Differential Diagnosis Malignancy Ewings Osteosarcoma Heteroptopic new bone Golden Rule Prevention from reinjury
5.12
Knee
Patello Femoral Stress Syndrome

Etiology Trauma Malalignment - biomechanics Combination Rapid growth Lateral force from TFL - VL Medial force - weaker VM Symptoms Anterior knee pain Pain on activity Difficulty with prolonged sitting Knee gives way May follow increase in training
Physical Exam Lateral patellar tightness No bony malalignment Treatment Training modification Strengthen medial quadriceps Stretch TFL Hamstrings - SLR to 12 lbs. Orthotics to alter mechanics If persists lat pat retinacular release 76.7% good to excellent
Osgood-Schilatter
Definition Overuse injury of the extensor mechanism of the knee Repetitive microtrauma to skeletally immature tib tubercle Avulsion of the developing ossification of the tibial tubercle High Risk Sports Kicking Jumping Squatting After growth spurt Symptoms Pain on palp over tt Swelling Exacerbation on resisted ext of knee X-ray/frag tibial tubercle Patella alta Treatment Pain relief NSAID Modality therapy Quadriceps stretch and strengthening Immobilization PRN 12% fail with ossicle May need to excise
Sinding Larsen Johansson Syndrome

Similar to Osgood-Schlatter Patellar tendon traction tendonitis Proximal attachment of the patellar tendon at the inferior pole of the patella Type of Jumpers knee
Symptoms Tenderness at inferior pole of patella X-ray: calcification at the inferior pole
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Treatment Non-operative care usually successful
Plica
Folds of synovium DDx of anterior knee pain in adolescent Acute Follows blunt injury (fall) Chronic Gradual onset of anterio-medial pain At start of new season Increase in exercise Growth spurt Biomechanical imbalance - pronation Symptoms Pain Swelling Pseudo-lock Held in flexion Refusal to extend Physcal Exam Palpable shelf above joint line Audible snap Treatment Modify activity Treat symptoms If persists after three months Arthroscopic plica division 83% good to excellent results
Meniscal Tears
Rare < 10 - 12 years of age May occur in adolescents Cause is significant injury Memorable event Acute hemarthrosis (pediatric) 45-50% had meniscal tear ACL tear also possible Arthroscope
Symptoms Gait abnormality Thigh atrophy Knee effusion Physical Exam Palpate for tenderness at joint line Range of motion Stability
Treatment Preserve meniscus Non-operative Stable, vertical, longitudinal tears Surgical repair - 7 mm length In the vascular zone Within 3-5 mm of periphery Partial menisectomy Major damage Central lesion Post-op rehab before return to activity
5.13 Tears
ACL INJURIES
Acute hemarthrosis - ages 7-12 47% had ACL tear Acute hemarthrosis - ages 13-18 65% had ACL tear
Figure 60.
Diagnosis History Physical exam Imaging Treatment Past Present Paradigm Activity modification Bracing Rehab Only 44% returned to competition Complaints included: effusion, pain, knee giving way Extra or intra-articular repair 70% return to competition
Acl Avulsion
Most common ACL injury in the skeletally immature Many result from athletics Falls from bicycles account for 50%
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Treatment Grade 1 - minimally displaced Grade 2 - hinged anteriorly, attached posterior Immobilize, knee extended or 30 flexed Grade 3 - completely detached Arthroscopy or ORIF
Medial Collateral Ligament Injury

