Intoeing is one of the most common pediatric gait disturbances. Prompted by parental concerns, it accounts for a large number of new patient specialist visits. Intoeing is not a diagnosis. It is a complaint and an objective finding on physical examination. In spite of the frequent occurrence of pediatric intoeing, clinical management is complicated by diagnostic confusion and difference of opinion on both the necessity for treatment and its effectiveness. Intoeing has been the topic of many publications directed both toward primary care physicians and parents. However, information expressed in these articles can be confusing to both groups. The essential question regarding the lower extremity causes of intoeing is whether they represent alterations in the shape and contour of a normal foot and limb or are true structural malformations.1-6 Some authors offer personal bias regarding the cause and treatment of intoeing. The opinions most often expressed are that treatment is not necessary, that most of the problems spontaneously correct on their own, and the benefits attributed to therapy are the result of natural resolution of the conditions as a part of their natural history.7-14 Other authors regard pediatric intoeing as alterations in physiologic developmental stages that have become pathological.5,15,16 Although there are many causes for intoeing, a careful systematic approach will yield a diagnosis and a treatment plan in most cases.17 Organizing the causes for intoeing is simply a matter of considering the anatomical area or areas of potential involvement. It is important to keep in mind that the more common causes of intoeing outside the foot are deviations of normal development while the abnormalities in the foot are purely pathological. An understanding of the natural history of the various pathologies is also crucial in order to offer a correct diagnosis and prognosis as well as facilitate the development of a successful treatment plan. There are really only two broad categories of pathology to consider. Intoeing is most often caused by static skeletal abnormalities in one or several parts of the lower extremity. Less frequently, intoeing may result from a movement disorder. On some occasions, intoeing is caused by a combination of these two. The history of the complaint is very helpful in pinpointing the cause of intoeing. Clinicians should place special emphasis on how old the child is when the symptoms first develop. When intoeing is noticed at birth, it is usually the result of some adducting deformity within the foot. These deformities include hallux varus, talipes equinovarus, metatarsus adductus and the various forms of pes cavus. When one first notices intoeing between the ages of 1 and 2, it is most likely caused by abnormality in the tibiofibular segment.18 Intoeing beginning after 18 months is most likely caused by femoral antetorsion (anteversion) and issues within the pelvis. The child’s neurological status is critical to the diagnosis and treatment of intoeing. The developmental history identifies issues that might place the fetus at risk for central nervous system damage. These issues might include bleeding during early pregnancy, premature labor, difficulty in delivery, meconium aspiration, intracranial hemorrhage and post-delivery seizures. Static encephalopathy (cerebral palsy) is associated with a number of foot deformities.19 Acquisition of the major motor milestones at the appropriate times is a good indicator of normal central nervous system development.20 If the history and physical examination show the child to be neurologically normal, the cause for intoeing is almost certainly a static skeletal abnormality. There are only three anatomical areas where one might note this pathology. These include deformities within the foot and issues with tibial torsion and femoral antetorsion (anteversion). Frequently, intoeing is caused by abnormalities in two or all three of these areas. The sum of the rotational components is known as the rotational or torsional profile.9,21 The overall position of the foot to the line of progression is the algebraic sum of all three of these areas. Most intoeing problems within the foot are congenital and are present at birth. Identification during neonatal examination and prompt treatment prevent long-term morbidity.22,23 Since the contour of the foot deviates from the normal, one can easily make the diagnosis by inspection alone. Part or all of the foot is adducted toward midline. In these cases, there are four conditions to consider.
When Hallux Varus Plays A Role
Hallux varus. There are three forms of hallux varus. The most frequent form is abnormality of the abductor hallucis muscle. The muscle may be contracted or there may be abnormal insertion into the base of the first proximal phalanx, causing it to act as an adductor of the great toe instead of adducting and plantarflexing. It may be an isolated deformity or it may be a residual deformity in an otherwise successfully treated metatarsus adductus or talipes equinovarus. Adduction of the hallux is particularly noticeable during gait. This is referred to as the “wandering great toe” syndrome. The second (and much less common) form of hallux varus is a teratological deformity associated with a number of developmental abnormalities of the first ray. These first ray abnormalities include incomplete tibial polydactyly, fibrous remnants of tibial polydactyly and the longitudinal epiphyseal bracket sequence.24-31 In the third form of hallux varus, there is an increased interval between the first and second toes, a slightly adducted first metatarsal, a hallux abductus angle of zero, and the first metatarsophalangeal joint is squared off and stable.
Can Metatarsus Adductus Contribute To Intoeing?