Caused by valgus or external rotation force at knee Mostly from contact sports: Tackle football/rugby Physical Exam Valgus instability in 30 flexion Valgus stress radiographs Treatment Non-operative as good as surg Full WB ASAP, early ROM exercises
Ankle Injuries
Anatomic considerations explain higher incidence of physeal ankle fractures as compared to sprains in the skeletally immature. Ligaments insert below physis Physis weaker than: Bone Ligament Types Salter-Harris Types I and II - rapid healing, thick periosteal sleeve Types III and IV - high-risk Juvenile Tillaux Intraarticular SH III Anterior tibio-fibular ligament avulses lateral distal tibial epiphysis
Figure 61.
Triplane Fracture Comminuted epiphyseal fracture Tillaux with SH II of posterior, distal tibial metaphysis High-risk Salter-Harris Injuries Tillaux
Occur after medial growth plate has closed Would cause diastasis in adults External rotation force to supinated foot Treatment Reduce with internal rotation of tibia and pressure on fragment ORIF if gap > 3mm High-Risk Salter Injuries Triplane and Tillaux High-risk sports Skateboarding Baseball (sliding) Triplane treatment Similar to Tillaux ORIF
Ankle Sprains
16% of sports injuries Majority 15 - 19 years of age Under 15 with open plates assume SH injury Especially if injury is rotational Tenderness at distal tibial or fibular physis (15 mm proximal to tip of fibula) Treatment If severe - two weeks walking cast Prevent further injury Progressive motion Strengthening with proprioceptive training
Osteochondral Injuries
Dome of talus - Bernt-Hardy classification DDx chronic ankle pain - CT/MRI useful Lateral lesion More often traumatic Persistent symptoms Caused by inversion/dorsiflexion Medial lesion Caused by inversion/plantarflexion with lateral rotation of the tibia Types I-III - treatment is immobilization
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Figure 62.
Figure 63.
Severs Apophysitis
Traction apophysitis Tight triceps surae and plantar fascia Open calcaneal apophysis Symptoms during growth spurt Study of 85 cases - onset 7 -16 years of age
High Risk Sports Soccer Basketball Treatment Activity modification Triceps surae stretching Heel raises Heel cushioning Orthotics to accomplish raising and cushioning and cupping of heel Shoes with more counter support
Stress Fractures
Overuse injury - excessive, repetitive force Common sites in children Proximal tibia (51%) Diaphyseal may go to fx. Distal fibula (20%) Navicular Metatarsal (2%) Sesamoids
High-Risk Sports Running Football Gymnastics Ballet Ice-skating (fibula)
Differential Diagnosis Osteomyelitis Osteogenic sarcoma Stress fractures Symptoms Gradual onset of local pain Increased by activity Relieved by rest (or dull ache) Local tenderness Swelling Diagnosis Bone scan - multiple foci of inc. uptake MRI Plain film- periosteal rxn Treatment Activity modification Non WB - rest 4-6 weeks Immobilize Foot orthoses Cushioning Weight-distribution
Freibergs Infraction
AVN of metatarsal epiphysis - usually 2nd Repetitive microtrauma Stages Sclerosis Resorption Subchondral fracture Collapse Reformation Freibergs Infraction End stage - regenerative changes with spurring High-heels aggravate
Figure 64.
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Treatment Short-leg cast for acute symptoms Activity modification Shoe modification Orthoses Surgery
Jones Fracture
DDX - avulsion fracture of the tuberosity Avulsion by lateral band of plantar fascia May be apophysis 9-11 in females 11-14 in males Parallel to shaft Jones - transverse fracture of metaphysis 1.5 cm from tuberosity
Figure 65.
Incidence Ages 15 -21 70% of Jones fractures 17% of tuberosity fractures Younger than 15 Higher incidence of tuberosity fractures Treatment Of Jones Non-WB short-leg cast ORIF in competitive athlete
Tarsal Coalition
May present as injury ages 8-12 8-12 year old, C-N bar most likely Adolescent, subtalar, middle facet
Figure 66.
Symptoms Rigid pes valgus Pain in subtalar/midfoot
Aggravated by activity Gait may be antalgic Higher incidence of ankle sprains Types Synostosis Synchondrosis Syndesmosis Treatment Peroneal block Cast Orthoses If persists surgical correction
Shin Splints
Symptoms Anteromedial (PT) or anterolateral pain (AT) Local tenderness distal 2/3 of tibia Progressive during activity Persists after activity Differential Diagnosis Periostalgia/periostitis Stress fracture Chronic compartment syndrome High-Risk Sports Basketball Gymnastic dismounts Grand jette in ballet Running Sprinting Distance Contributing Factors Muscle weakness/tightness Poor shoes Training errors Surface Regimen change Biomechanical malalignment Anterior tibial Supinator Over-working to oppose pronation Pulled from tibia with pronation Treatment RICE NSAID prn PT - strengthen/stretch
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Modify training Avoid increases in frequency or intensity Modify activity Cross-training With decreased pain return to activity Orthotics Shoe changes - after 500 miles - 40% loss
5.14
Osteochondroses
2nd metatarsal head Vascular disruption & trauma Female age 10-15 Unilateral - 90%
Friebergs Disease
Clinical Manifestations Local pain, dull, aching Tenderness and swelling X-ray Findings Flattening of met. Head distal Head irreg. With increased density Fragmentation Widening of joint space Thickening of cortex shaft Treatment Immobilization BK cast 4-6weeks. Prevent further trauma and collapse Orthotic Surgical
Treves Disease
Hallucial sesamoids Age 8 12 Rare confused with osteitis Clinical Manifestations Pain in region of sesamoids Pain ROM of hallux X-ray Findings Appearance of aseptic necrosis Pitting with fuzzy new bone formation Treatment Restriction of wt bearing Orthotic with dispersion Dancers pad Surgical Prognosis favorable
Iselins Disease
Apophysis base of 5th met. Appears parallel to long axis of bone R/O fx. transverse or oblique Peroneus brevis attaches at this site DDx - Os versaliarum Manifestation Pain and swelling Caused by increased tension (inversion sprain) or direct blow Up to 13 yrs of age of ossification
Clinical
X-ray Findings Fragmentation Treatment Rest Off to partial weight bearing Self limiting relief of symptoms
Haglunds Disease
Accessory tarsal navicular Prominent fragmentation Pain over medial aspect of foot Male Trauma and tension Cast followed by orthotic Surgical late
Thiemanns Disease
Proximal epiphysis of hallux Differentiate from traumatic conditions with good history Inc. incidence of other orthopedic problems Immobilization, protected weight bearing
Severs Disease
Calcaneal apophysis May not exist as a disease entity 8 14 yrs. old males Closure from 15 18 yrs R/O fracture infection, Stills disease Manifestations Limping Pain and tenderness inferior medial and lateral aspects of the calcaneus Males, may be obese Equinus present Soft tissue swelling
Clinical
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X-ray Findings Same as normal Sclerosis Fragmentation Irregularity Multiple ossification centers Treatment Severe cases BK cast 4 6 wks. with slight PF of ankle Milder cases restriction of activity with heel lifts/orthoses Orthoses with cushioning
Koehlers Disease
Navicular Coincides with ossification process Age 3 7 years Males 75% Unilateral Manifestations Limping, local pain & tenderness over the navicular Trauma Biomechanically induced Mild swelling
Clinical
X-ray Findings Flattened, squashed, discoid Fuzzy fragmented, sclerotic Normal variant multiple ossification centers X-ray changes may be normal variation in the sequence of navicular ossification Treatment Cast immobilization Reduced activities Orthotics Complete recovery is typical Miscellaneous Talus Diaz or Mouchets Cuneiforms Buschkes
5.15
Toe Walking
Toe walking is a normal variant in the gait pattern of children for the first three to six months of independent ambulation.
Differential Diagnosis
Cerebral Palsy abnormal muscle tone, hyperreflexia (lower greater than upper), clonus, extensor plantar response, unstable, falls frequently Congenital contracture of heel cord -The tendinous portion is shorter than normal with the muscle bellies extending further down than usual. These children often stand on their toes before beginning to ambulate and have limited ankle dorsiflexion with the knee flexed and extended. Limited range of motion of hamstrings or hip flexors. Muscular Dystrophy late walker, frequent falling, (+) Gowers sign, begins toe walking at 3 4 years of age, waddling gait, lumbar lordosis Spina bifida Minimal brain dysfunction, attention deficit disorder, schizophrenia Diastematomyelia toe walking begins at two to three years of age and worsens; spinal cord tethered in spinal canal; cavus deformity common; foot ulceration, bladder and bowel problems. Charcot-Marie Tooth difficulty in walking, paresthesias in legs, muscle cramps; toe walking begins later; vibratory and position sense lost early; early weakness of intrinsics, ankle dorsiflexors, and peroneals; progressive pes cavus and foot drop; check other family members Idiopathic well coordinated, runs with minimal tripping and falling; can achieve a heel toe or foot flat gait at lower walking speeds; neurologic exam normal, younger child has good ankle range of motion, older child may have limited range (acquired shortening from functional equinus); began toe walking at onset of walking
Evaluation Of Toe Walker

History pre, peri-, and postnatal history; decreased or absent fetal movements, low birth weight, prematurity. When did child begin toe walking? Is toe walking intermittent or all the time? Unilateral or bilateral? (Hemiparesis?) developmental milestones -abnormal psychological behavior unusual walking pattern in other family members Physical Exam range of motion at ankle, knee and hip; gait analysis Neurologic Exam sensory, vibration, position sense, muscle power (Gowers sign) deep tendon reflexes, weakness of ankle dorsiflexors (if child cant heel walk, have child lean against wall and dorsiflex feet against resistance) Radiographs if ankle range of motion is limited with knee flexed and extended, rule out bony block Special Diagnostic Tests e.g. NCV, EMG, muscle biopsy reserved for children in which muscle weakness cannot be ruled out clinically and when toe walking appears after a period of normal gait spinal MRI if a suspicion
Treatment
Serial below knee stretching casts (three to six weeks) to increase ankle range of motion. Articulating ankle-foot orthoses Reverse gait plates or flat rigid shoe plate and high topped sneakers need adequate ankle range of motion Heel lifts Discourage jolly jumpers and walkers Surgical intervention
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5.16
Pediatric Neuromuscular Disorders

Cerebral Palsy Static encephalopathy 7.5 per 1,000 live births, UMN Clinical syndrome characterized by a chronic, non-progressive disorder of motor control, resulting in abnormality of posture, movement and tone Three criteria Fixed, non-progressive brain lesion or lesions Original lesion a result of pre-, peri-, or postnatal trauma or anoxia Lack of motor control results in abnormal coordination of movement and posture; may also see mental retardation, convulsions, sensory disturbance, speech impediment, defects of hearing, language or eyesight Risk factors Prematurity and low birth weight* Metabolic (hypoglycemia, hyperbilirubinemia) CVA Infections (toxoplasmosis, rubella) Cerebral malformation CP classification Spastic- most common group, includes diplegia, hemiplegia, and quadriplegia Extrapyramidal (includes choreoathetosis and dystonia) Hypotonic Ataxic Mixed
Figure .
Clinical features In infants may see hypotonia, persistence of primitive neonatal reflexes, poor development of more mature reflexes, toe walking, strong hand preference (hemi) Older children hypertonicity, increased DTRs, Babinsky, delayed gross motor milestones, abnormal gait, drooling, strabismus, difficulty with feeding and speech, mental retardation, seizures, adductor grab, clonus Types Spastic diplegic more involvement of legs than arms, spastic crouch, equinovalgus foot deformity Spastic quadriplegic involvement of all four limbs, usually more severely involved than diplegic, may never walk, difficulty in feeding, speech and drooling, frequent pneumonia, mental retardation, seizures, strabismus Hemiplegic involvement of unilateral arm and leg, early hand preference, unilateral toe walking or circumduction of limb, unilateral Babinsky
Choreoathetoid hypotonic until age two, slow, writhing, involuntary movements of flexion and extension, pronation and supination of fingers and hands and sometimes toes and feet, abnormal movements of face, tongue, and palate, facial grimaces, difficulties with speech and feeding, may be very late in walking (8 or 10 years of age) Dystonia sustained twisted posture involving trunk and proximal limb Ataxia poor coordination, wide based gait
Spina Bifida
Incomplete closure of the bony elements of spine with or without extrusion of contents of the spinal canal through bony defect Spina bifida occulta Defect of fusion of posterior vertebral arch without disruption of underlying meninges and cord, 10% of pediatric population, asymptomatic, low mid-back hairy tuft, dimple or teratotoma Spina bifida aperta 1 in 1,000 live births, most common in lumbar and lumbosacral area Types Meningocoele distention of meninges Myelomeningocoele distention of meninges and cord Myelocoele distention of meninges and cord with lack of closure of cord in defective area Clinical Paralysis and loss of sensation below lesion level (ulcerations, fractures) Lack of bladder and bowel control Hydrocephalus Hip dislocations, scoliosis and foot deformities (equinovarusmost common)
Diastemtomyella
Congenital malformation in which spinal cord is divided longitudinally into 2 hemicords by a bony, fibrous, or cartilaginous spicule from the posterior aspect of a vertebral body; spicule transfixes spinal cord or cauda equina (tethered cord syndrome), stopping its normal ascent during growth of the vertebral column; neurologic deficit below level of lesion Clinical picture Various skin defects near midline at lesion level (usually lumbar) 30% of cases show no skin defect Late in walking or abnormal gait (limp) Chief complaint may be poor posture associated with leg length discrepancy or foot size difference Scoliosis common Cavovarus foot, ulcerations of feet Urinary incontinence Early diagnosis by MRI, followed by release of cord tethering; prevents further deformity but does not reverse existing deformity 75 % of cases female
Muscular Dystrophies
Duchenne MD Most common and most severe, x-linked recessive, high mutation rate Male to female, 9:1 Onset usually apparent by age 3 Weak fetal movements in last trimester
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Delayed motor milestones, difficulty climbing stairs, use arms to rise from chair Difficulty or unable to run or hop, frequent falling Gowers sign, waddling gait, toe walking DTRs disappear early except ankle Cardiac involvement, 50% mental retardation Symmetrical involvement first of pelvis, then shoulders 3 to 5 years later pseudohypertrophy of calves, unable to walk by 12, death teen to third decade Pes planus secondary to tight heel cord early stage, equinovarus later stage, lumbar lordosis Elevated serum enzyme levels, especially CPK 30-300 X normal Beckers MD X-linked recessive Benign form, onset 5-20, slow progression, otherwise similar to Duchenne Limb Girdle MD Progressive weakness and atrophy of mm of shoulder and pelvic girdle and proximal limbs during 20s or 30s, weakness of neck flexors and extensors Autosomal recessive Fascioscapulohumeral MD Autosomal dominant, onset 20s First facial weakness (whistling, sipping, keeping eyes closed) shoulder girdle weakness and scapular winging (cant raise arms above head), eventually anterolateral leg weakness (foot drop) Slow progression
Polymyositis
Non-hereditary, inflammatory myopathy In presence of skin rash, dematomyositis Dermatomyositis symmetrical weakness of proximal limb mm and neck flexors, rash (butterfly distribution, heliotrope, erythematous, scaly extensor surfaces of joints especially ankles, (medial malleolus), elbows, knees, knuckles and dorsal finger near nail bed; later stage- skin tight and glossy with subcutaneous calcium deposits In children, no association with malignancy
Neurofibromatosis
Von Recklinghausens disease hereditary Most common of the neurocutaneous dysplasias Three classic signs in childhood: 1) caf au lait spots 2) multiple soft tissue tumors (some malignant, seizures associated with intracranial tumors) 3) skeletal changes e.g. kyphoscoliosis, vertebral body defects, local gigantism
Peripheral Neuropathies
Guillain Barre syndrome (post-infectious polyneuritis) Rapid onset following an illness Distal weakness that ascends 50% cranial nerve involvement, DTRs absent, sensory deficit minimal Most children recover completely Charcot Marie Tooth type I HMSN 50% of all cases of childhood hereditary neuropathies Clinical picture
Peroneals (foot slap), tib ant and intrinsics, calf, hand intrinsics stork leg and pes cavovarus Decrease vibration and position sense, DTRs absent at ankles Nerve hypertrophy Decreased NCV hallmark of disease* Peroneal muscular atrophy type II HMSN Zxonal degeneration of peripheral nerve, NCV normal Clinically similar to CMT Dejerine Sottas disease type III HMSN Similar to CMT Scoliosis, pupillary abnormalities Refsums type IV HMSN Anorexia, gait abnormalities, icthyosis, eye problems, anosmia, hearing deficit, pes cavus Deficiency in fatty acid, metabolism, reduce dietary phytanic acid Riley Day syndrome HSN (familial dysautonomia) Onset in infancy, autonomic dysfunction, Jewish children of eastern European descent Failure to respond to pain Toxic Neuropathies Sciatic neuropathy Result of injection into buttocks, near sciatic nerve Paralysis within days Long term effects: limb growth retardation, pes cavus, trophic ulceration Antibiotic-induced, antimetabolite, heavy metal (e.g. lead exposure, seizures, headache and ataxia in Children under five, dropfoot in children over five)
Poliomyositis (infantile paralysis)