Metatarsus adductus. Metatarsus adductus is the most common foot deformity associated with intoeing. The medial border of the foot is concave with its apex near the first metatarsocuneiform joint. The lateral side is convex with the apex at the fifth metatarsal base. Physical examination determines whether the forefoot deformity is rigid or flexible. Evaluation of the rearfoot shows either a normal or moderately pronated peritalar complex with no ankle equinus. The clinician may see several forefoot patterns. The deformity may be purely transverse. This is the most common form and is best described as metatarsus adductus. Less commonly, the forefoot may be adducted transversely and rotated into varus against the rearfoot. On very rare occasions, the forefoot may be rotated into pure varus. A particularly complicated form known as skewfoot has a rigid adductovarus forefoot deformity with severe rearfoot hyperpronation.32,33 There is some debate about the spontaneous correction of metatarsus adductus.34 The frequency is unknown. However, there is no question about the fact that some metatarsus adductus persists into later childhood and can result in significant deformity.35 There is also some difference of opinion regarding the long-term effects of metatarsus adductus. Shoe fitting problems may become issues. Hallux valgus deformity occurring with metatarsus adductus is difficult to manage.36-39
A Guide To The Various Types Of Talipes Equinovarus
Talipes equinovarus. Talipes equinovarus is a congenital three plane foot and ankle deformity. There are four types of talipes equinovarus. The idiopathic type is the most common of the four but there are some studies suggesting peripheral nerve and muscle etiologies.40-44 Some recent studies are contradictory.45 The positional (sometimes called postural) form of talipes equinovarus may be the result of in-utero molding or muscle imbalance caused by other more specific etiologies. Prognosis and the need for additional workup depend on the type. Purely positional forms respond quickly to treatment and the prognosis for successful reduction is excellent. Those resulting from muscle imbalance have a more guarded prognosis and a higher recurrence rate. The teratological form is associated with arthrogryposis and is a part of a more generalized skeletal developmental complex. The syndromic type of talipes equinovarus is associated with other named clinical entities in which talipes equinovarus is a regular or an occasional feature. The clinical appearance is similar for all of the forms of talipes equinovarus. The forefoot is adducted while all or part of the medial column is plantarflexed. The peritalar complex is inverted, adducted and plantarflexed. The ankle joint is in equinus. Depending on the type and the underlying etiology, the foot may be rigid or flexible.
What About Pes Cavus?
Cavus deformity. Pes cavus is almost always the result of muscle imbalance and neurological abnormality.46-48 Causes include cerebral palsy, hereditary sensory and motor neuropathy, muscular dystrophies and spinal cord abnormality. The unique feature of cavus deformity is increased arch height. However, it is rare for the deformity to be confined entirely to the sagittal plane. In most cases, all or part of the medial column is in equinus and the peritalar complex is inverted. This causes the forefoot to adduct toward the midline of the body. In addition to the structural deformity produced by pes cavus, varying degrees of anterolateral compartment weakness with dominance of tibialis posterior will produce an additional dynamic adduction of the forefoot.
Understanding The Evolution Of Tibial Torsion
Tibial torsion is the anatomical relationship of the distal end of the tibia to the proximal end. Simply put, tibial torsion is defined as the relationship between the knee and ankle joint axes. This association is not constant throughout life. At birth, the ankle joint axis is internally rotated about 25 degrees to the knee axis. There is a gradual external rotation of the ankle joint axis so it becomes externally rotated approximately 10 to 15 degrees to the knee axis by 12 months of age. It continues to externally rotate rapidly until about 2 years of age. Target values at this age are 18 to 25 degrees. There is a small amount of additional external rotation from the age of 2 until about 4 to 5 years of age.49 At that point, almost 95 percent of the adult value has been achieved. The right side is usually about 3 to 5 degrees more externally rotated than the left. Internal tibial torsion and tibia varum frequently occur together. Internal tibial torsion is the most common cause for intoeing from the time a toddler begins to walk up until about 18 months. The change in gait is very characteristic with internal rotation of the foot to the line of progression while the knee joint axis is either in the coronal plane or externally rotated to it.