Etiology- one of three polioviruses attacks GI and respiratory tract and spreads to CNS (lower motor neuron) Incidence- rarer because of immunizations Acute phase - 5-10 days, acute illness during which paralysis may occur, fever, headache, nuchal rigidity, muscle tenderness, weakness asymmetric and scattered, bulbar poliomyelitis Convalescent phase- 16-month period following acute phase varying degrees of spontaneous recovery Chronic phase- rest of patients life following convalescent period Steppage gait- weakness of peroneal and anterior tibial Lower extremity deformities often include flexion, abduction, and lateral rotation of hip, paralysis of quadriceps, flexion and valgus deformity of knee, leg length discrepancy Feet - severe pes valgus on weight bearing, cavus foot, and claw toes off weight bearing
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5.17
Pediatric Pharmacology
Children are not little adults Parents will be involved *Concise instructions Metabolic rate varies Weight, height, body morphology and body surface area are factors Larger proportion of surface area to body volume. *Surface area increases less rapidly
General Considerations
Drug Considerations
Appropriate medication Established drugs over latest & greatest Dosage Toxicity Overdosage Dosage forms Strength Route of administration
Problems
Contraindications Allergy Age parameters Drug interactions Food interactions Dosage Toxicity Overdosage Syrup of Ipecac if necessary to induce vomitting
Dosage
Should be individualized Smallest amount to give the best therapeutic effect May be based upon weight, age, or body surface area Metabolic rate is a factor *Fever increases metabolic rate Obesity and edema are factors
Frieds Rule
Patient less than one year old Based on age Age in Months Adult Dose 150
Youngs Rule
Patient two years or older Based upon age
Age in Years Age in Years 12
Adult Dose
Clarkes Rule
Patient two years or older Based upon weight Weight in Pounds Adult Dose 150
Body Surface Area

Most accurate Calculate utilizing the West nomogram Correlates height and weight with body surface area Manufacturer suggests dose per square meter (m_) Can calculate based upon adult dosage
Manufacturers Recommended Dosage

PDR (Physicians Desk Reference) Utilize given formulation
Antibiotics
Oral Antibiotics Penicillin Gram (+) Best for streptococcus B lactamase resistant PCNs Dicloxicillin Oxacillin Methicillin Cloxicillin Amoxicillin/Ampicilin Broader spectrum H. influenza P. mirabilis Klebsiella Enterococcus E. coli Not B lactamase resistant Augmentin Same spectrum as ampicillin Better at enterococcus Some anaerobes, especially B. Fragilis DOC for animal bites including human Better tasting for children Suspension Chewable tablets Cephalasporins Broad spectrum
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Good gram (+) and adequate gram (-) Variable B lactamase resistant Duricef (Cefadroxil) Suspension Keflex (Cephalexin) Suspension and solution Erythromycin Good gram (+) including staphylococcus Good for penicillin allergy M. pneumonia, Legionella, Chlamydia GI upset common Suspension Tetracycline Some gram (+) and gram (-) Rickettsia m. pneumonia, chlamydia Avoid milk products Contraindicated under 8 years of age Ciprofloxacin A fluroquinolone Good gram (+) including staphylococcus Occasional MRSA Very good gram (-) including pseudomonas Contra-indicated under 16 years of age Topical Anitbiotics Bacitracin Staphylococcus and streptococcus Cream and ointment Bactroban (mupirocin) Ointment 2% Staphylococcus and streptococcus Specifically indicated for impetigo Neosporin Polymyxin B and neomycin Cream and ointment Ointment also has Bacitracin Silvadene cream 1% (silver sulfadiazine) Excellent coverage Betadine (povidone iodine) Excellent coverage Solution, cream, and ointment
Analgesics
Acetaminophen (Tylenol, Tempra) Most common Relatively safe and well-tolerated Chewable and solution
Analgesic and anti-pyretic NOT anti-inflammatory Narcotics
Non-Steriodal Anti-Inflammatories
Tolectin (Tolmetin sodium) NSAID indicated for pediatrics Ibuprofen (Motrin, Advil) Different strengths Childrens formulations Syrups and elixirs Naprosyn (Naproxen) Indicated for JRA Suspension Acetylsalicylic acid ASA Many forms Generally safe
Topical Steriods
Utilized for dermatological inflammatory conditionsdermatitis, eczema, inflammatory tinea pedis Use the highest potency for the shortest time Generally, use only low or intermediate strength in pediatrics Different vehicles Avoid occlusion in pediatrics Avoid overuse or prolonged use Steroid atrophy ulceration Potential for hypothalamic-pituitary-adrenal axis suppression Potential for Cushings syndrome Avoid intertriginous areas Contraindicated in varicella
Topical Steriods
Ultra high potency Diprolene (augmented betamethasone) Ultravate Temovate High potency Betamethasone diproprionate Betamethasone 0.05% Lidex (fluocinonide) Intermediate potency Betamethasone valerate Betamethasone 0.025% Elocon Low potency Hydrocortisone Dexamethasone
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Anti-Fungus
Orals for severe cases only, check PDR for guidelines Most are broad spectrum Tineas, e.floccosum, candida Use the vehicle that is most effective Solution, lotion, creme Should use for four weeks
Topical Anti-Fungus
Lotrimin Solution, lotion and crme Lotrisone crme formulation(combines steroid) Spectazole crme Once a day Loprox Crme and lotion Lamisil Two week treatment
5.18
Skeletal Syndromes and Systemic Disorders in Pediatric Orthopedics
Skeletal Dysplasias
Skeletal dysplasias involve basic and systemic abnormalities of bone and cartilage growth and development, usually causing short stature. Diagnosis of Skeletal Dysplasias Height and proportion Birth length Current height and percentile Most skeletal dysplasias produce adult height under 60 inches. Mean adult height in achondroplasia for males is 52 in. (+2 SD = 56 in.) and for females is 50 in. (+2 SD = 52 in.). Mean adult height in diastrophic dwarfism is 42 in. Body proportion is determined by comparing limb and trunk lengths. Limb height lower segment = symphysis to soles of feet. Trunk height upper segment = total height minus lower segment. For a graph of normal values by age, see the Harriet Lane Handbook. Another approach to determining body proportion is to subtract total height from arm span (fingertip to fingertip). Values for normal stature by this measure are 2 cm (13/16 in.) (before age 8), +1 cm (+3/8 in.) (adult females), and + 5 cm (+2 in.) (adult males). Limb segment ratios are best calculated from x-rays. Normal ratio of radius to humerus is 75%. Normal ratio of tibia to femur is 82% Types of disproportion include rhizomelic (short humerus and femur), mesomelic (short hands and feet). Dysmorphism is morphologic variation of bone and soft tissue that may characterize a specific disorder Depressed nasal bridge often seen in achondroplasia Long philtrum suggest trichorhinophalangeal dysplasia
Short broad thumb suggest multiple epiphyseal dysplasia V-shaped phalanges suggest trichorhinophalangeal dysplasia Hitchhikers thumb and abducted great toe indicates diastrophic dysplasia Radiographic evaluation should include these five key studies Lateral skull and cervical spine Lateral lumbar spine Anteroposterior pelvis Anteroposterior knees Anteroposterior hand and wrist Family evaluation Construct pedigree of at least all first-degree relatives. If family history is negative, consider the following: New mutation Gonadal mutation Recessive trait Nonpaternity Laboratory evaluation is usually not indicated but can be useful if prior work up is negative. It should include the following studies: Chemistry profile Endocrine evaluation Urine work up for storage disorder
Achondroplasia
Achondroplasia is autosomal dominant but usually due to frequent new mutation. It is the most common skeletal dysplasia. Major features Mid-face hypoplasia Rhizomelic dwarfism Genu varum (variable) Three- to three-month delay in motor milestones Thoracolumbar kyphosis, often resolving with growth Spinal stenosis. This is greatest in lumbar spine and distally but may affect entire spine, including foramen magnum, and cause severe developmental delay Height Final height for males is 46-56 in., and for females, 44-55 in.
Pseudoachondroplasia
Although these patients are also rhizomelic, the epiphyseal involvement in this syndrome causes basic differences from achondroplasia. Major features Rhizomelic shortening of extremities Variable knee deformities (varus on one side, valgus on the other) Mild platyspondyly, minimal scoliosis, no stenosis Odontoid hypoplasia, C1-C2 instability Epiphyseal deformation; eventual degeneration Ligamentous laxity
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Diastrophic Dysplasia
Autosomal recessive Major features Cauliflower ear develops at approximately six months Rhizomelic shortening of extremities Contractures of major joints with later degenerative joint disease (DJD) Hands: hitchhikers thumb, symphalangism Dislocated hips (occasionally) Equinovarus foot deformities Cervical spina bifida with kyphosis; sometimes resolves Scoliosis of thoracic and lumbar spine
Spondyloepiphyseal Dysplasia Congenita

Autosomal dominant with frequent new mutations Major features Odontoid hypoplasia or Os odontoideum; may have instability Platyspondyly, scoliosis Coxa vara, epiphyseal irregularity, DJD
Spondyloepiphyseal Dysplasia Tarda

Variable transmission; diagnosis late in childhood Major features Irregular ossification, DJD Hips may resemble Perthes disease but are bilaterally synchronous. Scoliosis Occasional cervical instability
Multiple Epiphyseal Dysplasia

Autosomal dominant Major features Variable, usually mild short stature due to short limbs Irregular epiphyseal ossification with deformity, pain, DJD Hips, knees, and ankles are most involved Usually presents in late childhood to adulthood
Metatropic Dysplasia
Major features: Epiphyseal or metaphyseal enlargement: knobby joint with contractures Cervical stenosis, instability Scoliosis, kyphosis, later onset Coccygeal tail Thoracic hypoplasia; may cause respiratory compromise Initially short-limb dwarfism; becomes short-trunk type with onset of scoliosis
Chondrodysplasia Punctata (Conradi-Hnermann syndrome)

Autosomal dominant Major features
Multiple asymmetric epiphyseal calcifications Good prognosis
Multiple Osteocartilaginous Exostoses

Autosomal dominant Clinical appearance features mild short stature. Categories of problems: Local impingement on tendons, nerves, spinal canal and ribs Asymmetric growth in two-bone segments leading to valgus knees, ankles, elbows, and wrists and possi bly to radial head dislocation Leg length inequality (usually <4 cm) Risk of malignant degeneration (about 1% of patients) Radiographic features Osteochondromas in metaphysis, pointing away from joint Cortex of osteochondroma is confluent with that of host bone May be sessile or pedunculated Treatment Resect lesions only when symptomatic. Resection does not predictably increase forearm rotation Correct knee and ankle valgus when greater than 10 Monitor in adulthood every two years with bone scan
Dysplasia Epiphysealis Hemimelica (Trevors disease)

Definition: epiphyseal osteochondroma; no genetic pattern Clinical features Presents in first decade Restricted joint motion Enlarged joint or locked joint Knee, foot, and ankle are most commonly involved Radiographic features include multiple opacity in exostotic cartilage; these eventually coalesce Treatment: resection, attempting to preserve normal cartilage
Multiple Enchondromas (Olliers disease)

Clinical presentation Angular deformity Bony irregularity Limb length inequality Radiographic features Diffuse enchondromas in metaphysis; occasionally epiphyses. Usually asymmetric Treatment *Angular or length correction of limb *Monitor for malignancy, especially in Maffuccis syndrome
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Cleidocranial Dysplasia
Autosomal dominant Persistently open skull sutures with bulging calvarium Hypoplasia or aplasia of clavicles Wide symphysis pubis Hip abnormalities Short middle phalanx of fifth finger Syringomyelia may be present
Dyschondrosteosis
Major features: Madelungs deformity Relative shortening of forearm and leg Females predominate
5.19
OTHER SYNDROMES INVOLVING SHORT STATURE
Cornelia de Lange Syndrome Major features Synophrys (single confluent eyebrow) Down-turned mouth Mandibular spur, in infancy Hirsutism Gastroesophageal reflux Small for gestational age, with continued growth retardation Motor and intellectual delay Cardiac abnormalities Orthopedic involvement Upper-extremity anomalies in almost all patients Micromelia, phocomelia Decreased number of fingers Lobster claw hand Proximally placed thumb Elbow anomalies Lower extremities Miscellaneous foot deformities and contracture Avascular necrosis of femoral head in 10% Treatment Correct lower-extremity abnormalities if limiting ambulation. Individualized treatment for upper extremities
Riley-Day Familial Dysautonomia Ashkenazi Jews only; autosomal recessive Sympathetic over activity is key feature Major features Deficient sensation of pain and proprioception Gastroesophageal reflux, pneumonia Variable life expectancy Orthopedic abnormalities and implications Scoliosis or kyphosis before age eight; poor brace tolerance; fuse early Fractures due to osteopenia or dyscoordination Avascular necrosis of femoral head, distal femur, talus Hip dysplasia Nail-patella Syndrome Autosomal dominant, normal life expectancy Orthopedic features Nails grooved, small, or absent, especially on thumb Multiple knee anomalies: patella tripartite, small, or absent; lateral femoral condyle hypoplastic; osteochondritis dissecans of lateral femur and talus Elbow: capitellar hypoplasia, cubitus valgus, flexion contracture Iliac horns
Sclerosing Bone Disorders