When Intoeing Originates In The Femur And The Acetabulum
In order to understand the causes of intoeing originating in these two anatomical areas, it is necessary to review some terminology as well as some developmental issues. Clinicians often use the terms antetorsion and anteversion synonymously. Taken interchangeably, they usually describe the relationship between the head and neck of the femur at the proximal end to the plane of the knee joint axis at the distal end. More specifically, these terms describe the relationship between the proximal and distal end of the femur. The head-neck-greater trochanteric axis almost always runs in an anteromedial direction to the knee axis. The opposite, retrotorsion or retroversion, almost never occurs, and is probably nonphysiologic. The relationship between the proximal and distal ends of the femur changes throughout life. In neonates, the proximal axis is rotated anteriorly about 35 to 40 degrees.50 Over the first two years of life, this angle decreases to a range of 20 to 25 degrees. All other components of the lower extremity being normal, if the head-neck-greater trochanteric axis is rotated 20 to 25 degrees anterior to the knee axis, the limb is neither internally nor externally rotated. The patella is directed forward. If the angle exceeds 25 degrees, the limb is internally rotated when the femoral head is seated in anatomical position in the acetabulum. This means that femoral antetorsion or anteversion in excess of normal produces obligate internal rotation of the limb and an intoeing gait. The literature uses the term antetorsion as well as anteversion interchangeably to describe this relationship. There is another use of the term anteversion that one must consider. The head-neck-greater trochanteric axis will form an angle with the coronal plane when the femoral head is seated in the acetabulum in any position. If the thigh is externally rotated in the acetabulum, this axis runs in an anteromedial direction. Clinicians also use the term anteversion to describe this position. It should be noted, however, that this form of anteversion produces an externally rotated limb with an out- toeing gait. If the entire limb is internally rotated, the head-neck-greater trochanteric axis is directed posteromedially and is called retroversion. This produces an intoeing gait. It is important to remember that this form of anteversion and retroversion is not anatomically fixed, and changes from moment to moment. The position of the head in the acetabulum is influenced by normal muscle activity as well as muscle imbalance and contracture. It is a fact that the infant femur has an antetorsion value (anteromedial head-neck axis with respect to the distal femur) of approximately 30 degrees. In spite of this high value that should produce intoeing, the typical position of the lower extremities of infants is one of flexion, abduction and external rotation. Even though the normal infant value is larger than the adult value of antetorsion, the limb is not internally rotated. The infant’s thighs can only internally rotate about 20 degrees but can externally rotate about 50 degrees. The exact reason for this apparent paradox is not fully understood. It has been theorized that rotation is limited by tightness of the hip capsular ligaments but this remains unverified. Another possible explanation is that the acetabulum of the infant and young child is directed more posterolaterally (retroverted) than the adult acetabulum. The literature is not in agreement on this point. The most common reason for intoeing over the age of 2 years is an abnormally large value of femoral antetorsion. The physical findings are very characteristic. Gait examination shows internal rotation of the patella and the entire lower extremity distal to the knee when the patient walks. The feet are internally rotated to the line of progression. When the hip is extended, internal thigh rotation exceeds 50 degrees and external rotation is less than 25 degrees. In hip flexion, internal rotation remains at 50 degrees to 60 degrees but external rotation does not exceed 45 degrees. The clinician can palpate the greater trochanter directly through the skin and muscle. The examiner can internally and externally rotate the limb while he or she feels the lateral surface of the greater trochanter. With a little experience, the podiatrist can estimate the position of the distal femur when the head, neck and greater trochanter are in the patient’s frontal or coronal plane. The amount of internal rotation of the distal femur needed to level the proximal femur is the angle of antetorsion. Another concept one should consider is the position of the acetabulum on the pelvis. The acetabulum is oblique on all three body planes. It usually faces in an anterior, downward and lateral direction. Thigh rotation is limited by soft tissue around the capsule as well as bony blocking. This is particularly true of external rotation, which is restricted by the capsular ligaments as well as by the posterior rim of the acetabulum. If the acetabulum faces in a more forward direction, this will alter thigh rotation in both extension and in flexion so there would be more internal rotation and less external rotation. It is hypothesized that the position of the acetabulum with respect to the rest of the pelvis may change over time. This might explain why infants have significant restriction of internal rotation but exaggerated external rotation when compared to adults. If the acetabulum were more posteriorly directed (retroverted), this would explain the exaggerated external rotation that characterizes infants and toddlers. However, the literature is sharply divided on whether this phenomenon actually exists.51,52 Abnormal acetabular anteversion and retroversion may also play a role in other hip diseases.53-56 This is particularly true for developmental hip dysplasia and dislocation.54,57-59 Total joint surgeons are well aware of malposition of the acetabular component during hip replacement surgery, and take great pains to position the cup antomically so the patient is not left with an abnormal intoeing or outtoeing gait.60-64
Insights On Addressing Structural Deformities That Cause Intoeing