Fibrodysplasia Ossificans Progressiva Progressive, disabling heteroptopic ossification or ankylosis Characteristic shortening or valgus of great toe Ossification starts as tender, hard nodule; progresses proximal to distal, posterior to anterior Do not biopsy - this may accelerate the process Genetics: usually a spontaneous mutation, but it may be transmitted as autosomal dominant Progressive Diaphyseal Dysplasia Clinical features: pain, fatigue, muscle atrophy Radiographic features: symmetrically widened, sclerotic diaphyses; epiphyses spared; tibia and femur most commonly involved Treatment: osteotomies only if there is marked deformity Melorheostosis A syndrome involving asymmetric, extraosseous, longitudinal hyperostotic streaks; limb pain and softtissue contracture. Treatment: analgesics, bracing, contracture releases, and bone shortening Osteopathia Striata Linear intraosseous metaphyseal striations Autosomal dominant Asymptomatic No treatment required Osteopoikilosis Multiple symmetric intraosseous epiphyseal or metaphyseal spots Autosomal dominant Asymptomatic
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Marfanoid Disorders
Marfan Syndrome This disorder of fibrillin has multiple effects on the skeleton and connective tissue. Because some features may be seen in the general population, the following diagnostic criteria have been developed. Diagnostic criteria. Positive family history or skeletal involvement. Involvement of two other systems - at least one must be a major manifestation (see * below) System involvement (*indicates major manifestation) Skeletal Anterior chest deformity Dolichostenomelia (long, narrow limbs) Arachnodactyly (long, narrow digits) Vertebral column deformity (kyphosis, scoliosis) Tall stature High, narrowly arched palate Increased appendicular joint mobility Protrusio acetabuli Ocular Ectopia lentis (superolateral lens dislocation) Flat cornea Retinal detachment Myopia Cardiovascular Ascending aortic aneurysm with dilation of valsalva sinuses Aortic dissection, usually ascending segment Aortic valve regurgitation Mitral valve regurgitation Abdominal aortic aneurysm Pulmonary Spontaneous pneumothorax Apical bleb Skin Striae atrophicae (stretch marks) Hernia Central nervous system Dural ectasia Learning disability Hyperactivity Implications Monitor aortic and cardiac status Beta blocker for aortic dilation Restrict from vigorous exertion Counsel regarding genetics Treat skeletal deformity if symptomatic
Homocystinuria
Homocystinuria may be mistaken for Marfan syndrome, but it is most readily distinguished by mental retardation. It has the following major features: Mental retardation Dislocated lens (inferomedial) Arachnodactyly Joint stiffness Cavus feet Scoliosis or kyphosis Diagnosis: urine amino acid screen Treatment: vitamin B6 administration, methionine restriction
Congenital Contractural Arachnodactyly

This is also a Marfan look-alike; so much so that Marfans original patient had this syndrome. Clinical features include: Face: oval with recessed jaw, flattened ear Eyes: occasional intraocular coloboma Heart: congenital septal and valve defects Skeleton Flexion contracture that partially improves with time Hands: contracture of proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints Scoliosis: appears by mid-childhood
Achard Syndrome
Clinical features include: Arachnodactyly Generalized ligamentous laxity Mandibular hypoplasia
Stickler Syndrome (Hereditary Arthro-Ophthalmopathy)

Etiology. A mutation in type II collagen. Abraham Lincoln may have had hereditary arthroophthalmopathy. Clinical features Progressive myopia beginning in first decade Retinal detachment Abnormal epiphyseal development, eventual DJD Mild joint hypermobility in some cases Marfanoid habitus in some cases Autosomal dominant
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Arthrogryposis Or Contracture
Arthrogryposis Multiplex Congenital This is the classic contractural syndrome. The etiology is unknown; it is probably multifactorial. Major features are all skeletal: It may affect all four limbs, upper extremities only, or lower extremities only. Involvement is usually greatest distally within each limb. Hips are frequently dislocated. Contractures are usually into abduction and external rotation Knees: flexion more common than extension Clubfoot and vertical talus are common, often resistant to cast treatment Upper extremities: extended at elbows, adducted, stiff fingers Spine: paralytic scoliosis, torticollis Implications for treatment Range of motion can be shifted but not increased Osteotomies most useful near end of growth Fractures common after manipulation or cast Larsen Syndrome Orthopedic features Dislocated hips, hyper-extended or dislocated knees Clubfeet Normal muscle mass Elbow dislocations Cervical kyphosis and instability Thoracic and lumbar scoliosis Non-orthopedic features Flattened face, depressed nasal bridge Cleft palate Freeman-Sheldon (Whistling face) Syndrome Small mouth and chin (may cause difficulty with intubation) Arthrogrypotic, flexed and ulnar-deviated fingers Clubfeet or vertical talus Scoliosis or kyphosis Mbius Syndrome Congenital facial diplegia Variable absence of shoulder girdle muscles Clubfeet and hand contractures or anomalies Pterygium Syndromes Multiple pterygium syndrome Static disorder with flexion contractures and webs at all flexion creases Short stature Congenital spinal anomalies Popliteal pterygium syndrome Webs only across perineum and knees Facial malformations Contractures are due to a single cord from ischium to calcaneus, with the nerve bow-strung across the joint
Vascular Abnormalties
Kippel-Trenaunay-Weber Syndrome Clinical features Cutaneous hemangioma (port-wine stain) Varicose veins Limb hemi-hypertrophy: often non-linear growth pattern Treatment Initially treated with compressive therapy May have specific indications for surgery Maffucci Syndrome Major features: Multiple enchondromas Cavernous hemangiomas Risk of sarcomatous transformation Sturge-Weber Syndrome Major features: Port-wine hemangioma in trigeminal distribution Neurologic sequelae due to meningeal hemangioma Blue-Rubber Bleb Nevus Syndrome Autosomal dominant Clinical features Bluish cavernous hemangiomas on trunk and upper arms; may bleed from GI tract locations; may cause pain Regional hyperhidrosis Kasabach-Merritt Syndrome Clinical features: Solitary or multiple cavernous hemangiomas on trunk or extremities Consumptive coagulopathy secondary to hemangiomas Ataxia-Telangiectasia (Louis-Bar Syndrome) Clinical features: Telangiectasia on conjunctivae, face, neck, and arms Progressive ataxia Genetics: autosomal dominant
Overgrowth Syndromes
Generalized bodily overgrowth Prader-Willi syndrome Partial deletion of chromosome 15 Major findings Infantile hypotonia Obesity beginning after age 1 Mental retardation Cryptorchidism Short stature Eyes slant upward and lateral
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Orthopedic findings Developmental dysplasia of the hip in 10% Scoliosis in 50% Small hands and feet Bardet-Biedl Syndrome Etiology unknown; genetics probably autosomal recessive Major findings Trunical obesity Mental retardation Hypogonadism Retinitis pigmentosa Renal abnormalities Orthopedic abnormalities: postaxial polydactyle (feet more than hands) Beckwith-Wiedemann Syndrome Autosomal dominant Major findings Large stature Omphalocele Macroglossia (may partially regress) Hypoglycemia Multiple organ enlargement; risk of Wilms tumor Orthopedic abnormalities Leg length inequality Neurologic damage if hypoglycemia not controlled Polydactyly, idiopathic scoliosis, radial head dislocation variable Asymmetric Overgrowth Idiopathic hemihypertrophy Skeletal findings One side of body larger in all dimensions Growth proportionate over time Lower extremities most often affected; trunk and upper extremities may be affected Genitourinary system Wilms tumor (nephroblastoma) in approximately 5% Medullary sponge kidney Renal malposition Vascular system: aortic, cerebral vascular, or congenital heart abnormalities Russell-Silver syndrome Short stature Sall, triangular face; may be asymmetric Genitourinary system and genital malformations Orthopedic features Hemihypertrophy Other miscellaneous skeletal findings Goldenhar syndrome Major features Epibulbar dermoids
Preauricular skin tags, facial asymmetry Orthopedic abnormalities Congenital vertebral anomalies Other aspects of VATER syndrome association Implications: Monitor for scoliosis; be aware of difficult intubation. Klippel-feil syndrome Key feature: cervical spine fusions; may have stenosis, instability Possible skeletal associations Congenital or idiopathic scoliosis of lower spine (60% of patients) Sprengels deformity (30% of patients) Upper extremity or hand anomalies Non-skeletal association Genitorinary or renal malformations Hearing impairment Cardiac anomalies Facial asymmetry Implications Screen early for hearing impairment, genitourinary malformations (ultrasound) Counsel regarding activity and anesthesia if neck is unstable Proteus syndrome A hemartomatous disorder affecting all three germ layers Characterized by its variability; named for the Greek god able to change shape at will Macrodactyly and asymmetric tissue overgrowth are key feature Diagnosis can be established by adding up the points assigned to each criterion below for a total score Diagnostic criteria Points Definitive diagnosis is made if score is 13 points or higher; questionable diagnosis is 10-13 points; diagnosis excluded is less than 10 points Macrodactyly, hemihypertrophy, or both5 Thickening of skin4 Lipomas and subcutaneous tumors4 Verrucous epidermal nevus3 Macrocephaly, irregular skull2.5 Other minor abnormalities1
Neurofibromatosis Neurofibromatosis is the most prevalent skeletal disorder to be caused by a single gene defect. It is a hemartomatous disorder, probably of neural crest origin. Diagnosis is established when the patient meets at least two of the following NIH criteria. Cafe au lait spots (five or more spots>1.5 cm after puberty or >0.5 cm before puberty) Subcutaneous neurofibroma Positive biopsy Positive family history (first-degree relative affected) Skeletal manifestations *Long bone pseudarthrosis *Dystrophic curve of spine *Elephantiasis neuromatosa Optic glioma
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Two or more Lisch nodules (hamartomas in iris) Axilliary or inguinal freckling Features of dystrophic spinal curve Severe apical rotation or wedging Paravetebral mass Spindling of transverse process Thinning of rib Enlargement of the foramen Vertebral scalloping Orthopedic implications Dystrophic curves require more aggressive treatment than non-dystrophic curves. (Fuse if>30 degrees; anterior and posterior fusion if>70 degrees of if kyphosis>50 degrees. Explore fusion postoperatively.) Preoperative CT scan or myelogram on all dystrophic curves Rule out sarcoma if unexplained pain or localized growth occurs
Ehlers-Danlos Syndromes
This group of connective tissue abnormalities include at least 11 different subtypes. Many other patients do not fit precisely into one of the groups. Osteogenesis Imperfecta A group of disorders of type II collagen causing bone fragility and in some cases blue sclerae, hearing loss, and abnormal dentin. The osseous fragility tends to improve after puberty Silence types Type I Variable osseous fragility (minimal through moderately severe) Distinctly blue sclerae (at all ages) Presenile hearing loss Autosomal dominant Type II (lethal perinatal osteogenesis imperfecta) Extremely severe osseous fragility, with stillbirth or neonatal death Subgroup A: Radiographs show broad, crumpled long bones and broad ribs with continuous beading. Autosomal dominant or new mutation Subgroup B: Radiographs show broad, crumpled long bones; ribs show discontinuous beading or are not beaded. Autosomal recessive Subgroup C: Radiographs show thin, fractured long bones with thin, beaded ribs Autosomal recessive Type III Autosomal recessive Fractures at birth, then progressive deformity Normal sclerae and hearing Type IV Moderate osseous fragility Normal sclerae (blue in infancy) Variable deformity of long bones and spine Autosomal dominant Note: The value of opalescent dentin for subcategorization of osteogenesis imperfecta is uncertain
5.20
Malformations of the Hand and Foot