The management of the various foot deformities that cause intoeing has been well studied and well reported in the literature. Most of the problems are structural in nature and require changing the morbid anatomy in order to produce a good functional result. It is beyond the scope of this article to discuss these various treatments in detail but there are some key points to keep in mind in regard to treatment. Hallux varus has so much morbid anatomy that nonoperative treatments usually fail. When hallux varus is caused by abnormality of the insertion of the abductor hallucis muscle, the treatment of choice is surgical management. Techniques include transfer of the abductor hallucis and simple release. The various forms of polydactyly require expert surgical reconstruction. When one treats metatarsus adductus at the appropriate age, it will respond well to serial casting.65 Clinicians can achieve the best results through early intervention before the age of 6 months.66,67 Casting may still be beneficial up until the age of 2. However, once the patient is older than 2, the success rate falls dramatically. The use of shoes and splints as the sole treatment for metatarsus adductus is controversial. I have not had success with them. Serial casting remains the treatment of choice. Unfortunately, many untreated children over two years of age will have an objectionable degree of metatarsus adductus but not so severe that it justifies surgery.68 At one point, tarsometatarsal release was a popular procedure for metatarsus adductus but it is rarely used today because of the arthrosis that develops at the tarsometatarsal joints. Presently, surgeons employ various forms of abducting metatarsal osteotomies to salvage residual metatarsus adductus. In regard to talipes equinovarus, it is best to manage this with closed reduction. At the time of this writing, the most successful technique is the one outlined by Ponseti.69 The technique is elegantly illustrated in Ponseti’s monograph.70 With careful casting technique and attention to detail, many of these infants will respond to the point that the only surgical intervention needed may be a simple tendo-Achilles release. Since the rediscovery of Ponseti’s technique, the need for more aggressive surgery has been reduced.71 A small number may require more extensive posteromedial release with the understanding that this is salvage surgery. The best results are those that clinicians achieve via nonoperative means.72-76 The technique of closed reduction is also applicable for older infants.77 Pes cavus is almost always the result of muscle imbalance. With careful investigation, one can identify an underlying etiology. Nonoperative management is very likely to fail because the etiology results in progressive deformity. Most of these children will require aggressive surgery. Procedures include plantar release, medial column dorsiflexing osteotomy, lateral calcaneal displacement osteotomy and muscle rebalancing by tibialis anterior and posterior transfer.
Treating Tibial Torsion: What You Should Know
Internal tibial torsion has a natural history for spontaneous correction. However, there are no guarantees that the problem will spontaneously resolve. Therefore, one should closely monitor each case. Once the child fails to follow the natural history of spontaneous correction, the clinician should initiate active intervention. A number of factors influence the likelihood of spontaneous correction. These factors include the age of the child, the severity and whether it is unilateral or bilateral. When it comes to children over the age of one year, clinicians should consider these patients at risk for failure to achieve spontaneous correction. Persistence of the deformity after 15 months of age should cause additional concern about the likelihood of spontaneous correction and the clinician should begin vigorous therapy. There are no data to suggest that in-shoe orthoses do anything to alter the natural history of tibial torsion. In-shoe orthotics only operate during stance phase of gait. Since this is a structural problem above the level of the ankle, it is a swing phase gait disturbance. There is no effect that an in-shoe orthotic could have in altering the abnormal anatomy. Some physicians still employ type D heel stabilizers and reverse Roberts orthoses but there are no data to support their use. Since they are designed to produce late stance phase abduction by pronating the foot at a time that it should be supinating, their use seems physiologically illogical. Use of these devices should be discouraged. There are a number of bars commercially available for the management of tibial torsion. They work by preventing positioning of the extremities that perpetuate the deformity. They are not designed to force the tibias into external rotation. They work best in toddlers under the age of 15 months and have their greatest benefit during sleep. Once children have passed 15 months in age, the success rate with bars begins to fall. At that point, the surgeon should consider serial casting for the deformity. The technique requires an above the knee cast with the knee flexed about 45 to 50 degrees. The purpose of the cast is to produce an external rotatory force on the proximal tibia in order to convert the function of the tibial physes from pressure loaded physes to rotational physes. In theory, this allows for remodeling of the tibia about its own long axis. Keeping in mind that there is often a discrepancy between chronological and developmental ages, the success of serial casting for tibial torsion begins to fall off dramatically as the child reaches the age of 2. Once the child passes this age, the definitive treatment is tibial derotational osteotomy. However, one should delay this treatment until the natural history of continued external rotation has run its course. In regard to persistent severe tibial torsion after the age of 8 years, surgeons may correct this with a supramalleolar tibial rotation osteotomy.67,78
Other Pertinent Pointers On Treatment
Treatment of femoral antetorsion is frustrating because there are no simple modalities that have been proven to alter the natural history. Orthoses and other treatment modalities designed to force the thighs into external rotation are uniformly unsuccessful. Additionally, more vigorous therapy carries a theoretical risk of injury to the proximal femur and the hip. In-shoe orthoses fail to produce gait improvement or modify the natural history of antetorsion. Since the gait disturbance produced by femoral antetorsion occurs during swing phase, no in-shoe orthosis will alter the intoeing produced by antetorsion. The only conservative measure that has ever been shown to improve this condition is avoiding the W-sitting position. Femoral derotation osteotomy is the only proven treatment for the management of femoral antetorsion. Since the long-term risks of persisting intoeing from femoral antetorsion are neither well-known nor considered to be serious, it is difficult to determine how far and how aggressively one should pursue clinical management in neurologically normal children. Since femoral derotation involves osteotomy of the femur and implantation of hardware, the risk of surgery may well outweigh any benefits derived from the procedure. However, one may consider a femoral osteotomy for severe femoral antetorsion (greater than 50 degrees) in patients older than 8 years of age if internal rotation exceeds 85 degrees and external rotation is less than 10 degrees.67,79 Children with cerebral palsy and other neurological disease are candidates for derotational osteotomy because their antetorsion does not follow the natural history of improvement. Additionally, femoral antetorsion in conjunction with coxa valga produces an unstable hip.
At first glance, intoeing seems like an overwhelming issue. However, clinicians should consider that there are only a few conditions that can produce an intoeing gait. In organizing the clinical approach, the examiner should keep in mind there are only three anatomical locations that can result in intoeing. In children under 1 year of age, most intoeing is caused by deformities within the foot itself. Metatarsus adductus remains the most common cause. When patients are between 1 and 2 years of age, tibial torsion is the most common reason for intoeing. Treatment is best delayed until after 1 year of age. After that time, the likelihood of spontaneous correction decreases. One may utilize bars to maintain the limb in an externally rotated position. If this modality has not produced a successful result by the time the child reaches 15 or 16 months of age, more aggressive therapy via serial casting is indicated. Managing femoral antetorsion is very frustrating because there is no nonoperative treatment other than keeping the child out of the W-sitting position. In-shoe orthoses do not influence this problem at all. Not only do they not have any effect on the anatomical abnormality, in-shoe orthotics can only operate during the stance phase of gait. Intoeing produced by femoral antetorsion occurs during swing phase. One must balance the benefits of surgical derotation against the risks of infection and nonunion as well as the extensive rehabilitation needed after operation. Since there are scant data to suggest that mild intoeing leads to adverse long-term consequences, very few neurologically normal children should be subject to the femoral rotational osteotomy. This is not the case for the neurologically abnormal. As a group of patients, they do not follow the natural history of spontaneous correction. Rather, they not only fail to spontaneously correct but, in many cases, the condition becomes worse. Since there is an association between femoral antetorsion and coxa valga, more severe cases carry the risk of hip subluxation and dislocation. A systematic diagnostic approach and recognition of the indications and limitations of available therapy will go a long way toward successful management of intoeing. Dr. Harris is a Clinical Associate Professor in the Department of Orthopaedics And Rehabilitation at the Loyola Medical Center in Maywood, Ill. He is a Fellow of the American College of Foot and Ankle Surgeons. References 1. Bruce RW Jr. Torsional and angular deformities. Pediatr Clin North Am 1996;43:867-81. 2. Churgay CA. Diagnosis and treatment of pediatric foot deformities. Am Fam Physician 1993;47:883-9. 3. Furdon SA, Donlon CR. Examination of the newborn foot: positional and structural abnormalities. Adv Neonatal Care 2002;2:248-58. 4. Killam PE. Orthopedic assessment of young children: developmental variations. Nurse Pract 1989;14:27-30, 32-4, 36. 5. Li YH, Leong JC. Intoeing gait in children. Hong Kong Med J 1999;5:360-366. 6. Yngve DA. Gait problems in children. A matter of rotation. Postgrad Med 1984;76:56-64. 7. Briggs RG, Carlson WO. The management of intoeing: a review. S D J Med 1990;43:13-6. 8. Karol LA. Rotational deformities in the lower extremities. Curr Opin Pediatr 1997;9:77-80. 9. Lincoln TL, Suen PW. Common rotational variations in children. J Am Acad Orthop Surg 2003;11:312-20. 10. Ryan DJ. Intoeing: a developmental norm. Orthop Nurs 2001;20:13-8. 11. Staheli LT. Torsional deformity. Pediatr Clin North Am 1986;33:1373-83. 12. Staheli LT. Rotational problems of the lower extremities. Orthop Clin North Am 1987;18:503-12. 13. Staheli LT, Corbett M, Wyss C, King H. Lower-extremity rotational problems in children. Normal values to guide management. J Bone Joint Surg Am 1985;67:39-47. 14. Staheli LT. Torsion — Treatment indications. Clin Orthop Relat Res 1989;247:61-6. 15. Accadbled F, Cahuzac JP. [“In-toeing and out-toeing”]. Rev Prat 2006;56:165-71. 