Terminology Extentpartial or complete Simpleskin only Complexsynostosis Polysyndactylyhidden duplicated skeletal structures Isolated syndactyly Of the five types, long-ring syndactyly is the most common Look for duplicated phalanges, abnormalities of metacarpals or metatarsals Autosomal dominant Minimal risk of associated anomalies Poland syndrome Simple syndactyly of variable number of fingers Short fingers (absent or hypoplastic middle phalanges) Absent sternocostal head of pectoralis major Acrocephalosyndactylies Apert syndrome Complete complex syndactyly D2-D4 with common nail, progressive interphalangeal (IP) synostosis of hands and feet, medial deviation of great toe, and tarsal synostosis. Craniosynostosis Occasional cervical fusions, usually without deformity Crouzon syndrome Craniosynostosis Calcaneocuboid coalition, cervical spine fusion Many other syndromes, such as Saethre-Chotzen, Carpenter Congenital constriction bands (e.g., Streeters bands) A distal (aracral) syndactyly Thumb rarely involved Cutaneous rings or amputations May have distal paresis or deformity (e.g., clubfoot)
Polydactyly
Ulnar: frequently isolated, especially in African-American children Radial: more frequently associated with syndromes, especially radial ray defects
Radial Clubhand
This is a spectrum ranging from hypoplasia to complete absence of preaxial parts. It may be isolated or associated with the following conditions. Blood dyscrasias Fanconis syndrome: anemia to progressive pancytopenia, not present at birth; one-third of patients have renal anomalies; often fatal Thrombocytopenia-absent radius (TAR) syndrome: neonatal thrombocytopenia; usually improves with time; frequent knee anomalies Congenital heart defects. Holt-Oram syndrome: variable cardiac and preaxial deficiency, most commonly atrial septal defect and hypoplastic thumb. Craniofacial anomalies (Nager syndrome)
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Congenital scoliosis VATER syndrome (vertebral anomalies, anal atresia, tracheoesophageal fistual (TEF), esophageal atresia, renal and rectal anomalies) Goldenhar syndrome (oculo-auriculo-vertebral dysplasia) Klippel-Feil syndrome Implications Examine previous chest and abdominal films for vertebral anomalies, or take new radiographs Evalute face, jaw, and palate CBC and platelet count Ask about feeding (esophageal abnormalities) Listen to heart, possibly by echocardiography Evaluate genitourinary systems: urinalysis, possibly echocardiography Perform chromosome analysis if multiple anomalies are found outside of the particular syndrome.
Ulnar Clubhand
Usually a mild dysgenesis; few frequent associations; may be seen with Cornelia de Lange syndrome Amputated Limbs Single: usually an isolated anomaly but may be associated with idiopathic scoliosis Congenital ring constriction syndrome: non-genetic, variable rings with two or more of the following findings: Grooves in skin, occasionally with lymphatic or vascular impairment Transverse amputation with proximal limb normal Syndactyly (distal with proximal fenestrations) Clubfeet Craniofacial defects
Syndromes Due To Teratogens

Fetal Aalcohol Syndrome Growth disturbance (of both length and weight) through childhood CNS dysfunction and decreased head size; learning deficit or attention deficit disorder or mental retar dation Dysmorphic face (mild): (a) small eyes, (b) flat philtrum, (c) thin upper lip Orthopedic features Contractures (elbows, metacarpophalangeal [MP] and IP joints) Miscellaneous synostosis Hip dislocations, clubfeet Congenital cervical fusion (most often C2-C3) Fetal Hydantoin Syndrome (Due To Maternal Use Of Phenytoin) Growth retardation: mild Mental retardation: mild Face: hypertelorism, cleft lip Hands: hypoplasia or absence of phalanges, mostly distal
Chromosome Abnormalities
Down Syndrome Trisomy, mosaicism, or translocation of chromosome 21
Major findings Mental retardation (variable) Congenital heart defects: atrioventriculum communis, ventricular septal defect GI anomalies Short stature Leukemia (1%), seizures, diabetes, hypothyroidism (less frequent) Orthopedic findings Delayed walking (age 1_ to 5) Ligamentous laxity C1-C2 or occiput: C1 laxity (x-ray at about age four and yearly if atlanto-dens interval [ADI] >5 mm; fuse if signs of myelopathy exist) Scoliosis, idiopathic type Hip dislocations: acute, subacute, or habitual Slipped capital femoral epiphysis (SCFE) Perthes disease Patellar subluxation or dislocation Metatarsus adductus or hallux valgus Turner Syndrome Monosomy X Major findings Low birth weight and persistent growth retardation Normal intelligence Low hairline and webbed neck Renal and cardiac anomalies, coarctation Absent or hypoplastic gonads Orthopedic Genu valgum, cubitus valgus Scoliosis, idiopathic Noonan Syndrome Turner-like phenotype but normal chromosomes Major findings Mental retardation Hypertelorism, ptosis, downward-slanting eyes Increased severity of scoliosis, end-plate changes Klinefelter Syndrome Genetics: 47 XXY Clinical features Asthenic habitus, long legs Failure of secondary sexual development Scoliosis Proximal radioulnar synostosis Cri Du Chat Syndrome Genetics: 5P Clinical findings Profound mental retardation Multiple hand and foot anomalies Scoliosis, congenital
Pediatric Podiatry
505

Chapter 5 Pediatric Podiatry

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Chapter 5 Pediatric Podiatry

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5 Pediatric Podiatry

Russell Volpe, DPM

5.13 5.14 5.15 5.16

420 The 2005 Podiatry Study Guide

422 The 2005 Podiatry Study Guide

424 The 2005 Podiatry Study Guide

Tendoachilles notch Small, bean-shaped heel

426 The 2005 Podiatry Study Guide

5.2 Metatarsus Definition

Determining Metatarus Adductus

428 The 2005 Podiatry Study Guide

430 The 2005 Podiatry Study Guide

Figure 16. Serial Maniopulations and Holding Plaster Immobilization

Serial Plaster Immobilization of Congenital Foot Deformities

Purpose of the Cast

432 The 2005 Podiatry Study Guide

434 The 2005 Podiatry Study Guide

Left Foot - Left Hand

Internal Tibial Position - Corrective Position

Talipes Calcaneovalgus-Corrective Position

Talipes Equinovarus - Left Hand (Clinician)

436 The 2005 Podiatry Study Guide

Exam Positioning of a Child

438 The 2005 Podiatry Study Guide

Tips for Assessment

General Exam Tips

Lower Extremity Exam

Collapsing Pes Plano Valgus

440 The 2005 Podiatry Study Guide

Flatfoot As Pathology In The Literature

Why Treat The Pes Planovalgus Foot?

Planal Dominance As A Management Concept

442 The 2005 Podiatry Study Guide

Planal Dominance On X-ray

Childhood And Adolescence

Development of Flat Foot

444 The 2005 Podiatry Study Guide

Differential - Pes Valgus

Criteria For Selection

446 The 2005 Podiatry Study Guide

448 The 2005 Podiatry Study Guide

NORMAL AND PATHOLOGIC GAIT IN CHILDREN

Two Year Old Gait

Three Year Old Gait

Final Determinants Of Gait

Age Parameters For Motor Maturity

450 The 2005 Podiatry Study Guide

Caf au lait spots Bony abnormalities Muscle mass

Techniques To Bring Out Pathlogy

Non-Neurologic Abnormal Gait

452 The 2005 Podiatry Study Guide

Neurologic Abnormal Gait

454 The 2005 Podiatry Study Guide

Rotational and Angular Disorders in Children

Rotational Deformities - Overview

456 The 2005 Podiatry Study Guide

Exam - Malleolar Position

Exam - Hip Range Of Motion

Exam - Ryders Test

Explaining The Diagnosis

Treatment Of Underlying Deformity

458 The 2005 Podiatry Study Guide

Wheaton brace - leg extender

Management Theory - Bars And Casts