16. Correll J, Berger N. [Diagnosis and treatment of disorders of the foot in children]. Orthopade 2005;34:1061-72; quiz 1073-4. 17. Sass P, Hassan G. Lower extremity abnormalities in children. Am Fam Physician 2003;68:461-8. 18. Dietz FR. Intoeing — fact, fiction and opinion. Am Fam Physician 1994;50:1249-59, 1262-4. 19. Bleck EE. Forefoot problems in cerebral palsy-diagnosis and management. Foot Ankle 1984;4:188-94. 20. Rethlefsen SA, Healy BS, Wren TA, Skaggs DL, Kay RM. Causes of intoeing gait in children with cerebral palsy. J Bone Joint Surg Am 2006;88:2175-80. 21. Staheli LT. In-toeing and out-toeing in children. J Fam Pract 1983;16:1005-11. 22. Gore AI, Spencer JP. The newborn foot. Am Fam Physician 2004;69:865-72. 23. Hart ES, Grottkau BE, Rebello GN, Albright MB. The newborn foot: diagnosis and management of common conditions. Orthop Nurs 2005;24:313-21; quiz 322-3. 24. Blauth W. [The treatment of congenital foot abnormalities]. Z Orthop Ihre Grenzgeb 1989;127:3-14. 25. Chiang H, Huang SC. Polydactyly of the foot: manifestations and treatment. J Formos Med Assoc 1997;96:194-8. 26. Falliner A, Blauth W, Olason AT. [Hallux varus congenitus]. Z Orthop Ihre Grenzgeb 1988;126:239-49. 27. Glickman SH, Cornfield RH. Surgical reconstruction of a congenital foot deformity: hallux varus with brachymetatarsia of the first metatarsal. J Foot Surg 1990;29:499-503. 28. Masada K, Tsuyuguchi Y, Kawabata H, Ono K. Treatment of preaxial polydactyly of the foot. Plast Reconstr Surg 1987;79:251-8. 29. Mubarak SJ, O'Brien TJ, Davids JR. Metatarsal epiphyseal bracket: treatment by central physiolysis. J Pediatr Orthop 1993;13:5-8. 30. Sobel E, Levitz S, Cohen R, Giorgini R, Jules KT. Longitudinal epiphyseal bracket: associated foot deformities with implications for treatment. J Am Podiatr Med Assoc 1996;86:147-55. 31. Vispo Seara JL, Krauspe R. [Hallux varus congenitus]. Z Orthop Ihre Grenzgeb 1998;136:542-7. 32. Peterson HA. Skewfoot (forefoot adduction with heel valgus). J Pediatr Orthop 1986;6:24-30. 33. Tonnis D. [Skewfoot ]. Orthopade 1986;15:174-83. 34. Farsetti P, Weinstein SL, Ponseti IV. The long-term functional and radiographic outcomes of untreated and non-operatively treated metatarsus adductus. J Bone Joint Surg Am 1994;76:257-65. 35. Wan SC. Metatarsus adductus and skewfoot deformity. Clin Podiatr Med Surg 2006;23:23-40, vii-viii. 36. Ferrari J, Malone-Lee J. A radiographic study of the relationship between metatarsus adductus and hallux valgus. J Foot Ankle Surg 2003;42:9-14. 37. Mahan KT, Jacko J. Juvenile hallux valgus with compensated metatarsus adductus. Case report. J Am Podiatr Med Assoc 1991;81:525-30. 38. Okuda R, Kinoshita M, Morikawa J, Jotoku T, Abe M. Adult hallux valgus with metatarsus adductus: a case report. Clin Orthop Relat Res 2002:179-83. 39. Trepal MJ. Hallux valgus and metatarsus adductus: the surgical dilemma. Clin Podiatr Med Surg 1989;6:103-13. 40. Ahmed M, Ahmed N, Khan KM, Umer M, Rashid H, Hashmi P, Umar M. Sensory hypoinnervation in club foot. J Bone Joint Surg Br 2004;86:1163-9. 41. Bill PL, Versfeld GA. Congenital clubfoot: an electromyographic study. J Pediatr Orthop 1982;2:139-42. 42. Feldbrin Z, Gilai AN, Ezra E, Khermosh O, Kramer U, Wientroub S. Muscle imbalance in the aetiology of idiopathic club foot. An electromyographic study. J Bone Joint Surg Br 1995;77:596-601. 43. Loren GJ, Karpinski NC, Mubarak SJ. Clinical implications of clubfoot histopathology. J Pediatr Orthop 1998;18:765-9. 44. Nadeem RD, Brown JK, Lawson G, Macnicol MF. Somatosensory evoked potentials as a means of assessing neurological abnormality in congenital talipes equinovarus. Dev Med Child Neurol 2000;42:525-30. 45. Herceg MB, Weiner DS, Agamanolis DP, Hawk D. Histologic and histochemical analysis of muscle specimens in idiopathic talipes equinovarus. J Pediatr Orthop 2006;26:91-3. 46. Michlitsch MG, Rethlefsen SA, Kay RM. The contributions of anterior and posterior tibialis dysfunction to varus foot deformity in patients with cerebral palsy. J Bone Joint Surg Am 2006;88:1764-8. 47. Schwend RM, Drennan JC. Cavus foot deformity in children. J Am Acad Orthop Surg 2003;11:201-11. 48. Wines AP, Chen D, Lynch B, Stephens M. Foot deformities in children with hereditary motor and sensory neuropathy. J Pediatr Orthop 2005;25:241-4. 49. Kristiansen LP, Gunderson RB, Steen H, Reikeras O. The normal development of tibial torsion. Skeletal Radiol 2001;30:519-22. 50. Cordier W, Katthagen BD. [Femoral torsional deformities]. Orthopade 2000;29:795-801. 51. Jacquemier M, Jouve JL, Bollini G, Panuel M, Migliani R. Acetabular anteversion in children. J Pediatr Orthop 1992;12:373-5. 52. Weiner LS, Kelley MA, Ulin RI, Wallach D. Development of the acetabulum and hip: computed tomography analysis of the axial plane. J Pediatr Orthop 1993;13:421-5. 53. Kim SS, Frick SL, Wenger DR. Anteversion of the acetabulum in developmental dysplasia of the hip: analysis with computed tomography. J Pediatr Orthop 1999;19:438-42. 54. Li PL, Ganz R. Morphologic features of congenital acetabular dysplasia: one in six is retroverted. Clin Orthop Relat Res 2003:245-53. 55. Song KS, Choi IH, Sohn YJ, Shin HD, Leem HS. Habitual dislocation of the hip in children: report of eight additional cases and literature review. J Pediatr Orthop 2003;23:178-83. 56. Tonnis D, Heinecke A. [Decreased acetabular anteversion and femur neck antetorsion cause pain and arthrosis. 2: Etiology, diagnosis and therapy]. Z Orthop Ihre Grenzgeb 1999;137:160-7. 57. Duffy CM, Taylor FN, Coleman L, Graham HK, Nattrass GR. Magnetic resonance imaging evaluation of surgical management in developmental dysplasia of the hip in childhood. J Pediatr Orthop 2002;22:92-100. 58. Jacquemier M, Bollini G, Jouve JL, Volot F, Panuel M, Bouyala JM. [Acetabular anteversion in congenital luxation of the hip]. Rev Chir Orthop Reparatrice Appar Mot 1995;80:22-7. 59. Lin CJ, Lin YT, Lai KA. Intraoperative instability for developmental dysplasia of the hip in children 12 to 18 months of age as a guide to Salter osteotomy. J Pediatr Orthop 2000;20:575-8. 60. Honl M, Schwieger K, Salineros M, Jacobs J, Morlock M, Wimmer M. Orientation of the acetabular component: a comparison of five navigation systems with conventional surgical technique. J Bone Joint Surg Br 2006;88:1401-5. 61. Muller O, Reize P, Trappmann D, Wulker N. Measuring anatomical acetabular cup orientation with a new X-ray technique. Comput Aided Surg 2006;11:69-75. 62. Minoda Y, Kadowaki T, Kim M. Acetabular component orientation in 834 total hip arthroplasties using a manual technique. Clin Orthop Relat Res 2006;445:186-91. 63. Rittmeister M, Callitsis C. Factors influencing cup orientation in 500 consecutive total hip replacements. Clin Orthop Relat Res 2006;445:192-6. 64. Wines AP, McNicol D. Computed tomography measurement of the accuracy of component version in total hip arthroplasty. J Arthroplasty 2006;21:696-701. 65. Katz K, David R, Soudry M. Below-knee plaster cast for the treatment of metatarsus adductus. J Pediatr Orthop 1999;19:49-50. 66. Bleck EE. Metatarsus adductus: classification and relationship to outcomes of treatment. J Pediatr Orthop 1983;3:2-9. 67. Staheli LT. Torsion--treatment indications. Clin Orthop Relat Res 1989:61-6. 68. Asirvatham R, Stevens PM. Idiopathic forefoot-adduction deformity: medial capsulotomy and abductor hallucis lengthening for resistant and severe deformities. J Pediatr Orthop 1997;17:496-500. 69. Silvani S. The Ponseti technique for treatment of talipes equinovarus. Clin Podiatr Med Surg 2006;23:119-35, viii-ix. 70. Ponseti IV. Congenital Clubfoot Fundamentals of treatment. Oxford: Oxford University Press, 1996:140. 71. Eberhardt O, Schelling K, Parsch K, Wirth T. [Treatment of congenital club foot with the Ponseti method]. Z Orthop Ihre Grenzgeb 2006;144:497-501. 72. Bensahel H, Jehanno P, Delaby JP, Themar-Noel C. [Conservative treatment of clubfoot: the Functional Method and its long-term follow-up]. Acta Orthop Traumatol Turc 2006;40:181-6. 73. Hulme A. The management of congenital talipes equinovarus. Early Hum Dev 2005;81:797-802. 74. Morcuende JA. Congenital idiopathic clubfoot: prevention of late deformity and disability by conservative treatment with the Ponseti technique. Pediatr Ann 2006;35:132-6. 75. Radler C, Suda R, Manner HM, Grill F. [Early results of the Ponseti method for the treatment of idiopathic clubfoot. Z Orthop Ihre Grenzgeb 2006;144:80-6. 76. Scher D. The Ponseti method for treatment of congenital clubfoot. Curr Opin Pediatr 2006;18:22-5. 77. Bor N, Herzberg JE, Frick SL. Ponseti management of clubfoot in older infants. Clin Orthop Relat Res 2006;444:224-8. 78. Savva N, Ramesh R, Richards RH. Supramalleolar osteotomy for unilateral tibial torsion. J Pediatr Orthop B 2006;15:190-3. 79. Gordon JE, Pappademos PC, Schoenecker PL, Dobbs MB, Luhmann SJ. Diaphyseal derotational osteotomy with intramedullary fixation for correction of excessive femoral anteversion in children. J Pediatr Orthop 2005;25:548-53. For further reading, see “A Comprehensive Review Of Pediatric Orthoses” in the October 2002 issue of Podiatry Today or “How To Recognize Pediatric Gait Abnormalities” in the April 2002 issue.
CE Exam #149 Choose the best single answer to the following questions. 1. If the history and physical examination show the child with intoeing to be neurologically normal, the cause for intoeing is almost certainly … a) hallux varus b) due to tibial torsion c) a static skeletal abnormality d) due to an abnormally large value of femoral antetorsion 2. What is the most common foot deformity associated with intoeing? a) Talipes equinovarus b) Metatarsus adductus c) Pes cavus d) None of the above 3. In regard to the clinical appearance of all forms of talipes equinovarus, which of the following statements is true? a) The peritalar complex is not plantarflxed. b) The forefoot is adducted while all or part of the medial column is plantarflexed. c) The patient always has a flexible foot in these cases. d) All of the above 4. All other components of the lower extremity being equal, if the head-neck-greater trochanteric axis is rotated __ to __ degrees anterior to the knee axis, the limb is neither internally nor externally rotated. a) 10, 15 b) 30, 45 c) 20, 25 d) 5, 10 5. True or false: The typical position of the lower extremities of infants is one of flexion, abduction and external rotation. a) True b) False 6. In regard to serial casting for metatarsus adductus, clinicians can achieve the best results via early intervention before the age of … a) 18 months b) 6 months c) 1 year d) 2 years 7. In regard to talipes equinovarus, it is best to manage this with … a) ankle-foot orthoses b) in-shoe orthoses c) closed reduction d) none of the above 8. Which of the following statements is true about pes cavus among children with intoeing? a) It is almost always the result of muscle imbalance. b) It has a natural history for spontaneous correction. c) Nonoperative management succeeds in the vast majority of cases. d) All of the above 9. Which of the following statements is true about the use of bars for managing tibial torsion? a) They work best in children over the age of 3. b) They are designed to force the tibia into external rotation. c) They have their greatest benefit while patients are alert and active. d) None of the above 10. What is the only proven treatment for the management of femoral antetorsion? a) In-shoe orthoses b) Physical therapy c) Femoral derotation osteotomy d) None of the above Instructions for Submitting Exams Fill out the enclosed card that appears on the following page or fax the form to the NACCME at (610) 560-0502. Within 60 days, you will be advised that you have passed or failed the exam. A score of 70 percent or above will comprise a passing grade. A certificate will be awarded to participants who successfully complete the exam. Responses will be accepted up to 12 months from the publication date.